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As with no other doping drug, growth hormones are still surrounded by an aura of mystery. Some call it a wonder drug which causes gigantic strength and muscle gains in the shortest time. Others con-sider it completely useless in improving sports performance and ar-gue that it only promotes the growth process in children with an early stunting of growth. Some are of the opinion that growth hor-mones in adults cause severe bone deformities in the form of over-growth of the lower jaw and extremities. And, generally speaking, which growth hormones should one take -the human form, the synthetically manufactured version, recombined or genetically pro-duced form- and in which dosage? All this controversy about growth hormones is so complex that the reader must have some basic information in order to understand them. The growth hor-mone is a polypeptide hormone consisting of 191 amino acids. In humans it is produced in the hypophysis and released if there are the right stimuli (e.g. training, sleep, stress, low blood sugar level). It is now important to understand that the freed HGH (human growth hormone) itself has no direct effect but only stimulates the liver to produce and release insulin-like growth factors and so-matomedins. These growth factors are then the ones that cause vari-ous effects on the body The problem, however, is that the liver is only capable of producing a limited amount of these substances so that the effect is limited. If growth hormones are injected they only stimulate the liver to produce and release these substances and thus, as already mentioned, have no direct effect.
During the mid 1980's only the human, biologically-active form was available as exogenous sour-cc of intake. It was obtained from the hypophysis of dead corpses, an expensive and costly procedure. In 1985 the intake of human growth hormones was linked with the very rare Creutzfeld-Jakob disease, an invariably fatal brain disease characterized by progressive dementia. In response, manufacturers removed this version from the market. Today, human growth hor-mones are no longer available for injection. Fortunately, science has not been asleep and has developed the synthetic growth hormone which is genetically produced either from Escherichia coli (E coli) or from the transformed mouse cell line. It has been available in nu-merous countries for years (see list with Trade Names
.
The use of these STH somatotropic hormone compounds offers the athlete three performance-enhancing effects. STH (somatotropic hormone) has a strong anabolic effect and causes an increased pro-tein synthesis which manifests itself in a muscular hypertrophy (enlargement of muscle cells) and in a muscular hyperplasia (in-crease of muscle cells.) The latter is very interesting since this in-crease cannot be obtained by the intake of steroids. This is probably also the reason why STH is called the strongest anabolic hormone. The second effect of STH is its pronounced influence on the burning of fat. It turns more body fat into energy, leading to a drastic reduc-tion in fat or allowing the athlete to increase his caloric intake. Third, and often overlooked, is the fact that STH strengthens the connective tissue, tendons, and cartilages, which could be one of the main reasons for the significant increase in strength experienced by many athletes. Several bodybuilders and powerlifters report that through the simultaneous intake with steroids STH protects the athlete from injuries while increasing his strength. You will say that this sounds just wonderful. What is the problem, however, since there are still some who argue that STH offers nothing to athletes? There are, by all means, several athletes who have tried STH and who were sadly disappointed by its results. However, as with many things in life, there is a logical explanation or perhaps even more than one:
1.The athlete simply has not taken a sufficient amount of STH regularly and over a long enough period of time. STH is a very expensive compound and an effective dosage is unaffordable by most people.
2.When using STH the body also needs more thyroid hormones, insulin, corticosteroids, gonadotropins, estrogens and - what a surprise! - androgens and anabolics. This is also the reason why STH, when taken alone, is considerably less effective and can only reach its optimum effect by the additive intake of steroids, thyroid hormones, and insulin, in particular. But we must point out in this case that STH has a predominately anabolic effect. There are three hormones which are needed at the same time in order to allow for maximum anabolic effect. These are STH, insulin, and an LT-3 thyroid hormone, such as, for example, Cytomel. Only then can the liver produce and release an optimal amount of somatomedin and insulin-like growth factors. This anabolic effect can be further enhanced by taking a substance with an anticatabolic effect. These substances are---everybody should probably know by now-anabolic/androgenic steroids or Clenbuterol. Then a synergetic effect takes place. Are you still wondering why pro bodybuilders are so incredibly massive but, at the same time, totally ripped while you are not? It is "Polypharmacy at its finest," as W Nathaniel Phillips described to the point in his bookAnabolic Reference Guide (5th Issue, 1990). But coming back once more to the "anabolic formula": STH, insulin, and L-T3. Most athletes have tried STH during preparation for a competition in that phase when the diet is calorie-reduced. The body usually reacts by reducing the release of insulin and of the L- T3 thyroid hormone. And, as was described under point 2, this is not an advantageous condition when STH is expected to work well. Well, we almost forgot. Those who combine Clenbuterol with STH should know that Clenbuterol (like Ephedrine) reduces the body's own release of insulin and L-T3. True, this seems a little complicated and when reading it for the first time it might be a little confusing; however it really is true: STH has a significant influence on several hormones in the human body; this does not allow for a simple ad-ministration schedule. As said, STH is not cheap and those who intend to use it should know a little more about it. If you only want to burn fat with STH you will only have to remember user infor-mation for the part with the L-T3 thyroid hormone as is printed by Kabi Pharmacia GmbH for their compound Genotropin: "The need of the thyroid hormone often increases during treatment with growth hormones. "
3. Since most athletes who want to use STH can only obtain it if prescribed by a physician, the only supply source remains the black market. And this is certainly another reason why some athletes might not have been very happy with the effect of the purchased com-pound. How could he, if cheap HCG was passed off as expensive STH? Since both compounds are available as dry substances, all that would be needed is a new label of Serono's Saizen or Lilly's Humatrope on the HCG ampule. It is no longer fun when somebody is paying $200 for 5000 I.U. of HCG, only worth $12, and thinking that he just purchased 4 I.U. of STH. And if you think this happens only to novices and to the ignorant, ask Ben Johnson. "Big Ben," who during three tests within five days showed an above-limit testosterone level, was not a victim of his own stupidity but more likely the victim of fraud. 'According to statistics by the German Drug Administration, 42% of the HGH vials confiscated on the North American black market are fakes." (Der Spiegel, no. 11, 1993.) One can only say, "Poor Ben." Even Deutsche Apothekerzeitung is aware of this problem. The magazine wrote in its issue no. 26 of 07/01/93 in the article "Wachstumshormon--Praparate: Arzneimittelf5lschungen in Bodybuilder-Szene": "The currently-known cases are traded with Dutch or Russian labels... in addition to a display of labels in the Dutch or Russian lan-guage the fakes are distinguished from the original product, in-sofar as the dry substance is not present as lyophilic but present as loose powder. The fakes confiscated so far use the name "Humatrope 16" under the name of Lilly Company (with Dutch denomination) or "Somatogen" (in Russian)." Nowhere can this much money be made except by faking STH. Who has ever held original growth hormones in his hand and known how.they should look?
4. In a few very rare cases the body reacts by developing-antibodies to the exogenous STH, thus making it ineffective.
Before discussing the extremely difficult matter of dosage and intake the following question suggests itself: Generally speaking who is taking growth hormones? A whole lot of athletes as the following quotation suggests: "Charlie Francis, the Canadian athletic trainer of Ben Johnson tells how he improved the performance of Ben and numerous other Olympic athletes by the use of growth hormones in 1983. Francis also had conclusive evidence that the U.S.-American field and track athletes were using growth hormones. In a 1989 interview with a pro bodybuilder, an interview not meant for publication, this massive athlete made clear that he was convinced that almost all professional top athletes were using Protropin. He also said that it did not bother him if the IFBB were to introduce doping tests for men in 1990 as long as there would be no testing for growth hormones (Anabolic Reference Update, June 1989, no. 11). "it is highly suspected that the top Ms. 0 competitors use this product to help them attain their incredibly rippled muscles while still looking like women." (Anabolic Reference Guide, 5th Issue, 1990, W N. Phillips.) Most top bodybuilders using Growth Hormone (GH) feel that insulin activates it. One top pro was rumored to have been using 12 I. U. of GH per day in preparation for his last WBF contest. He swears that GH only works with insulin." (Muscle Media 2000 ' October/ November 1993, no. 34.)" And shortly before the 1984 Olympic Games in Los Angeles, U.S. researchers succeeded in synthetically manufacturing the hormone. This hormone which cannot be detected with current testing methods immediately prepared American athletes throughout the country for the games in California. After reports of success the drug became the secret runner on the doping market. The football pro Lyle Alzado, who died of brain tumor, shortly before his death confessed that he had taken HGH for 16 weeks - and he claimed that 80% of all American football pros do so, too. Ben Johnson, who in 1988 in Seoul was caught with anabolics, admitted to the investigating committee of the Canadian government that he had tried the Growth Hormone. He had paid $ 10,000 for ten bottles of HGH. According to Johnson, his physician, George Astaphan, had also designed programs for his colleagues Mark McKoy, Angella Issajenko, and Desai Williams. Hurdle sprinter Juli Rochelean who toddy runs records for Switzerland under the name Baumann procured HGH on the black market of the bodybuilder scene in Montreal... Among women Gail Devers won the 100 meters (1992 Olympic Games in Barcelona, the auth.) after havingjust overcome a severe thyroid condition, a well-known side effect of taking HGH. Such suspicions are reinforced by current market data. The two U.S. companies Genentech and Eli Lilly produced about 800 million dollars of HGH in 1992. Genentech alone reported an eleven percent production increase compared to last year. Chemists incessantly emphasize that the drug should only be manufactured for use by persons with stunted growth. The U.S.Food and Drug Administration, however, sees it differently: the U.S. government currently includes HGH on the list of forbidden drugs and 'threatens up to five years of,prison for illegal possession of the drug." (Der Spiegel, no. I I of 03/15/93). "Many of the top strength athletes use HGH and the cost of its use ran as high as $30,000/year for one particular pro bodybuilder. Short term users (8 week duration) will spend up to $150 per daily dosage. And because the top athletes are rumored to use it, HGH lust in the lower ranks has become more rampant." (Daniel Duchaine, Underground Steroid Handbook 2.)
The question of the right dosage, as well as the type and duration of application, Is very difficult to answer. Since there is no scientific research showing how STH should be taken for performance improvement, we can only rely on empirical data, that is experimental values. The respective manufacturers indicate that in cases of hypophysially stunted growth due to lacking or insufficient release of growth hormones by the hypophysis, a weekly average dose of 0.3 I.U./week per pound of body weight should be taken. An athlete weighing 200 pounds, therefore, would have to inject 60 I.U. weekly. The dosage would be divided into three intramuscular injections of 20 I.U. each. Subcutaneous injections (under the skin) are another form of intake which, however, would have to be injected daily, usually 8 I.U. per day. Top athletes usually inject 4-16 I.U~day. Ordinarily, daily subcutaneous injections are preferred Since STH has a half-life time of less than one hour, it is not surprising that some athletes divide their daily dose into three or four subcutaueous injections of 2-4 I.U. each. Application of regular, small dosages seems to bring the most effective results. This also has its reasons: When STH is injected, serum concentration in the blood rises quickly, meaning that the effect is almost immediate. As we know, STH stimulates the liver to produce and release somatomedins and insulin-like growth factors which in turn effect the desired results in the body. Since the liver can only produce a limited amount of these substances, we doubt that larger STH injections will induce the liver to produce instantaneously a larger quantity of somatomedins and insulin-like growth factors. it seems more likely that the liver will react more favorably to smaller dosages.
If the STH solution is injected subcutaneously several consecutive times at the same point of injection, a loss of fat tissue is possible. Therefore, the point of injection, or even better, the entire side of the body, should be continuously changed in order to avoid a loss of local fat tissue (lipoathrophy) in the injection cell. One thing has manifested itself over the years: The effect of STH is dosage-dependent. This means either invest a lot of money and do it right or do not even begin. Half-hearted attempts are condemned to failure. Minimum effective dosages seem to start at 4 I.U. per day. For comparison: the hypophysis of a healthy, adult releases 0.5-1.5 I.U. growth hormones daily. The duration of intake usually depends on the athlete's financial resources. Our experience is that STH is taken over a prolonged period, from at least six weeks to several months. It is interesting to note that the effect of STH does not stop after a few weeks; this usually allows for continued improvements at a steady dosage. Bodybuilders who have had positive results with STH have reported that the built-up strength and, in particular, the newlygained muscle system were essentially maintained after discontinuance of the product. The American physician, Dr. William N. Taylor, confirms this statement in his book Anabolic Steroids and the Athlete, where on page 75 he writes: "Evidence for increased muscle number (hyperplasia) in athletes stems from their statements that the increased muscular size and strength remain after the HGH therapy has been discontinued. In fact, there may be further muscular size and strength gains as the training-induced hypertrophy continues in the month beyond."
It remains to be clarified what happens with the insulin and LT-3 thyroid hormone. Athletes who take - STH in their build-up phase usually do not need exogenous insulin. It is recommended, in this case, that the athlete eats a complete meal every three hours, result ing in 6-7 meals daily. This causes the body to continuously release insulin so that the blood sugar level does not fall too low. The use of LT-3 thyroid hormones, in this phase, is carried out reluctantly by athletes. In any case, you must have a physician check the thyroid hormone level during the intake of STH. Simultaneous use of ana bolic/androgenic steroids and/or Clenbuterol is usually appropri ate. During the preparation for a competition the use of thyroid hormones steadily increases. Sometimes insulin is taken together with STH, as well as with steroids and Clenbuterol. Apart from the high damage potential that exogenous insulin can-have in non-diabetics, incorrect use will simply and plainly make you FAT! Too much insulin activates certain enzymes which convert glucose into glycerol and finally into triglyceride. Too little insulin, especially dur ing a diet, reduces the anabolic effect of STH. The solution to this dilemma- Visiting a qualified physician who advises the athlete during this undertaking and who, in the event of exogenous in sulin supply, checks the blood sugar level and urine periodically. According to what we have heard so far, athletes usually inject intermediately-effective insulin having a maximum duration of effect of 24 hours once a day. Human insulin such as Depot-H Insulin Hoechst is generally used. Briefly-effective insulin with a maximum duration of effect of eight hours is rarely used by athletes. Again a human insulin such as H-Insulin Hoechst is preferred.
The undesired effect of growth hormones, the so-called side effects, are also a very interesting and hotly-discussed issue. Above all it must be said: STH has none of the typical side effects of anabolic/ androgenic steroids including reduced endogenous testosterone production, acne, hair loss, aggressiveness, elevated estrogen level, virilization symptoms in women, and increased water and salt retention. The main side effects that are possible with STH are an abnormally small concentration of glucose in the Wood (hypoglycemia) and an inadequate thyroid function. In some cases antibodies against growth hormones are developed but are clinically irrelevant. What about the horror stories about Acromegaly, bone deformation, heart enlargement, organ conditions, gigantism, and early death- In order to answer this question a clear differentiation must be made between humans before and after puberty. The growth plates in a person continue to grow in length until puberty. After puberty neither an endogenous hypersection of growth hormones nor an excessive exogenous supply of STH can cause additional growth in the length of the bones. Abnormal size (gigantism) initially goes hand in hand with remarkable body strength and muscular hardness in the afflicted; later, if left untreated, it ends in weakness and death. Again, this is only possible in pre-pubescent humans who also suffer from an inadequate gonadal function (hypogonadism). Humans who suffer from an endogenous hypersecretion after puberty and whose normal growth is completed can also suffer from Acromegaly. Bones become wider but not longer. There is a progressive growth in the hands and feet, and enlargement of features due to the growth of the lower jaw and nose. Heart muscle and kidneys can also gain in weight and size. In the beginning all of this goes hand in hand with increased body strength and muscular hardness; it ends, however, in fatigue, weakness, diabetes, heart conditions, and early death.
What the authorities like to do now is to present extreme cases of athletes suffering from these malfunctions in order to discourage others and to drum into athletes the fact that with the exogenous supply of growth hormones they would suffer the same destiny This, however, is very unlikely, as reality has proven. Among the numerous athletes using STH comparatively few are seven feet tall Neanderthalers with a protruded lower jaw, deformed skull, clawlike hands, thick lips, and prominent bone plates who walk around in size 25 shoes in order to avoid any misunderstandings, we do not want to disguise the possible risks of exogenous STH use in adults and healthy humans, but one should at least try to be open-minded. Acromegaly, diabetes, thyroid insufficiency, heart muscle hypertrophy, high blood pressure, and enlargement of the kidneys are theoretically possible if STH is used excessively over prolonged periods of time; however, in reality and particularly when it comes to the external attributes, these are rarely present. Tests have shown no causal relation between treatment with somatropin and a possible higher risk of leukemia. Some athletes report headaches, nausea, vomiting, and visual disturbances during the first weeks of intake. These symptoms disappear in most cases even with continued intake. The most common problems with STH occur when the athlete intends to inject insulin in addition to STH. We know two competing German bodybuilders who, because of improper insulin injections, fell into comas lasting several weeks.
The substance somatropin is available as a dried powder and before injecting it must be mixed with the enclosed solution-containing ampule. The ready solution must be injected immediately or stored in the refrigerator for up to 24 hours. It is usually recommended that the compound be stored in the refrigerator. With the exception of the remedy Saizcn the biological activity of growth hormones is usually not impaired when storing the dry substance at 15-25ºC (room temperature); however, a cooler place (2-8?C is preferable. On the black market the price for 4 I.U. each of the compounds Genotropin, Humatrope, Norditropin, and Saizen, in Europe is $80 - 120 for a prick-through vial including the solution ampule. As already mentioned, there are many fakes. It is noted that for the U.S.-American growth hormone compounds, the substance con tent is not given in 1-U. (International Units) but in mg (milligrams). Since I mg corresponds to exactly 2.7 I.U. the 5 mg solution of the compound Humatrope by Lilly contains exactly 13.5 I.U. of Somatropin. The 10 mg solution of the Protropin compound by Genentech therefore contains 27 I.U. of Somatropin. In American powerlifting and bodybuilding circles Humatrope is usually preferred over Protropin. The reason is that Humatrope is synthesized from a chain of 191 amino acids and thus is identical to the amino acid sequence of the human growth hormone. Protropin, on the other hand, consists of 192 amino acids, one amino acid too many. This might be the explanation for why more antibodies are developed with Protropin than with Humatrope. Growth hormones are on the doping list but they are not yet detectable during doping tests.
During the mid 1980's only the human, biologically-active form was available as exogenous sour-cc of intake. It was obtained from the hypophysis of dead corpses, an expensive and costly procedure. In 1985 the intake of human growth hormones was linked with the very rare Creutzfeld-Jakob disease, an invariably fatal brain disease characterized by progressive dementia. In response, manufacturers removed this version from the market. Today, human growth hor-mones are no longer available for injection. Fortunately, science has not been asleep and has developed the synthetic growth hormone which is genetically produced either from Escherichia coli (E coli) or from the transformed mouse cell line. It has been available in nu-merous countries for years (see list with Trade Names
. The use of these STH somatotropic hormone compounds offers the athlete three performance-enhancing effects. STH (somatotropic hormone) has a strong anabolic effect and causes an increased pro-tein synthesis which manifests itself in a muscular hypertrophy (enlargement of muscle cells) and in a muscular hyperplasia (in-crease of muscle cells.) The latter is very interesting since this in-crease cannot be obtained by the intake of steroids. This is probably also the reason why STH is called the strongest anabolic hormone. The second effect of STH is its pronounced influence on the burning of fat. It turns more body fat into energy, leading to a drastic reduc-tion in fat or allowing the athlete to increase his caloric intake. Third, and often overlooked, is the fact that STH strengthens the connective tissue, tendons, and cartilages, which could be one of the main reasons for the significant increase in strength experienced by many athletes. Several bodybuilders and powerlifters report that through the simultaneous intake with steroids STH protects the athlete from injuries while increasing his strength. You will say that this sounds just wonderful. What is the problem, however, since there are still some who argue that STH offers nothing to athletes? There are, by all means, several athletes who have tried STH and who were sadly disappointed by its results. However, as with many things in life, there is a logical explanation or perhaps even more than one:
1.The athlete simply has not taken a sufficient amount of STH regularly and over a long enough period of time. STH is a very expensive compound and an effective dosage is unaffordable by most people.
2.When using STH the body also needs more thyroid hormones, insulin, corticosteroids, gonadotropins, estrogens and - what a surprise! - androgens and anabolics. This is also the reason why STH, when taken alone, is considerably less effective and can only reach its optimum effect by the additive intake of steroids, thyroid hormones, and insulin, in particular. But we must point out in this case that STH has a predominately anabolic effect. There are three hormones which are needed at the same time in order to allow for maximum anabolic effect. These are STH, insulin, and an LT-3 thyroid hormone, such as, for example, Cytomel. Only then can the liver produce and release an optimal amount of somatomedin and insulin-like growth factors. This anabolic effect can be further enhanced by taking a substance with an anticatabolic effect. These substances are---everybody should probably know by now-anabolic/androgenic steroids or Clenbuterol. Then a synergetic effect takes place. Are you still wondering why pro bodybuilders are so incredibly massive but, at the same time, totally ripped while you are not? It is "Polypharmacy at its finest," as W Nathaniel Phillips described to the point in his bookAnabolic Reference Guide (5th Issue, 1990). But coming back once more to the "anabolic formula": STH, insulin, and L-T3. Most athletes have tried STH during preparation for a competition in that phase when the diet is calorie-reduced. The body usually reacts by reducing the release of insulin and of the L- T3 thyroid hormone. And, as was described under point 2, this is not an advantageous condition when STH is expected to work well. Well, we almost forgot. Those who combine Clenbuterol with STH should know that Clenbuterol (like Ephedrine) reduces the body's own release of insulin and L-T3. True, this seems a little complicated and when reading it for the first time it might be a little confusing; however it really is true: STH has a significant influence on several hormones in the human body; this does not allow for a simple ad-ministration schedule. As said, STH is not cheap and those who intend to use it should know a little more about it. If you only want to burn fat with STH you will only have to remember user infor-mation for the part with the L-T3 thyroid hormone as is printed by Kabi Pharmacia GmbH for their compound Genotropin: "The need of the thyroid hormone often increases during treatment with growth hormones. "
3. Since most athletes who want to use STH can only obtain it if prescribed by a physician, the only supply source remains the black market. And this is certainly another reason why some athletes might not have been very happy with the effect of the purchased com-pound. How could he, if cheap HCG was passed off as expensive STH? Since both compounds are available as dry substances, all that would be needed is a new label of Serono's Saizen or Lilly's Humatrope on the HCG ampule. It is no longer fun when somebody is paying $200 for 5000 I.U. of HCG, only worth $12, and thinking that he just purchased 4 I.U. of STH. And if you think this happens only to novices and to the ignorant, ask Ben Johnson. "Big Ben," who during three tests within five days showed an above-limit testosterone level, was not a victim of his own stupidity but more likely the victim of fraud. 'According to statistics by the German Drug Administration, 42% of the HGH vials confiscated on the North American black market are fakes." (Der Spiegel, no. 11, 1993.) One can only say, "Poor Ben." Even Deutsche Apothekerzeitung is aware of this problem. The magazine wrote in its issue no. 26 of 07/01/93 in the article "Wachstumshormon--Praparate: Arzneimittelf5lschungen in Bodybuilder-Szene": "The currently-known cases are traded with Dutch or Russian labels... in addition to a display of labels in the Dutch or Russian lan-guage the fakes are distinguished from the original product, in-sofar as the dry substance is not present as lyophilic but present as loose powder. The fakes confiscated so far use the name "Humatrope 16" under the name of Lilly Company (with Dutch denomination) or "Somatogen" (in Russian)." Nowhere can this much money be made except by faking STH. Who has ever held original growth hormones in his hand and known how.they should look?
4. In a few very rare cases the body reacts by developing-antibodies to the exogenous STH, thus making it ineffective.
Before discussing the extremely difficult matter of dosage and intake the following question suggests itself: Generally speaking who is taking growth hormones? A whole lot of athletes as the following quotation suggests: "Charlie Francis, the Canadian athletic trainer of Ben Johnson tells how he improved the performance of Ben and numerous other Olympic athletes by the use of growth hormones in 1983. Francis also had conclusive evidence that the U.S.-American field and track athletes were using growth hormones. In a 1989 interview with a pro bodybuilder, an interview not meant for publication, this massive athlete made clear that he was convinced that almost all professional top athletes were using Protropin. He also said that it did not bother him if the IFBB were to introduce doping tests for men in 1990 as long as there would be no testing for growth hormones (Anabolic Reference Update, June 1989, no. 11). "it is highly suspected that the top Ms. 0 competitors use this product to help them attain their incredibly rippled muscles while still looking like women." (Anabolic Reference Guide, 5th Issue, 1990, W N. Phillips.) Most top bodybuilders using Growth Hormone (GH) feel that insulin activates it. One top pro was rumored to have been using 12 I. U. of GH per day in preparation for his last WBF contest. He swears that GH only works with insulin." (Muscle Media 2000 ' October/ November 1993, no. 34.)" And shortly before the 1984 Olympic Games in Los Angeles, U.S. researchers succeeded in synthetically manufacturing the hormone. This hormone which cannot be detected with current testing methods immediately prepared American athletes throughout the country for the games in California. After reports of success the drug became the secret runner on the doping market. The football pro Lyle Alzado, who died of brain tumor, shortly before his death confessed that he had taken HGH for 16 weeks - and he claimed that 80% of all American football pros do so, too. Ben Johnson, who in 1988 in Seoul was caught with anabolics, admitted to the investigating committee of the Canadian government that he had tried the Growth Hormone. He had paid $ 10,000 for ten bottles of HGH. According to Johnson, his physician, George Astaphan, had also designed programs for his colleagues Mark McKoy, Angella Issajenko, and Desai Williams. Hurdle sprinter Juli Rochelean who toddy runs records for Switzerland under the name Baumann procured HGH on the black market of the bodybuilder scene in Montreal... Among women Gail Devers won the 100 meters (1992 Olympic Games in Barcelona, the auth.) after havingjust overcome a severe thyroid condition, a well-known side effect of taking HGH. Such suspicions are reinforced by current market data. The two U.S. companies Genentech and Eli Lilly produced about 800 million dollars of HGH in 1992. Genentech alone reported an eleven percent production increase compared to last year. Chemists incessantly emphasize that the drug should only be manufactured for use by persons with stunted growth. The U.S.Food and Drug Administration, however, sees it differently: the U.S. government currently includes HGH on the list of forbidden drugs and 'threatens up to five years of,prison for illegal possession of the drug." (Der Spiegel, no. I I of 03/15/93). "Many of the top strength athletes use HGH and the cost of its use ran as high as $30,000/year for one particular pro bodybuilder. Short term users (8 week duration) will spend up to $150 per daily dosage. And because the top athletes are rumored to use it, HGH lust in the lower ranks has become more rampant." (Daniel Duchaine, Underground Steroid Handbook 2.)
The question of the right dosage, as well as the type and duration of application, Is very difficult to answer. Since there is no scientific research showing how STH should be taken for performance improvement, we can only rely on empirical data, that is experimental values. The respective manufacturers indicate that in cases of hypophysially stunted growth due to lacking or insufficient release of growth hormones by the hypophysis, a weekly average dose of 0.3 I.U./week per pound of body weight should be taken. An athlete weighing 200 pounds, therefore, would have to inject 60 I.U. weekly. The dosage would be divided into three intramuscular injections of 20 I.U. each. Subcutaneous injections (under the skin) are another form of intake which, however, would have to be injected daily, usually 8 I.U. per day. Top athletes usually inject 4-16 I.U~day. Ordinarily, daily subcutaneous injections are preferred Since STH has a half-life time of less than one hour, it is not surprising that some athletes divide their daily dose into three or four subcutaueous injections of 2-4 I.U. each. Application of regular, small dosages seems to bring the most effective results. This also has its reasons: When STH is injected, serum concentration in the blood rises quickly, meaning that the effect is almost immediate. As we know, STH stimulates the liver to produce and release somatomedins and insulin-like growth factors which in turn effect the desired results in the body. Since the liver can only produce a limited amount of these substances, we doubt that larger STH injections will induce the liver to produce instantaneously a larger quantity of somatomedins and insulin-like growth factors. it seems more likely that the liver will react more favorably to smaller dosages.
If the STH solution is injected subcutaneously several consecutive times at the same point of injection, a loss of fat tissue is possible. Therefore, the point of injection, or even better, the entire side of the body, should be continuously changed in order to avoid a loss of local fat tissue (lipoathrophy) in the injection cell. One thing has manifested itself over the years: The effect of STH is dosage-dependent. This means either invest a lot of money and do it right or do not even begin. Half-hearted attempts are condemned to failure. Minimum effective dosages seem to start at 4 I.U. per day. For comparison: the hypophysis of a healthy, adult releases 0.5-1.5 I.U. growth hormones daily. The duration of intake usually depends on the athlete's financial resources. Our experience is that STH is taken over a prolonged period, from at least six weeks to several months. It is interesting to note that the effect of STH does not stop after a few weeks; this usually allows for continued improvements at a steady dosage. Bodybuilders who have had positive results with STH have reported that the built-up strength and, in particular, the newlygained muscle system were essentially maintained after discontinuance of the product. The American physician, Dr. William N. Taylor, confirms this statement in his book Anabolic Steroids and the Athlete, where on page 75 he writes: "Evidence for increased muscle number (hyperplasia) in athletes stems from their statements that the increased muscular size and strength remain after the HGH therapy has been discontinued. In fact, there may be further muscular size and strength gains as the training-induced hypertrophy continues in the month beyond."
It remains to be clarified what happens with the insulin and LT-3 thyroid hormone. Athletes who take - STH in their build-up phase usually do not need exogenous insulin. It is recommended, in this case, that the athlete eats a complete meal every three hours, result ing in 6-7 meals daily. This causes the body to continuously release insulin so that the blood sugar level does not fall too low. The use of LT-3 thyroid hormones, in this phase, is carried out reluctantly by athletes. In any case, you must have a physician check the thyroid hormone level during the intake of STH. Simultaneous use of ana bolic/androgenic steroids and/or Clenbuterol is usually appropri ate. During the preparation for a competition the use of thyroid hormones steadily increases. Sometimes insulin is taken together with STH, as well as with steroids and Clenbuterol. Apart from the high damage potential that exogenous insulin can-have in non-diabetics, incorrect use will simply and plainly make you FAT! Too much insulin activates certain enzymes which convert glucose into glycerol and finally into triglyceride. Too little insulin, especially dur ing a diet, reduces the anabolic effect of STH. The solution to this dilemma- Visiting a qualified physician who advises the athlete during this undertaking and who, in the event of exogenous in sulin supply, checks the blood sugar level and urine periodically. According to what we have heard so far, athletes usually inject intermediately-effective insulin having a maximum duration of effect of 24 hours once a day. Human insulin such as Depot-H Insulin Hoechst is generally used. Briefly-effective insulin with a maximum duration of effect of eight hours is rarely used by athletes. Again a human insulin such as H-Insulin Hoechst is preferred.
The undesired effect of growth hormones, the so-called side effects, are also a very interesting and hotly-discussed issue. Above all it must be said: STH has none of the typical side effects of anabolic/ androgenic steroids including reduced endogenous testosterone production, acne, hair loss, aggressiveness, elevated estrogen level, virilization symptoms in women, and increased water and salt retention. The main side effects that are possible with STH are an abnormally small concentration of glucose in the Wood (hypoglycemia) and an inadequate thyroid function. In some cases antibodies against growth hormones are developed but are clinically irrelevant. What about the horror stories about Acromegaly, bone deformation, heart enlargement, organ conditions, gigantism, and early death- In order to answer this question a clear differentiation must be made between humans before and after puberty. The growth plates in a person continue to grow in length until puberty. After puberty neither an endogenous hypersection of growth hormones nor an excessive exogenous supply of STH can cause additional growth in the length of the bones. Abnormal size (gigantism) initially goes hand in hand with remarkable body strength and muscular hardness in the afflicted; later, if left untreated, it ends in weakness and death. Again, this is only possible in pre-pubescent humans who also suffer from an inadequate gonadal function (hypogonadism). Humans who suffer from an endogenous hypersecretion after puberty and whose normal growth is completed can also suffer from Acromegaly. Bones become wider but not longer. There is a progressive growth in the hands and feet, and enlargement of features due to the growth of the lower jaw and nose. Heart muscle and kidneys can also gain in weight and size. In the beginning all of this goes hand in hand with increased body strength and muscular hardness; it ends, however, in fatigue, weakness, diabetes, heart conditions, and early death.
What the authorities like to do now is to present extreme cases of athletes suffering from these malfunctions in order to discourage others and to drum into athletes the fact that with the exogenous supply of growth hormones they would suffer the same destiny This, however, is very unlikely, as reality has proven. Among the numerous athletes using STH comparatively few are seven feet tall Neanderthalers with a protruded lower jaw, deformed skull, clawlike hands, thick lips, and prominent bone plates who walk around in size 25 shoes in order to avoid any misunderstandings, we do not want to disguise the possible risks of exogenous STH use in adults and healthy humans, but one should at least try to be open-minded. Acromegaly, diabetes, thyroid insufficiency, heart muscle hypertrophy, high blood pressure, and enlargement of the kidneys are theoretically possible if STH is used excessively over prolonged periods of time; however, in reality and particularly when it comes to the external attributes, these are rarely present. Tests have shown no causal relation between treatment with somatropin and a possible higher risk of leukemia. Some athletes report headaches, nausea, vomiting, and visual disturbances during the first weeks of intake. These symptoms disappear in most cases even with continued intake. The most common problems with STH occur when the athlete intends to inject insulin in addition to STH. We know two competing German bodybuilders who, because of improper insulin injections, fell into comas lasting several weeks.
The substance somatropin is available as a dried powder and before injecting it must be mixed with the enclosed solution-containing ampule. The ready solution must be injected immediately or stored in the refrigerator for up to 24 hours. It is usually recommended that the compound be stored in the refrigerator. With the exception of the remedy Saizcn the biological activity of growth hormones is usually not impaired when storing the dry substance at 15-25ºC (room temperature); however, a cooler place (2-8?C is preferable. On the black market the price for 4 I.U. each of the compounds Genotropin, Humatrope, Norditropin, and Saizen, in Europe is $80 - 120 for a prick-through vial including the solution ampule. As already mentioned, there are many fakes. It is noted that for the U.S.-American growth hormone compounds, the substance con tent is not given in 1-U. (International Units) but in mg (milligrams). Since I mg corresponds to exactly 2.7 I.U. the 5 mg solution of the compound Humatrope by Lilly contains exactly 13.5 I.U. of Somatropin. The 10 mg solution of the Protropin compound by Genentech therefore contains 27 I.U. of Somatropin. In American powerlifting and bodybuilding circles Humatrope is usually preferred over Protropin. The reason is that Humatrope is synthesized from a chain of 191 amino acids and thus is identical to the amino acid sequence of the human growth hormone. Protropin, on the other hand, consists of 192 amino acids, one amino acid too many. This might be the explanation for why more antibodies are developed with Protropin than with Humatrope. Growth hormones are on the doping list but they are not yet detectable during doping tests.
C
Citruscide
Guest
fuuuuuuuuuuuuuuuuuuuuuuuck that was long....
I would have just said it promotes growth in skeletal muscles (and eventually soft), increases elasticity in skin, improves vision, reduces body fat, improves thought process and memory skills, heightened energy and hmm... oh yeah, it can actually heal injured joints
C-ditty
I would have just said it promotes growth in skeletal muscles (and eventually soft), increases elasticity in skin, improves vision, reduces body fat, improves thought process and memory skills, heightened energy and hmm... oh yeah, it can actually heal injured joints
C-ditty
bumpo
New member
powerforward
Well-known member
long but maybe some use for you, print it out then read it.
Human Growth Hormone (HGH)
Clinical Outcomes Study
The Effect of a Program of Hormone Modulation, Low Glycemic Nutrition and Exercise Instruction on Select Outcomes Indicative of Disease Risk and Subjective Impression of Quality of Life in a Private Practice Setting.
Introduction.
Testosterone supplementation (T) in men improves strength (1-4) and increases de novo protein synthesis as well as muscle mass (5-7). T has also been shown to decrease body fat (7-9) and particularly visceral body fat (8), increase libido in normal men (10) and increase libido and sexual performance in hypogonadal men.(11-13). Mood is also improved with T in both hypogonadal(14-15) and older community dwelling men(16). Higher endogenous testosterone has been correlated in many studies with a reduction in a number of cardiovascular risk factors, among them lower - blood pressure, total cholesterol (TC), LDL-cholesterol (LDL), triglycerides (TG), visceral body fat, waist-hip ratio (WHR), serum insulin, fasting and post-prandial glucose, higher HDL-cholesterol (HDL) and greater insulin sensitivity (17-23). In several studies where T has been shown to increase cardiovascular risk, levels of T achieved were supraphysioligic(24-28).
Levels of dehydroepiandrosterone sulfate (DHEAS) correlate inversely with depression(29-30) and supplementation with DHEA (D) results in improvement(31-35). D also directly stimulates immune responsiveness in humans(36) in animals(37)and in vitro(38,39). In men, D has been shown to improve body composition in some studies(40-42) but not in others(43,44). DHEAS levels have been shown to correlate inversely with hippocampal atrophy in the elderly(45) and D was shown in one study to improve memory in depressed patients of middle and older age(46).
Growth hormone deficiency (GHD) is associated with the following, all of which can be significantly reversed with replacement of human growth hormone (G): a decrease in lean body mass(47-51), bone density(52-58), skin thickness(59), sense of well-being(60-65), rate of wound healing(66-70), immune responsiveness(71,72),and aerobic capacity(73,74) . In addition, GHD is associated with an increase in the following, all of which have been reduced in clinical trials of G: (LDL) (75) , atherosclerosis (65,76-82), total body fat(47-51) , hospitalization rate and sick days from work(83).
The benefits of Estrogen replacement therapy have been well described in terms of reducing risk of coronary disease (79,84-88), osteoporosis (94-97), and Alzheimer's Disease (89-93).
There is evidence that progesterone (P) replacement therapy in both the perimenopausal and post-menopausal periods is effective in reducing risk of osteoporosis through osteoblast stimulation (98-100) .
A diet of low glycemic index (LGID) has been shown to lower LDL(101-103) and TG (104,105), raise HDL(105-107), improve both glycemic control(102,108) and insulin sensitivity in non-insulin dependent diabetes(109), and reduce coronary artery disease (CAD) risk in women.(110)
And certainly it is no surprise that physical exercise is capable of increasing muscle mass (111,112) decreasing body fat(111-113) and lowering the waist-hip ratio (WHR).(113) One well-published risk of GH therapy is an increase in glucose levels with associated insulin resistance.(114-118) One recent study showed improvement in insulin sensitivity in obese, insulin resistant individuals using GH along with a low calorie diet compared to a low calorie diet alone(119).
The above litany of benefits, many of which are attributable to, and overlap among several of the above potential interventions, are demonstrated in controlled clinical trials isolating one intervention and measuring one or more related outcomes. Our practice incorporates all of the above interventions in three categories: LGID, regular exercise and hormone supplementation.
Hypothesis
We hypothesized that applying these three modalities simultaneously to an uncontrolled private patient population where the subject is autonomous and compliance is variable will improve select outcomes of disease risk and in the subjective view of the patient, enhance quality of life. We further hypothesize that the tendency of G to increase insulin resistance and serum glucose will be offset by the LGID, exercise and perhaps some benefit from testosterone. We collected data on 78 men and 29 women on our program to determine how selected parameters of disease risk were altered. We measured the following outcomes related to disease risk before commencing and after 197 to 274 days on a program: HA1C, TC, LDL, HDL, TG, TC/HDL (CRR), TG/HDL, body fat percentage (%BF), WHR, bone mineral density (BMD), and prostate specific antigen (PSA) in men.
In our practice we have found that quality of life (QOL) issues are at least as important to our patients as longevity. The benefit of an aging control program should also include some means of measuring QOL. Since one's impression of his or her own QOL is largely subjective, a subjective survey would seem appropriate as a means of measuring changes in QOL. We sent a 2- part survey randomly to patients currently on our program and recorded all responses. Part 1 inquired of side effects and part 2 of perceived benefits. In this paper we report the changes seen in the above-mentioned objective outcomes as well as the results of our side effects and benefits survey given to patients currently on our program.
Materials and Methods
All subjects were patients enrolled in the Cenegenics Program between February of 2000 and March of 2001. Data was collected retrospectively on enrolled patients who qualified by having not been on any hormone therapy prior to the trial period, having remained on a constant set of hormones for the study duration, having not been on any prescription drug known to affect the outcomes being measured, and having had their follow-up blood draws, dexa scan, and physical measurements taken also during the study period. Most of our patients were disqualified for one or more of these reasons. One exception to the above criteria was that women previously on estrogens and/ or progesterone or progestins were admitted. All subjects had their baseline studies done within the 3 weeks prior to commencing their program. Both baseline and follow-up blood draws were done fasting. Blood testing was routinely performed by Quest Diagnostics in Salt Lake City, Utah, but other commercial labs were sometimes used at the subject's discretion. Normal ranges for the various labs used were identical.
Subjects were initially seen at Cenegenics for a baseline evaluation that included a standard history and physical examination including measurement of WHR, breast and digital rectal examination with stool hemoccult. Pap smears and mammograms were not done but were required to be on record within the past 12 months and annually thereafter for all women on GH or estrogen. % BF, lean body mass and bone density were measured by DXA scan. Baseline DXA scanning was done by Cenegenics on a Lunar DPX-IQ Imaging Densitometer. If a follow-up scan was done at a different facility it was disqualified for difference in either technique or precise anatomical location. Baseline blood test results were available at the time of the initial visit. Subjects met for 90 to 120 minutes with a physician for the exam, evaluation of all data and formulation of a hormone program. The physician instructed the subjects on the benefits and risks of each hormone as well as potential side effects and the synergy of nutrition, exercise and hormone supplementation. Initial dosing of hormones was not formula based and was determined solely by the judgment of the physician based on his experience. Each subject met for a similar period of time with a nutritionist for a comprehensive diet analysis, explanation of the physiologic effect of a low glycemic diet, and instruction on healthy and harmful fats. Moderate intake of polyunsaturated and monounsaturated fats was encouraged without a specific requirement in grams or calorie percentage. Patients were encouraged to use green and yellow vegetables (excluding corn, carrots and beets) and the lower glycemic fruits as sole sources of carbohydrate. Sugars and starches were strongly discouraged. A calculation of daily protein requirement based on lean body mass and activity level was performed. Emphasis was placed on motivating the patient through education rather than imposing strict dietary rules. An evaluation was made of physical restrictions and/or disability, followed by the recommendation of a specific exercise plan. The subjects then met for 15 to 30 minutes with a registered nurse who instructed them on the administration of all prescribed hormones including self-injection. Subjects were encouraged to call in to speak with the physician, nurse or nutritionist at any time they had questions, doubts or symptoms. The first follow-up blood draw was scheduled 6 weeks after the initial visit. Subjects reviewed the results in a teleconference with their physician and dose was adjusted in an effort to attain or maintain the serum level in the "Cenegenics Optimal Range" (COR). The COR was arbitrarily chosen by the following guidelines: Estradiol: mid-range for the early follicular phase; Progesterone: upper normal for the follicular phase yet below normal for the luteal phase; T: upper 40% of the normal range for men (not age defined); IGF-1: upper 40% of the normal range for men and women for the age bracket of 39 to 54; DHEAS: upper 30% of the normal range for a young adult. The only drug therapy used to effect hormone levels was anastrazole, an aromatase inhibitor, used for men whose estradiol rose above the normal range with the administration of T. The dose of anastrazole was estimated with the goal of keeping estradiol levels in the upper ½ of the normal range for men. Subsequent blood draws were scheduled approximately 12 weeks after the first follow-up blood draw.
For data collection and reporting, the subjects were divided into five groups: Men on androgens (A) (D orally and T as testosterone cypionate by weekly IM injection), men on A plus G (recombinant human growth hormone by subcutaneous injection 6 mornings per week), women on A (D orally and T as compounded transdermal testosterone cream or gel) plus hormone replacement therapy (HRT) (oral progesterone plus transdermal estradiol, or triest [estradiol, estriol, estrone] or biest [estradiol, estriol]), women on A plus G, and women on A plus HRT plus G. Patients were assigned to a particular group based on their personal selection of a hormone program after consulting with the physician. Doses are not reported. Since the patients were managed according to their serum level for each hormone, the dose varied widely. The intent of the study was not to correlate the outcomes to a specific dose, but to correlate the outcomes with the change in serum level in the context of the program. The average study period was defined as the number of days from the first day of hormone therapy to the date of the last blood draw within the first 9 months of the patient's program. Since the data was collected retrospectively and the timing of the blood draw was strongly influenced by patient preference, the average study period varied for each group. It ranged from 197 to 274 days. The average study period for each group is shown in Table 1.
Table 1
RESULTS
Table 2 shows the change in serum hormone levels as well as the change in PSA for both groups of men - those on A, and those on A plus G. Estradiol level was not shown in these men because it was kept in the normal range with the use of anastrazole.
The change in levels of the various administered hormones for women are shown in Tables 3 and 4. Estradiol and progesterone levels were not followed in women who were not taking them. The normal range of testosterone, free testosterone, DHEAS and insulin-like growth factor-1 (IGF-1) were different for those aged 50 and over versus those under 50.
Table 5 shows the change in HA1C for all the groups. In addition, calculations were done to show the change in all men and all women, regardless of which hormone program they were on. We also calculated the change for all subjects, for all men and for all women, separating these three categories further into those receiving or not receiving G.
Table 6 shows the percentage change for each group in TC, LDL, HDL, TG, TG/HDL and CRR. Table 7 shows the percent change in weight, LBM, % BF and WHR in four out of the five groups. We were unable to obtain follow up data for women on A plus G.
Table 2
Table 3
Table 6
Table 7
Table 8 shows the change in bone density that occurred over the course of the program in only four groups. No follow up data was available for women on A plus G. The fifth column shows the percent better than predicted of total body bone density for each of the four groups. The purpose is to show how well the patients in each category fared in comparison to the expected change in bone density matched to their age and period of time between scans. Peer reviewed papers were used to obtain a range of expected bone loss per year matched for sex and age to our groups. Based on these data, the rates of expected decline in bone density that we used in comparison to those actually experienced in our population were: for men, 1% per year; for women on A+G+HRT (average age 67), 1.5% per year; for women on A+HRT (average age 53, perimenopausal), 3% per year.
Table 13 illustrates an effect we noticed on HDL cholesterol by raising testosterone levels above the normal range in women.
Side effects that occurred while on the program are recorded for men on Table 9 and for women on Table 10. This survey was sent to all patients on the program. The response rate was low, partly because we had only a very small window of time to receive the answers back. The survey was sent only to those who were currently on the program. It would therefore, exclude anyone who had dropped out of the program due to side effects.
Perceived benefits of the program based on a subjective survey filled out by patients currently on the program are shown on Table 11 for women, and Table 12 for men. Although statistical analysis was not done, it did appear that a majority of the women who responded positively were on growth hormone.
Side effects that occurred while on the program are recorded for men on Table 9 and for women on Table 10. This survey was sent to all patients on the program. The response rate was low, partly because we had only a very small window of time to receive the answers back. The survey was sent only to those who were currently on the program. It would therefore, exclude anyone who had dropped out of the program due to side effects.
Perceived benefits of the program based on a subjective survey filled out by patients currently on the program are shown on Table 11 for women, and Table 12 for men. Although statistical analysis was not done, it did appear that a majority of the women who responded positively were on growth hormone.
Conclusion
These data support the hypothesis that the many benefits seen in controlled trials of hormone replacement, low glycemic nutrition and exercise in the realm of reduced disease risk and quality of life, can be delivered in the private practice setting with minimal side effects that are easily managed.
Discussion
The first issue of note is that attaining more youthful serum levels of the sex hormones and IGF-1 is achievable and largely predictable. We overshot both our goal and the normal range only for T and only in one group- women on A + G + HRT. This was apparently not without consequence as shown in Table 13, due to the decline in HDL. T has been implicated to lower HDL levels in women(120,121). Reducing the T dose, fine-tuning the diet, or even using cholesterol-modifying agents are options for dealing with this. Also notable is the relatively high level of HDL in these women both before and after T administration. The rise in T levels in women is partially affected by D. (122,123)
DHEAS levels were below the goal in most women as a result of dose restriction due to the occurrence of acne. This is of limited significance due to the arbitrary nature of the goal range. In no group did we achieve our goal for IGF-1. This was a function of cost, but often also, a result of adequate clinical response as perceived by the patient, at a level below the goal range, obviating the need to reach the goal range.
The substantial improvement in disease risk outcomes seen in tables 4-10 and the subjective benefit shown in tables 11 and 12 cannot be attributed to G or any single or group of hormones, or even to one modality. They can only be attributed to the comprehensive program. For example, studies without calorie restriction unanimously demonstrate a rise in HA1C with the use of G well beyond what we experienced (114-118). Yet there were at least three interventions working to lower HA1C: LGID (102,108), exercise (113), and T (7). It is gratifying that we saw a reduction in HA1C in most groups on G and only a minimal increase in women on G. Certainly our patients were consuming more calories than the subjects in Nam’s study (119) where patients on a daily restriction of 25 kcal/ kg and G lost more fat and became more insulin sensitive than those on the same diet without G.
Every category of women on G experienced, on average, an increase in HA1C, even though their percentage increase in IGF-1 was slightly less than that in men. We can speculate that they were less compliant with nutrition and exercise. Another possibility is less effect of T (7), since their serum level on the program was roughly 8.5% that of men.
In both groups of men, serum PSA increased between 27 and 30%. These percentages seem somewhat misleading since the baseline values were so low (1.23 and 1.67) and the normal range is relatively wide (0-4.0). The actual increases in PSA were only 0.37 in men on A and 0.45 in men on A + G. Our data conflict with that of Cooper (124) who saw no change in PSA in his study of 31 healthy men age 21 to 39 using intramuscular T at up to 500mg per week for 15 weeks. Although his trial was of much shorter duration than our approximate 33 weeks, his dose was up to 12 times ours. This leads us to believe that the difference in results is attributable to the subjects’ age differences. His eldest was 39 and our average age was 56. Only 7.5% of men currently on our program experienced new nocturia (Table 12). These are not necessarily the same men for whom PSA values are reported. In our 4-year history we have had only one patient drop out for urinary symptoms, a 68 year old with severe BPH who returned to the program after a trans-urethral resection.
Dihydrotestosterone (DHT) levels in our male subjects increased very modestly and remained normal. We were unable to maintain this control of DHT in our early history of using transdermal T without the aid of finasteride. No finasteride was used in any of the subjects reported herein. All our male subjects are encouraged to use saw palmetto, stinging nettle and pygeum but we are unable to report on compliance.
There was a slight increase in IGF-1 in both groups not on G, one group in each gender (Tables 2 and 3). This is likely a T and D effect. Testosterone administration in eugonadal (125) and hypogonadal (126) men has been shown to raise IGF-1. D supplementation has been shown to raise IGF-1 modestly in both men and women (127). In those on G, our post treatment IGF-1 increased only modestly, partially due to our conservative approach but most importantly because subjects were satisfied with their perceived clinical response at these modestly increased levels. If they requested a higher dose it was given provided their IGF-1 had not exceeded 360 ng/ml (upper normal for the 39 to 54 year old adult as provided by Quest Diagnostics). The dose of G ranged between 5 and 10 units per week and averaged 7. The weekly dose was divided into 6 morning injections to afford the least possible risk of suppressing the early morning spike in pituitary activity. Our approach differs from the standard endocrine procedure of evening injections in the pituitary deficient where there is little or no morning activity to suppress. Because the risks of long-term administration of G are incompletely defined, we attempt to use the lowest possible dose that reasonably satisfies the patient, with the absolute upper limit of IGF-1 at 360 ng/ml. We find we seldom need approach that level.
The improvement seen in serum lipids may be the benefit that is most shared among the various interventions. G has been shown to reduce LDL as well as TC in patients with GHD (65,76). Cuneo showed this to be true with 6 months treatment (65). In a 12-month trial, also on GHD patients, Borson-Chazot noted only a transient improvement in LDL and TC at 6 months with return to baseline at 12 months, yet reported a decrease in carotid intima-media thickness in the same group at 12 months (77). Our trial ended between 6 and 12 months, consistent with the interval where improvement in TC and LDL was seen in both studies.
O’Neal, however, saw improvement in TC and LDL after 24 months of G in GHD patients(78). He did, however, note an increase in lipoprotein (a), which we did not measure. The improvement in serum lipids in men was also likely supported by T. (17,18,22-24,26)
Table 7 illustrates that weight and %BF dropped and LBM increased in all subjects except women on A + HRT. We’re unable to explain the increase in %BF and decrease in lean body mass in women on A + HRT, other than that follow-up measurements were obtained in only two subjects. No one from the group of women on A + G was available for follow-up measurements. The greatest rise in LBM was seen in men on A + G, as would be expected (1,5,6,47-51). WHR decreased in three of four groups, and increased negligibly in women on A + G + HRT. We were pleased with the overall effect on body composition, particularly if we overlook the group with only two subjects. Men on A lost more body fat than men on A + G. This is inconsistent with the data from the NIA data that showed an additive effect of the two hormones on fat loss in elderly men.(128) One explanation is that in the NIA study there were no components of nutrition or exercise, which clearly can have a profound differential influence among groups, particularly given the small numbers in our groups.
Table 8 shows the improvement in bone density of 1.4 to 2.4% over the predicted for four groups. Again we were unable to collect follow-up data on women on A + G. Although the results appear mixed when reading the change in T score, one must take into account normal bone loss for age and sex over the given time studied. Most studies report a 1% annual loss for men and 1 to 3% for women with the exception of women in the perimenopausal period where bone loss is reported to be 3% or more per year (129-132). We therefore, used 1% as the expected bone loss per year for all groups of men and 1.5% for women except women on A + G. Since those women averaged 53 in age, we used the low end of the perimenopausal expected decline, or 3%. We factored the expected bone loss per year over the number of months between DXA scans.
Our side effect survey ( tables 9 and 10) pertains to a different group of subjects than those discussed above, although there was some overlap. It was sent randomly to patients currently on our program and therefore excluded those who had dropped out, making it less objective. The occurrence of testicular atrophy in 25% of men was the most frequent adverse event. This was surprisingly well tolerated because men were forewarned but also because they were so appreciative of the benefits of T. Human chorionic gonadotropin (HCG) was used to reverse it. The benefit of HCG was incomplete but substantial. Arthralgias were the second most common at 20% with swelling of hands or feet at 10%. These are well known side effects of G related to its antinatruretic effect and are dose dependent (60,65,83,128); they were easily reversed in our population by abstaining from G for 1 week and resuming at a dose reduced by 15%. Weight gain occurred in 15% of respondents. This fits with the antinatruretic effect of G but is likely also related to the anabolic effect of T (1,5,6). Nipple discomfort is likely related to the rise in estradiol (E2) that often accompanied the rise in T level. It was easily controlled by bringing E2 back down to the upper normal range with a very low dose aromatase inhibitor. 10% of our patients experienced some level of erectile dysfunction while on a program. This is less than or equal to the norm expected for men over 40.(133,134) The National Health and Social Life Survey reported a prevalence rate for erectile dysfunction of 11% for ages 40 to 49 years and 18% for ages 50 to 59 years.(134) In our practice new erectile dysfunction has never proven to be more than transient and therefore is thought to be either psychological or related to fluctuations in T or estradiol levels. Acne, seen in 7.5%, in our experience is a common side effect of D and is dose dependent. Nocturia and hair loss might both be considered related to a rise in DHT and PSA, although in our study group the rise in both was slight and they remained normal (Table 2).
Table 10 represents symptoms reported by women on our program that could represent side effects. The most common at 27.3% was weight gain. To this we assign the same discussion as for men in the above paragraph. Looking at the data from our other study population shown in Table 10, we see that of the 8 women, there was a net loss in BF% and a net gain in LBM. This would support the likelihood of weight gain being a result of gains in LBM and water. The next most common symptom was acne, which we discussed in the above paragraph. Hot flashes, abnormal vaginal bleeding and nipple soreness can usually be attributed to physiologic response to non-optimal levels of estradiol or progesterone. They require measurement and adjustment in dosage followed by the appropriate work-up if unsuccessful, the scope of which is beyond this paper. Swollen joints, swelling of hands and feet and arthralgias we would again attribute to fluid retention from G, which is discussed in the above paragraph. Decreased libido was reported by 9.1% of women. We’re at a loss to explain this. As you can see from Table 11, libido increased in 62% of these same women and sexual performance improved in 55%. T is credited in a number of studies to enhance libido and sexual performance in postmenopausal women
Tables 11 and 12 represent the positive side of our survey. These data speak for themselves and detailed discussion of their relation to individual aspects of our program would be redundant. Suffice it to say that we were gratified to see the high percentages of patients who felt they had improved in so many outcomes so critical to quality of life.
Human Growth Hormone (HGH)
Clinical Outcomes Study
The Effect of a Program of Hormone Modulation, Low Glycemic Nutrition and Exercise Instruction on Select Outcomes Indicative of Disease Risk and Subjective Impression of Quality of Life in a Private Practice Setting.
Introduction.
Testosterone supplementation (T) in men improves strength (1-4) and increases de novo protein synthesis as well as muscle mass (5-7). T has also been shown to decrease body fat (7-9) and particularly visceral body fat (8), increase libido in normal men (10) and increase libido and sexual performance in hypogonadal men.(11-13). Mood is also improved with T in both hypogonadal(14-15) and older community dwelling men(16). Higher endogenous testosterone has been correlated in many studies with a reduction in a number of cardiovascular risk factors, among them lower - blood pressure, total cholesterol (TC), LDL-cholesterol (LDL), triglycerides (TG), visceral body fat, waist-hip ratio (WHR), serum insulin, fasting and post-prandial glucose, higher HDL-cholesterol (HDL) and greater insulin sensitivity (17-23). In several studies where T has been shown to increase cardiovascular risk, levels of T achieved were supraphysioligic(24-28).
Levels of dehydroepiandrosterone sulfate (DHEAS) correlate inversely with depression(29-30) and supplementation with DHEA (D) results in improvement(31-35). D also directly stimulates immune responsiveness in humans(36) in animals(37)and in vitro(38,39). In men, D has been shown to improve body composition in some studies(40-42) but not in others(43,44). DHEAS levels have been shown to correlate inversely with hippocampal atrophy in the elderly(45) and D was shown in one study to improve memory in depressed patients of middle and older age(46).
Growth hormone deficiency (GHD) is associated with the following, all of which can be significantly reversed with replacement of human growth hormone (G): a decrease in lean body mass(47-51), bone density(52-58), skin thickness(59), sense of well-being(60-65), rate of wound healing(66-70), immune responsiveness(71,72),and aerobic capacity(73,74) . In addition, GHD is associated with an increase in the following, all of which have been reduced in clinical trials of G: (LDL) (75) , atherosclerosis (65,76-82), total body fat(47-51) , hospitalization rate and sick days from work(83).
The benefits of Estrogen replacement therapy have been well described in terms of reducing risk of coronary disease (79,84-88), osteoporosis (94-97), and Alzheimer's Disease (89-93).
There is evidence that progesterone (P) replacement therapy in both the perimenopausal and post-menopausal periods is effective in reducing risk of osteoporosis through osteoblast stimulation (98-100) .
A diet of low glycemic index (LGID) has been shown to lower LDL(101-103) and TG (104,105), raise HDL(105-107), improve both glycemic control(102,108) and insulin sensitivity in non-insulin dependent diabetes(109), and reduce coronary artery disease (CAD) risk in women.(110)
And certainly it is no surprise that physical exercise is capable of increasing muscle mass (111,112) decreasing body fat(111-113) and lowering the waist-hip ratio (WHR).(113) One well-published risk of GH therapy is an increase in glucose levels with associated insulin resistance.(114-118) One recent study showed improvement in insulin sensitivity in obese, insulin resistant individuals using GH along with a low calorie diet compared to a low calorie diet alone(119).
The above litany of benefits, many of which are attributable to, and overlap among several of the above potential interventions, are demonstrated in controlled clinical trials isolating one intervention and measuring one or more related outcomes. Our practice incorporates all of the above interventions in three categories: LGID, regular exercise and hormone supplementation.
Hypothesis
We hypothesized that applying these three modalities simultaneously to an uncontrolled private patient population where the subject is autonomous and compliance is variable will improve select outcomes of disease risk and in the subjective view of the patient, enhance quality of life. We further hypothesize that the tendency of G to increase insulin resistance and serum glucose will be offset by the LGID, exercise and perhaps some benefit from testosterone. We collected data on 78 men and 29 women on our program to determine how selected parameters of disease risk were altered. We measured the following outcomes related to disease risk before commencing and after 197 to 274 days on a program: HA1C, TC, LDL, HDL, TG, TC/HDL (CRR), TG/HDL, body fat percentage (%BF), WHR, bone mineral density (BMD), and prostate specific antigen (PSA) in men.
In our practice we have found that quality of life (QOL) issues are at least as important to our patients as longevity. The benefit of an aging control program should also include some means of measuring QOL. Since one's impression of his or her own QOL is largely subjective, a subjective survey would seem appropriate as a means of measuring changes in QOL. We sent a 2- part survey randomly to patients currently on our program and recorded all responses. Part 1 inquired of side effects and part 2 of perceived benefits. In this paper we report the changes seen in the above-mentioned objective outcomes as well as the results of our side effects and benefits survey given to patients currently on our program.
Materials and Methods
All subjects were patients enrolled in the Cenegenics Program between February of 2000 and March of 2001. Data was collected retrospectively on enrolled patients who qualified by having not been on any hormone therapy prior to the trial period, having remained on a constant set of hormones for the study duration, having not been on any prescription drug known to affect the outcomes being measured, and having had their follow-up blood draws, dexa scan, and physical measurements taken also during the study period. Most of our patients were disqualified for one or more of these reasons. One exception to the above criteria was that women previously on estrogens and/ or progesterone or progestins were admitted. All subjects had their baseline studies done within the 3 weeks prior to commencing their program. Both baseline and follow-up blood draws were done fasting. Blood testing was routinely performed by Quest Diagnostics in Salt Lake City, Utah, but other commercial labs were sometimes used at the subject's discretion. Normal ranges for the various labs used were identical.
Subjects were initially seen at Cenegenics for a baseline evaluation that included a standard history and physical examination including measurement of WHR, breast and digital rectal examination with stool hemoccult. Pap smears and mammograms were not done but were required to be on record within the past 12 months and annually thereafter for all women on GH or estrogen. % BF, lean body mass and bone density were measured by DXA scan. Baseline DXA scanning was done by Cenegenics on a Lunar DPX-IQ Imaging Densitometer. If a follow-up scan was done at a different facility it was disqualified for difference in either technique or precise anatomical location. Baseline blood test results were available at the time of the initial visit. Subjects met for 90 to 120 minutes with a physician for the exam, evaluation of all data and formulation of a hormone program. The physician instructed the subjects on the benefits and risks of each hormone as well as potential side effects and the synergy of nutrition, exercise and hormone supplementation. Initial dosing of hormones was not formula based and was determined solely by the judgment of the physician based on his experience. Each subject met for a similar period of time with a nutritionist for a comprehensive diet analysis, explanation of the physiologic effect of a low glycemic diet, and instruction on healthy and harmful fats. Moderate intake of polyunsaturated and monounsaturated fats was encouraged without a specific requirement in grams or calorie percentage. Patients were encouraged to use green and yellow vegetables (excluding corn, carrots and beets) and the lower glycemic fruits as sole sources of carbohydrate. Sugars and starches were strongly discouraged. A calculation of daily protein requirement based on lean body mass and activity level was performed. Emphasis was placed on motivating the patient through education rather than imposing strict dietary rules. An evaluation was made of physical restrictions and/or disability, followed by the recommendation of a specific exercise plan. The subjects then met for 15 to 30 minutes with a registered nurse who instructed them on the administration of all prescribed hormones including self-injection. Subjects were encouraged to call in to speak with the physician, nurse or nutritionist at any time they had questions, doubts or symptoms. The first follow-up blood draw was scheduled 6 weeks after the initial visit. Subjects reviewed the results in a teleconference with their physician and dose was adjusted in an effort to attain or maintain the serum level in the "Cenegenics Optimal Range" (COR). The COR was arbitrarily chosen by the following guidelines: Estradiol: mid-range for the early follicular phase; Progesterone: upper normal for the follicular phase yet below normal for the luteal phase; T: upper 40% of the normal range for men (not age defined); IGF-1: upper 40% of the normal range for men and women for the age bracket of 39 to 54; DHEAS: upper 30% of the normal range for a young adult. The only drug therapy used to effect hormone levels was anastrazole, an aromatase inhibitor, used for men whose estradiol rose above the normal range with the administration of T. The dose of anastrazole was estimated with the goal of keeping estradiol levels in the upper ½ of the normal range for men. Subsequent blood draws were scheduled approximately 12 weeks after the first follow-up blood draw.
For data collection and reporting, the subjects were divided into five groups: Men on androgens (A) (D orally and T as testosterone cypionate by weekly IM injection), men on A plus G (recombinant human growth hormone by subcutaneous injection 6 mornings per week), women on A (D orally and T as compounded transdermal testosterone cream or gel) plus hormone replacement therapy (HRT) (oral progesterone plus transdermal estradiol, or triest [estradiol, estriol, estrone] or biest [estradiol, estriol]), women on A plus G, and women on A plus HRT plus G. Patients were assigned to a particular group based on their personal selection of a hormone program after consulting with the physician. Doses are not reported. Since the patients were managed according to their serum level for each hormone, the dose varied widely. The intent of the study was not to correlate the outcomes to a specific dose, but to correlate the outcomes with the change in serum level in the context of the program. The average study period was defined as the number of days from the first day of hormone therapy to the date of the last blood draw within the first 9 months of the patient's program. Since the data was collected retrospectively and the timing of the blood draw was strongly influenced by patient preference, the average study period varied for each group. It ranged from 197 to 274 days. The average study period for each group is shown in Table 1.
Table 1
RESULTS
Table 2 shows the change in serum hormone levels as well as the change in PSA for both groups of men - those on A, and those on A plus G. Estradiol level was not shown in these men because it was kept in the normal range with the use of anastrazole.
The change in levels of the various administered hormones for women are shown in Tables 3 and 4. Estradiol and progesterone levels were not followed in women who were not taking them. The normal range of testosterone, free testosterone, DHEAS and insulin-like growth factor-1 (IGF-1) were different for those aged 50 and over versus those under 50.
Table 5 shows the change in HA1C for all the groups. In addition, calculations were done to show the change in all men and all women, regardless of which hormone program they were on. We also calculated the change for all subjects, for all men and for all women, separating these three categories further into those receiving or not receiving G.
Table 6 shows the percentage change for each group in TC, LDL, HDL, TG, TG/HDL and CRR. Table 7 shows the percent change in weight, LBM, % BF and WHR in four out of the five groups. We were unable to obtain follow up data for women on A plus G.
Table 2
Table 3
Table 6
Table 7
Table 8 shows the change in bone density that occurred over the course of the program in only four groups. No follow up data was available for women on A plus G. The fifth column shows the percent better than predicted of total body bone density for each of the four groups. The purpose is to show how well the patients in each category fared in comparison to the expected change in bone density matched to their age and period of time between scans. Peer reviewed papers were used to obtain a range of expected bone loss per year matched for sex and age to our groups. Based on these data, the rates of expected decline in bone density that we used in comparison to those actually experienced in our population were: for men, 1% per year; for women on A+G+HRT (average age 67), 1.5% per year; for women on A+HRT (average age 53, perimenopausal), 3% per year.
Table 13 illustrates an effect we noticed on HDL cholesterol by raising testosterone levels above the normal range in women.
Side effects that occurred while on the program are recorded for men on Table 9 and for women on Table 10. This survey was sent to all patients on the program. The response rate was low, partly because we had only a very small window of time to receive the answers back. The survey was sent only to those who were currently on the program. It would therefore, exclude anyone who had dropped out of the program due to side effects.
Perceived benefits of the program based on a subjective survey filled out by patients currently on the program are shown on Table 11 for women, and Table 12 for men. Although statistical analysis was not done, it did appear that a majority of the women who responded positively were on growth hormone.
Side effects that occurred while on the program are recorded for men on Table 9 and for women on Table 10. This survey was sent to all patients on the program. The response rate was low, partly because we had only a very small window of time to receive the answers back. The survey was sent only to those who were currently on the program. It would therefore, exclude anyone who had dropped out of the program due to side effects.
Perceived benefits of the program based on a subjective survey filled out by patients currently on the program are shown on Table 11 for women, and Table 12 for men. Although statistical analysis was not done, it did appear that a majority of the women who responded positively were on growth hormone.
Conclusion
These data support the hypothesis that the many benefits seen in controlled trials of hormone replacement, low glycemic nutrition and exercise in the realm of reduced disease risk and quality of life, can be delivered in the private practice setting with minimal side effects that are easily managed.
Discussion
The first issue of note is that attaining more youthful serum levels of the sex hormones and IGF-1 is achievable and largely predictable. We overshot both our goal and the normal range only for T and only in one group- women on A + G + HRT. This was apparently not without consequence as shown in Table 13, due to the decline in HDL. T has been implicated to lower HDL levels in women(120,121). Reducing the T dose, fine-tuning the diet, or even using cholesterol-modifying agents are options for dealing with this. Also notable is the relatively high level of HDL in these women both before and after T administration. The rise in T levels in women is partially affected by D. (122,123)
DHEAS levels were below the goal in most women as a result of dose restriction due to the occurrence of acne. This is of limited significance due to the arbitrary nature of the goal range. In no group did we achieve our goal for IGF-1. This was a function of cost, but often also, a result of adequate clinical response as perceived by the patient, at a level below the goal range, obviating the need to reach the goal range.
The substantial improvement in disease risk outcomes seen in tables 4-10 and the subjective benefit shown in tables 11 and 12 cannot be attributed to G or any single or group of hormones, or even to one modality. They can only be attributed to the comprehensive program. For example, studies without calorie restriction unanimously demonstrate a rise in HA1C with the use of G well beyond what we experienced (114-118). Yet there were at least three interventions working to lower HA1C: LGID (102,108), exercise (113), and T (7). It is gratifying that we saw a reduction in HA1C in most groups on G and only a minimal increase in women on G. Certainly our patients were consuming more calories than the subjects in Nam’s study (119) where patients on a daily restriction of 25 kcal/ kg and G lost more fat and became more insulin sensitive than those on the same diet without G.
Every category of women on G experienced, on average, an increase in HA1C, even though their percentage increase in IGF-1 was slightly less than that in men. We can speculate that they were less compliant with nutrition and exercise. Another possibility is less effect of T (7), since their serum level on the program was roughly 8.5% that of men.
In both groups of men, serum PSA increased between 27 and 30%. These percentages seem somewhat misleading since the baseline values were so low (1.23 and 1.67) and the normal range is relatively wide (0-4.0). The actual increases in PSA were only 0.37 in men on A and 0.45 in men on A + G. Our data conflict with that of Cooper (124) who saw no change in PSA in his study of 31 healthy men age 21 to 39 using intramuscular T at up to 500mg per week for 15 weeks. Although his trial was of much shorter duration than our approximate 33 weeks, his dose was up to 12 times ours. This leads us to believe that the difference in results is attributable to the subjects’ age differences. His eldest was 39 and our average age was 56. Only 7.5% of men currently on our program experienced new nocturia (Table 12). These are not necessarily the same men for whom PSA values are reported. In our 4-year history we have had only one patient drop out for urinary symptoms, a 68 year old with severe BPH who returned to the program after a trans-urethral resection.
Dihydrotestosterone (DHT) levels in our male subjects increased very modestly and remained normal. We were unable to maintain this control of DHT in our early history of using transdermal T without the aid of finasteride. No finasteride was used in any of the subjects reported herein. All our male subjects are encouraged to use saw palmetto, stinging nettle and pygeum but we are unable to report on compliance.
There was a slight increase in IGF-1 in both groups not on G, one group in each gender (Tables 2 and 3). This is likely a T and D effect. Testosterone administration in eugonadal (125) and hypogonadal (126) men has been shown to raise IGF-1. D supplementation has been shown to raise IGF-1 modestly in both men and women (127). In those on G, our post treatment IGF-1 increased only modestly, partially due to our conservative approach but most importantly because subjects were satisfied with their perceived clinical response at these modestly increased levels. If they requested a higher dose it was given provided their IGF-1 had not exceeded 360 ng/ml (upper normal for the 39 to 54 year old adult as provided by Quest Diagnostics). The dose of G ranged between 5 and 10 units per week and averaged 7. The weekly dose was divided into 6 morning injections to afford the least possible risk of suppressing the early morning spike in pituitary activity. Our approach differs from the standard endocrine procedure of evening injections in the pituitary deficient where there is little or no morning activity to suppress. Because the risks of long-term administration of G are incompletely defined, we attempt to use the lowest possible dose that reasonably satisfies the patient, with the absolute upper limit of IGF-1 at 360 ng/ml. We find we seldom need approach that level.
The improvement seen in serum lipids may be the benefit that is most shared among the various interventions. G has been shown to reduce LDL as well as TC in patients with GHD (65,76). Cuneo showed this to be true with 6 months treatment (65). In a 12-month trial, also on GHD patients, Borson-Chazot noted only a transient improvement in LDL and TC at 6 months with return to baseline at 12 months, yet reported a decrease in carotid intima-media thickness in the same group at 12 months (77). Our trial ended between 6 and 12 months, consistent with the interval where improvement in TC and LDL was seen in both studies.
O’Neal, however, saw improvement in TC and LDL after 24 months of G in GHD patients(78). He did, however, note an increase in lipoprotein (a), which we did not measure. The improvement in serum lipids in men was also likely supported by T. (17,18,22-24,26)
Table 7 illustrates that weight and %BF dropped and LBM increased in all subjects except women on A + HRT. We’re unable to explain the increase in %BF and decrease in lean body mass in women on A + HRT, other than that follow-up measurements were obtained in only two subjects. No one from the group of women on A + G was available for follow-up measurements. The greatest rise in LBM was seen in men on A + G, as would be expected (1,5,6,47-51). WHR decreased in three of four groups, and increased negligibly in women on A + G + HRT. We were pleased with the overall effect on body composition, particularly if we overlook the group with only two subjects. Men on A lost more body fat than men on A + G. This is inconsistent with the data from the NIA data that showed an additive effect of the two hormones on fat loss in elderly men.(128) One explanation is that in the NIA study there were no components of nutrition or exercise, which clearly can have a profound differential influence among groups, particularly given the small numbers in our groups.
Table 8 shows the improvement in bone density of 1.4 to 2.4% over the predicted for four groups. Again we were unable to collect follow-up data on women on A + G. Although the results appear mixed when reading the change in T score, one must take into account normal bone loss for age and sex over the given time studied. Most studies report a 1% annual loss for men and 1 to 3% for women with the exception of women in the perimenopausal period where bone loss is reported to be 3% or more per year (129-132). We therefore, used 1% as the expected bone loss per year for all groups of men and 1.5% for women except women on A + G. Since those women averaged 53 in age, we used the low end of the perimenopausal expected decline, or 3%. We factored the expected bone loss per year over the number of months between DXA scans.
Our side effect survey ( tables 9 and 10) pertains to a different group of subjects than those discussed above, although there was some overlap. It was sent randomly to patients currently on our program and therefore excluded those who had dropped out, making it less objective. The occurrence of testicular atrophy in 25% of men was the most frequent adverse event. This was surprisingly well tolerated because men were forewarned but also because they were so appreciative of the benefits of T. Human chorionic gonadotropin (HCG) was used to reverse it. The benefit of HCG was incomplete but substantial. Arthralgias were the second most common at 20% with swelling of hands or feet at 10%. These are well known side effects of G related to its antinatruretic effect and are dose dependent (60,65,83,128); they were easily reversed in our population by abstaining from G for 1 week and resuming at a dose reduced by 15%. Weight gain occurred in 15% of respondents. This fits with the antinatruretic effect of G but is likely also related to the anabolic effect of T (1,5,6). Nipple discomfort is likely related to the rise in estradiol (E2) that often accompanied the rise in T level. It was easily controlled by bringing E2 back down to the upper normal range with a very low dose aromatase inhibitor. 10% of our patients experienced some level of erectile dysfunction while on a program. This is less than or equal to the norm expected for men over 40.(133,134) The National Health and Social Life Survey reported a prevalence rate for erectile dysfunction of 11% for ages 40 to 49 years and 18% for ages 50 to 59 years.(134) In our practice new erectile dysfunction has never proven to be more than transient and therefore is thought to be either psychological or related to fluctuations in T or estradiol levels. Acne, seen in 7.5%, in our experience is a common side effect of D and is dose dependent. Nocturia and hair loss might both be considered related to a rise in DHT and PSA, although in our study group the rise in both was slight and they remained normal (Table 2).
Table 10 represents symptoms reported by women on our program that could represent side effects. The most common at 27.3% was weight gain. To this we assign the same discussion as for men in the above paragraph. Looking at the data from our other study population shown in Table 10, we see that of the 8 women, there was a net loss in BF% and a net gain in LBM. This would support the likelihood of weight gain being a result of gains in LBM and water. The next most common symptom was acne, which we discussed in the above paragraph. Hot flashes, abnormal vaginal bleeding and nipple soreness can usually be attributed to physiologic response to non-optimal levels of estradiol or progesterone. They require measurement and adjustment in dosage followed by the appropriate work-up if unsuccessful, the scope of which is beyond this paper. Swollen joints, swelling of hands and feet and arthralgias we would again attribute to fluid retention from G, which is discussed in the above paragraph. Decreased libido was reported by 9.1% of women. We’re at a loss to explain this. As you can see from Table 11, libido increased in 62% of these same women and sexual performance improved in 55%. T is credited in a number of studies to enhance libido and sexual performance in postmenopausal women
Tables 11 and 12 represent the positive side of our survey. These data speak for themselves and detailed discussion of their relation to individual aspects of our program would be redundant. Suffice it to say that we were gratified to see the high percentages of patients who felt they had improved in so many outcomes so critical to quality of life.
