Quotations About HGH From
The International Medical Community II

Articles on this page give medical opinions on HGH Therapy.

The List of Medical and Scientific Articles presented here is for educational and informational purposes only. No dietary supplement product discussed in this website is intended to treat, cure, diagnose or mitigate any disease.

1. Beshyah SA, Shati M, et al. Cardiovascular effects of growth hormone replacement therapy in hypopituitary adults. Euro J Endocrin (1994) 130: 451-8

Study of 36 AGHD patients. Conclusion: “six months of GH replacement therapy in hypopituitary adults had favorable cardiovascular effects, including increased exercise tolerance and improved diastolic function.”

2. Cano A, Castelo-Branco C, Tarin JJ. Effect of Menopause and Different Combined Estradiol-progestin Regiments on Basal and Growth Hormone, Insulin-like Growth Factor-1, Insulin-like Growth Factor Binding Protein (IGFBP-1), and IGFBP-3 Levels. Fertil Steril (Feb 1999) 71: 261-7.

The administration of oral, but not transdermal, E2 at the usual clinical doses used in postmenopausal women decreased IGF-1 levels and the response of GH to GHRH in older women. No substantial changes were detected in IGFBP-1, IGFBP-3, insulin, or C peptide levels.

3. Chyatte SB, Rudman D, et al. Human Growth Hormone in Myopathy: Myotonic Dystrophy, Duchenne Muscular Dystrophy, and Limb-Girdle Muscular Dystrophy. Southern Med J (Feb 1974) 67(No 2): 170-2

Small prospective controlled study showing: “positive results with GH in adult dystrophies, but not Duchenne’s.”

4. Dubois-Dalcq M, Murray K, et al. Why are growth factors important in oligodendrocyte physiology? Pathologie Biologie (2000) 48: 80-6

A review article of factors involved in oligodendrocyte repair and development. IGF-1 is one of, if not, the major factors: “Administration of IGF-1 to these EAE rats increases oligodendrocyte numbers, myelin gene expression and enhances myelin synthesis in the lesions, while it decreases brain inflammatory cells and improves the clinical status of treated animals.”

5. Fernholm R, Bramnert M, et al. Growth Hormone Replacement Therapy Improves Body Composition and Increases Bone Metabolism in Elderly Patients with Pituitary Disease. J Clin Endocrinol and Metab (2000) 85: 4104-4112

Placebo controlled study of AGHD. Conclusion: “Elderly patients with GHD respond to replacement therapy in similar manner as younger subjects, with an improvement in body composition and an increase in markers for bone metabolism. Side effects are few, and elderly GHD patients can be offered treatment. As long-term risks are unknown, GH doses should be titrated to keep IGF-1 within the age-related physiological range.”

6. Gudmundur J, Rosen T, et al. Two Years of Growth Hormone (GH) Treatment Increases Bone Mineral Content and Density in Hypopituitary Patients with Adult-Onset GH Deficiency. J Clin Endocrinol Metab (1996) 81: 2865-2873

Two-year study measuring changes in BMD, BMC, PICP and ICTP in a group of 44 AGHD patients. All parameters improved by the end of the study and were not appreciated until 18mos into the study, supporting the conclusion: “GH treatment induced a sustained increase in overall bone remodeling activity, which resulted in a net gain in BMD that was more marked in those subjects with a low pretreatment z-score.”

7. Rosen T, Bengtsson BA. Premature Mortality Due to Cardiovascular Disease in hypopituitarism. Lancet (1990) 336: 285-88

Retrospective study of 333 consecutive patients supporting an increase in mortality from cardiovascular disease with AGHD.

8. Rosen T, Johannsson G, at al. Consequences of Growth Hormone Deficiency in Adults and the Benefits and Risks of Recombinant Human Growth Hormone Treatment—A Review Paper. Horm Res (1995) 43: 93-99

Review article defining clinical AGHD: overweight, abnormal body composition (excess body fat and a decrease in the extracellular water volume), low bone mineral content, lipid abnormalities, decreased insulin sensitivity and decreased fibrinolysis. Conclusion: “Most of these symptoms and signs are reversed during GH replacement therapy. There is no evidence suggesting that this replacement therapy causes any unfavorable long-term side effects.”

9. Serri O, St-Jacques P, et al. Alterations of Monocyte Function in Patients with Growth Hormone (GH) Deficiency: Effect of Substitutive GH Therapy. J Clin Endocrinol Metab (1999) 84: 58-63

Twelve AGHD patients were followed for 3 months on GH therapy. Conclusion: “Our results demonstrate that markers of monocyte activation are increased in patients with GHD and GH replacement partly reduces these abnormalities. Reduction of cellular activation of monocytes by GH therapy could potentially contribute to reduce the risk of cardiovascular events in patients with GHD.

10. Slonim AE, Bulone L, at al. A Preliminary Study of Growth Hormone Therapy for Crohn’s Disease. N Engl J Med (2000) 342: 1633-7

A double blind placebo controlled study of 37 patients with Crohn’s disease. GH was administered in extremely high dosage (5mg/day for 1 week, then reduced to 1.5mg/day thereafter). The authors concluded: “Our preliminary study suggests that growth hormone may be a beneficial treatment for patients with Crohn’s disease.” There were very significant improvements in the disease activity index with reduction in the amount and number of medications. Additionally, there were no significant alterations in the insulin, glucose or lipid profiles in these patients.

Growth Hormones and IGF-1 References:

1. Skjaerbaek C, Vahl N, et. al.. Serum Free Insulin-like Growth Factor-1 in growth hormone-defcient Adults before and After Growth Hormone Replacement. Euro J Endocrinology (1997) 137: 132-137.

Free IGF-1 are decreased in GHD, but measurements of free IGF-1 in a single, fasting serum sample do not offer a better separation of patients with GHD from individuals with normal GH status than can be achieved by measurement of total IGF-1.

2. Rosen, CJ. Growth Hormone and Aging. Endocrine (2000) 12 (2): 197-201. Growth Hormone and Aging. Endocrine (Apr 2000) 12 (2): 197-201.

Defines other causes of IGF-1 deficiency, e.g., malnutrition (receptors are down regulated despite elevated GH levels), insulin deficiency, acute catabolic stress (acute trauma, infection, surgery, etc.), and exogenous glucocorticoid and estrogens. Also, cautions against treating somatopause because of perceived risk of neoplasia.

3. Cano A, Castelo-Branco C, Tarin JJ. Effect of Menopause and Different Combined Estradiol-progestin Regiments on Basal and Growth Hormone, Insulin-like Growth Factor-1, Insulin-like Growth Factor Binding Protein (IGFBP)-1, andIGFBP-3 Levels. Fertil Steril (Feb 1999) 71: 261-7.

The administration of oral, but not transdermal, E2 at the usual clinical doses used in postmenopausal women decreased IGF-1 levels and the response of GH to GHRH in older women. No substantial changes were detected in IGFBP-1, IGFBP-3, insulin, or C peptide levels.

4. Marcus R. Recombinant human growth hormone as potential therapy for osteoporosis. Bailliere’s Clinical Endoreinology and Metabolism (July 1998) 12 (2): 251-259

Review article with the conclusion: GH enhances lumbar bone density and appears to maintain femoral density. Author suggests that IGF-1 therapy may be more effective therapy than GH. Studies reported were too short to draw that conclusion (see reference 17).

5. Abs R, Bengtssont B, et al. GH Replacement in 1034 growth hormone deficient hypopituitary adults: demographic and clinical characteristics, dosing and safety. Clinical Endo (1999) 50: 703-713

Study basically shows safety of GH in AGHD without increase in tumor recurrence or diabetes in patients treated for more the 800 patient years. Also, IGF-1 was used and shown to be the method of choice for titration of rhGH therapy.

6. Clemmons D R. Commercial Assays Available for Insulin-Like Growth factor-1 and Their Use in Diagnosing Growth Hormone Deficiency. Horm Res (2001) 55 (suppl 2): 73-79.

Study employs the immunoradiometric (IRMA) sandwich assay with antibodies specific to IGF-1. These assays are found to be quick and accurate, and produce a high degree of specificity. The addition of acid-ethanol extraction or saturation with IGF-II improves reliability. “Despite the problems, IGF-1 measurement is currently the best indirect method available for screening and monitoring patients with GHD

7. Diamandi A, Khosravi MJ, et al. Filter Paper Blood Spot Assay of Human Insulin-Like Growth Factor I (IGF-I) and IGF-Binding Protein-3 and Preliminary Application in the Evaluation of Growth Hormone Status. J Clin Endocrinol Metab (1998) 83: 2296-2301

Authors developed blood spot assays for IGF-1 and IGFBP- 3 and compared them to conventional methodologies. They found that dried blood spot showed a greater than 1 month stability at –20C, 4C and RT and retained more than 65% of the immunoreactivity after approximately 1 month at 37C. “We conclude that blood collected on filter paper is ideal for IGF-I and IGFBP-3 analysis and may find applications in pediatric and large scale infant screening programs.”

Oral Estrogen Effect on IGF-1 Levels

By Jay H Mead MD

1. Fonseca E, Ochoa R, et al. Increased serum levels of growth hormone and insulin-like growth factor-1 associated with simultaneous decrease of circulation insulin in postmenopausal women receiving hormone replacement therapy. Menopause (1999) 6 (1): 56-60.

Study concludes that conjugated equine estrogen 0.625mg/day (HRT) PO increased GH and IGF-1 levels, while lowering insulin levels in postmenopausal women. There was no evidence that this was correlated to reversal of GH metabolic effects.

2. Cano A, Castelo-Branco C, Tarin JJ. Effect of Menopause and Different Combined Estradiol-progestin Regiments on Basal and Growth Hormone, Insulin-like Growth Factor-1, Insulin-like Growth Factor Binding Protein (IGFBP-1), and IGFBP-3 Levels. Fertil Steril (Feb 1999) 71: 261-7.

The administration of oral, but not transdermal, E2 at the usual clinical doses used in postmenopausal women decreased IGF-1 levels and the response of GH to GHRH in older women. No substantial changes were detected in IGFBP-1, IGFBP-3, insulin, or C peptide levels.

3. Grace YW, KAM et al. Estrogens Exert Route- and Dose-Dependent Effects on Insulin-Like Growth factor (IGF-1)-Binding Protein-3 and Acid-Labile Subunit of the IGF Ternary Complex. J Clin Endocrinol and Metab (2000) 85: 1918-1922

Conclusion: “Exogenous oral estrogen exerts inhibitory effects on all three components of the IGF-1 ternary complex. These effects are route and dose dependent, but independent of endogenous GH status. These findings indicate that IGFBP-3 and ALS are directly or indirectly estrogen-sensitive hepatic proteins”.

4. Cook DM, Ludlam WH, et al. Route of Estrogen Administration Helps Determine Growth Hormone (GH) Replacement Dose in GH-Deficient Adults. J Clin Endocrinol Metab (1999) 84: 3956-3960

Retrospective study comparing two groups of AGHD women: those taking oral E2 and those not taking oral E2. Note: transdermal application of E2 patients was included in the latter group. Conclusion: Women taking oral estrogen need about twice the amount to normalize IGF-1 than women using transdermal estrogen. We believe that the difference is related to an effect of oral estrogen on hepatic IGF-1, the major source of circulating serum IGF-1. A potential cost savings of GH could be realized if women needing GH replacement therapy and exogenous estrogen chose transdermal rather than oral treatment.

5. Friend KE, Hartman ML, et al. Both Oral and Transdermal Estrogen Increase Growth Hormone Release in Postmenopausal Women—A Clinical Research Center Study. J Clin Endocrin and Metab (1996) 81: 2250-56

Don’t be fooled by the title. What has actually been shown here is that extremely high non-physiologic dosing of transdermal E2 approximated the same effect on IGF-1 levels as the standard oral dosage. The main flaw in the study is the attempt to increase the serum levels equally with transdermal administration. In so doing, an excessive dose was required—we know that saliva is the only accurate way to measure levels of transdermal steroid hormone administration. Additionally, this study demonstrates that oral E2 is very efficiently converted to estrone and SHBG is increased disproportionately. Despite the excessive transdermal dosage the IGF-1 reduction was less than oral route, though not statistically significant.

6. Bellantoni MF, Harman SM, et al. Effects of Progestin-Opposed Transdermal Estrogen Administration on Growth Hormone and Insulin-Like Growth Factor-I in Postmenopausal Women of Different Ages. J Clin Endocrinol Metab (1991) 72: 172-178

A DB PC study showing that transdermal estradiol (tERT) does not lower IGF-1 levels with 0.05, 0.1 and 0.15 mcg patches. Of interest is the decreased responsiveness of the pituitary gland for release of GH with tERT. The authors speculated that MPA may have played a role.

7. Weissberger AJ, Ho KKY, et al. Contrasting Effects of Oral and Transdermal Routes of Estrogen Replacement Therapy on 24-Hour Growth Hormone (GH) Secretion, Insulin-Like Growth Factor I, and GH-binding Protein in Postmenopausal Women. J Clin Endocrinol Metab (1991) 72: 374-381

An excellent prospective study of 19 woman comparing PO and tERT. Conclusion: “The route of administration is a major determinant of the effects of exogenous estrogens on the GH/IGF-1 axis. Oral estrogen administration inhibits hepatic IGF-1 synthesis and increases GH secretion through reduced feedback inhibition. Reduced GH secretion in the menopause is not explained by estrogen deficiency since GH secretion is not restored by the attainment of physiological E2 concentrations using the transdermal route. The contrasting route dependent IGF-1 responses have important implications for the long-term benefit of hormone replacement therapy in the menopause.” Additionally, there was an increase in IGF-1 levels in the tERT group over baseline.

8. HO KKY, Weissberger AJ. Impact of Short-Term Estrogen Administration on Growth Hormone Secretion and Action: Distinct Route-Dependent effects on Connective and Bone Tissue Metabolism. J Bone and Mineral Res (1992) 7(7): 821-827

A 3 month prospective study comparing bone metabolism parameters in two groups of postmenopausal women (N=7, each group) receiving either PO or transdermal estrogen. Conclusions: “Transdermally delivered estrogen stimulates IGF-1 production, increases osteoblastic function, and stimulates bone and non-bone collagen synthesis. When delivered orally, estrogen reduces IGF-1 and inhibits osteoblastic function; both routes suppress urinary calcium loss. Estrogen administration confers distinct route-dependent effects on connective and bone tissue metabolism; the specific effects on fibroblast and osteoblast function suggest IGF-1 dependency. The divergent effects on indices of bone turnover and connective tissue metabolism suggest that the route of estrogen replacement therapy may have different effects on the integrity of structural tissue in the menopause.

IGF-1 and Remyelination

By Jay H Mead MD

1. Dubois-Dalcq M, Murray K, et al. Why are growth factors important in oligodendrocyte physiology? Pathologie Biologie (2000) 48: 80-6

A review article of factors involved in oligodendrocyte repair and development finds that IGF-1 is one of, if not, the major factor. Conclusion: “Administration of IGF-1 to these EAE rats increases oligodendrocyte numbers, myelin gene expression and enhances myelin synthesis in the lesions, while it decreases brain inflammatory cells and improves the clinical status of treated animals.”

2. Webster, Henry deF. Growth factors and myelin regeneration multiple sclerosis. Multiple Sclerosis (1997) 3: 113-120

A review study of growth factors involved with myelin regeneration in EAE. Conclusion: “Our recent observations on gene expression of IGF-1 related proteins in several demyelination models and on IGF-1 treatment of EAE strongly suggest that this growth factor acts directly on oligodendroglia in the lesions. It upregulates their synthesis of myelin-related proteins, increases regeneration of myelin and promotes the proliferation of oligodendroglia-like cells. An additional, unexpected benefit of IGF-1 administration in EAE is the reduction of some of the BBB defects and inflammatory responses, which cause immune-mediated demyelination. If trials show that IGF-1 has similar actions in MS, it will be useful therapeutically.”

3. Ludwin SK. Central Nervous System Remyelination: Studies in Chronically Damage Tissue. Ann Neurol (1994) 36: S143-5

A review article validating that toxin induced (Cuprizone) plaque formation in the mouse MS model is reversible with withdrawal of the toxin. This reversibility is dependent upon the recovery of the oligodendrocytes, which is a function of the duration of injury. The implication for potential reversibility for MS patients is tremendous.

4. Mason JL, Ye P, al et. Insulin-Like Growth Factor-1 Inhibits Mature Oligodendrocyte Apoptosis During Primary Demyelination. J Neuroscience (Aug 2000) 20 (15): 5703-8

This article includes an in-vivo mouse study and review of literature. Two groups, a wild type mouse strain and a strain (IGF-1 tg) that continuously expresses IGF-1 were challenged by a neurotoxin (Cuprizone). The IGF-1 tg mice showed minimal apoptosis of mature oliogodendrocytes and essentially full recovery from the toxic insult, whereas, the wild type mice showed dramatic apoptosis and delayed recovery. The implication for patients with multiple sclerosis is tremendous: “Our data suggest that inhibiting the death of mature oliogodendrocytes not only prevents their depletion, but it may prevent the formation of chronic plaques in demyelinating diseases such as multiple sclerosis.”

5. Mason JL, Jones JJ, et al. Mature Oligodendrocyte Apoptosis Precedes IGF-1 Production and Oligodendrocyte Progenitor Accumulation and Differentiation During Demyelination/Remyelination. J Neurosci Res (2000) 66: 251-262

Mouse study demonstrating: 1) mature oligodendrocytes are almost completely depleted within the Cuprizone induced lesions by apoptosis; 2) oligodendrocyte progenitors proliferate and accumulate in a time course that overlaps with active remyelination; 3) oligodendrocyte progenitors mature within the lesions; 4) the expression of IGF-1 parallels the accumulation and differentiation of oligodendrocyte progenitors within the lesion. The implication for neurodegenerative conditions such as multiple sclerosis is: the demyelinating process is not due to an autoimmune inflammatory process, but from apoptosis (programmed cell death) secondary to a toxic exposure. And, that IGF-1 levels may play a role in the remyelination process.

6. Matsushima GK, Morell P. The Neuotoxicant, Cuprizone, as a Model to Study Demyelination in the Central Nervous System.

Mouse study demonstrating: 1) mature oligodendrocytes are almost completely depleted within the Cuprizone induced lesions by apoptosis; 2) oligodendrocyte progenitors proliferate and accumulate in a time course that overlaps with active remyelination; 3) oligodendrocyte progenitors mature within the lesions; 4) the expression of IGF-1 parallels the accumulation and differentiation of oligodendrocyte progenitors within the lesion; 5) microglia and astrocytes produce IGF-1, and; 6) Interleukin-1 release by the microglia may be an initiating for IGF-1 production and release. The implication for neurodegenerative conditions such as multiple sclerosis is: the demyelinating process is not due to an autoimmune inflammatory process, but from apoptosis (programmed cell death) secondary to a toxic exposure. And, that IGF-1 levels may play a role in the remyelination process. A good discussion on the possible mechanisms of Cuprizone injury.

7. Cammer W. The Neurotoxicant, Cuprizone, Retards the Differentiation of Oligodendrocytes in Vitro. J Neuro Sci (1999) 168: 116-120

In-vitro rodent study that demonstrated the neurotoxic activity of cuprizone, and the mechanism of injury. Conclusion: “Cuprizone inhibited the maturation of oligodendrocytes without diminishing the numbers of precursors, and appeared to affect the mitochondria in those cells.” The author speculated on the potential benefits of protecting the injured mitochondria, “measures that might protect oligodendrocytes from energy deficits may protect against demyelination during future studies in vivo and in vitro.”

IGF-I Additional References

1. Ghigo E, Arvat E, et al. Diagnostic and therapeutic uses of growth hormone-releasing substances in adult and elderly subjects. Bailliere’s Clin Endo and Met (Jul 1998) 12(2): 341-358

This study validates the use of GHRH provocation testing (with arginine) for the diagnosis of AGHD instead of ITT, and that injectable rhGH is the most effective replacement strategy. The cutoff limit for diagnosis needs to be adjusted for the particular provocation test, e.g., arginine with GHRH is 16 ug/l with less than 9 ug/l as the criteria for severe deficiency.

2. Frackelton JP, Christenson RL. Mercury Poisoning and Its Potential Impact on Hormone Regulation and Aging: Preliminary Clinical Observations Using a New Therapeutic Approach. J Advancement in Med (1998) 11(1): 9-25

James Frackelton MD is one the nation most respected chelators. He discusses the pathophysiology of mercury poisoning and the potential impact on aging by reducing GH levels. Bio-aging formula is presented.

3. Marcus R. Recombinant human growth hormone as potential therapy for osteoporosis. Bailliere’s Clinical Endocrinology and Metabolism (July 1998) 12 (2): 251-259

Review article with the conclusion: GH enhances lumbar bone density and appears to maintain femoral density. Author suggests that IGF-1 therapy may be more effective therapy than GH. Studies reported were too short to draw that conclusion (see reference 17).

4. Strasburger CJ, Bidlingmaier M, et al. Normal values of Insulin-Like Growth Factor and Their Clinical Utility in Adults. Horm Res (2001) 55(suppl 2):100-105

Review article. Conclusions: Abnormal circulating IGF-1 levels are a suitable parameter to aid in the diagnosis of GHD or acromegaly in adults, particularly if they are below 40 years of age. A determination of accurate normative values is, however, essential to this process. Normative values are assay specific and individuals with confounding disease must be excluded from these data. IGFBP-3 levels should also be monitored in adult patients receiving GH replacement therapy. In addition to IGF-1, ALS is a useful parameter for diagnosing and monitoring acromegaly.

5. Diamandi A, Khosravi MJ, et al. Filter Paper Blood Spot Assay of Human Insulin-Like Growth Factor I (IGF-I) and IGFBinding Protein-3 and Preliminary Application in the Evaluation of Growth Hormone Status. J Clin Endocrinol Metab (1998) 83: 2296-2301

Authors developed blood spot assays for IGF-1 and IGFBP-3 and compared them to conventional methodologies. They found that dried blood spot showed a greater than 1 month stability at –20C, 4C and RT and retained more than 65% of the immunoreactivity after approximately 1 month at 37C. “We conclude that blood collected on filter paper is ideal for IGF-I and IGFBP-3 analysis and may find applications in pediatric and large scale infant screening programs.”

6. Alexander D, Appleton R, et al. Epidemiology of Acromegaly in the Newcastle Region. Clin Endocrinol (1980) 12: 71-79

Survey study showing increased mortality for acromegalic individuals. The expected cardiovascular and pulmonary complications were reported. Also, their survey showed an increase in cancer for males (expected 1.3, observed 6), but not in females (expected 2.3, observed 1). Reporting bias is a possible explanation of this unusual result.

7. Bengtsson B, Eden S, et al. Epidemiology and Long-term Survival in Acromegaly. Acta Med Scand (1988) 223: 327-35

Retrospective study of 166 acromegalic patients. Results show the expected mortality due to cardiovascular disease. The interesting finding is an increase in cancer deaths of 15/100K compared to the expected rate of 5.6/100K. The cancer deaths were mixed: ependymoma, cancinoid, melanoma, lymphoma/leukemia, breast, lung, renal, stomach, adrenal and prostate. A previous study showed an increased risk of colon cancer—none were identified in this study. The hypothesis suggested relates to the overall growth inducing effects of GH.

8. Lieman HJ, Tovaghgol E, et al. Effects of Aging and Estradiol Supplementation on GH Axis Dynamics in Women. J Clin Endocrinol Metab (2001) 86: 3918-3923

Prospective study of pre and postmenopausal women. Conclusion: “Moderate doses of transdermal estradiol supplementation do not exert a great effect on the somatotropic axis in women. Age and body composition appear to be the predominant influences on GH activity in women.”

9. Cook DM. Adult growth hormone deficiency syndrome: a personal approach to diagnosis, treatment and monitoring. Growth Horm & IGF Res (1999) 9: 129-133

Excellent review of the diagnosis and treatment of AGHD, including side effects.

10. Rudman D, Hoskote S, et al. Hyposomatomedinemia in the Nursing Home Patient. J Am Geriatr Soc (1986) 34:427-30

Prospective study demonstrating somatomedin C to be inversely correlated with age in the independent elderly; yet, statistically significantly lower levels seen in the nursing home patients was not explained by age.

11. Rudman D, Feller AG, et al. Effects of Human Growth Hormone in Men Over 60 Years Old. N Engl J Med (1990) 323:1-6

Highly quoted prospective study showing for the first time the effects of GH administration to men age 60. GH was given (0.03mg/kg three times/week) to 12 men for 6mos. Compared to the control group, the study group showed an 8.8% increase in lean body mass, a 14.4% decrease in adipose-tissue mass, a 7.1% increase in skin thickness, and a 1.6% increase in average lumbar vertebral bone density.

12. Slonim AE, Bulone L, at al. A Preliminary Study of Growth Hormone Therapy for Crohn’s Disease. N Engl J Med (2000) 342: 1633-7

A double blind placebo controlled study of 37 patients with Crohn’s disease. GH was administered in extremely high dosage (5mg/day for 1 week) then reduced to 1.5mg/day thereafter. The authors concluded: “Our preliminary study suggests that growth hormone may be a beneficial treatment for patients with Crohn’s disease.” There were very significant improvements in the disease activity index with reduction in the amount and number of medications. Additionally, there were no significant alterations in the insulin, glucose or lipid profiles in these patients.

13. Salomon F, Cuneo RC, et al. The Effects of Treatment with Recombinant Human Growth Hormone on Body Composition and Metabolism in Adults with Growth Hormone Deficiency. N Engl J Med (1989) 321: 1797-803

A double blind placebo controlled trial with 24 subjects. The study clearly showed injectable GH to improve lean body mass and reduces fat mass in AGHD patients.

14. Ho KY, Weissberger AJ, et al. The Pharmacokinetics, Safety and Endocrine Effects of Authentic Biosynthetic Human Growth Hormone in Normal Subjects.

A small (N5) and short term (5days), yet informative study using a relatively new Bio-hGH. The phamacokinetics of IGF-1, sodium and the pituitary-thyroid axis are assessed. The results as follows are consistent with other Bio-hGH products: 1) there is a sustained release of IGF-1, which did return to baseline for 10 days following cessation of hGH supplementation. 2) hGH serum levels peaked at approximately 3.3h. 3) Subjects gained approximately 1kg during study, and 4) T3 levels increased while TSH levels dropped.

15. Gotherstrom G, Svensson J, et al. A Prospective Study of 5 Years of GH Replacement Therapy in GH-Deficient Adults: Sustained Effects on Body Composition, Bone Mass, and Metabolic Indices. J Clin Endocrinol Metab (2001) 86: 4657-65

Prospective 5 yr study of 118 AGHD men and woman. The data supports the authors’ conclusions: “5yr of GH substitution in GH-deficient adults is safe and well tolerated. The effects on body composition, bone mass and metabolic indices were sustained. The effects on body composition and low density lipoprotein cholesterol were seen after 1 yr, whereas the effects on bone mass, triglycerides, and hemoglobin A1c were first observed after years of treatment.”

Also See:
HGH, What Doctors Say I
HGH, The Master Hormone of Youth
Anti-Aging: A case study!