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Part 3 - Hormone Replacement Therapy

This page contains educational resources for hormone replacement therapy. 


Additional Resources for Hormone Replacement Therapy

This page contains treatments details specific to hormone replacement therapy at Peach. This page is not meant to diagnose or recommend. If you have any questions, please contact us at one our facilities. 

Beneficial effects of long-term GH replacement therapy on quality of life in adults with GH deficiency.

Objective: Quality of life tends to be adversely affected in adults with GH deficiency. The aim of this study was to examine changes in quality of life in a large group of GH-deficient adults receiving long-term GH replacement therapy.

Design: The study was conducted in two stages. The first stage was a prospective, open trial of GH replacement therapy in 71 GH-deficient adults, during which GH was administered for 20-50 months. For the second stage, a further 90 patients were recruited to create a population of 161 GH-deficient adults, all of whom had received GH replacement therapy for more than 12 months. This population was investigated retrospectively, using a questionnaire designed specifically for this study.

Patients: All patients were GH deficient and showed a peak GH response of less than 3.0 micrograms/l during an insulin tolerance test in which blood glucose levels dropped to 2.2 mmol/l or below.

Measurements: The quality of life of patients in the prospective stage was assessed using the Nottingham Health Profile (NHP) parts I and II, and the Psychological General Well-Being (PGWB) index. In the retrospective study patients completed a specially developed questionnaire, designed to determine whether changes in quality of life were sudden or gradual, and whether quality of life continued to change after GH had been administered for more than 12 months.

Results: In the prospective stage, mean overall score on the NHP I improved significantly during the first 6 months of GH therapy, and remained at its new level thereafter. Scores in all areas of the NHP II improved significantly between baseline and 20-50 months, as did the total score and five of six area scores on the PGWB index. The total PGWB score and three area scores improved significantly between 6 or 12 months and 20-50 months. In the retrospective stage, 92.7% of the patients reported that they had experienced positive effects of GH therapy. In 30.3% of patients, however, such effects did not become apparent until GH had been administered for more than 6 months. Almost 60% of patients felt that their condition was still improving.

Conclusions: These results indicate that the previously reported beneficial effects of GH therapy on quality of life in GH-deficient adults are sustained during long-term therapy. In addition, they suggest that, once started, GH therapy should be continued for at least 6 months before judgements are made regarding its efficacy in improving quality of life.

Wiren, L., Bengtsson, B., & Johannsson, G. (1998). Beneficial effects of long-term GH replacement therapy on quality of life in adults with GH deficiency. Clinical Endocrinology, 48(5), 613-620. doi:10.1046/j.1365-2265.1998.00462.x

Direct effects of sex steroid hormones on adipose tissues and obesity.

Sex steroid hormones are involved in the metabolism, accumulation and distribution of adipose tissues. It is now known that oestrogen receptor, progesterone receptor and androgen receptor exist in adipose tissues, so their actions could be direct. Sex steroid hormones carry out their function in adipose tissues by both genomic and nongenomic mechanisms. In the genomic mechanism, the sex steroid hormone binds to its receptor and the steroid-receptor complex regulates the transcription of given genes. Leptin and lipoprotein lipase are two key proteins in adipose tissues that are regulated by transcriptional control with sex steroid hormones. In the nongenomic mechanism, the sex steroid hormone binds to its receptor in the plasma membrane, and second messengers are formed. This involves both the cAMP cascade and the phosphoinositide cascade. Activation of the cAMP cascade by sex steroid hormones would activate hormone-sensitive lipase leading to lipolysis in adipose tissues. In the phosphoinositide cascade, diacylglycerol and inositol 1,4,5-trisphosphate are formed as second messengers ultimately causing the activation of protein kinase C. Their activation appears to be involved in the control of preadipocyte proliferation and differentiation. In the presence of sex steroid hormones, a normal distribution of body fat exists, but with a decrease in sex steroid hormones, as occurs with ageing or gonadectomy, there is a tendency to increase central obesity, a major risk for cardiovascular disease, type 2 diabetes and certain cancers. Because sex steroid hormones regulate the amount and distribution of adipose tissues, they or adipose tissue-specific selective receptor modulators might be used to ameliorate obesity. In fact, hormone replacement therapy in postmenopausal women and testosterone replacement therapy in older men appear to reduce the degree of central obesity. However, these therapies have numerous side effects limiting their use, and selective receptor modulators of sex steroid hormones are needed that are more specific for adipose tissues with fewer side effects

Mayes, J. S., & Watson, G. H. (2004). Direct effects of sex steroid hormones on adipose tissues and obesity. Obesity Reviews, 5(4), 197-216. doi:10.1111/j.1467-789x.2004.00152.x

OHSU Researchers Uncover Cause, Possible Treatment For Abdominal Fat In Postmenopausal Women

  • Researchers determined that the drop in estrogen levels commonly associated with menopause is likely linked to an increase in cortisol. 
  • There untrested women with higher cortisol levels also witnessed an increase in abdominal fat when compared with women receiving the therapy. 
  • Findings suggest that estrogen replacement protects women from developing high cortisol levels and increased abdominal fat. 
  • We believe that by preventing the rise in cortisol, we can delay or prevent weight issues and the many weight associated disorder in these women 
  • After one month of therapy these women who previously had elevated levels of cortisol experienced a decrease in cortisol levels close to that of premenopausal women. 

(n.d.). Retrieved February 12, 2017, from

Effect of DHEA on abdominal fat and insulin action in elderly women and men: a randomized controlled trial.

Context: Dehydroepiandrosterone (DHEA) administration has been shown to reduce accumulation of abdominal visceral fat and protect against insulin resistance in laboratory animals, but it is not known whether DHEA decreases abdominal obesity in humans. DHEA is widely available as a dietary supplement without a prescription.

Objective: To determine whether DHEA replacement therapy decreases abdominal fat and improves insulin action in elderly persons.

Design and setting: Randomized, double-blind, placebo-controlled trial conducted in a US university-based research center from June 2001 to February 2004.

Participants: Fifty-six elderly persons (28 women and 28 men aged 71 [range, 65-78] years) with age-related decrease in DHEA level.

Intervention:  Participants were randomly assigned to receive 50 mg/d of DHEA or matching placebo for 6 months.

Main outcome measures:  The primary outcome measures were 6-month change in visceral and subcutaneous abdominal fat measured by magnetic resonance imaging and glucose and insulin responses to an oral glucose tolerance test (OGTT).

Results:  Of the 56 men and women enrolled, 52 underwent follow-up evaluations. Compliance with the intervention was 97% in the DHEA group and 95% in the placebo group. Based on intention-to-treat analyses, DHEA therapy compared with placebo induced significant decreases in visceral fat area (-13 cm2 vs +3 cm2, respectively; P = .001) and subcutaneous fat (-13 cm2 vs +2 cm2, P = .003). The insulin area under the curve (AUC) during the OGTT was significantly reduced after 6 months of DHEA therapy compared with placebo (-1119 muU/mL per 2 hours vs +818 muU/mL per 2 hours, P = .007). Despite the lower insulin levels, the glucose AUC was unchanged, resulting in a significant increase in an insulin sensitivity index in response to DHEA compared with placebo (+1.4 vs -0.7, P = .005).

Conclusion: DHEA replacement could play a role in prevention and treatment of the metabolic syndrome associated with abdominal obesity.

Villareal, D. T., & Holloszy, J. O. (2004). Effect of DHEA on Abdominal Fat and Insulin Action in Elderly Women and Men. Jama, 292(18), 2243. doi:10.1001/jama.292.18.2243