OBJECTIVES: Although several studies have shown beneficial short-term effects of recombinant human growth hormone (rHGH) therapy in adult GH deficient (GHD) patients, few data are available on large groups of patients treated for more than one year. In addition, the optimal dose of rHGH for each patient and the baseline parameters that predict which patients will benefit most from therapy or will have adverse events are not entirely elucidated.

DESIGN: 148 adult GHD patients were enrolled in a multicentre 2-year rHGH replacement study which was placebo controlled for the first six months. rHGH (Genotropin/Genotonorm Pharmacia & Upjohn) was given in a dose of 0.25 IU/kg/week sc (1-5 IU/m2/day).

MEASUREMENTS: Every 3-6 months body composition was measured using body impedance analysis and general well being was assessed using the Nottingham Health Profile (NHP) and social self-reporting questionnaire. At the same time patients had a full clinical examination and blood was sampled for glucose, HbA1c, IGF-1, creatinine, full blood count, thyroid hormones and liver function tests.

RESULTS: With rHGH therapy IGF-1 levels increased from -2.00 + 2.60 SDS to 1.47 + 2.6 SDS after six months (P<0.001), continued to rise despite no change in dose in 1.84 + 2.8 SDS after one year and remained constant thereafter (1.98 + 2.4 after 2 years). 56% of patients ultimately attained supranormal IGF-1 levels (+2 SD), 22% had levels below the mean, of which 9% were below -2 SD. Within 3 months lean body mass (LBM) increased by +5.09% (P<0.001), total body water (TBW) by 5.40% (P<0.001), while body fat (BF) dropped by -10.89% (P<0.001) and waist circumference by -1.42% (P<0.004). These effects were maintained during the first year of therapy, but the effect was attenuated after 24 months: LBM, + 3.91% (P<0.001); TBW, +3.28%, P<0.001, BF, -6.42% (P<0.001) and waist -2.22% (P<0.009). Individual differences in response were large and could not be predicted by any of the baseline parameters, except for a better response in males. Treatment resulted in a large and progressive improvement on the NHP scale, especially energy, emotions and sleep, but a similar change was also found in patients during placebo treatment. With rHGH the number of full days of sick leave/6 months decreased from 12.17+3.90 days (SEM) to 7.15+3.50 days after six months (P=0.009), 2.93+1.55 days after 12 months (P=0.01), 0.39 + 0.17 days after 18 months (P<0.001) and 3.3 +2.51 days after 24 months (P=0.26). Similarly, the hospitalization rate went down from 14.9% to 7% after 6 months and remained at this level thereafter (P=0.12). About one third of patients on rHGH experienced fluid-related adverse events, most often within the first 3 months. They usually disappeared spontaneously or responded well to dose reduction. Cumulative dropout rates were 29% after 1 year and 38% after two years. Two thirds of these patients stopped treatment because of insufficient subjective improvement. Neither dropouts nor fluid retention could not be predicted by any of the baseline parameters.

CONCLUSIONS: We confirmed in a large group of patients the beneficial effects of rHGH therapy on body composition, metabolic parameters and general well being and found a consistent drop in number of sick days and hospitalization rate. These effects were maintained during two years of therapy, except for attenuation in body composition changes after 24 months. The high incidence of fluid-related adverse events suggests that it may be better to start with lower doses of rHGH and to increase the dose more slowly over a number of weeks. The finding of sub-optimal high or low IGF-I levels in many patients reinforces guidelines not to give rHGH in a weight-dependent dose but to titrate it individually for each patient.

OBJECTIVE: Adults with growth hormone (GH) deficiency are often osteopenic. Short-term GH replacement therapy has been shown to improve bone mineral density (BMD). However, whether the increases in BMD are progressive with time is still unclear. We therefore examined long-term changes in BMD with GH treatment in GH-deficient adults over a period of 6 years.

DESIGN: Open prospective GH therapeutic study.

PATIENTS: Twelve GH-deficient patients (four women, eight men) with a mean age of 42.5 years (range 24-61 years) at the beginning of GH replacement. Eleven patients suffered in addition from LH/FSH insufficiency, eight from TSH insufficiency and eight from ACTH insufficiency. Before the start of GH substitution, the insufficient anterior pituitary axes were fully substituted for an average of 9.8 years (range 2-22 years). Average daily GH does was 2.4 IU (SD 0.86).

MEASUREMENTS: BMD and bone area were measured at annual intervals at the lumbar spine and at the proximal femur using dual-X-ray absorptiometry.

RESULTS: Under GH substitution, serum insulin-like growth factor I concentrations increased by 140 microg/l compared to pretherapeutic values (P=0.0003). BMD at the lumbar spine increased by 0.16 g/cm2 (P=0.0005), corresponding to a mean increase of 15.9% or an increase of BMD Z-score by 1.53 SD. Increases in BMD were independently observed from years 3 to 6 by a mean of 5.8% (P=0.0087). This increase was paralleled by an increase in the area of the lumbar vertebrae. Bone area also increased at selected sites of the proximal femur, but there was no consistent increase in BMD at the proximal femur.

CONCLUSION: GH therapy in GH-deficient adults is able to progressively increase BMD and bone area at the lumbar spine over a period of at least 6 years. However, our study has several limitations, making it necessary to confirm these findings in further long-term studies.

Journal of Endocrinology
Clanget C, Seck T, Hinke V, Wuster C, Ziegler R, Pfeilschifter J
July 2001, Vol, 55 No. 1 93

ABSTRACT Aging is associated with reduced GH, IGD-1, and sex steroid axis activity and with increased abdominal fat. We employed a randomized, double-masked, placebo-controlled, noncross-over design to study the effects of 6 months of administration of GH alone (20 microg/kg BW), sex hormone alone (hormone replacement therapy in women, testosterone enanthate in men), or GH + sex hormone on total abdominal area, abdominal sc fat, and visceral fat in 110 healthy women (n=46) and men (n=64), 65-88 year old (mean, 72 year). GH administration increased IGF-1 levels in women (P=0.05) and men (P=0.0001), with the increment in IGF-1 levels being higher in men (P=0.05). Sex steroid administration increased levels of estrogen and testosterone in women and men, respectively (P= 0.05). In women, neither GH, hormone replacement therapy, nor GH + hormone replacement therapy altered total abdominal area, sc fat, or visceral fat significantly. In contrast, in men, administration of GH and GH + testosterone enanthate decreased total abdominal area by 3.9% and 3.8%, respectively, within group and vs. placebo (P=0.05). Within-group comparisons revealed that sc fat decreased by 10% (P=0.01) after GH, and by 14% (P=0.0005) after GH + testosterone enanthate. Compared with placebo, sc fat decreased by 14% (P=0.05) after GH, by 7% (P=0.05) after testosterone enanthate, and by 16% (P+0.0005) after GH + testosterone enanthate. Compared with placebo, visceral fat did not decrease significantly after administration of GH, testosterone enanthate, or GH + testosterone enanthate. These date suggest that in healthy older individuals, GH and/or sex hormone administration elicits a sexually dimorphic response on sc abdominal fat. The generally proportionate reductions we observed in sc and visceral fat, after 6 months of GH administration in healthy aged men, contrast with the disproportionate reductions of visceral fat reported after a similar period of GH treatment of nonelderly GH deficient men and women. Whether longer term administration of GH or testosterone enanthate, alone or in combination, will reduce abdominal fat distribution-related cardiovascular risk in healthy older men remains to be elucidated.

Journal of Clinical Endocrinology and Metabolism Article
Munzer T, Harman SM, Hees P, Shapiro E, Christmas C, Bellantoni MF, Stevens TE, O'Conner KG, Pabst KM, St Clair C, Sorkin JD, Blackman MR August 2001, Vol, 86 No. 8 3604

The role of insulin-like growth factor 1 (IGF-1) in prostate development is currently under thorough investigation because it has been claimed that IGF-1 is a positive predictor of prostate cancer. To assess the effect of GH and IGF-1 levels on prostate pathophysiology, 46 acromegalic (30 in active disease, ten cured from acromegaly, and six affected from GH deficiency) and 30 aged-matched male controls, free from previous or concomitant prostate disorders, underwent pituitary, androgen, and prostate hormonal assessments and transrectal ultrasonography. Compared to control values, GH (P<0.0001), IGF-1 (P<0.0001), and IGFBP-3 (P<0.001) levels were increased, whereas testosterone (P<0.0001) and dihydrotestosterone levels (P<0.0001) were reduced in active acromegalic patients. Hypogonadism was present in 28 of the 46 acromegalic patients (60.8%). The anteroposterior (P<0.05), and transverse (P<0.0001) prostate diameters and the transitional zone volume (P<0.05) were increased in acromegalic patients compared to those in controls. Prostate volume (PV) was significantly higher in untreated acromegalic patients than in controls (41.7 + 3.2 vs. 21.9 + 1.4 mL; P<0.0001), cured patients (23.6 + 1.6 mL; P<0.0001), and GH-deficient patients (17.5 + 1.1 mL; P<0.0001). In the patients, PV was correlated with disease duration (r=0.606; P<0.0001) and age (r=0.496; P<0.0001), whereas in controls it was correlated with age (r=0.476; P<0.01) and IGF-1 levels (r=-0.448; P<0.05). Benign prostate hyperplasia (PV > 30 mL) was found in 58% of the acromegalics and 26.6% of the controls. When grouped by age (<40, 40-60, and >60 yr), PV was increased in elderly patients compared to younger patients (P<0.05) and to controls (P<0.01). The prevalence of structural abnormalities, including calcifications, nodules, cysts, and vesicle inflammation, was significantly increased in patients compared to controls (78.2% vs. 23.3%; x2= 5.856; P<0.05). No clinical, transrectal ultrasonography, or cytological evidence of prostate cancer was detected in acromegalic or control subjects. In conclusion, chronic excess of GH and IGF-1 cause prostate overgrowth and further phenomena of rearrangement, but not prostate cancer.

Journal of the Clinical Endocrinology & Metabolism
AnnaMarie Colao, Paolo Marzullo, Stefano Spiezia, Diego Ferone, Assunta Giaccio, Gaetana Cerbone, Rosario Pivonello, Carolina Di Somma, and Gaetano Lombardi March 8, 1999, Vol. 84, No. 6

The long-term effects of GH replacement in adult GH-deficient (GHD) patients have not yet been clarified. We studied 21 GHD adults who originally took part in a randomized, double blind, placebo-controlled trial of GH treatment in 1987. After completion of that trial, ten patients received continuous GH replacement for the subsequent ten years, whereas 11 did not. A group of 11 age-and sex-matched normal controls were also studied in 1987 and 1997. Lean body mass, as assessed by total body potassium measurement and computed tomography scanning of the dominant thigh, increased in the GH-treated group (P< 0.01 for both) only (P< 0.05 between groups for total body potassium). Low-density lipoprotein cholesterol decreased in the GH-treated group (P < 0.05) only. Carotid intima media thickness was significantly greater (P < 0.05) in the untreated group than in the GH-treated group. Assessment of psychological well being, using the Nottingham Health Profile, revealed improvement in overall score, energy levels, and emotional reaction in the GH-treated group compared with those in the untreated group (P < 0.02). In conclusion, GH treatment for ten years in GHD adults resulted in increased lean body and muscle mass, a less atherogenic lipid profile, reduced carotid intima media thickness, and improved psychological well-being.

Journal of Clinical Endocrinology & Metabolism
J. Gibney, J.D. Wallace, T. Spinks, L. Schnorr, A. Ranicar, R.C. Cuneo S. Lockhart, K.G. Burnand, F. Salomon, P.H. Sonksen, D. Russell-Jones August, 1999, Vol. 84(8)

Acquired growth hormone (GH) deficiency results from the destruction of normal pituitary and/or hypothalamic tissue, usually from a tumor or secondary to surgical and/or radiation therapy. Diagnostic criteria and clinical sequelae of GH deficiency, although well established in children, are currently areas of active investigation in the adult. It is now apparent that acquired GH deficiency is associated with significant changes in body composition, bone density, lipid metabolism, cardiovascular function and physical performance. In addition, new information is now available on the use of low doses of recombinant human growth hormone (rHGH) to reverse the sequelae of GH deficiency in adults.

The Growth Hormone Deficiency Syndrome
Acquired GH deficiency is characterized by weight gain, increased fat mass and decreased lean body mass. In one recent study, total body fat was shown to be increased by 7% in this population while lean body mass was decreased to a similar degree (1). The increased fat mass is found in a truncal distribution, thereby increasing the waist: hip ratio. In addition, triglyceride levels are increased and HDL levels decreased. The increased lipid levels may explain, in part, the observation of increased vascular wall thickness, as measured by carotid ultrasonography, in this population. These factors all likely contribute to the increased incidence of cardiovascular mortality seen in patients with GH deficiency (2).

Muscle mass and muscle strength are diminished in GH-deficient patients. In the heart, these changes are manifested by a reduced left ventricular mass, decreased fractional shortening of cardiac myocytes, and decreased cardiac output. Such abnormalities may contribute to the striking decline in exercise capacity in this population. In one recent study, exercise capacity, as assessed by cycle ergometry was decreased by 20-25% compared to normal controls (3). Bone density is also known to be reduced in the GH-deficient patient. In a recent study, cortical bone density and spinal (trabecular) bone density were 2.8 and 1.5 standard deviations below the mean for age and sex matched controls (4).

Finally, patients with GH deficiency appear to have impaired psychological well being and potentially significant neuropsychiatric manifestations, such as lack of concentration and memory impairment. Self-rating questionnaires consistently demonstrate reduced vitality, fatigue, social isolation and depression (5). However, it is unknown whether this impairment in psychological well-being is associated specifically with GH deficiency or is due to another factor associated with hypopituitarism.

Recombinant Human Growth Hormone Therapy
Recombinant human growth hormone may become a novel therapeutic option for adults with acquired GH deficiency. Recent studies indicate that many of the metabolic and psychological abnormalities associated with GH deficiency can be reversed with GH replacement, even at low doses, which are not associated with side effects.

Body Composition
GH therapy results in profound changes in body composition: fat mass is reduced while lean body mass increases. Growth hormone, at the relatively low dose of 0.003 mg/kg was shown to normalize lean body mass over 6 months in 24 adults with GH deficiency (1). The improvement in lean body mass is associated with increased protein synthesis, muscle mass and muscle function. Total body fat mass also decreases after 6 months of GH administration. The decline in fat mass is most significant in visceral and trunk locations as compared to the arms, neck and legs, suggesting that GH replacement therapy will reverse the truncal redistribution of fat mass associated with GH deficiency and impact on cardiovascular risk (6).

Lipid Metabolism
GH replacement in adults may have a beneficial effect on lipids. In a recent study, it was reported that short courses of GH reduced LDL cholesterol and this reduction correlated with increased mRNA expression of the LDL receptor in the liver (7). The potential benefit of this interaction has yet to be investigated in longer term clinical trials, but it must be noted that dramatic changes in serum lipid levels are not consistently seen with GH administration.

Bone Density
The potential role of GH in the maintenance of the skeleton has recently been investigated. GH is known to stimulate osteoblast proliferation and thymidine incorporation in vitro. Furthermore, GH stimulates systemic and local production of Insulin Like Growth Factor I, another known bone mitogen. In a recent study, GH replacement was shown to increase significantly bone Gla-protein, a sensitive indicator of osteoblast function (8). Less consistent changes in bone density have been demonstrated with GH administration. However, in a recent study using the sensitive techniques of quantitative tomography and single photon absorptiometry, significant increases of 5% and 4% were demonstrated in spinal and cortical bone density over 12 months of therapy in GH-deficient adults (4). It thus appears that GH administration may act to reverse the osteopenia present in the GH-deficient patient.

Cardiovascular Function
Improvements in exercise capacity and cardiac function have been demonstrated among GH-deficient patients receiving GH replacement in several recent studies. Such patients show increased oxygen uptake and power output during cycle ergometry associated with increased skeletal muscle mass and improved cardiac function. Echocardiography has shown that left ventricular mass index, fractional shortening and fiber shortening velocity all improve after 6 months of low dose GH therapy (8).

Side Effects Associated with Low-Dose GH Replacement
The dose of rHGH is an important consideration in the therapy of acquired GH-deficiency. Large, pharmacological doses of GH are often associated with the clinical sequelae of GH excess, including fluid retention and hypertension. However, increasingly smaller, physiological, doses of rHGH are currently being used for replacement in GH- deficient patients without such sequelae. At a dose of 0.03 mg/kg/week, Bengtsson et al. demonstrated only minor side effects including fluid retention and mild arthralgias in the majority of patients but did report carpal tunnel syndrome in one patient (6). In all cases, further reduction of the GH dosage resulted in amelioration of side effects. In another recent study in which a smaller dose of GH was used, 0.01 mg/kg was administered three times per week without any reported side effects (8). It remains unknown, however, whether chronic administration of GH at doses which keep IGF-I levels within the normal range will also improve key metabolic variables.

Future Directions
Growth hormone deficiency is an important cause of excess morbidity and even mortality. Evidence from a number of smaller studies indicates that GH replacement will improve body composition, lipid metabolism, bone density, cardiovascular function and psychological well being. Important issues remaining are the precise clinical definition of partial vs. complete GH deficiency in such patients and clarifying the best tests to make this diagnosis. In addition, it is unclear whether some of the observed beneficial effects reflect pharmacological GH therapy rather than physiologic GH replacement. Nevertheless, it is apparent that small doses, unassociated with sequelae of GH excess, may suffice to achieve the desired metabolic results. Definitive recommendations on dosage and the long term effects of GH therapy, particularly on cardiovascular morbidity and mortality, will be determined by the prospective studies now underway at the MGH and other centers around the country.

References:
1. Salomon F, Cuneo RC, Hesp R et al. The Effects of Treatment with Recombinant Human Growth Hormone on Body Composition and Metabolism in Adults with Growth Hormone Deficiency. New England Journal of Medicine 1989;321:1797-1803.
2. Bengtsson BA. The Consequences of Growth Hormone Deficiency in Adults. Acta Endocrinologica 1993;128 (Suppl 2):2-5.
3. Cuneo RC, Salomon F, Wiles CM et al. Growth Hormone Treatment in Growth Hormone Deficient Adults. II. Effects on Exercise Performance. Journal of Applied Physiology 1991;70:695-700.
4. O'Halloran DJ, Tsatsoulis A, Whitehouse RW et al. Increased Bone Density after Recombinant Human Growth Hormone (GH) Therapy in Adults with Isolated GH Deficiency. Journal of Clinical Endocrinology and Metabolism 1993;76:1344-1348.
5. McGauley GA, Cuneo RC, Salomon F et al. Psychological Well-Being Before and After Growth Hormone Treatment in Adults with Growth Hormone Deficiency. Hormone Research 1990;33 (suppl 4):52-54.
6. Bengtsson BA, Eden S, Lonn L et al. Treatment of Adults with Growth Hormone (GH) Deficiency with Recombinant Human GH. Journal of Clinical Endocrinology and Metabolism 1993;76;309-317.
7. Johnston DG, Bengtsson BA. Workshop Report: the Effects of Growth Hormone and Growth Hormone Deficiency on Lipids and the Cardiovascular System. Acta Endocrinologica 1993;128 (Suppl 2): 69-70.
8. Amato G, Carella C, Fazio S et al. Body Composition, Bone Metabolism, and Heart Structure and Function in Growth Hormone (GH)-Deficient Adults Before and After GH Replacement Therapy at Low Doses. Journal of Clinical Endocrinology and Metabolism 1993;77:1671-1676.

A better solution
Many women experience significant changes in their health before, during and after menopause. Many of these health problems are associated with hormone imbalances that can be overcome with natural therapies or HRT (hormone replacement therapy)- whether it be using traditional or bio-identical hormones. Hormones are powerful chemical messengers that circulate throughout the bloodstream to specific target cells where they generate biological responses. The interdependent relationship between adrenal function and sex hormones has a profound effect on many organ systems. Women have traditionally used “synthetic” estrogens and progestins (traditional HRT) to protect against osteoporosis and heart disease. These “synthetic” hormones offer some protection against heart disease and osteoporosis but have many unwanted side effects. Because of these side effects many women abandon traditional HRT very soon after starting. This has led to a strong interest in the use of bio-identical hormone replacement therapy (BHRT).

What are Bio-Identical Hormones?
Bio-identical (BHRT) hormones are derived from natural plant sources to produce molecules which are physiologically identical to hormones made in the human body. Bio-identical hormones are chemically processed from precursors found in yams or soy plants, yet they are identical to the hormones produced by the human body.

Hence the term “bio-identical plant-derived hormone.” These hormones are able to follow normal metabolic pathways so that essential active metabolites are formed in response to hormone replacement therapy.
Synthetic hormones are chemically altered and are not identical in structure or activity to the naturally occurring hormones in the body.

No two women are alike, of course, and the value of bio-identical hormone replacement therapy is that it can be adapted to fit your individual body and hormone levels. In fact, hormones can be made in a variety of strengths and dosage forms including capsules, topical creams and gels,
suppositories and sublingual troches or lozenges. With the help of your doctor and a compounding pharmacist, a woman can start and maintain a bio-identical hormone replacement regimen that closely mimics what her body has been doing naturally for years.

BHRT includes estrogens (estrone, estradiol & estriol), progesterone, testosterone, DHEA and pregnenolone (and many metabolites).

Benefits of BHRT include:

1. fewer side effects compared with traditional HRT
2. protection against heart disease
3. reduced risk of breast cancer , and
4. improved lipid profile.

Hormone related symptoms or problems occur throughout the feminine life cycle:

Goals of Natural HRT
Alleviate the symptoms caused by the natural decrease in production of hormones by the body.

• Give the protective benefits which were originally provided by naturally occurring hormones.
• Re-establish a hormonal balance.
  
  The three types of hormones typically prescribed for natural hormone replacement therapy (HRT) are estrogens, progesterone and androgens.
  The precise components of each woman’s therapy need to be determined after physical examination, medical history,
  and laboratory testing are considered. Close monitoring is essential to ensure that appropriate dosage adjustments are made.

“Natural Hormones” are used to correct hormone imbalance during each cycle of human life. This imbalance can be established by blood or saliva testing and treated with
(a) Traditional HRT., e.g., oral contraceptives or HRT,
(b) NHRT (using bio-identical hormones) or
(c) natural therapies, e.g., herbals or homoeopathics.

Lisa Everett (Int. Jnl. Of P’ceutical Compounding Vol 2 No 1 ’98) confirms a few essential truths about HRT. Seeking the meaning of life is a worthwhile endeavour. As the axiom goes…. ‘anything worthwhile does not come easily’…and so it is that our journey through hormone imbalance remains a task.

• The first rule is that there is no simple answer to HRT;
• Each patient is a unique individual….thus standardising a drug or dose has potential for harm;
• Hormone imbalances cannot be treated with hormones alone. Educating the patient on hormones (be it synthetic or “natural”), diet, nutrition, lifestyle & spirit are all of paramount importance.

Where do I go for help?
Your doctor will assess your current hormone status by either a blood , saliva test, or a questionnaire. If your doctor is not familiar with this treatment, ask them to call us for further information.

After determining the level of hormonal imbalance, the doctor can prescribe natural hormones

• in various combinations, e.g., progesterone cream, triest & progesterone troches,
• in various dosage forms, e.g., cream, troche/lozenge, capsule, pessary, gel or oil.
Where more than one hormone is deficient, they can be incorporated into one dosage form, e.g., DHEA & testosterone troche. In effect, the doctor prescribes a complete NHRT supplement tailored for the individual patient in a dosage form suitable for that patient.

Which dosage form do I use?
Your doctor will prescribe the most appropriate dosage form for you. The types of dosage forms available include:

Transdermal Cream
Hormones are compounded in a cream or gel to be applied to hormone sensitive areas on the skin for absorption via adipose tissue. The areas for application are breasts, tummy, inner part of the arms or legs. This allows the hormone to reach the target tissue (similar to hormone patches) avoiding rapid breakdown by the liver allowing a much lower strength to be used. It is a good idea to apply the cream on various areas of the skin, or rotate daily to avoid overload of the receptor sites. Please ensure that the hands are washed before and after application.

Troches
Troches are sublingual lozenges made to dissolve in the mouth and absorbed by the salivary mucus, avoiding first pass liver metabolism. Troches are probably the most favorable dosage form particularly if more than one hormone is deficient.

Place your recommended dosage ( a whole or half troche ) between gum & cheek or under the tongue to allow for slow absorption via the saliva so that the active hormone will be absorbed straight into the blood stream. Avoid sucking the troche quickly as you would want maximum absorption into your body.

Capsules
Capsules are a convenient method of administration. Natural hormones are micronised and can be compounded with slow release ingredients to prevent rapid liver metabolism.

Pessaries
Pessaries are useful where high doses of hormone are required intra-vaginally for a short duration e.g. triest pessaries for dry vagina. Take the pessary or suppository (for rectal use) out of the wrapping before insertion with your finger. The best time to use a pessary or supposi-tory is whilst lying down.

As every woman is unique, our approach is for the patient, pharmacist, and doctor to work together to customise hormone replacement therapy.

What is compounding?
Compounding is the preparation of medicine by a pharmacist for an individual patient according to a doctor’s prescription. The practice predates the manufacture by mass production of drugs.

In every field of medicine, there are some patients who don’t respond to traditional methods of treatment.

Sometimes they need medicine at strengths that are not manufactured by drug companies. Sometimes they simply need a different method of ingesting a medication.

Ask your doctor or pharmacist today about customised compounding, tailoring your hormone needs for you.

Most compounding medicine can be covered by your private medical insurance, depending on the type of cover you have.

“By studying the organic patterns of heaven and earth a fool can become a sage. So by watching the times and seasons of natural phenomena, we can become true philosophers” ( Li Chu’uan 735 A.D.)

SOURCE/REFERENCE:International Jnl of Pharmaceutical Compounding;

“What Your Doctor May Not Tell You About Menopause”
by John R. Lee M.D .

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