I hear ya Wilson6. There is now good evidence that long term tamoxifen treatment causes and increase in female fat:
Body composition measurements using DXA and other techniques in tamoxifen-treated patients.
Ali PA, al-Ghorabie FH, Evans CJ, el-Sharkawi AM, Hancock DA.
Department of Medical Physics and Radiotherapy, Singleton Hospital, Swansea, U.K.
Tamoxifen is an anti-oestrogenic drug which is widely used in the treatment of patients with breast cancer. There is increasing interest in using the drug both for benign breast disease and as a chemo-preventative agent of the drug in women at high risk of breast cancer. Despite the fact that the acute side-effects of the drug are few, its agonistic and antagonistic oestrogenic effects are not fully known and may have some undesirable effects for patients treated with the drug for several years. A number of studies carried out recently indicate a varying degree of change in bone mineral content following treatment with tamoxifen. These studies concentrated mainly on bone mineral density measurements only and non of them reported the effects of tamoxifen on lean body mass and fat mass. In this study we measured lean body mass and fat mass in tamoxifen-treated females and a comparison group to determine the difference between the two groups. Twenty-six women receiving tamoxifen (20 mg/d) have participated in this study. The control group comprised 31 healthy women of a similar age. Total body bone mineral (TBBM) was measured using a dual-energy X-ray absorptiometry (DXA) (Hologic INV., Waltham, U.S.A.). Similarly, regional and total body soft tissue (lean and fat tissue) were measured using the DXA system. In addition to DXA measurements, percentage body fat (%BF) was measured using total body potassium counting (TBK), skinfold anthropometry (SF), infrared interactance (i.r.) and bioelectric impedance analysis (BIA). Results from DXA alone showed that there were no significant differences between the two groups for TBBM, regional and total body lean tissue mass. However, there was a significant difference between the two groups (P < 0.05) for %BF measurement. Similarly there was a significant difference between the two groups (P < 0.05) for %BF measured by other body composition techniques. Although there is no other research reported on the effects of tamoxifen on %BF, this retrospective study indicates that tamoxifen may lead to increase in fat content in women who are subjected to this treatment. We conclude that this observation is probably related to the agonistic oestrogenic effect of Tamoxifen on body fat. To our knowledge this deleterious effect has not been reported before and it should be taken into consideration when comprising different types of anti-oestrogenic drugs. Furthermore, patients should be warned about this side-effect when they are prescribed Tamoxifen.
And on the GH front, there is evidence that GH reduces adipose lipoprotein lipase activity (LPL), and may marginally increase hormone sensitive lipase, but there is a paucity of evidence showing that this translates into increased fat loss: Again we have a case where the biochemistry seems plausible but the real world results just don't pan out:
Regulation of lipoprotein lipase and hormone-sensitive lipase activity and gene expression in adipose and muscle tissue by growth hormone treatment during weight loss in obese patients.
Richelsen B, Pedersen SB, Kristensen K, Borglum JD, Norrelund H, Christiansen JS, Jorgensen JO.
Department of Endocrinology and Metabolism C, Aarhus Amtssygehus, Aarhus University Hospital, Denmark.
We investigated the effect of weight loss together with GH treatment on the activity and gene expression of LPL and hormone-sensitive lipase (HSL) in AT and muscle tissue. A very-low-calorie diet ([VLCD] 740 kcal/d) was given to 18 obese women (body mass index [BMI] > 35 kg/m2) and half of them were treated with GH (0.04 IU/kg) for 4 weeks in a randomized double-blind placebo-controlled study. Subcutaneous fat and muscle biopsies were taken before and after 4 weeks. Weight loss after 4 weeks was similar in the 2 groups, with a reduction of 4.5% (placebo) and 4.6% (GH) and a reduction of FM by 7.4% and 9.0% ([NS] nonsignificant). The weight loss resulted in a small and NS reduction of AT-LPL activity by 20% +/- 12% in the placebo group, but in the GH group, AT-LPL was significantly reduced by 65% +/- 8% (P < .01). Muscle LPL (M-LPL) activity was not affected by the weight loss alone, but a significant reduction was observed in the GH group (20.4% +/- 10%, P < .05). AT-HSL activity was significantly enhanced after weight loss, but GH had no additional effect on this minor increment. This is in accordance with the finding that the increment in free fatty acid (FFA) after weight loss was similar in the 2 groups. GH treatment was associated with a significant reduction of high-density lipoprotein (HDL) cholesterol (P < .05). In conclusion, GH significantly inhibited AT-LPL activity but had no additional effect on the hypocaloric-induced loss of FM, indicating that under such circumstances, AT-LPL does not directly regulate adipose tissue mass. GH was not found to have opposite effects on the activity of LPL in adipose tissue and muscle, since GH treatment reduced them both (by 65% and 20%, respectively). The VLCD-induced weight loss was associated with a minor enhanced activity of AT-HSL with no independent effect of GH. Thus, concerning body weight, FM, and lipolytic activity, treatment with GH offers no extra benefits during a VLCD for 4 weeks.
Let's just say this whole area of supplementation is still very controversial. I mean, for instance, tamoxifen also decreases LPL activity but leads to an overall INCREASE in fat mass in some women.
One thing to keep in mind with all of this science (and pseudo-science) is that obese and post menopausal women may not respond the same as young, very lean weight training females.