Longterm use of FEMARA (LETROZOLE)

Without having all the details as why or what you're doing with this type of drug regimen, your main concern should be to keep estrogen levels within a normal range.

Lowering Oestrogen will not increase fat loss.

lipids, and extremely low estrogen (which causes I wide variety of serious problems). Very bad idea IMO.

It should be common knowledge that messing with your lipid profile too much for too long will cause pretty serious problems. I think a lot of the more serious users (abusers) run into problems not because of just the AAS abuse but the AI abuse. People tend to forgot these can be just as harmful as the AAS themselves.

I'm having a hard time reading post with Governor's avatar.

Posted by: Alpine

It should be common knowledge that messing with your lipid profile too much for too long will cause pretty serious problems. I think a lot of the more serious users (abusers) run into problems not because of just the AAS abuse but the AI abuse. People tend to forgot these can be just as harmful as the AAS themselves.

I agree. One guy on elite had some very, very serious problems with running dex for long periods and at high doses. I believe he was in the hospital for a while, and had a heart attack or something, which they attibuted directly to his use of AI for such long periods. Make a thread on elite, im sure he will post and tell you his story, or you can search if you are plat.

Posted by: bigtee

I'm having a hard time reading post with Governor's avatar.

letrozole supposedly does not effect your lipid profile.

Posted by: Gino_ny2az

letrozole supposedly does not effect your lipid profile.

Any drug that is going to lower the amount of estrogen in your system is going to have hazardous effects on the your lipid profile.

Posted by: Gino_ny2az

letrozole supposedly does not effect your lipid profile.

Effect of letrozole on the lipid profile in postmenopausal women with breast cancer.

Elisaf MS, Bairaktari ET, Nicolaides C, Kakaidi B, Tzallas CS, Katsaraki A, Pavlidis NA.

Department of Internal Medicine, Medical School, University of Ioannina, GR 451 10 Ioannina, Greece.

Hormonal therapy plays a central role in the overall treatment of breast cancer. Aromatase inhibitors can inhibit the aromatase enzyme system resulting in a reduction of oestrogens. letrozole is a non-steroidal aromatase inhibitor that effectively blocks aromatase activity without interfering with adrenal steroid biosynthesis. The drug can significantly reduce the levels of plasma oestrogens, which remain suppressed throughout the treatment. Data are scarce concerning the influence of these drugs on serum lipid levels. In the present study, we evaluated the effects of letrozole on the serum lipid profile in postmenopausal women with breast cancer. A total of 20 patients with breast cancer were treated with letrozole, 2.5 mg once daily. After an overnight fast, serum lipid parameters (total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides, apolipoproteins A1, B and E and lipoprotein (a)) were measured before treatment and at 8 and 16 weeks afterwards. A significant increase in total cholesterol (P=0.05), LDL cholesterol (P<0.01) and apolipoprotein B levels (P=0.05) in the serum, as well as in the atherogenic risk ratios total cholesterol/HDL cholesterol (P<0.005) and LDL cholesterol/HDL cholesterol (P<0.005) was noticed after letrozole treatment. We conclude that letrozole administration in postmenopausal women with breast cancer has an unfavourable effect on the serum lipid profile.

aromasin could be a safer choice but in my opinion it is not a good idea to use AI for an extensive period because the important role of estrogens, even in male. AI must only be used to keep them in the normal range in heavy testosterone's cycles. For smaller cycles, oral formestane (250 to 500mg ED) could be another option with less risks to crash too much estrogen levels.
Remember that estrogens are important in brain, bone, for lipid metabolism ... they are also expected to play a role in androgenic receptors synthesis.

Posted by: ready2explode

Any drug that is going to lower the amount of estrogen in your system is going to have hazardous effects on the your lipid profile.

Not if you have high supraphysiological amounts of test, and actually not in most males in general. Also, keep in mind that studies on post menopausal women do not necessarily apply to bodybuilders using steroids. If you are using high amounts of testosterone, letrozole is a better choice,and actually even without using exogenous test it may offer lowered LDL levels and higher insulin sensitivity. You can't take these figures of 98% suppression in PM women and apply them to steroid users! We had a long discussion on cholesterol levels and aromatase inhibitors here awhile ago. Someone should find the link.

Look at this study done on boys with GH deficiency with anastrozole. There was no use of exogenous test in this study and lipid profiles remained unchanged:

J Pediatr Endocrinol Metab. 2004 Dec;17(12):1597-606. Related Articles, Links

An open label 12-month pilot trial on the effects of the aromatase inhibitor Anastrozole in growth hormone (GH)-treated GH deficient adolescent boys.

Mauras N, Welch S, Rini A, Klein KO.

Nemours Children's Clinics in Jacksonville, FL, USA. [email protected]

OBJECTIVE: To investigate whether 12 mo treatment with the aromatase inhibitor anastrozole can achieve sustained suppression of estrogen production and delay epiphyseal fusion in growth hormone deficient (GHD) adolescent males. STUDY DESIGN: 20 adolescents with GHD were recruited (mean age +/- SE: 14.7 +/- 0.5 yr). Ten continued on GH (control group), and 10 on GH and anastrozole (Rx group) for 12 mo. RESULTS: After 12 mo E2 concentrations declined 60% in the Rx group (from 1.8 +/- 0.5 to 0.7 +/- 0.3 pg/ml, p <0.05) whereas they increased in controls (from 1.2 +/- 0.7 to 1.8 +/- 0.7, p <0.05). Testosterone increased 117% in the Rx group (from 304 +/- 31 to 626 +/- 64 ng/dl), 47% in controls (from 274 +/- 89 to 398 +/- 51) (p = 0.03, ANOVA between groups). IGF-I increased 42% in controls (454 +/- 22 to 711 +/- 109 ng/ml, p <0.05), but remained invariant in the Rx group (446 +/- 29 to 540 +/- 80, p = NS). Bone markers, plasma lipids, insulin, glucose, and liver function tests were all unchanged between groups with no differences either in body composition or bone mineral density accrual. There were no differences in growth velocity, height SDS, bone age advancement, predicted adult height or testicular volumes between groups after 12 mo. CONCLUSIONS: Anastrozole treatment potently decreases estrogen concentrations in adolescent males with GHD while allowing normal virilization, without deleterious effects on body composition, plasma lipids, bone metabolism or the tempo of puberty. Twelve months of treatment, however, did not increase predicted adult height. Further studies are needed to ascertain whether more prolonged estrogen blockade is helpful in the treatment of growth retardation in puberty.

and with letrozole:

J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):345-56. Related Articles, Links
Click here to read
Novel treatment of short stature with aromatase inhibitors.

Dunkel L, Wickman S.

Hospital for Children and Adolescents, University of Helsinki, PO Box 281, Helsinki 00029 HUS, Finland. [email protected]

Estrogens have an essential role in the regulation of bone maturation and importantly in the closure of growth plates in both sexes. This prospective, randomized, placebo-controlled study was undertaken to evaluate whether suppression of estrogen synthesis in pubertal boys delays bone maturation and ultimately results in increased adult height. A total of 23 boys with constitutional delay of puberty (CDP) received a conventional, low-dose testosterone treatment for inducing progression of puberty. Eleven of these 23 boys were randomized to receive a specific and potent P450-aromatase inhibitor, letrozole, for suppression of estrogen action, and 12 boys were randomized to receive placebo. Estradiol concentrations in the letrozole-treated boys remained at the pretreatment level during the administration of letrozole, whereas the concentrations increased during the treatment with testosterone alone and during spontaneous progression of puberty. Testosterone concentrations increased in all groups, but during the letrozole treatment, the increase was more than fivefold higher than in the group treated with testosterone alone. The inhibition of estrogen synthesis delayed bone maturation. The slower bone maturation in the boys treated with testosterone and letrozole, despite higher androgen concentrations, than in the boys treated with testosterone indicate that estrogens are more important than androgens in regulation of bone maturation in pubertal boys. During the 18 months follow-up, an increase of 5.1 cm in predicted adult height was observed in the boys who received testosterone and letrozole, but no change was seen in the boys who received testosterone alone or in the untreated boys. This finding indicates that an increase in adult height can be attained in growing adolescent boys by inhibiting of estrogen action.

And the coup de grace:

Eur J Endocrinol. 2002 Mar;146(3):339-46. Related Articles, Links
Click here to read
The role of sex steroids in the regulation of insulin sensitivity and serum lipid concentrations during male puberty: a prospective study with a P450-aromatase inhibitor.

Wickman S, Saukkonen T, Dunkel L.

Hospital for Children and Adolescents, University of Helsinki, PL281, FIN-00029 HUS, Helsinki, Finland. [email protected]

OBJECTIVE: Our purpose was to study the sex steroid-mediated changes in serum insulin and lipid concentrations in boys during puberty. DESIGN AND METHODS: We treated boys with constitutional delay of puberty either with testosterone plus placebo or with testosterone plus an aromatase inhibitor, letrozole, which inhibits the conversion of androgens to oestrogens. We demonstrated previously that during treatment with testosterone plus letrozole the increase in testosterone concentration was more than 5-fold higher than during treatment with testosterone plus placebo. The concentrations of 17beta-oestradiol, IGF-I and IGF-binding protein-3 increased during testosterone-plus-placebo treatment, but during testosterone-plus-letrozole treatment the concentrations remained unchanged. These divergent changes in the two groups enabled us to study the effects of sex steroids and GH on insulin sensitivity and lipid concentrations. RESULTS: The insulin concentration in the testosterone-plus-placebo-treated group did not change. In contrast, in the testosterone-plus-letrozole-treated group, the concentration decreased during letrozole treatment, indicating improved insulin sensitivity. Changes in insulin and IGF-I concentrations within 12 and 18 months were correlated. In the testosterone-plus-placebo-treated group, the high-density lipoprotein cholesterol concentration did not change but in the testosterone-plus-letrozole-treated group the concentration decreased. The concentrations of low-density lipoprotein cholesterol (LDL-cholesterol) and triglycerides did not change in either of the groups. CONCLUSIONS: The findings indicate that androgens do not directly alter insulin sensitivity in boys during puberty. In contrast, the observations suggest tight regulation of glucose--insulin homeostasis by GH in boys at this stage. Furthermore, our findings indicate that sex steroids do not significantly participate in the regulation of serum concentrations of LDL-cholesterol or triglycerides in boys during early and mid-puberty.

There you have it: no exogenous test, but LDL remained unchanged with letrozole in boys. Anastrozole appeared to have no effect on lipids in the previous study I posted.