40butpumpin said:
I thought what was detrimental to the lipid profile was the reduction or near elimination of Estrogen. If what the doc says is true then this is obviously incorrect because Aromasin is even more effective than Arimidex at lowering E. There must be something else going on here that has yet to be explained/understood. Realgains, Huck, do you have any input on this?
The reduction of estrogen is what causes a decrease of HDL, since estrogen decreases hepatic lipase activity which causes the breakdown of HDL.
Androgens increase hepatic lipase...
Aromatase inhibitors alone are not that hard on your lipid profile, some AS are a lot worse...
If an aromatase inhibitor is used with an aromatizable AS, it will cause a further decrease of HDL because no excess estrogen will be formed to counteract the increase of hepatic lipase caused by androgens.
Any effective aromatase inhibitor would have impact...
The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity.
Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD.
Department of Medicine, Miriam Hospital, Providence, RI.
Stanozolol, an oral 17 alpha-alkylated androgen, increases hepatic triglyceride lipase activity (HTGLA) and decreases high-density lipoprotein cholesterol (HDL-C) levels, whereas intramuscular testosterone has comparatively little effect. In the present study, we tested the hypothesis that aromatization of androgen to estrogen blunts the lipid and lipase effects of exogenous testosterone.
Fourteen male weightlifters received testosterone enanthate (200 mg/wk intramuscularly), the aromatase inhibitor testolactone (250 mg four times per day), or both drugs together in a randomized cross-over design. Serum testosterone level increased during all three drug treatments, whereas estradiol level increased only with testosterone alone (+47%, P < .05), demonstrating that testolactone effectively inhibited testosterone aromatization.
Testosterone decreased HDL-C(-16%, P < .05), HDL2-C(-23%, NS), and apoprotein (apo) A-I (-12%, P < .05) levels, effects that were consistently but not significantly greater with simultaneous testosterone and testolactone administration (HDL-C, -20%; HDL2-C, -30%; apo A-I, -15%; P < .05 for all). In contrast, both testosterone regimens decreased HDL3-C levels by 13% (P < .05 for both). HTGLA increased 21% during testosterone treatment and 38% during combined testosterone and testolactone treatment (P < .01 for both). Lipoprotein lipase activity (LPLA) increased only during combined testosterone and testolactone treatment (+31%, P < .01), suggesting that estrogen production may counteract the effects of testosterone on LPLA.
Testolactone alone had little effect on any lipid, lipoprotein, apoprotein, or lipase concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
Physiological levels of estradiol stimulate plasma high density lipoprotein2 cholesterol levels in normal men.
Bagatell CJ, Knopp RH, Rivier JE, Bremner WJ.
Medical Service, Seattle Veterans Affairs Medical Center, Washington 98108.
Premenopausal women have a lower risk of coronary artery disease than men or postmenopausal women; estrogens are thought to contribute to this lower risk. Administration of exogenous estrogen to post-menopausal women increases plasma high density lipoprotein (HDL) cholesterol and may reduce mortality from coronary disease in users. Although many investigations have examined the roles of estrogen in the regulation of lipoproteins in women, little attention has been directed to estrogen regulation of lipids in men. We designed a paradigm to study the role of physiological levels of estradiol (E2) on plasma lipoproteins in healthy men. We used a GnRH antagonist, Nal-Glu, to suppress endogenous steroid hormones in healthy men. We then administered testosterone (T) enanthate (100 mg, im, weekly) to restore T levels to the baseline range, and we administered an aromatase inhibitor, testolactone (Teslac), to prevent the normal conversion of T to E2, thereby producing a selective estrogen deficiency state in normal young men. As controls, we administered Nal-Glu and T along with placebo Teslac to a separate group of men; a third group of men received all placebo medications. We found that in men who received Nal-Glu plus T plus Teslac, E2 levels were profoundly suppressed during treatment, whereas T levels remained in the baseline range. Plasma HDL cholesterol, particularly, the HDL2 fraction, decreased significantly in response to the low serum E2 level. Plasma apoprotein-AI levels also decreased significantly. Plasma LDL and triglyceride levels did not change. All hormone and lipoprotein parameters returned to baseline within 4 weeks after treatment ended. In men who received Nal-Glu plus T, plasma HDL and apoprotein-AI decreased, but these decreases did not achieve statistical significance. Only a small decrease in HDL2 cholesterol was seen in these men. There were no hormonal or lipid changes in the placebo group. We conclude that in men, physiological levels of E2 are important in maintaining plasma levels of HDL cholesterol, especially the HDL2 fraction. These observations suggest that estrogen, in the amount normally produced in men, may offer some degree of protection against cardiovascular disease in males, as they do in women.
Here are a few studies performed on male subjects:
Anastrozole (1 mg ED for 10 weeks):
http://jcem.endojournals.org/cgi/content/full/85/7/2370
..eight males (aged 15–22 yr; four adults and four late pubertal) had isotopic infusions of [13C]leucine and 42Ca/44Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex (1 mg ED)
...Anastrozole treatment was well tolerated by all subjects.
Glucose and insulin concentrations remained unchanged during these studies, as did plasma lipid concentrations, blood chemistries, and cell blood counts...
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2.5 mg of letrozole ED + 1 mg/kg of test once every 4 weeks for
12 MONTHS
http://jcem.endojournals.org/cgi/content/full/86/10/4887
The boys in the T-treated group (12 boys) received T enanthate (1 mg/kg, im, every 4 wk, six times). The T- plus-letrozole-treated group (13 boys) received T enanthate (as above) and, in addition, an aromatase inhibitor, letrozole 2.5 mg, orally, once a day for 12 months
Safety
The concentrations of total cholesterol, low and high density lipoprotein cholesterol, triglycerides, transaminases, the leukocyte count, and the bone density were determined during the follow-up. In these safety parameters, no changes sufficient to indicate discontinuation of the treatment were observed in any of the boys. Letrozole was well tolerated; no side-effects were observed.
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http://jcem.endojournals.org/cgi/content/full/86/6/2869
Fifteen eugonadal men over 65 yr were treated for 9 weeks with 2.0 mg/day of anastrozole, an aromatase inhibitor
... After 9 weeks of aromatase inhibition,
total cholesterol decreased significantly by 7 ± 10% (P = 0.016), and HDL cholesterol decreased by 7 ± 9% (P = 0.013). Calculated LDL showed a small decrease that was not statistically significant ...
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