StoneColdNTO said:
Here's how mine changed; Jan 03 was 6 months since a cycle, Aug 03 was 4 weeks after cycle ended with 1 mg Arimidex EOD. Cycle was 437 mg/week of Test Enanthate
LIPID PROFILE...Jan 03.........Aug 03........Normal Values
Cholesterol.........4.67............4.17............[<5.2]mmol/L
Triglyceride.........1.12............1.64............[<2.3]mmol/L
HDL Cholesterol..0.99............0.85............[>.90]mmol/L
LDL ""..............3.17............2.57............[<3.4]mmol/L
Total Chol/HDL Ratio.4.7.............4.9................*
*males; avg=5,less than 3.5(low risk), greater than 9(high risk)
In your case it dropped by >7 %.
Arimidex alone is not the same as arimidex + test.
Androgens in general lower HDL ... They lower HDL by increasing hepatic lipase activity (which causes breakdown of HDL).
Estrogens have the opposite effect, they lower HL activity, so HDL goes up - that's the reason why aromatizable AS don't suppress your HDL as much as AS which don't aromatize.... because that estrogen caused by aromatization can counteract the effect of androgen....
A few examples:
Test + teslac vs. teslac alone
Metabolism 1993 Apr;42(4):446-50 Related Articles, Links
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.
...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.
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Test vs. stanozolol
Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.
Thompson PD, Cullinane EM, Sady SP, Chenevert C, Saritelli AL, Sady MA, Herbert PN.
Department of Medicine, Miriam Hospital, Providence, RI 02906.
Oral anabolic steroids produce striking reductions in serum concentrations of high-density lipoprotein (HDL) cholesterol. We hypothesized that this effect related to their route of administration and was unrelated to their androgenic potency. We administered oral stanozolol (6 mg/d) or supraphysiological doses of intramuscular testosterone enanthate (200 mg/wk) to 11 male weight lifters for six weeks in a crossover design. Stanozolol reduced HDL-cholesterol and the HDL2 subfraction by 33% and 71%, respectively. In contrast, testosterone decreased HDL-cholesterol concentration by only 9% and the decrease was in the HDL3 subfraction. Apolipoprotein A-I level decreased 40% during stanozolol but only 8% during testosterone treatment. The low-density lipoprotein cholesterol concentration increased 29% with stanozolol and decreased 16% with testosterone treatment. Stanozolol, moreover, increased postheparin hepatic triglyceride lipase activity by 123%, whereas the maximum change during testosterone therapy (+25%) was not significant. Weight gain was similar with both drugs, but testosterone was more effective in suppressing gonadotropic hormones. We conclude that the undesirable lipoprotein effects of 17-alpha-alkylated steroids given orally are different from those of parenteral testosterone and that the latter may be preferable in many clinical situations.