Arimidex has little impact on your lipid profile (read the studies I posted above) when compared to AS.
In study 1 young males used arimidex at 1 mg ED for 2 months and experienced no change in their lipid profiles.
The other study was performed on older men, 2 mg Arimidex was used for 9 weeks and their HDL was reduced by 7 % which still is not nearly as bad when compared to what AS can do to it.
Also, your biggest problem on cycle is reduced HDL, and tamoxifen will do nothing to correct that:
from:
http://circ.ahajournals.org/cgi/content/full/103/11/1497
..The decreases in LDL-C in the treated TVD and NCA groups did not reach significance compared with the untreated TVD group, whereas decreases in HDL-C were significant (P=0.05 and P=0.015, respectively; Figure 3A). Overall, there was no significant effect of tamoxifen on LDL:HDL ratio. Triglyceride levels showed substantial decreases in response to tamoxifen, reaching significance in the NCA group....
Horm Res 2002;57(5-6):187-91 Related Articles, Links
Effects of tamoxifen on lipid profile and coagulation parameters in male patients with pubertal gynecomastia.
RESULTS: Total cholesterol and lipoprotein(a) showed moderate but significant decreases from baseline. Low-density lipoprotein and high-density lipoprotein cholesterol concentrations as well as triglyceride and apolipoprotein B levels became lower, but these changes were not statistically significant...
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AS & plasma lipids:
One of the reasons that AS are so hard on your HDL is that they increase hepatic lipase, - which causes breakdown of HDL.
17AA's seem to be particulary hard on your HDL.
Rev Clin Esp 2000 Mar;200(3):133-8 Related Articles, Links
43 cycles of anabolic steroid treatment studied in athletes: the uses and secondary effects
Inigo MA, Arrimadas E, Arroyo D.
Servicio de Analisis Clinicos, Hospital del Servicio Andaluz de Salud de La Linea, Cadiz.
...Forty-three therapy courses with anabolic steroids among 39 male athletes were studied. Diet and training were standardized for all participants. A verification was made that the test group started from a basal state. RESULTS: Duration of therapy was 6 weeks and the mean total dose was 2,928 mg. Significant differences were found in the test group regarding basal and post-therapy values for: transaminases (AST: 29.8 vs 45.0 IU/l, p < 0.001. ALT: 32.9 vs 51.4 IU/l, p < 0.01), cholesterol,
HDL-cholesterol (31.4 vs 19.7 mg/dl, p < 0.01), LDL-cholesterol (145.9 vs 173.5 mg/dl, p < 0.01)...
JAMA 1989 Feb 24;261(8):1165-8 Related Articles, Links
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.
Int J Sports Med 1991 Aug;12(4):413-8 Related Articles, Links
Influence of anabolic steroids on body composition, blood pressure, lipid profile and liver functions in body builders.
Kuipers H, Wijnen JA, Hartgens F, Willems SM.
Dept. of Physiology, University of Limburg, Maastricht, The Netherlands.
The effects of anabolic steroids on body composition, blood pressure, lipid profile and liver functions were studied in male body builders who received
a weekly i.m. injection of nandrolone-decanoate (100 mg) or placebo for 8 weeks in a double blind way. In addition, 5 body builders received the same dosage of nandrolone-decanoate or placebo, in a double blind cross-over design during two 8-week periods, interspersed by 12 weeks. [/B]Anabolic steroids induced a 25-27% decrease in HDL-cholesterol, which was virtually reversed 6 weeks after cessation of drug use[/B]. In the SAD group an increase in diastolic blood pressure was observed, which returned to pre-anabolic values approximately 6 weeks after cessation of drug administration. No deleterious effects of anabolic drugs on plasma activity of liver enzymes were found. Increases in lean body mass were found in all groups, though the increase in the subjects who received anabolic steroids was superior to that in the placebo-treated subjects. The increase in lean body mass suggests increases in muscle mass.
Int J Sports Med 1985 Feb;6(1):24-9 Related Articles, Links
Physical health and fitness of an elite bodybuilder during 1 year of self-administration of testosterone and anabolic steroids: a case study.
Alen M, Hakkinen K.
An adult male bodybuilder of international level, who had decided to complement his training by self-administering the androgenic hormones (actually 53 mg/day), volunteered as a subject for investigation of his physical health and fitness over a training period of 1 year including only a 4-week abstinence from drugs in the middle of the year. The subject was able to gain greatly in fat-free weight (from 83 to 90 kg), in mean fiber area of the VL muscle (enlargement of 11.4% after a half year's training), and in maximal strength (from 5145 to 5948 N). The high level of serum testosterone and low level of serum SHBG observed tend to strengthen suggestions of the anabolic effects of androgenic steroids during training. The subject's health status was affected. A high serum E2 level during the use of androgens, atrophic testicles, and low LH, FSH, and T levels after drug withdrawal indicate that sustained testosterone/anabolic steroid administration affects the function of the pituitary and leads to long-lasting impairment of testicular endocrine function, and consequently to azoospermia and cynegomastia.
The observed decrease in serum HDL-cholesterol (from 1.59 to 0.44 mmol/l) and in HDL2-cholesterol (from 0.42 to 0.01 mmol/l) may indicate a higher risk for atherogenesis.
Int J Sports Med 1985 Jun;6(3):139-44 Related Articles, Links
Serum lipids in power athletes self-administering testosterone and anabolic steroids.
Alen M, Rahkila P, Marniemi J.
The purpose of the present investigation was to study the effects of testosterone and anabolic steroids on serum lipids in power athletes. Altogether 11 national top-level adult athletes completed the study. Five of them volunteered for the study group and the rest for controls. The follow-up consisted of 9 months of a strength training period.
During the first 6 months, the subjects in the study group self-administered androgenic steroids on an average of 57 +/- 24.9 mg/day.
The most interesting observation was the extremely low high-density lipoprotein (HDL) and HDL2 cholesterol concentrations of the androgen users. After 8 weeks of training, the study group had significantly (P less than 0.05) lower HDL cholesterol concentrations than the control group (0.53 +/- 0.11 and 1.14 +/- 0.19 mmol/l, respectively). This difference remained significant from 8 to 32 weeks of training. No systematic changes were observed in the control group.
The HDL2 cholesterol concentration decreased by about 80% (P less than 0.01) and HDL3 cholesterol by about 55% (P less than 0.01) from the onset values in the study group. A substantial decrease in HDL cholesterol to total cholesterol and in HDL2 cholesterol to HDL3 cholesterol ratios were also noticed under the influence of exogenous androgens. The results of this study suggest that the sustained use of testosterone and anabolic steroids have a marked unfavorable effect on the pattern of HDL cholesterol in the serum of male power athletes.
Notice the increase in hepatic lipase in this study (> 300 %)
Metabolism 1983 Apr;32(4):413-20 Related Articles, Links
Studies on the metabolic mechanism of reduced high density lipoproteins during anabolic steroid therapy.
Haffner SM, Kushwaha RS, Foster DM, Applebaum-Bowden D, Hazzard WR.
To explore the mechanism whereby stanozolol, a 17 alpha-methyl androgenic anabolic steroid, depresses high density lipoproteins (HDL), 6 subjects, aged 46-71 yr (4 postmenopausal women and 2 men), underwent paired studies of 125I-HDL turnover (including HDL2 and HDL3 and Apo A-I and A-II) and postheparin plasma (PHP) lipolytic activity (hepatic triglyceride lipase, HTGL, and lipoprotein lipase LPL) before and during treatment with
stanozolol, 6 mg/day. While total cholesterol and triglyceride levels did not change during stanozolol,
HDL-cholesterol decreased from 59 +/- 18 mg/dl (x +/- SD) to 29 +/- 7 mg/dl (p less than 0.01) and low density lipoprotein (LDL)-cholesterol increased from 160 +/- 36 mg/dl to 181 +/- 42 mg/dl (p less than 0.02). PHP-HTGL increased from 111 +/- 47 nmole/min/ml to 369 +/- 202 nmole/min/ml (p less than 0.04), while PHP-LPL did not change. At baseline the residence time of HDL2 (4.00 +/- 1.04 day) was shorter than that of HDL3 (6.79 +/- 1.00 day) (p less than 0.001). Residence times of both declined on stanozolol, to 3.25 +/- 0.83 day and 4.00 +/- 0.29 day, respectively (0.1 less than p less than 0.2); however, only the reduction in residence time of HDL3 was statistically significant (p less than 0.001). At baseline the residence time of apo A-I (4.93 +/- 1.32 day) was shorter than that of A-II (6.85 +/- 1.98 day) (p less than 0.025); on stanozolol these declined to 3.19 +/- 0.41 (p less than 0.02) and 5.10 +/- 1.13 (p = 0.07), respectively, still significantly different from each other (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
Hepatic lipase is not the only mechanism responsible for reduction of HDL:
Metabolism 1997 Sep;46(9):992-6 Related Articles, Links
Effects of short-term stanozolol administration on serum lipoproteins in hepatic lipase deficiency.
Bausserman LL, Saritelli AL, Herbert PN.
Lipid Research Laboratory, Miriam Hospital, Brown University Medical School, Providence, RI, USA.
We have identified a kindred in Providence, RI, deficient in hepatic triglyceride lipase (HL). The two affected brothers have coronary heart disease and elevated levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoprotein [apo] A-I. The lipoprotein lipase (LPL) activity is normal. We and others have postulated that the effects of oral anabolic steroids on HDL metabolism are mediated by HL. To test this hypothesis, we treated these
two men and two controls with the oral androgen stanozolol (6 mg/d) for 2 weeks. Consistent with other reports,
HL activity increased a mean of 277% in controls with a concomitant decrease in HDL cholesterol (49%), HDL2 cholesterol (90%), HDL3 cholesterol (16%), and apo A-I (41%) and no change in apo A-II. Although stanozolol failed to induce HL activity in the HL-deficient man, HDL cholesterol, HDL2 cholesterol, and apo A-I were reduced a mean of 20%, 48%, and 32%, respectively. In contrast to controls, HDL3 cholesterol (46%) and apo A-II (14%) increased in HL-deficient subjects. Stanozolol treatment also increased LPL activity (124% +/- 86%, n = 4) and decreased lipoprotein(a) ([Lp(a)] 66% +/- 3%, n = 3) in the three men with detectable levels. The data indicate that in addition to stimulation of HL activity, stanozolol treatment changes HDL cholesterol concentration and subfraction distribution by other mechanisms.
A single 50 mg injection of stanozolol reduced HDL and increased LDL for one month after injection.
Thromb Res 1982 Oct 1;28(1):27-36 Related Articles, Links
The effect of intramuscular stanozolol on fibrinolysis and blood lipids.
Small M, McArdle BM, Lowe GD, Forbes CD, Prentice CR.
The effects of a
single 50 mg intramuscular injection of the anabolic steroid stanozolol (Stromba) on fibrinolysis, blood coagulation and lipids was evaluated in 12 healthy male volunteers. Significantly increased plasminogen activator levels (p less than 0.05) was noted 24 hours following the injection and these remained elevated for one week. Plasminogen levels increased significantly by day two (p less than 0.01) and remained elevated for three weeks.
HDL cholesterol fell (p less than 0.01) and both total and LDL cholesterol increased (p less than 0.05) when measured one month post injection. Stanozolol appears to have therapeutic potential as an activator of the fibrinolytic system when given by intramuscular injection.
You should quit focusing on aromatase inhibitors/SERMs as cause/solution of the problem.
Avoid using 17AA's, use moderate amount of injectables.
Also, you should be aware that tamox may interact with aromatase inhibitors, - I've seen on study in which tamox reduced plasma letrozole by 30 %...
