Effect of AAS, SERMs & aromatase inhibitors on plasma lipids in men


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Anastrozole (1 mg ED for 10 weeks):


..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...


2.5 mg of letrozole ED + 1 mg/kg of test once every 4 weeks for 12 MONTHS


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


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.



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 ...


Effects of tamoxifen on lipid profile and coagulation parameters in male patients with pubertal gynecomastia.

Novoa FJ, Boronat M, Carrillo A, Tapia M, Diaz-Cremades J, Chirino R.

Department of Endocrinology, Hospital Universitario Insular, Las Palmas de Gran Canaria, Spain. jnovoa@cicei.ulpgc.es

BACKGROUND/AIM: The estrogenic actions of tamoxifen on lipid profiles and hemostasis have been extensively demonstrated in women. Due to limited experience with this drug in males, it is uncertain whether these effects are also present in men. The aim of our study was to assess the response of blood lipids, lipoproteins, and coagulation parameters in a group of men taking tamoxifen. METHODS: We studied 15 healthy boys with pubertal gynecomastia who were given 10 mg tamoxifen per day. Total testosterone, sex-hormone-binding globulin, estradiol, serum lipids, apolipoprotein B, apolipoprotein A-I, lipoprotein(a), fibrinogen, antithrombin III, von Willebrand factor, and markers of activated coagulation and fibrinolysis were determined at baseline and 1 and 3 months after beginning of the tamoxifen treatment. 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. Among clotting parameters, antithrombin III was reduced, and von Willebrand factor increased significantly. Markers of activated coagulation and fibrinolysis remained unchanged throughout the period of therapy. CONCLUSIONS: The effects of tamoxifen on blood lipids and hemostasis we found in this group of healthy young men were qualitatively similar, but lesser than those previously described in women. Copyright 2002 S. Karger AG, Basel



..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....


J Lipid Res 2002 Mar;43(3):383-91 Related Articles, Links

Estrogen receptor-mediated repression of human hepatic lipase gene transcription.

Jones DR, Schmidt RJ, Pickard RT, Foxworthy PS, Eacho PI.

Lilly Research Laboratories, Cardiovascular Research Division, Eli Lilly and Company, Indianapolis, IN 46285, USA.

Estrogen replacement therapy in women decreases hepatic lipase (HL) activity, which may account for the associated increase in HDL cholesterol. To investigate whether estrogen decreases HL transcription, transient cotransfection assays with HL promoter and estrogen receptor-alpha (ERalpha) expression constructs were performed in HepG2 cells. 17beta-estradiol (E(2)) decreased transcription driven by the -1557/+41 human HL promoter by up to 50% at 10(-7) M. Mutation of ERalpha by deletion of its transactivation domains or ligand-binding domain eliminated E(2)-induced repression of the promoter, whereas deletion of the DNA-binding domain of ERalpha resulted in a 7-fold activation by E(2). The E(2)-induced repression was maintained after mutation of a potential estrogen-response element in the promoter. The region of estrogen responsiveness was localized to -1557/-1175 of the HL promoter by deletion analysis. Mutation of an AP-1 site at -1493 resulted in a partial loss of E(2)-induced repression, similar to that caused by deletion of nucleotides -1557 to -1366. Gel shift assays with nuclear extracts from E(2)-treated HepG2 cells stably expressing ERalpha demonstrated an increase in binding to an AP-1 consensus oligonucleotide. The AP-1 activator, phorbol 12-myristate 13-acetate, inhibited the HL promoter by greater than 50%. Collectively, the data suggest that estrogen represses the transcription of the HL gene, possibly through an AP-1 pathway.


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.

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)


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.


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.


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.


Int J Obes Relat Metab Disord 1995 Sep;19(9):614-24

Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men.

Lovejoy JC, Bray GA, Greeson CS, Klemperer M, Morris J, Partington C, Tulley R.

Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808-4124, USA.

OBJECTIVE: To compare the effects of testosterone enanthate (TE), anabolic steroid (AS) or placebo (PL) on regional fat distribution and health risk factors in obese middle-aged men undergoing weight loss by dietary means.

DESIGN: Randomized, double-blind, placebo-controlled clinical trial, carried out for 9 months with primary assessments at 3 month intervals.Due to adverse blood lipid changes, the AS group was switched from oral oxandrolone (ASOX) to parenteral nandrolone decaoate (ASND) after the 3 month assessment point. SUBJECTS: Thirty healthy, obese men, aged 40-60 years, with serum testosterone (T) levels in the low-normal range (2-5 ng/mL).

There was a significant decrease in HDL-C, and increase in LDL-C in the ASOX group,....


N Engl J Med 1975 Jun 19;292(25):1314-7 Related Articles, Links

Effect of oxandrolone treatment on the activity of lipoprotein lipase, hepatic lipase and phospholipase A1 of human postheparin plasma.

Ehnholm C, Huttunen JK, Kinnunen PJ, Miettinen TA, Nikkila EA.

The effect of a synthetic steroid, oxandrolone, on total postheparin plasma lipolytic activity, postherpain hepatic lipase activity, lipoprotein lipase and phospholipase A1 was studied in seven patients with hypertriglyceridemia. The mean total postheparin lipolytic activity increased 100 per cent during oxandrolone tratement (p smaller than 0.05). This change was caused mainly by postheparin hepatic lipase, whose activity increased on the average more than 2.5 times (p smaller than 0.001). The change in postheparin plasma-lipoprotein-lipase activity was insignificant. A highly significant correlation (r equals +0.87, p smaller than 0.01) was observed between the activities of postheparin hepatic lipase and phospholipase A1 before and during oxandrolone treatment. No relation was observed between serum triglyceride level and various postheparin lipase activities, or between the changes induced by oxandrolone in the level of serum lipids and the activities of postheparin lipases. We conclude that oxandrolone increases the activities of postheparin plasma hepatic lipase and phospholipase A1 but has little influence on lipoprotein lipase.


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)


Effects of an oral androgen on muscle and metabolism in older, community-dwelling men.

Schroeder ET, Singh A, Bhasin S, Storer TW, Azen C, Davidson T, Martinez C, Sinha-Hikim I, Jaque SV, Terk M, Sattler FR.

Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles 90033, USA.

To determine whether oxymetholone increases lean body mass (LBM) and skeletal muscle strength in older persons, 31 men 65-80 yr of age were randomized to placebo (group 1) or oxymetholone 50 mg (group 2) or 100 mg (group 3) daily for 12 wk. For the three groups, total LBM increased by 0.0 +/- 0.6, 3.3 +/- 1.2 (P < 0.001), and 4.2 +/- 2.4 kg (P < 0.001), respectively. Trunk fat decreased by 0.2 +/- 0.4, 1.7 +/- 1.0 (P = 0.018), and 2.2 +/- 0.9 kg (P = 0.005) in groups 1, 2, and 3, respectively. Relative increases in 1-repetition maximum (1-RM) strength for biaxial chest press of 8.2 +/- 9.2 and 13.9 +/- 8.1% in the two active treatment groups were significantly different from the change (-0.8 +/- 4.3%) for the placebo group (P < 0.03). For lat pull-down, 1-RM changed by -0.6 +/- 8.3, 8.8 +/- 15.1, and 18.4 +/- 21.0% for the groups, respectively (1-way ANOVA, P = 0.019). The pattern of changes among the groups for LBM and upper-body strength suggested that changes might be related to dose. Alanine aminotransferase increased by 72 +/- 67 U/l in group 3 (P < 0.001), and HDL-cholesterol decreased by -19 +/- 9 and -23 +/- 18 mg/dl in groups 2 and 3, respectively (P = 0.04 and P = 0.008). Thus oxymetholone improved LBM and maximal voluntary muscle strength and decreased fat mass in older men.


Testosterone dose-response (20 weeks)

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. Anabolic steroids induced a 25-27% decrease in HDL-cholesterol, which was virtually reversed 6 weeks after cessation of drug use. 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