Severe depression of high-density lipoprotein cholesterol levels in weight lifters and body builders by self-administered exogenous testosterone and anabolic-androgenic steroids

Webb, O L; Laskarzewski, Peter M.; Glueck, Charles J.

doi:10.1016/0026-0495(84)90222-1

Cited by 120 publications

(41 citation statements)

References 6 publications

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“…The recent demonstration that administration of anabolic androgens can result in a marked decrease in HDL cholesterol is also consistent with this possibility (5).…”

supporting

confidence: 56%

Biphasic effects of estrogen on apolipoprotein synthesis in human hepatoma cells: mechanism of antagonism by testosterone.

Tam¹,

Archer²,

Deeley³

1986

Proc. Natl. Acad. Sci. U.S.A.

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Treatment of HepG2 cells with various concentrations of 17 beta-estradiol has revealed two distinct thresholds for induction of different apolipoproteins. Maximal increases in apolipoprotein AI and CII (apoAI and apoCII) secretion can be obtained with initial concentrations of hormone of 20 nM or greater, while a similar induction of apoB and apoE requires in excess of 500 nM. Both responses involve alterations in the concentrations of apolipoprotein mRNAs. Analyses of the kinetics of accumulation of the apolipoproteins in response to high concentrations of hormone indicate that induction of apoB and apoE occurs coordinately, but it lags behind that of apoAI and apoCII by 5-6 hr. This lag can be eliminated by preexposing the cells to low concentrations of hormone. The ability to induce apoAI and apoCII and the kinetics with which they respond to low levels of estrogen correlate with levels of nuclear type I estrogen binding sites, while increases in apoE and apoB synthesis in response to high concentrations of hormone correlate with the induction of type II sites. Testosterone alone has no effect on the rates of apolipoprotein secretion, but it does increase the concentration of estrogen required to maximally induce apoCII and apoAI by a mechanism that involves high-affinity androgen receptors. This effect may be attributable to the testosterone-dependent induction of a cytoplasmic moderate-affinity estrogen-binding component.

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“…The recent demonstration that administration of anabolic androgens can result in a marked decrease in HDL cholesterol is also consistent with this possibility (5).…”

supporting

confidence: 56%

Biphasic effects of estrogen on apolipoprotein synthesis in human hepatoma cells: mechanism of antagonism by testosterone.

Tam¹,

Archer²,

Deeley³

1986

Proc. Natl. Acad. Sci. U.S.A.

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“…Some studies have shown that AAS causes a reduction 37 in the plasmatic concentration of vascular protective HDL 38 and an increase in vascular aggressive LDL. 37 However, the effects of physiological levels of testosterone were not consistent: testosterone replacement in men is reported to be associated with decreased HDL, 39 no change in HDL levels, 40 and a favorable effect on HDL levels. 41 In addition, the administration of nandrolone decanoate (100 mg/kg, intramuscularly), once per week for 6 weeks did not change HDL or LDL levels of 24 volunteers.…”

Section: Discussionmentioning

confidence: 99%

Vascular Sensitivity to Phenylephrine in Rats Submitted to Anaerobic Training and Nandrolone Treatment

et al. 2005

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Abstract-The effect of anaerobic physical training and nandrolone treatment on the sensitivity to phenylephrine in thoracic aorta and lipoprotein plasma levels of rats was studied. Sedentary and trained male Wistar rats were treated with vehicle or nandrolone (5 mg/kg IM; twice per week) for 6 weeks. Training was performed by jumping into water (4 sets, 10 repetitions, 30-second rest, 50% to 70% body weight load, 5 days/week, 6 weeks). Two days after the last training session, the animals were killed and blood samples for lipoprotein dosage were obtained. Thoracic aorta was isolated and concentration-effect curves of phenylephrine were performed in intact endothelium and endothelium-denuded aortic rings in the absence or presence of N G -L-arginine-methyl ester. No changes were observed in endotheliumdenuded aortic rings. However, in endothelium-intact thoracic aorta, anaerobic physical training induced subsensitivity to phenylephrine (pD 2 ϭ7.11Ϯ0.07) compared with sedentary group (7.55Ϯ1.74), and this effect was canceled by the inhibition of nitric oxide synthesis. No difference was observed between trained (7.22Ϯ0.07) and sedentary (7.28Ϯ0.09) groups treated with nandrolone. Anaerobic training induced an increase in high-density lipoprotein levels in vehicle-treated rats, but there were no changes in nandrolone-treated groups. Training associated with nandrolone induced an increase in low-density lipoprotein levels but no change in the other groups. If altering endotheliumdependent vasodilatation is considered to be a beneficial adaptation to anaerobic physical training, it is concluded that nandrolone treatment worsens animals' endothelial function, and this effect may be related to lipoprotein blood levels. Key Words: aorta Ⅲ endothelium Ⅲ exercise Ⅲ lipoproteins Ⅲ nitric oxide Ⅲ phenylephrine Ⅲ rats A nabolic androgenic steroids (AAS) are formed from testosterone or one of its derivatives and present both anabolic and androgenic effects. Although the therapeutic indications of AAS are hypogonadism and protein metabolism deficiency, high doses of AAS are frequently used by persons in good health to improve physical performance and appearance, and this practice results in serious health risks. 1 With regard to the cardiovascular system, it is well known that AAS can cause stroke, 2 ischemic heart disease, myocardial infarction, 3 electrocardiographic alterations, 4 and sudden cardiac death. 5 However, there are few studies about their effects on vascular reactivity. Ferrer et al 6 observed an inhibition of endothelium-dependent and endotheliumindependent relaxation in the aortic rings of rabbits treated with nandrolone. Vasoconstrictor responses to angiotensin and tyramine, but not to noradrenaline, and vasodepressor responses to acetylcholine are reduced in testosterone-treated dogs. 7 Although it is well documented that postexercise hypotension results from a decrease in systemic vascular resistance after aerobic exercise, both in humans and animals, 8 there are no data about the vascular effects of anaero...

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“…Additionally, those interested in enlarging skeletal muscle mass beyond that obtainable by ordinary training activities often resort to anabolic steroid use. The use of anabolic steroids is associated with lowering of serum HDL-cholesterol concentrations (56,57).…”

Section: Discussionmentioning

confidence: 99%

An independent, inverse association of high-density-lipoprotein-cholesterol concentration with nonadipose body mass

Pietrobelli

Lee

Capristo

et al. 1999

The American Journal of Clinical Nutrition

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Background: Increasing body mass index (BMI) is associated with progressively lower serum HDL-cholesterol concentrations, although the underlying body-composition compartment accounting for this unfavorable lipid change remains uncertain. Objective: Because growing evidence favors a role of lean tissue in HDL homeostasis, the hypothesis was tested that non-adipose tissue components of body mass explain the inverse association of HDL cholesterol and BMI. Design: Fasting serum lipid concentrations and body composition [total, subcutaneous, and visceral adipose tissue; adipose tissue-free mass (ATFM); and skeletal muscle by whole-body magnetic resonance imaging and body cell mass by 40 K counting) were evaluated in healthy adults. Body-composition compartments were expressed as height 2 -normalized indexes. Results: An inverse correlation was observed between serum HDL cholesterol and BMI in women (n = 68; R 2 = 0.08, P = 0.023) and men (n = 61; R 2 = 0.07, P = 0.046). Significant inverse correlations (P = 0.005-0.02) were also observed between HDL cholesterol and nonadipose components (ie, ATFM, skeletal muscle, and body cell mass) but not between HDL cholesterol and any adipose tissue component. The association between HDL cholesterol and ATFM remained significant after serum triacylglycerol was controlled for. When BMI was entered into the HDL cholesterol-ATFM regression model, BMI was not a significant independent variable. The strongest correlate of serum triacylglycerol was visceral adipose tissue (P = 0.002 for both women and men). Conclusions: Lean tissues and body cell mass appear to account in part for the long-observed inverse association of HDL cholesterol and BMI. These observations suggest a link between nonadipose tissue compartments and the greater cardiovascular risk associated with high BMI.Am J Clin Nutr 1999;69:614-20.

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Severe depression of high-density lipoprotein cholesterol levels in weight lifters and body builders by self-administered exogenous testosterone and anabolic-androgenic steroids

Cited by 120 publications

References 6 publications

Biphasic effects of estrogen on apolipoprotein synthesis in human hepatoma cells: mechanism of antagonism by testosterone.

Biphasic effects of estrogen on apolipoprotein synthesis in human hepatoma cells: mechanism of antagonism by testosterone.

Vascular Sensitivity to Phenylephrine in Rats Submitted to Anaerobic Training and Nandrolone Treatment

An independent, inverse association of high-density-lipoprotein-cholesterol concentration with nonadipose body mass

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