Lipid profile of body builders with and without self-administration of anabolic steroids

Fröhlich, Jiří; Kullmer, T.; Urhausen, Axel; Bergmann, RL; Kindermann, Wilfried

doi:10.1007/bf02396586

Cited by 27 publications

(15 citation statements)

References 26 publications

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“…Other laboratory parameters of lipid metabolism that might be impaired are a decrease in lipoprotein (a) (Cohen et al 1996;Fröhlich et al 1989;Hislop et al 2001;Lenders et al 1988;Lippi et al 1997;Zmuda et al 1996) and apolipoprotein A-I and A-II (Fröhlich et al 1989;Zuliani et al 1989) and an elevation of the apolipoprotein B level Zuliani et al 1989). …”

Section: Lipid Metabolismmentioning

confidence: 97%

“…However, the chronic abuse of AAS has been shown to induce profound alterations in serum lipid concentrations. There is a decrease of the vasoprotective HDL level (Ebenbichler et al 2001;Fröhlich et al 1989;Glazer 1991;Hislop et al 2001;Karila 2003;Sader et al 2001) and an elevation of the vasoaggressive low-density lipoprotein (LDL) (Fröhlich et al 1989;Glazer 1991;Hurley et al 1984;Webb et al 1984), resulting in a decreased HDL/LDL ratio. These alterations of lipid parameters seem to be especially associated with stanozolol (Applebaum-Bowden et al 1987;Sloane and Lee 2007) and oxymetholone (Pavlatos et al 2001).…”

Section: Lipid Metabolismmentioning

confidence: 99%

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Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships

Büttner

Thieme²

2009

Handbook of Experimental Pharmacology

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Side effects of anabolic steroids with relevance in forensic medicine are mainly due to life-threatening health risks with potential fatal outcome and cases of uncertain limitations of criminal liability after steroid administration. Both problems are typically associated with long-term abuse and excessive overdose of anabolic steroids. Side effects may be due to direct genomic or nongenomic activities (myotrophic, hepatotoxic), can result from down-regulation of endogenous biosynthesis (antiandrogenic) or be indirect consequence of steroid biotransformation (estrogenic).Logically, there are no systematic clinical studies available and the number of causally determined fatalities is fairly limited. The following compilation reviews typical abundant observations in cases where nonnatural deaths (mostly liver failure and sudden cardiac death) were concurrent with steroid abuse. Moreover, frequent associations between structural characteristics and typical side effects are summarized.

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Section: Lipid Metabolismmentioning

confidence: 97%

Section: Lipid Metabolismmentioning

confidence: 99%

Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships

Büttner

Thieme²

2009

Handbook of Experimental Pharmacology

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“…Das Verhältnis HDL 2 -Cholesterin/HDL 3 -Cholesterin war reduziert, was auf einen stärkeren Abfall von HDL 2 -Cholesterin hinweist. Apolipoprotein A-I war ebenfalls abgefallen [1,5,8,15,37,40,46,48,50,52,58,62,83,100,109,113]. Als wesentlicher Mechanismus für den markanten Abfall von HDL-Cholesterin unter AAS wird ein beschleunigter Katabolismus der gefäß-protektiven Cholesterinfraktion, zurückzuführen auf eine angestiegene Aktivität der hepatischen Triglyzeridlipase, angenommen [5,52].…”

Section: Lipoproteineunclassified

“…Als wesentlicher Mechanismus für den markanten Abfall von HDL-Cholesterin unter AAS wird ein beschleunigter Katabolismus der gefäß-protektiven Cholesterinfraktion, zurückzuführen auf eine angestiegene Aktivität der hepatischen Triglyzeridlipase, angenommen [5,52]. Die gefäßaggressive LDL-Cholesterin-Fraktion steigt in den meisten Studien leicht an, während Gesamtcholesterin und Triglyzeride unverändert bleiben [15,37,40,50,83,100,109]. Erhöhte Konzentrationen von Lipoprotein (a) fallen unter AAS ab, was als günstiger Effekt interpretiert werden kann [15,48,83].…”

Section: Lipoproteineunclassified

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Kardiovaskuläre Nebenwirkungen von anabol-androgenen Steroiden

Kindermann

2006

Herz

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The intake of anabolic-androgenic steroids (AAS) leads to an increase in skeletal muscle mass and is prohibited as a doping measure in sport. AAS abuse is not limited to competitive athletes. It is also prevalent in subjects who do body building or resistance training for cosmetic reasons only. Out of the numerous and partly serious side effects, the cardiovascular ones are presented here. An increase in left ventricular muscle mass is well documented, and some researchers have even reported concentric hypertrophy. By contrast, resistance training without AAS intake does not lead to increased ventricular wall thickness. AAS do not affect the systolic function of the left ventricle, whereas diastolic function might be impaired. Different ultrastructural myocardial alterations have been documented in animal studies. In addition, AAS can induce arterial hypertension. Blood clotting and fibrinolysis are negatively affected, and several case studies of thrombi exist in young strength athletes. Changes in the concentration of blood lipoproteins, particularly a reduction in vessel-protective HDL cholesterol, can lead to early atherosclerosis. Many case reports exist about cardiac deaths in seemingly healthy subjects-most often body builders and other strength athletes. In fatal and nonfatal myocardial infarctions patent coronary arteries were proven frequently. Besides the prothrombotic effects of AAS, an impaired endothelial function and vasospasms are discussed hypothetically as pathomechanisms. Also, cardiomyopathies can occur due to AAS abuse. On the basis of the described possible cardiovascular side effects, it can be concluded that in cases of sudden cardiac deaths in young athletes, a misuse of AS should be excluded.

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Androgenic Anabolic Steroid Abuse and the Cardiovascular System

Vanberg

Atar²

2009

Handbook of Experimental Pharmacology

122

120

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Abuse of anabolic androgenic steroids (AAS) has been linked to a variety of different cardiovascular side effects. In case reports, acute myocardial infarction is the most common event presented, but other adverse cardiovascular effects such as left ventricular hypertrophy, reduced left ventricular function, arterial thrombosis, pulmonary embolism and several cases of sudden cardiac death have also been reported. However, to date there are no prospective, randomized, interventional studies on the long-term cardiovascular effects of abuse of AAS. In this review we have studied the relevant literature regarding several risk factors for cardiovascular disease where the effects of AAS have been scrutinized:(1) Echocardiographic studies show that supraphysiologic doses of AAS lead to both morphologic and functional changes of the heart. These include a tendency to produce myocardial hypertrophy (Fig. 3), a possible increase of heart chamber diameters, unequivocal alterations of diastolic function and ventricular relaxation, and most likely a subclinically compromised left ventricular contractile function. (2) AAS induce a mild, but transient increase of blood pressure. However, the clinical significance of this effect remains modest. (3) Furthermore, AAS confer an enhanced pro-thrombotic state, most prominently through an activation of platelet aggregability. The concomitant effects on the humoral coagulation cascade are more complex and include activation of both pro-coagulatory and fibrinolytic pathways. (4) Users of AAS often demonstrate unfavorable measurements of vascular reactivity involving endothelial-dependent or endothelial-independent vasodilatation. A degree of reversibility seems to be consistent, though. (5) There is a comprehensive body of evidence documenting that AAS induce various alterations of lipid metabolism. The most prominent changes are concomitant elevations of LDL and decreases of HDL, effects that increase the risk of coronary artery disease. And finally, (6) the use of AAS appears to confer an increased risk of life-threatening arrhythmia leading to sudden death, although the underlying mechanisms are still far from being elucidated. Taken together, various lines of evidence involving a variety of pathophysiologic mechanisms suggest an increased risk for cardiovascular disease in users of anabolic androgenic steroids.

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Lipid profile of body builders with and without self-administration of anabolic steroids

Cited by 27 publications

References 26 publications

Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships

Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships

Kardiovaskuläre Nebenwirkungen von anabol-androgenen Steroiden

Androgenic Anabolic Steroid Abuse and the Cardiovascular System

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