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Steroids and Lipoprotein Metabolism

Steroids should only be taken under close supervision of a doctor. The information provided here should not be taken as medical advice.

A commonly reported consequence of ASS use is an unfavourable decrease in high-density lipoprotein (HDL) cholesterol and increase in low-density lipoprotein (LDL) cholesterol. According to Thiblin and Petersson (2005) changes in lipid profiles are the only complication of ASS that receives definitive support from the investigations.

Lowering of HDL-cholesterol is thought to be an independent risk factor for cardiovascular disease and can be closely correlated by an increase in LDL-cholesterol. A study by Crook et.,al (1992) on the effects of the anabolic steroid dananzol on lipoprotein lp(a) levels in women found that levels of LDL cholesterol and apo B were increased by 38% and 49%, respectively (P < 0.001). In contrast, HDL cholesterol and apo AI levels were reduced by 48% and 42%, respectively (P<0.001) (Crook et.,al (1992). Subjects were not randomised due to ethical restraints but were on supraphysiologic doses (600mg/d).

Bonetti et.,al (2008) echoed those results with a study on the adverse effects of ASS over a two year period. They found that HDL-cholesterol (baseline 56.94 ± 13.54) was reduced at 18 (41.86 ± 14.17) (P< 0.01) and 24 (43.82 ± 18.67) (P < 0.05) months. They concluded that this was an important long-term side affect and can be associated with and increased cardiovascular risk.

The effects of ASS on apoliproteins and lipoproteins were also well investigated by Hartgens et al., (2004). The study included one group of 9 strength athletes on 8 weeks of ASS and another group of 10 strength athletes on between 12 and 16 weeks of drug use. The control consisted of 16 subjects training without ASS.

Lipoprotein

Figure 5: (Source: Hartgens et al., 2004, p256)

The results in figure 4 show significant decreases in all HDL-cholesterol following 8 weeks of ASS use. Not shown in the table is an increase in LDL-cholesterol. All lipoprotein variables slowly returned to normal but had not returned to baseline concentrations 6 weeks after cessation. The subjects on ASS for between 12 and 16 weeks showed similar results but lipoprotein concentrations remained lower. There was also significant reductions in the serum concentration of the atherogenic lipoprotein (P<0.001) and apolipoprotein (P<0.001) (Hartgens et al., 2004) .

The reduction of serum Lp (a) found in the study is important as this is recommended for patients with atherosclerosis. Crook et.,al (1992) found that serum Lp(a) levels fell by 78.6% ± 24.0% in women treated with danazol (P<0.001). This is supported by the findings of Cohen et. Al (1996) who found that serum Lp(a) levels above 30 mg · dl-1 was significantly lower in AAS subjects than non-AAS subjects. They also found that HDL-C levels were significantly lower and LDL-C levels significantly higher in the AAS group. In addition, Kuipers et al. (1991) found that ASS induced a 25-27% decrease in HDL-cholesterol but was reversed after 6 weeks of cessation of drug use.

There is clear evidence that ASS increases LDL-cholesterol and decreases HDL-cholesterol concentrations. The effect seems to be profound the longer the duration of steroid use. Concentrations should return to normal after short term use but this remains inconclusive at the current time. Long term ASS use in-particular could pose a cardiovascular risk to users and could induce heart complications. This risk should be explained to any athlete contemplating steroid use. Serum Lp (a) concentrations appear to decrease which could be beneficial and therefore warrants further study.

End of steroids and lipoprotein metabolism