The effects of long-term anabolic androgenic steroid use on blood lipids and apolipoproteins

The acute effects of anabolic androgenic steroids (AAS)
on blood lipid sub-fractions are regarded as being both
dramatic and consistent and have been extensively
reviewed by Glazer (1991: Archives of Internal Medicine,
151, 1925–1933), but the effects of long-term (420
years) AAS use on blood lipids are unstudied to date.
The aim of this study was to determine the effects of
such long-term AAS use on cholesterol subfractions
and their major apolipoproteins: Apo AI, Apo AII, Apo
B. Lipoprotein(a) was also measured as an independent
risk factor for cardiovascular disease.

The participants (n = 32) were matched for age and
were divided into four distinct age-matched groups:
long-term ( 420 years) AAS users (n = 8) who were still
using at the time of testing (Group A); long-term (420
years) AAS users who had been abstinent for a period of
more than 3 months (Group B); bodybuilding controls
who did not use any pharmacological ergogenic aids
(Group C); and sedentary male controls (Group D).
The AAS-using control group had abstained from AAS
use for a minimum of 12 weeks before examination.
Venous plasma blood samples were collected 12 h postprandial using the standard venepuncture method.
Cholesterol subfractions, apolipoproteins and lipoprotein(a) were measured using appropriate assays. Group differences were analysed using a one-way analysis of variance followed by a post-hoc Tukey test; a level of P 50.05 was selected to indicate statistical significance.

The mean body mass index (BMI) was significantly
higher in both groups of AAS users compared with the
controls (P5 0.01). The sedentary control group had
significantly higher body fat (P5 0.05). There were no
differences between groups for total cholesterol or
triglycerides. However, HDL-C and the HDLC:TOT-C
ratio were significantly lower (P 50.01), while LDL-C and the LDL:TOT-C ratio were significantly higher (P 50.01), in Group A. Both Apo AI and Apo AII were significantly lower (P5 0.01) in Group A than Groups C and D, but not Group B. Apo B was significantly higher (P5 0.05) in Group A than the other three groups. Although there were trends between Group B and Groups C and D, for Apo AI and Apo AII, they did not reach significance. Lipoprotein(a) was significantly higher (P5 0.05) in Groups A and B than Groups C and D.

The higher lipoprotein(a) concentrations, as found
in both groups of AAS users, does not conform with the
few previous reports and provides evidence for elevated
levels of lipoprotein(a) following long-term AAS use.
Although the synthesis and regulation of lipoprotein(a)
and LDL-C cholesterol concentrations in the blood
exist independently of each other, the elevation of both
factors confers an additive risk of cardiovascular disease
up to five-fold when both are abnormally high.
Considering the magnitude of the AAS-induced LDLC
elevation in this study, the potential for artherogenic
and thrombotic events among bodybuilders using
anabolic androgenic steroids is increased.