A Young, Fit Man With Low HDL is on the “Juice”
The Different Effects of Oral vs. Intramuscular Anabolic Steroids
I am occasionally asked to see a young male athlete with an HDL-cholesterol (HDL-C) well below 30 mg/dL. The diagnosis is usually obvious, because the patient is “cut” with well-defined muscles. He is also taking an over-the-counter (OTC) training powder that “really works”, but according to him absolutely does not contain any anabolic steroids. But, it does. I always get the name of the product and search the web. Occasionally I am lucky enough to find evidence that the product does indeed contain an oral anabolic steroid, but usually no such report is available. The products often do contain these steroids because the kids aren’t dumb, and they will not buy the product again if it does not bulk them up. Reportedly, the FDA chases these companies and takes their products off the market, but the companies simply change the name, repackage the powder and are back in business.
Oral anabolic steroids produce a prompt, large decrease in HDL-C. We compared the oral anabolic steroid, stanozolol, to intramuscular testosterone enanthate in a crossover design study of weightlifters. (1). The oral anabolic steroids reduced HDL cholesterol within a week of initiating the treatment. (Fig)
Figure — The time points are baseline, 1, 2, 4, & 6 weeks. The no-drug cross-over interval was 6–9 weeks. Doses were stanozolol 6 mg daily and testosterone 200 mg IM weekly. From Thompson et.al. (1)
That’s because oral steroids enter the portal circulation and go promptly to the liver, so-called first-pass hepatic metabolism. An oral AS in the liver increases hepatic triglyceride lipase (HTGL) which reduces HDL-C. The same first-pass-hepatic-metabolism principal explains why oral estrogen increases triglycerides whereas cutaneous or vaginal estrogen does not. Our injected testosterone produced more marked decreases in luteinizing hormone and follicular stimulating hormone than the oral stanozolol demonstrating that the testosterone had a more powerful androgenic effect, but still did little to HDL-C. Why?
First, the testosterone did not go through the liver so it had little effect on HTGL, and second, testosterone is aromatized to estrogen in fat cells and estrogen increases HDL. We repeated the testosterone injections, but blocked its conversion to estrogen using testolactone, an aromatase inhibitor. We showed a bigger decrease in HDL-C with testosterone when we simultaneously decreased estrogen production by giving the aromatase inhibitor.(2) That’s also why body builders taking testosterone often use aromatase inhibitors. It’s hard to win male body builder competitions with boobs.
The athletes with low HDL-C are often reluctant to stop the OTC product to see if their HDL-C increases. I encourage them to try a 2 to 3-week drug holiday, and the HDL-C usually increases promptly, making the diagnosis. With kids under 18, the parents can help the child decide to take a powder break.
By the way, stanozolol was the oral anabolic steroid used by Ben Johnson, the disqualified Canadian sprinter in the 1988 Olympic Games. I got to work as NBC’s sports medicine commentator at those Olympics in part because I still had hair, and also because we were studying how anabolic steroids affected HDL metabolism. I told NBC that stanozolol would probably be detected in someone at those Olympics. I knew that because Don Catlin, MD, who directed the drug testing lab at the 1984 Los Angeles Olympics, had developed a way to detect the previously undetectable stanozolol. Don measured our samples for several of our AS studies. (2)
1. P D Thompson 1, E M Cullinane, S P Sady, C Chenevert, A L Saritelli, M A Sady, P N Herbert. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA. 1989 Feb 24;261(8):1165–8. PMID: 2915439
2. Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD. The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity. Metabolism. 1993 Apr;42(4):446–50. PMID: 8487666
