A few years back, there was a rash of positive drug tests in the track and field world. Interestingly (and not surprisingly), many of them blamed tainted supplements.  “Coach, I swear, I was just taking protein powder and creatine… that’s it!”

Coach says, “What about those needles in your bag?” 
“Coach, that’s for B12 injections.”  
Yeah… well, if you believe that, you probably believe that folks speak English in South Beach, Miami, Fla. 
   

What actually was happening was that many of these athletes were taking some form of nandrolone. In the track and field world (actually the entire athletic world outside of bodybuilding), taking the nandrolones is a no-no because the stuff clings on to you like an old girlfriend with a fatal attraction.    

A recent investigation looked at the pharmacokinetics of nandrolone in serum and urine. The researchers investigated healthy young men after a single intramuscular injection of 50, 100, or 150 milligrams of nandrolone decanoate— hardly what I call whopping doses. In fact, the dose is something you might give your pet Beagle. Nonetheless, blood samples were collected before treatment and for up to 32 days after dosing. In addition, in the 50- and 150-milligram groups, 24-hour urine samples were collected before treatment and on days one, seven and 33 after treatment; in the 150-milligram group, additional samples were collected after three and six months.
  

  Serum concentrations and the area under the curve of nandrolone increased proportionally with the dose administered. In other words, the more you took, the more appeared in your blood. Good thing for needle technology, huh?
   

The peak serum concentration ranged from 2.14 ng/ml in the 50-mg group to 4.26 ng/ml in the 100-mg group and 5.16 nanograms per milliliter (ng/ml) in the 150-milligram group. The peak serum concentration was reached after 30 hours (50 and 100 milligrams) and 72 hours (150 milligrams), whereas the terminal half-life was seven to 12 days. In urine, pretreatment concentrations of 19-norandrosterone (19-NA) and/or 19-noretiocholanolone (19-NE) were detected in five of 37 subjects (14 percent). In the 50-milligram group, 19-NA and/or 19-NE could be detected at least until 33 days after injection in 16 of 17 subjects (94 percent).  But here’s the kicker. In the 150-milligram group, the members of which were presumed to not have previously used nandrolone, nandrolone metabolites could be detected for up to six months in eight of 12 subjects (67 percent) for 19-NE and in 10 of 12 subjects (83 percent) for 19-NA.1
   

So like I said, this stuff clings to you like Velcro.

T Lowers Adiponectin
    This story falls in the “keep an eye out for this” category. Adiponectin is a hormone that appears to burn fat in muscle cells and helps reverse insulin resistance, according to recent studies. For example, accumulation of fat in muscle cells is strongly associated with insulin resistance and perhaps adiponectin supplementation might be a viable way to treat insulin resistance and type 2 diabetes.  Where is adiponectin made? Well, believe it or not, Mr. Ripley, it’s from your fat cells. It’s a peptide hormone that’s affected by diet and yes, testosterone. Moderate alcohol intake is associated with higher adiponectin concentrations, whereas a carbohydrate-rich diet with a high glycemic load is associated with lower adiponectin concentrations in men with no history of cardiovascular disease.2 So drink your wine and stay away from bagels and white bread. However, let’s get back to testosterone and adiponectin.
     For off, we know that testosterone (T) administration to men increases lean body mass and decreases fat mass. A recent study measured adiponectin levels in 28 healthy men ages 18-35 years before and during treatment with a potent gonadotropin-releasing-hormone (GnRH) antagonist, acyline. Decreased T levels led to increased serum adiponectin within seven days. In a second study, 25 men aged 55-85 years were treated with three weeks of high-dose T (testosterone enanthate [TE], 600 milligrams per intramuscularly). With high serum T levels, adiponectin levels decreased significantly by day 21 of treatment (baseline 14.3 +/- 1.9 compared with 10.8 +/- 1.5 micrograms per milliliter, P <.05 vs baseline and placebo), BMI slightly increased and leptin levels were decreased. 
These scientists concluded that adiponectin levels increased within days of experimental T deficiency in normal men, and the increase in adiponectin is prevented by T replacement. Furthermore, supraphysiologic T administration results in decreased adiponectin levels. Thus, it looks like T, its metabolites, or both, directly suppress adipocyte production of adiponectin.3 Now, if this is the case, it would suggest that T administration by itself may, in fact, increase one’s risk of metabolic syndrome and other cardiovascular-related maladies. I think a follow-up investigation on T combined with exercise and the effects on adiponectin might show otherwise.4

     Low Dose HCG… We Knew that, Didn’t We?
    To jumpstart your twins in the nether regions, particularly after a cycle, injections of HCG seem to do the trick. A recent study determined the dose-response relationship between human chorionic gonadotropin (hCG) and intra-testicular testosterone (ITT) to ascertain the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 milligrams of T enanthate weekly in combination with either saline placebo or 125, 250, or 500 IU hCG every other day for three weeks. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and at the end of treatment.
    Did you read that, too? They stuck a friggin’ needle in there! Reading that makes me want to curl up into the fetal position.
    Baseline serum T (14.1 nmol/liter) was 1.2 percent of ITT (1,174 nmol/liter). LH and FSH were profoundly suppressed to five percent and three percent of baseline, respectively, and ITT was suppressed by 94 percent (1,234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose. Post-treatment ITT was 25 percent less than baseline in the 125 IU hCG group, seven percent less than baseline in the 250 IU hCG group and 26 percent greater than baseline in the 500 IU hCG group. This study shows that relatively low-dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.5

     COX Inhibitors Inhibit Aromatase, Too
    Ever since the congressional ban on prohormones, companies have been scrambling to fill the market void in this category.  Hence, the introduction of aromatase inhibitors. Why? Well, remember that estradiol (you know, the chick hormone) is made from androgens by the aromatase enzyme complex. And a recent investigation showed that COX inhibitors decrease aromatase mRNA expression and enzymatic activity in human breast cancer cells in culture. This would, in turn, suggest that these agents may be useful in suppressing local estrogen biosynthesis.6

    

Update on T for Chicks Who Don’t Eat

    Did you know that giving T to skinny women with anorexia nervosa (AN) is helpful? Well, yes indeed. We know AN is complicated by severe bone loss, cognitive function deficits and a high prevalence of major depression. A recent study randomized 33 women with AN and relative testosterone deficiency to transdermal testosterone (Intrinsa, Procter and Gamble Pharmaceuticals, Cincinnati, OH), 150 micrograms, 300 micrograms, or placebo, for three weeks. They found that depressed patients receiving testosterone improved from severely depressed to moderately depressed; the placebo group was unchanged. Spatial cognition also improved in the testosterone group, compared with placebo. Therefore, short-term low-dose testosterone may improve depressive symptoms and spatial cognition in women with AN.7 In other words, they think better and can probably drive a car in a remote area without asking for directions.

References
1.    Bagchus WM, Smeets JM, Verheul HA, De Jager-Van Der Veen SM, Port A, Geurts TB. Pharmacokinetic evaluation of three different intramuscular doses of nandrolone decanoate: analysis of serum and urine samples in healthy men. J Clin Endocrinol Metab, May 2005;90(5):2624-2630.
2.    Pischon T, Girman CJ, Rifai N, Hotamisligil GS, Rimm EB. Association between dietary factors and plasma adiponectin concentrations in men. Am J Clin Nutr, Apr 2005;81(4):780-786.
3.    Page ST, Herbst KL, Amory JK, et al. Testosterone administration suppresses adiponectin levels in men. J Androl, Jan-Feb 2005;26(1):85-92.
4.    Kriketos AD, Gan SK, Poynten AM, Furler SM, Chisholm DJ, Campbell LV. Exercise increases adiponectin levels and insulin sensitivity in humans. Diabetes Care, Feb 2004;27(2):629-630.
5.    Coviello AD, Matsumoto AM, Bremner WJ, et al. Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression. J Clin Endocrinol Metab, May 2005;90(5):2595-2602.
6.    Diaz-Cruz ES, Shapiro CL, Brueggemeier RW. Cyclooxygenase inhibitors suppress aromatase expression and activity in breast cancer cells. J Clin Endocrinol Metab, May 2005;90(5):2563-2570.
7.    Miller KK, Grieco KA, Klibanski A. Testosterone administration in women with anorexia nervosa. J Clin Endocrinol Metab, Mar 2005;90(3):1428-1433.
 

Jose Antonio, PhD is Chief Science Officer of Javalution Coffee Company (www.javalution.com) and the co-founder and CEO of the International Society of Sports Nutrition (www.sportsnutritionsociety.org).