By: Andy Abbate, Presented By Driven Sports
Often maligned, regularly misunderstood, and with an aura somewhat similar to Dr Jekyll and “Mrs Hyde”, nature’s female sex hormone is a hell of a lot like… Well, I’ll refrain from any comparisons to women (but I do love them crazy chicks). Yes, I am talking about estrogen. What is Estrogen?
It’s a duplicitous mystery hormone and while figuring it out completely is a life’s work, learning to control and manipulate it to your advantage is far easier, albeit still a growing, evolving challenge.
Sex Hormone Binding Globulin (SHBG): Who’s binding whom?
I think a common misunderstanding in fundamental endocrinology is the phrase “SHBG”, which implies no real specificity for testosterone over estrogen, although most associate it solely with testosterone. To clear the confusion, let’s quickly examine a method doctors use to determine the distinction: it’s called metabolic clearance (MCR), and it’s measured in liters per day. In healthy men, estradiol, the more genetically potent metabolite of estrogen, leaves the body at a MCR or 1,500 L/day, while testosterone rivals at 1,000 L/day (Becker et al., 1044). The larger number for estrogen suggests that testosterone is mostly bound to SHBG while estrogen is only weakly bound, with approximately 10% of the affinity versus testosterone (Becker et al., 1051). So supplementing with something like stinging nettle root (found in Driven Sports’ Activate Xtreme) has a far more profound effect on increasing free testosterone, which is genetically active, versus free estrogen.
We strength athletes have breast cancer research to thank for galvanizing estrogen receptor research, through which endocrinologists and physiologists have unraveled the mystery of estrogen-sensitive breast cancers and the estrogen receptor (ER). Further, ER subtypes alpha and beta were discovered along the way, which brings us to our goal: to use this information to manipulate estrogen.
ER-alpha is generally found in breast tissue and it’s notorious for bolstering hormone-sensitive breast cancer cell division, and it’s a common target for breast cancer drugs, but that doesn’t exonerate ER-beta. The molecular distinctions are outside the scope of this article, but keep in mind that while the receptors behave very differently on a molecular level, they are both directly involved in cell growth signaling.
The distinction is relevant to us because recent research suggests that targeting ER-beta agonism without activating its evil twin sister supports skeletal muscle anabolism (Velders et al., 2012). I know I’m not alone when I hypothesize that caffeic acid-phenylester (CAPE, which is found in Driven Sports’ Triazole), can be an extremely valuable addition to a natural athlete’s supplement arsenal. Further, CAPE antagonizes ER-alpha while activating ER-beta, propagating an anabolic cascade supporting strong muscles, joints, and bones while preventing unwanted estrogenic side effects. It’s a remarkable compound with a theory to match.
There are a few naturally occurring aromatase inhibitors on the supplement market that are sold on research that seems promising to the untrained eye, but surprise: it’s not so simple.
Most of us are aware that decreasing estrogen increases testosterone, but the hypothalamic middlemen (LH and FSH) don’t discriminate; they bring their own bag of tricks that can end up being counterproductive if your goal is decreasing estrogen. In short, FSH signals an increase in aromatase which can result in a proportional increase in estrogen, but this only happens when the AI isn’t strong enough to compensate for the increased aromatization. This translates to short-lived drop in estrogen (the tease) followed by a net increase, which may even be enough to aggravate existing gynecomastia.
It’s important that you see blood testosterone and/or estrogen levels before, during, and about a week after cessation of a potential aromatase inhibitor. Make sure you can view reliable blood-work on a purported AI before making a purchase.
Get Outta Those Genes
We’ve briefly covered estrogen’s cell signaling capabilities, which is genetic, but one of the reasons estrogen is such a mystery is because it carries a myriad of potential effects that don’t involve receptor binding and subsequent gene activation. Like the alpha/beta receptor distinction, these effects can also be either positive or negative.
The potential danger comes from a type of estrogen metabolite called a 4-hydroxy-estrogen quinone. These nasty little molecules interfere with DNA amino acid-amino acid interactions in such a way that can influence carcinogenic mutation in otherwise normal cells. However, if you’re a strength athlete you likely eat a balanced diet consisting of cruciferous vegetables, which contain compounds that inhibit the formation of the dangerous estrogen metabolites and induce the formation of potentially beneficial metabolites, which I’ll discuss in the next paragraph.
While you can certainly choose to supplement with the compound in mind, indole-3-carbinol, I recommend eating lots of broccoli instead for its nutrient rich profile and fibrous texture as well as its diindole-methane and indole-3-carbinol content.
An innocuous cousin from the same family of hydroxylated estrogens carries an interesting, non-hormonal effect that can have a considerably positive effect on brain function. Catechol estrogens, again, not the same ones that can cause cancer, interfere with the degradation of neurotransmitters like dopamine, serotonin, and norepinephrine in the liver and kidneys by inhibiting an enzyme called catechol-O-methyltransferase (COMT) (Becker et al., 756). This could potentially mean better overall cognitive function as a result of healthy estrogen metabolism and they have in fact been evidenced as synergistic with neurotransmitters in vitro (Ball et al., 1972).
In the brain, catechol estrogens are found in 10-fold higher concentrations than active estrogen and they may also act as mild anti-estrogens, promoting testosterone production and, as mentioned, contributing to catecholamine-mediated neurotransmission; however, the former (increased testosterone as a result of I3C supplementation) has not been supported as statistically significant in humans (Hild-Petito et al., 1988; Brown et al., 2002).
What is Estrogen? Estrogen is a part of your life, and no matter what you’ve experienced, it’s not evil. My advice to strength athletes is to seek understanding in the dichotomy between its benefits and its detriments: use the information to get bigger, stronger, and faster, while simultaneously avoiding over-thinking, which is unnecessarily exhausting. Also, eat your brocolli.
Becker K, Bilezikian J, Wellington H et al. Principles and Practice of Endocrinology and Metabolism. 2nd ed. Philadelphia: J.B. Lipponcott Company, 1999.
Ball P, Knuppen R, Haupt M et al. Interactions between estrogens and catecholamines. J Clin Endocrinol Metab 1972;34;736.
Hild-Petito S, Stouffer RL, Brenner RM. Immunocytochemical localization of estradiol and progesterone receptors in the monkey ovary throughout the menstrual cycle. Endocrinology 1988;123;2896.
Brown G, Vukovich M, Martini E, Kohut M, et al. Endocrine and lipid responses to chronic androstenediol-herbal supplementation in 30 to 58 year-old men. J Am Coll Nutr 2002;20;520-28