While there are many different belief systems on whether you should and or should not need to use one, this article will go in depth on why the author believes you should, along with scientific evidence to back this up.
It’s well known (at least I think it is) that estrogen is a carcinogen. In fact, it’s a Group 1 IARC classified estrogen, which means it’s a pretty potent one really. The risks of estrogen and carcinogenic activity are then again confirmed in ‘estrogen only’ conraceptive treatment(s). Although the data is somewhat confusing (as some data is on estrogen+progestagen treatment), the links to various forms of cancer rates increasing are pretty clear.
To quote from a paper looking at the effects of estrogen-only contraceptive treatment and estorgen+progestrogen contraceptive therapy:
“Four studies (one cohort study and three large case-control studies) reported increased risk of endometrial cancer with estrogen replacement therapy (Cushing et al. 1998, Shapiro et al. 1998, Persson et al. 1999, Weiderpass et al. 1999), and three of these studies reported strong positive associations between risk of endometrial cancer and duration of estrogen use.”
“Two of four case-control studies found that estrogen-only replacement therapy was associated with an increased risk of breast cancer (Heinrich et al. 1998, Magnusson et al. 1999).”
“One study found that estrogen therapy was associated with ovarian cancer (Purdie et al. 1999).”
“In 2009, IARC concluded there was sufficient evidence of the carcinogenicity of estrogen-only therapy in humans based on increased risks of endometrial cancer and ovarian cancer and limited evidence based on increased risk of breast cancer (Grosse et al. 2009). The findings for ovarian cancer were based on two meta-analyses (Greiser 2007, Zhou 2008). Since then, another meta-analysis has estimated a significant overall increase in ovarian cancer risk related to duration of use of estrogen-only therapy (Pearce et al. 2009)”.”
“In rodents, steroidal estrogens caused benign and malignant tumors, as well as pre-cancerous lesions, in a variety of organs, including the mammary gland and female reproductive tract (IARC 1999). Estrogenic compounds generally caused endometrial, cervical, and mammary-gland tumors in mice, mammary- and pituitary-gland tumors in rats, and kidney tumors in hamsters”.
I think you get my point…
Although there is mixed data in that study, the theory that estrogen is carcinogenic is overwhelming.
So what does that all tell us? It tells us that when exposed to estrogen (steroidal) that it can cause some serious problems. Yes, these studies are done on females (I didn’t miss that), but women are a hell of a lot more tolerable to estrogen than men are. Males are not designed for increased levels of estrogen at all, women are (during pregnancy for a start). Women’s levels can hit 500pg/ml, the top end of males is 50pg/ml 10x lower.
Estrogen’s role in males is important. It’s important for GH and IGF synthesis, bone density, lipid profile, glucose uptake and utilisation, AR sensitivity and activation, immune function, anti-inflammatory effects, and a host of other benefits. Without it, we (males) wouldn’t function properly.
There are studies of and against the importance of sex hormones in CHD and mortality, but the hypothesis is plausible. Why?
- Estrogens inhibit smooth muscle proliferation and decrease smooth muscle tone
- Their effects on lipid profiles
- High-affinity estradiol receptors are present in both vascular smooth muscle and endothelium
- Estrogens enhance the release of nitric oxide and prostacyclin from endothelial cells, thus inducing vasodilation
- Estrogens exert indirect effects on the cardiovascular system through their influence on lipoprotein metabolism and coagulation, fibrinolytic, and antioxidant systems
So one can not see the importance estrogen has on the cardiovascular system, CHD, therefore mortality rates. Here is a good solid article on estrgens links to CHD, found here.
How else does estrogen negatively effect males?
Well, recent research has confirmed its role in the most common form of cancer in males – prostate cancer. The basics of which are shown here. These are very recent findings and more research is to be done. However, the links and risks are evident, and whilst DHT was thought to play the main role (10 years ago), estrogen and also prolactin (which worsens prostate cancer) have been shown to have positive effects on expression and proliferation in cancerous prostate cells in vitro and vivo. On the plus side, Tamoxifen has been shown to inhibit expression and proliferation, much like it does in female breast cancer patients.
When I see someone argue that an AI just isn’t needed on a cycle, I think to myself, why is it not needed? Based on what? Because you haven’t got a gyno? The user may not experience side effects such as gyno, water retention, acne, but their estrogen level is surely as f*ck high.
Aromasin (Exemestane) at 10mg/ED will keep most people’s estrogen levels below 50pg/ml on cycle IMO.
It’s what I do and I am sensitive to estrogenic side effects (very). The common reason for not using an AI is, that it may limit gains made… But do they?
AI’s have little impact on IGF-1 levels and Exemestane does not have any effects at all, as shown here. If IGF-1 was somewhat lowered, we also need to understand that exogenous testosterone and other anabolic steroids are going to increase IGF-1 and further negate these effects. To understand how little effect AI’s have on IGF-1, read this study. To summarise: Nine young healthy men who received Femara at 2.5 mg daily for 28 days had a 15% reduction in IGF-1, a 24% reduction in leptin, and a 14% increase in LDL (bad cholesterol).
As for Exemestane on lipid levels, it has far less impact than other AI’s although it does not have the beneficial effects of SERMs. Some data, such as this one, it has no “no clinically significant effect on the serum lipids”. Another study stated, “Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels”
Here is one on young males that’s slightly more applicable, this study states, “Plasma lipids and IGF-I concentrations were unaffected by treatment.”
Finally, because of the Long Feedback Mechanism (google it), controlling estrogen means we can help control prolactin. So there is more of a reason to use AI when using 19-Nors (if you experience increased PRL). I’d also keep a D2-agonist on hand though.
My advice is to keep estrogen in “normal ranges”. That needs to be decided by trial and error (experimentation).
The key here is to keep it in the normal ranges when “on cycle”, not high off the charts and not too low. Too low – and we can experience a host of other side effects, from loss of libido, energy, joint problems, CNS function, anxiety, and erectile dysfunction.
It needs to be balanced and the only way you’re going to find out your estrogen level on cycle is BW. Have BW done when “on cycle” and taking the AI and see where you are at. Or have BW done on HRT (if you’re on HRT) and see where you’re at. Some doctors/endo’s prescribe AI’s because HRT can push estorgen high in those sensitive or estorgen dominant.
My advice: Aromasin on cycle 10mg/ED. It can be even lower when using DHT derived steroids because of their anti-estrogenic effects. This AI dose will change with the total dose of aromotasable compounds. Put simply, if you’re on compounds that aromatase – use more if you need to. 19-Nor’s will also affect this dose.