Over the course of the last few decades, estrogen has gone through the same kind of reputation slingshot as…well…Toyota.
First, estrogen was adored by all. Both health experts and women hailed estrogen-replacement therapy as the fountain of youth. A solution that would restore sanity, comfort and beauty to women entering menopause.
But when several studies came out showing that supplemental estrogen increased women’s risk of endometrial cancer by as much as 800%, along with increasing other health risks, estrogen lost its glamorous appeal…
Estrogen has now become the villain. As the latest term for estrogen-related problems, “estrogen dominance” implies, estrogen dominates your body with a vengeance, cracking the whip to get breast cancer cells to proliferate and igniting hot flashes to make you lose your cool.
But like most stereotypes, estrogen is both and neither of these. Because estrogen is not just one estrogen. It is many different compounds.
And the more you understand about the range of estrogenic compounds and how they behave in your body, the more you can gain control over your health and put estrogen in its – I mean, their – rightful place.
The True Identity of Villainous Estrogen Revealed…
See, yes indeed estrogen spurs cancer growth. In fact 60-65% of breast cancer is estrogen positive breast cancer, meaning estrogen stimulates the cancerous growth. This is even more predominant in older women with breast cancer.
And – yes, guilty as charged – estrogen is the pyromaniac making your temperature go bonkers at a moment’s notice during menopause.
Yes, it’s estrogen… but let’s be specific. The 17 beta-estradiol form is the strongest estrogen produced by the human body. And this form of estrogen seems to be associated with breast cancer and cell proliferation.
Estrone is another potent form of estrogen, but not nearly as strong as 17 beta-estradiol. The estrone form seems to be responsible for your menopausal conflagrations, as well as being associated with breast cancer growth.
The potency of these estrogens as well as the specifics of how they interact with your cells’ chemistry has everything to do with how they affect your body.
Let me explain…
Some Estrogens Stimulate And Others Inhibit
Hormones like estrogen take basically two steps before they affect your body. They’re like an ignition key. First they have to fit into the lock – or hormone receptor – on a cell. And then they have to actually turn the ignition to get things running.
The 17 beta-estradiol form does all of this. It fits into the estrogen receptors on cells and then turns on the ignition to start certain activities like starting DNA transcription to get cells to reproduce and grow. But there are other estrogens. And unlike the estrogens that turn certain cell functions on, some forms don’t have the wherewithal to turn the ignition.
But before you think that these other estrogens or estrogen-like compounds are duds – understand this: They serve a very specific purpose. When they sit in the ignition, they occupy the receptor, which in turn means the more powerful estrogen – like 17 beta-estradiol – can’t get in there to insert itself in the lock and turn the ignition on. They can’t signal your breast cells to start multiplying.
Instead, the more potent estrogens – without a keyhole to fit in – float around in the blood, powerless. Better yet, as your body notes the high levels of these estrogens in the bloodstream, it gets the message that there is too much. So your body starts to lower production of these powerful estrogens.
Weaker Estrogens Help Protect Against Cancer
One of these “weaker” estrogens is the hormone estriol. The placenta makes estriol during pregnancy. This form of estrogen is significantly weaker than 17 beta-estradiol.
And interestingly enough, not only does this hormone “lock out” 17 beta-estradiol, but has been shown to correlate with the remission of breast cancer. In fact in one study conducted by researcher H.M. Lemon, women who had high levels of this estrogen were less likely to get breast cancer. And in another study, when post-menopausal women with spreading breast cancer were given this form of estrogen, 37% of them experienced a remission or complete stop of the tumor’s growth.
The lesson here? All estrogens aren’t bad. In fact even 17 beta-estradiol is made for a reason – it helps your breasts grow during adolescence, for one. But your body has an elaborate system of checks and balances to keep these in potent ones reined in.
However, with stress, environmental pollutants, illness and even other medications, our bodies’ ability to keep this delicate dance of estrogens up can easily be compromised.
And for this nature has another answer – plants.
Pomegranate’s Phytoestrogens: Helpful Not Hazardous
Plants like soy, red clover, black cohosh and (yes, our favorite) pomegranate contain their own estrogens called phyoestrogens (”phyto” means plant) or compounds with estrogenic effects.
In fact pomegranate contains a wider variety of phytoestrogens than any other plant. And one of the phytoestrogens found in pomegranate is another very weak estrogen – 17 alpha-estradiol. This form of estrogen is actually a mirror image of 17 beta-estradiol. But while 17 beta-estradiol is the most potent of estrogens, 17 apha-estradiol is the mildest.
In vitro (laboratory petri dish) studies as well as studies on mice have shown that, indeed, this and other estrogens from pomegranate occupy the ignition switch so stronger estrogens can’t take affect.
And there are other pomegranate compounds that are not estrogens, yet they also compete with estrogens for those ignition spots. Researchers noted that the conjugated fatty acids found in pomegranate, such as punicic acid, shut out other estrogens from binding with receptor sites in a manner similar to the cancer drug tamoxifen. And alpha-eleostearic acid, newly identified in pomegranate, seemed especially potent in inhibiting estrogen-sensitive breast cancer cells.
But pomegranate goes even further in keeping your estrogen activity in check.
Other recent research indicates that pomegranate extracts not only block estrogen activity, but block the enzyme that makes estrogen from its precursor androgen. This makes pomegranate a potential aromatase inhibitor (AI), the name of a class of drugs used for the treatment of estrogen-positive breast cancer. And unlike AI drugs, pomegranate has none of the side effects like joint pain, heart problems or bone fractures.
Certainly, the research on breast cancer and pomegranate is still in its early stages. Most of the studies demonstrating pomegranate’s ability to not only block breast cancer development but also kill cancer cells are done in laboratories or on animals. To date, there are no clinical trials.
But the promise is hopeful. As Dr. Sherrill Sellman notes in her book Hormone Heresy: What Women MUST Know About Their Hormones,
“The ability of the many components found in the pomegranate fruit to help safely modulate and regulate hormones is certainly good news for women of all ages. These weaker and safer forms of estrogens… will not contribute to estrogen dominance.”
Women have turned to this fruit for generations to keep them in good health. And with no documented side effects. Quite the opposite, the evidence gives us plenty of indication that we can only benefit from getting more of this most medicinal fruit and its complex array of phytoestrogens and estrogen-like molecules.
Sources:
Berger GS et al. Exogenous estrogens and endometrial carcinoma: review and comments for the clinician. J Reprod Med. 1977 Apr; 18(4): 177-80
Estrogen Receptor Status May Determine Chemotherapy Use. http://news.med.cornell.edu/nyp_health/nyp_health_2006/estrogen-receptor-status-.shtml
Tran, HNA et al. Pomegranate (Punica granatum) seed linolenic acid isomers: Concentration-dependent modulation of estrogen receptor activity. Endocrine Research, 2010. 35(1): 1-16.
Sellman, Sherrill. Hormone Heresy: What Women MUST Know About Their Hormones. Bridger House Publishers, Hayden, ID, 2009.
Watson et al. Nongenomic actions of estradiol compared with estrone and estriol in pituitary tumor cell signaling and proliferation. FASEB Journal, September 2008, 22.
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