Soy is perhaps, second to chocolate, the food most closely associated with women. It is not only a vegetarian staple, which automatically makes it a womanly food, but it also acts as an estrogen in the body. Yet interpretations of what this means for the female body vary: is soy (and flax, another potent phytoestrogen) the fountain of youth, or is it a toxin?

What advice do we heed? What’s actually going on inside of our bodies?  It’s hard to tell.  But with just a bit of science the waters become less murky, and we can glimpse the truth of why eating soy, flax, and other phytoestrogens can be so risky.

What is a phytoestrogen?

Phytoestrogens are a class of chemicals that resemble estrogen, but are not identical to estrogen. The whole category is called xeno (= false) estrogens.  And then as a subclass come then phytoestrogens. Phyto means plant. Estrogen means estrogen. Phytoestrogens are plant estrogens.

There are, moreover, several varieties of phytoestrogens.  The primary kinds are coumestans, isoflavones, and lignans. Coumestans are found in split peas, pinto and lima beans, alfafa sprouts, and most importantly, red clover and clover sprouts. Isoflavones are found in soy (powerfully), green beans, alfafa sprouts, chick peas, peanuts, and red clover. Lignans include flax seed and sesame. Other less potent sources are rhy, wheat, oal and barley, nuts, and some fruits and vegetables. Note that there is often significant overlap of phytoestrogens between different foods.  Here is the most comprehensive and scientifically accurate list of phytoestrogen content of foods I have yet been able to find that is publicly available.  Here is the journal article (even more comprehensive) that gave birth to the bulk of the information out there.

Soy and flax are the most potent phytoestrogens by far.  Yet all legumes, seeds, and nuts are phytoestrogens. Please note, moreover, that phytoestrogens are orders of magnitude less potent than regular estrogen. This means that a healthfully functioning man or woman should be able to handle consuming phytoestrogens from time to time.  However, women with hormone balance issues, as well as people who regularly consume vegetable oils, nuts and soy, would do well to consider how potent their phytoestrogen intake can really be.

What is estrogen?

Estrogen is actually a catch-all term for a wide variety of chemicals with similar shapes and functions, such as estrone (E3) and estradiol (E2). During a woman’s reproductive years, estradiol levels are much higher than other estrogens, so for these women, referring to estrogen almost always means estradiol. During menopause, estradiol levels drop off, and the bulk of a woman’s estrogen content becomes E1 and E3. This is important because E2 is the form of estrogen the ovaries pump out, and is also what is has the greatest effect in a woman’s reproductive years on partitioning fat to the hips and thighs rather than the abdomen. Plummeting E2 is why many women experience increases in abdominal fat during menopause.

How does the body perform estrogen signalling?

Estrogen is a hormone, which means that it is one of the chemicals in the body that works primarily as a signal: it tells cells and organs what they should be doing.  The sex hormone signalling process “begins” in the pituitary (with overhead influence from the hypothalamus in the brain).  It is up to the pituitary to tell the ovaries what to do, and they, in turn, produce estrogen.

The hypothalamus and pituitary glands have estrogen receptors liberally positioned through them.  These receptors tell them how much estrogen is circling throughout the body at any given time.  Think of it like keys and locks: estrogen receptors are the locks, and estrogen molecules are the keys.   With more keys, more locks can be filled. With fewer keys, locks end up sitting there empty, and rusted.

When the locks are filled, the pituitary detects “estrogen sufficiency!” in the body, and it down-regulates the strength of the “please pump estrogen” signal it sends to the ovaries.  This makes the ovary produce less estrogen.  The whole purpose of this system is to maintain stable estrogen levels in the blood.  If estrogen levels get too high, then the pituitary (in a healthy body) tells the ovaries to back off.  If estrogen levels are low, the pituitary (in a healthy body) revs up estrogen production.

So is the problem that phytoestrogens, in resembling estrogen, bind to estrogen receptors and mess up hormone production?


Does it get more complicated?

You bet your sweet ass it does.


What the medical community recognizes phytoestrogens do

Phytoestrogens act as estrogen in the body.  But here’s the trick: while phytoestrogens have a pretty good ability to bind to estrogen receptors, they have less of an ability to give instructions the way true estrogen does.

This fact is so important it bears repeating.  Phytoestrogens look enough like estrogen to bind to estrogen receptors, but they do not look exactly like estrogen.  This makes their ability to perform estrogen functions inferior to true estrogen.

When we eat phytoestrogens, they enter our bloodstreams.  This means that, to many doctors, women with low estrogen levels should eat phytoestrogens. Phytoestrogens would signal “fullness” to the estrogen receptors, sure, but they would also perform the normal functions of estrogen in the body.  If a woman has low estrogen, the medical community doesn’t really think she can boost those levels by any means other than supplementing with food or with drugs, right?, so adding some phytoestrogen into her diet could do her nothing but good.  Like I said, she may be signalling estrogen ‘fullness’ to her hypothalamus and pituitary, but perhaps it would be worth it if it could boost estrogenic activity.

By the same token, many doctors argue that women with high estrogen levels also should supplement with phytoestrogens.  This is because the phytoestrogens would flood the estrogen receptors, which in turn wuld down-regulate estrogen production, without really increasing estrogenic activity too much.  Or so the theory goes.

In reality, however, women with low estrogen often suffer more from the binding of estrogen receptors than they might benefit from limited increase in estrogenic activity (particularly if by filling the estrogen receptors they actually reduce their already limited estrogen stores.)  Women with high estrogen levels clearly already have flooded receptors, so adding more estrogen into the mix is not necessarily going to help anybody.

The solution might be, then, to restore estrogen balance by other methods.  Increase fat mass, if underweight.  Decrease fat mass if overweight.  Exercise when it feels right.  Eat anti-inflammatory, paleo foods.  Sleep.  Etc. You can read about all of these in my book, available here.

Does it get even more complicated?


What we have dealt with so far are phytoestrogens and estrogen receptors.

What the body is actually dealing with are three primary types of phytoestrogens (plus dozens of sub-types): lignans, coumestans, and isoflavones, and two types of estrogen receptors: estrogen receptor alpha (ERa) and estrogen receptor beta (ERb).

Different estrogen receptors have different shapes, and are distributed unevenly throughout the body.  ERa is concentrated more heavily in the hypothalamus than ERb, for example.  ERb is concentrated more heavily in skin tissue.    It also varies for fat cells, for ovarian cells, for different types of brain cells.  It is a complicated mix.

Coumestans have a unique chemical shape (with two hydroxy groups in the same position as estradiol).   Coumestol has the same binding affinity for the ERb receptor as estrogen, but it has much less of an afinity for ERa.  This fact means that ERb’s will get filled up by coumestans, but ERa-heavy tissue might suffer a decrease in estrogen-like activity because estrogen production in general gets down-regulated by the hypothalamus, pituitary, and ovaries, etc, in response to the coumestol, thus making estrogen levels decrease in ERa tissues relative to ERb.  Additionally, the shape of coumestans means that coumestans have the ability to inhibit aromatase.  Aromatase is the process of converting testosterone to estrogen in cells.  This is a big deal for women with PCOS who have high testosterone and low estrogen levels.

Different isoflavones bind to different estrogen receptors differently (my head is spinning, too).   Some bind more strongly to ERa, and others to ERb (genistein, dihydrogenistein to ERb, equol to ERa).  Yet most importantly, many (though not all) isoflavanones that have been tested have the same binding affinity as actual estrogen, but half the receptor-dependent transcriptional power.   This is a powerful fact, that isoflavones have half of the ability to perform estrogenic function as they do to take up space.

There are so many different kinds of lignans that it’s best to just walk away and shake your head.

As a matter of fact, that notion applies I believe to all phytoestrogens.   Walk away and shake your head.  I have included this last section about estrogen receptors and phytoestrogens in this post not to incite anyone to figure out which plant they should be eating in order to fix which specific tissue in their body, but rather to demonstrate the enormous complexity of phytoestrogen biochemistry.

The takeaway

Phytoestrogen biochemistry is complicated.  Some studies have shown that phytoestrogens boost estrogen activity, and others have shown that they decrease estrogen activity.   This varies widely by the population studied, too.  What were the women’s estrogen levels beforehand?  Were they healthy women?  Fertile women?  Women who grew up eating soy?  Women who are routinely exposed to xenoestrogens?  There are too many questions still yet for real answers, yet above all I believe it indicates that we should step lightly around soy.

The fact of the matter is that while the medical community has yet to understand and come to grips with phytoestrogen biochemistry, it is clear that phytoestrogens can cause unnatural hormonal disruptions.  This is especially problematic for people with high or low estrogen levels or other reproductive issues.  If estrogen seems to be increasing by one measure in one type of receptor and in one type of tissue, it is possibly decreasing in others.  And vice versa.   This can do real damage, since it is impossible for us to understand what is going on in every kind of our tissues at once.

The solution, then, is in my opinion to minimize the influence entirely.  You are welcome to disagree.  Many doctors do.  Yet in my personal and research-based experience, soy is not a way to find hormone balance.  Even if it patches a leak for a long time, it may be creating other holes, and it will never repair the bottom of the ship.

Instead, as I mentioned briefly above, I believe that holistic healing, stress reduction, paleo foods, and weight management all fare much better for women in the long term, and definitely with fewer risks. You can find more about how to live a healthy, whole foods lifestyle in my book, Sexy By Nature.

This post did not even touch on breast and other estrogen-dependent cancers.  That pool of research is a conflicting box of vipers all on its own.  But I will cover it in due course.  Suffice to say, it is an uncertain and risky landscape.




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