Whey vs Soy... have we been tricked?

Nutrition Discussions Supplements
1

OK, so I have always considered soy protein a no-go because I’d heard that it contained phyto-estrogens…

However I just found an interesting article…

Daidzein is a key isoflavone found in soy that acts as a potent phyto-estrogen. It is structurally a very weak “pseudo-estrogen” (about 1000 times weaker than the body’s primary estrogen estradiol). This is good news to the bodybuilder because weak estrogens like daidzein will compete with stronger estrogens like estradiol for available receptor sites to “bind” to. By binding to the receptor sites daidzein then “blocks” the stronger estrogens from binding to and activating receptor sites. With the daidzein isolflavone attached, estrogen receptor sites remain inactive. This inactivity further minimizes the negative effects of estrogen in the body. Many researchers believe this effect is the reason soy protein is linked to a reduction in the risk for many forms of breast, endometrial, and prostate cancer. This mechanism works similarly to the prescription drug Nolvadex (tamoxifen citrate)–an anti-estrogen staple in the bodybuilding community.

http://www.timinvermont.com/fitness/soyvswhy.htm

The rest of the article outlines the benefits of soy over other proteins…

So what are your thoughts of the role of phyto-estrogens in the body??

2

I’d be very careful with your soy consumption. Judging by your Avatar, it’s beginning to have side effects on you!

3

I don’t get this argument. If daidzein is 1000 times weaker than normal estrogens this would be because it binds 1000 times weaker to the estrogen receptor, in which case it would not be able to outcompete endogenous estrogens (unless present at 1000-fold higher concentrations). If there is anything to this theory than it must be more complex than that. Even if this blocking effect is true, however, it would likely result in increased production of endogenous estrogens due to blocking estrogen receptor mediated negative feedback mechanisms (i.e. the body would ‘think’ it doesn’t have enough estrogens and thus produce more).

4

I thought I’d do a quick google search on soy and estrogen and the first link I found was this…

http://www.mothering.com/articles/growing_child/food/soy_story.html

While it is not intended for athletes, it is very in depth, extremely well referenced (111 citations) and offers a rebuttal page for those with comments, pro and con. For anyone currently consuming, or thinking about consuming, soy products, might want to take a quick peak at this.

5

Well whatever she’s consuming she’s still got bigger quads than me, haha!

I’ve never consumed soy personally, although I wonder why it’s such a baddy as a quick search for phyto-estrogens reveals that nuts and seeds contain the highest concentrations… but nuts are recommended for healthly test levels… so why is soy so bad??

6

Strength of signal is not the same as the strength of binding. That is, just because the phytoestrogen sends a weaker signal (once bound to the estrogen receptor), that doesn’t mean that it doesn’t bind at the same (or more, or less) level.

So the idea is that phytoestrogens act as competitive inhibitors to estrogens in the body; they tie up the receptor but send much less of a signal.

In premise, this means that they might reduce overall estrogenic signalling (b/c the receptor is tied up by the phytoestrogen but the signal being sent is weaker).

When I looked into soy for my protein book, what I basically found was that, like one of the links in this thread says,it has pros and cons.

On the pro side, it has a pretty decent amino acid profile (especially some of the isolates); on the con side, it doesn’t appear to support protein synthesis or growth as well as milk proteins when consumed after resistance training.

On the pro side, it may improve endogenous anti-oxidant status. On the con side, there is the issue of hormonal effects.

Some work has found a negative impact on hormones (e.g. lowered testosterone) above a certain amount of phytoestrogens (roughly 50-60 mg/day from memory). That’s maybe one serving (20-25 grams protein) of soy per day since a typica soy protein has about 2-3 mg phytoestrogens per gram protein.

Even this is variable. In one recent study, while one guy saw a massive drop in testosterone (he was starting off from a super high level), a few subjects showed a slight increase. So it gets complicated and there seems to be a lot of individual variance.

I think a lot of the concern over soy comes from the way we do things in the US. People hear that something is ‘healthy’ and that means ‘eat as much of it as you can put down’.

If something is good in small amounts, it must be great in large amounts, right?

Usually not.

If you look at actual soy intake among Asian cultures on a day to day basis, it isn’t massive (a point made in the second article linked). But Americans took the ‘some is good so more is better thing’ and soy is being included in a lot of foods. Many people are already getting soy in their daily diet without adding more via a protein powder.

And excessive amounts can cause problems (including impaired thyroid conversion, esp. in the context of low sodium diets).

As well, the increased conversion of T4 to T3 was only shown in animal models, not humans. So that claim in the elitefts article is incorrect.

Basically, a small amount is probably ok but large amounts can be problematic.

Lyle

7

That may be what the author(s) is (are) trying to make you believe, but it’s simply not true.

The affinity of daidzein for the estrogen receptor (ER) is, indeed, more than 1000 times lower than that of estrogen. As suggested, it will thus only outcompete the latter if present at a > 1000-fold higher concentration.

The strength of the signal caused by daidzein binding to estrogen receptor alpha (as measured by binding of the engaged receptor to the estrogen response element) is 30,000 fold weaker than that caused by estrogen. Daidzein binding to ER beta, however, produces a signal that is only about 50 times weaker. While the response to ER beta binding may be somewhat different to that of ER alpha binding, it is thus not correct to postulate that the relative signal strength induced by daidzein is less than its relative affinity for the ER. Moreover, daidzein can be metabolised to equol which then is also a strong agonist of ER alpha.

Where studies show an estrogen blocking effect, they used cells grown in the presence of very high doses of daidzein. The effect was that these cells increased their estrogen production because their estrogen receptors were blocked by the massive amounts of daidzein thus interfering with their ability to determine true estrogen concentrations and thereby eliminating negative feedback mechanisms.

8

Any thoughts on consuming phytoestrogens from other food sources… like nuts? Should all sources of phytoestrogens be controlled. I ask as Soy gets the wrap for high phytoestrogen concentration but I’ve read nuts and seeds are higher…??

9

Phytoestrogens, or the plant “version” of estrogen found in various edible foods, such as soy and soy protein, serve primarily as weak precursors to estrogen production. The isoflavones found in soy, for example, are similar in chemical structure to human estrogen, but Shippen notes that typically such estrogens have only about 1/500th the active effect of estradiol, the most active human estrogen.

“The fear of soy protein and phytoestrogens is absurd,” says reigning USA champ Tom Prince.“You need the proper receptor sites, and a significant amount of them, to produce estrogen in the body through ingestion of phytoestrogens.”

Men have fewer estrogen receptors than do women. Additionally, there is a technique for manipulating these sites in men so that genuine estrogen is minimized: Shippen suggests that high levels of phytoestrogens compete with the female hormone for receptor sites, block its actions – which can include some inhibition of pituitary functions – and stimulate the P450 system in the liver to more actively process and excrete excess estrogen.

Susan Kleiner, Ph.D, RD, author of Power Eating, notes that phytoestrogens tend to overwhelm estrogen in competing at the receptor site level. “That’s why we use phytoestrogens for both men and women who have hormonal-involved cancer,” such as prostate or breast cancer. So, the process is absolutely clear: If you want to block estrogen, take moderate amounts of isoflavones.Soy protein is a great source of isoflavones, providing that you can find a soy protein that has the isoflavones in it. "Isoflavones can be found in soy protein, but not always, " advises Kleiner. “High heat or chemical processing can damage and deplete phytoestrogens and isoflavones. Some soy protein powders I had analyzed had no isoflavones whatsoever, even though the label touted their benefits. .”

http://www.superiormuscle.com/forums/steroid-articles/40685-estrogen-testosterone-phytoestrogens

Can anyone guide me to any studies directly investigating phytoestrogen consumption and male androgens?? Thanks

10

Here are the first three studies I found using a pubmed search:

Genistein decreases androgen biosynthesis in rat Leydig cells by interference with luteinizing hormone-dependent signaling.

Hancock KD, Coleman ES, Tao YX, Morrison EE, Braden TD, Kemppainen BW, Akingbemi BT.

Department of Anatomy, Physiology and Pharmacology, Auburn University, Auburn, AL 36849, United States.

Testicular Leydig cells express estrogen receptors and are the predominant source of the male sex steroid hormone testosterone (T). Previous studies demonstrated that genistein acts through estrogen receptors in Leydig cells. In the present study, pre-treatment of Leydig cells isolated from 35 day-old male Long Evans rats with the epidermal growth factor receptor (EGFR) kinase inhibitor AG 1478 abrogated genistein inhibition of T biosynthesis. Also, incubation of Leydig cells in culture medium containing epidermal growth factor (EGF) decreased T secretion (control: 255+/-16; EGF: 190+/-17ng/10(6) cells, 24h) (P<0.05). However, T secretion by genistein-treated Leydig cells (0.1nM, 10muM; 24h) was rescued by post-treatment incubation with forskolin (control: 275+/-28 versus 325+/-35; 780+/-85; ng/10(6) cells, 3h) and dibutyryl cyclic adenosine 3’-5’-monophosphate (dbcAMP) (control: 370+/-65 versus 580+/-75; 2500+/-200; ng/10(6) cells, 3h) (P>0.05). Furthermore, post-treatment incubation with cholera toxin, an activator of G proteins, caused genistein-treated Leydig cells to produce similar T amounts as untreated control (control: 55+/-5 versus 52+/-2 and 47+/-4; ng/10(6) cells, 3h) (P>0.05). These observations imply that genistein action interferes with coupling of transmembrane luteinizing hormone receptors (LHR) with G proteins. Uncoupling of LHR from G proteins adversely affects adenylate cyclase function and impacts LH-dependent stimulation of Leydig cells. These findings have implications for testicular steroidogenesis in individuals exposed to genistein and soy-based products.

Publication Types:
Research Support, Non-U.S. Gov’t

PMID: 19059320 [PubMed - indexed for MEDLINE]

2: Climacteric. 2008 Oct;11(5):409-15.Related Articles, Links
Impact of soy supplementation on sex steroids and vascular inflammation markers in postmenopausal women using tibolone: role of equol production capability.

Törmälä R, Appt S, Clarkson TB, Mueck AO, Seeger H, Mikkola TS, Ylikorkala O.

Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Helsinki, Finland.

OBJECTIVES: Tibolone is often taken concurrently with soy. Tibolone, soy and equol-producing capacity each affect vascular health, whereas their concomitant effects are unknown. We studied the effects of soy on sex steroids and vascular inflammation markers in long-term tibolone users. METHODS: Postmenopausal women (n = 110) on tibolone were screened with a soy challenge to find 20 equol producers and 20 non-producers. All women were treated for 8 weeks in a cross-over trial with soy (52 g of soy protein containing 112 mg of isoflavones) or placebo. Serum estrone, 17beta-estradiol, testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEAS), sex hormone binding globulin (SHBG), C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and platelet-selectin (P-selectin) were assessed. RESULTS: Soy decreased (7.1%) the estrone level, significantly (12.5%) only in equol producers (from 80.2 +/- 10.8 to 70.3 +/- 7.0 pmol/l; p = 0.04). Testosterone was reduced (15.5%; from 586 +/- 62.6 to 495 +/- 50.1 pmol/l, p = 0.02) during soy treatment, and more markedly in equol producers than non-producers (22.1% vs. 10.0%). No changes appeared in SHBG, CRP or ICAM-1, but VCAM-1 increased (9.2%) and P-selectin decreased (10.3%) during soy treatment. CONCLUSIONS: Soy modified the concentrations of estrone, testosterone and some endothelial markers. Equol production enforced these effects. Soy supplementation may be clinically significant in tibolone users.

Publication Types:
Randomized Controlled Trial
Research Support, Non-U.S. Gov’t

PMID: 18781486 [PubMed - indexed for MEDLINE]

3: Cancer Causes Control. 2008 Dec;19(10):1085-93. Epub 2008 May 14.Related Articles, Links
Daidzein-metabolizing phenotypes in relation to serum hormones and sex hormone binding globulin, and urinary estrogen metabolites in premenopausal women in the United States.

Atkinson C, Newton KM, Stanczyk FZ, Westerlind KC, Li L, Lampe JW.

Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.

OBJECTIVE: Blood and urine concentrations of hormones are implicated in the etiology of some cancers. Small studies have assessed relationships between production of the daidzein metabolites equol and O-desmethylangolensin (ODMA) and hormones, but findings are unclear. We evaluated relationships between daidzein-metabolizing phenotypes and follicular phase concentrations of estrogens, androgens, sex hormone binding globulin (SHBG), and urinary estrogen metabolites in premenopausal women. METHODS: Two-hundred women collected a first-void urine sample after a 3-day soy challenge, and 191 and 193 provided fasting blood and spot urine samples, respectively, during days 5-9 of their menstrual cycle. Soy challenge urines were analyzed for isoflavones; serum was analyzed for estrogens, androgens, and SHBG; spot urines were analyzed for 2-hydroxyestrone and 16alpha-hydroxyestrone. Data were log-transformed and multiple regression analyses were conducted to assess relationships between daidzein-metabolizing phenotypes and hormones and SHBG. Data from 187 and 189 women were included in analyses of serum and urine hormones, respectively. RESULTS: 55 (27.5%) and 182 (91%) of the 200 women who provided a soy challenge urine sample were equol- and ODMA-producers (>87.5 ng/ml urine), respectively. In unadjusted analyses, equol-producers (n = 52) had lower free testosterone than equol non-producers (n = 137, p = 0.02). In adjusted analyses, there were no differences between producers and non-producers of either daidzein metabolite. CONCLUSIONS: In the absence of a soy intervention, we found no difference in serum or urine hormone concentrations between producers and non-producers of equol or ODMA.

11

Soy contains mainly isoflavones and nuts and seeds mainly lignans, and only the former bind to the estrogen receptor.