Phytoestrogens In Soy Vs. Estrogens In Milk

[Giraffe]

I just think people should get the facts straight so they can make informed choices.

Some things worth mentioning in this context...

The amount of E1 sulfate in milk is measured in pg/ml. "E1 sulfate increases from 30 pg/mL in non-pregnant cows to a maximum level of 1000 pg/mL [= 1 ng/ml = 100 ng/100 ml] in cows at 220 days of gestation." (source) The isoflavones in soy products are measured in mg/100 g. Serum testosterone levels in plasma are measured in pg/ml, isoflavones are measured in ng/ml (tables here).

pico= 10-12, nano = 10-9, milli = 10-3

As the content of estrogens (and progesterone!) in milk varies, so does the content of phytoestrogens in plant food.

The effects of phytoestrogens are complex, and results of studies (even in-vivo studies) inconsistent. There are effects that are not directly related to estrogen "receptors": Soy is a goitrogen. Progesteron acts on the "glycine receptor", decreasing excitation, genistein "antagonizes the inhibitory effect of glycine" (Ray Peat). Most soy is genetically modified crop which requires huge amounts of toxic pesticides ....

 

[Travis]

Giraffe makes a good point that hasn't been explicitly stated. The Estrogen concentrations in milk are lower than the soy isoflavones in soy. "Soy drink" on this table has a total isoflavone concentration of 7.01 mg/100g. If we assume the same density of water, we get 7.01 mg/100mL.

I have seen total estrogen values for milk at ~435 pg/mL, ~700 pg/mL, and a total of 1000 pg/mL for third trimester pregnant cows.

Taking the middle number I get:

700pg(x) = 7.01mg/(10²)
700pg(x) = 7.01(10³)μg/(10²)
700pg(x) = 7.01(10³)(10³)ng/(10²)
700pg(x) = 7.01(10³)(10³)(10³)pg/(10²)
700(x) = 701.(10⁻²)(10³)(10³)(10³)/(10²)
700(x) = 701(10⁵)
700(x) = 701(10⁵)
(x) = 701(10⁵) /700
(x) = (10⁵)

About 10⁵ times more isoflavones in soy 'milk' than estrogens in cow's milk! But if you look at the growth charts in Interaction of Phytoestrogens with Estrogen Receptors α and β, you can see that most of the phytoestrogens are about 10⁴ times weaker.

Maybe there is a study that directly compares estrogenic effects in mice fed either soy or cow's milk?

 

[Giraffe]

I have seen total estrogen values for milk at ~435 pg/mL, ~700 pg/mL, and a total of 1000 pg/mL for third trimester pregnant cows.

I think that 435 pg/ml is a mean value already.

But if you look at the growth charts in Interaction of Phytoestrogens with Estrogen Receptors α and β, you can see that most of the phytoestrogens are about 10⁴ times weaker.

If you argue that phytoestrogens are less potent than E2, than you also must take into account that the potency of E1 = 10% E2, E3 = 1/80 E2. The main estrogen metabilite in milk is 2OHE1. Don't know what to make of its potency; it is considered to be anti-estrogenic?! See what I am getting at?

Your approach is flawed. Even if we knew what the net effect of all these different substances is, the approach would be wrong. Not all of this gets absorbed, and substances are altered by the liver and by microorganisms in the gut.

Estradiol - Wikipedia
When taken orally, most estradiol is converted into estrone and estrone sulfate in the liver during first-pass metabolism. Oral estradiol administration produces a plasma estradiol-to-estrone ratio of about 1:5 to 1:7.

 

[Travis]

@Giraffe Just trying to put the concentrations and relative potency into perspective. It was that other guy that said Soy was 100 times more estrogenic, not me. I couldn't let that comment slide without evidence.

The gold standard for measuring estrogenicty, as far as I know, is testing uterine weights. You can't do this in people, but you can do this in rats. I'll see if I can find animal studies.

It would be impossible to reliably estimate how much gets absorbed or course. You could look at blood levels after soy consumption to get an idea.

@X3CyO I don't really worry too much about protein. The cronometer shows about 90% RDA for me when I just eat fruit and leaves; you could easily tip the balance with just more food.

You should get the cronometer and check it out! Everything has protein except for refined food. It adds up more than I had though before I started using the cronometer.

 

[Travis]

OK. I just read a rat study on cow's milk titled Uterotrophic effects of cow milk in immature ovariectomized Sprague–Dawley rats. The rats were broken up into three groups; one fed water (W), one fed traditional cow's milk (T), and one fed commercial cow's milk (C). They analyzed the estrogen contents¹ of the milks and found the commercial milk to have 184pg/mL and the traditional milk to have 123pg/mL. The progesterone content was 20ng/mL in the commercial milk and .2ng/mL in the traditional milk group. Water is of course assumed to be hormone-free.

A change in plasma estrogen concentration¹ was reported in the study groups. Table 3 shows these findings, and they are summarized below:

.........Water = 31.2 pg/mL
.Traditional = 71.1 pg/mL
Commercial = 79.3 pg/mL

There is a doubling of plasma estrogen concentration among the milk-fed groups! There were also changes is plasma progesterone concentration.

Now estrogen is known to effect the uterus more than any other organ. Here is what the authors say:

The relationship between estrogen and uterotrophic effects is well established. The role of estrogen in uterotrophic effects is regulated by the estrogen receptor [27]. In sexually immature rodents, estrogen stimulates DNA synthesis and cell proliferation in all uterine compartments...

For this reason, the authors measured the uterine weights of the rats [Table1]. The results were significant. The water fed rats had a dry uterine weight of 69mg, the traditional milk-fed rats had a uterine weight of 91mg, and the commercial milk-fed rats had a uterine weight of 112mg. This works out² to a weight increase over controls of:

.........Water = 0%
.Traditional = 32%
Commercial = 62%

And they report histological changes as well [Table5]. Before euthenasia the rats were injected with bromodeoxyuridine (BrdU), a synthetic nucleoside base. This molecule takes the place of thymidine in DNA replication, and it can be visualized by using advanced immunostaining techniques as outlined in the paper. The authors report more uterine DNA synthesis among the milk-fed groups. S-phase cells is short for synthesis-phase cells.

...(BrdU is a synthetic nucleoside that is an analog of thymidine and can be incorporated into the newly synthesized DNA of replicating cells). The C group had the highest percentage of labeled cells in both the uterine epithelium (8.9 ± 1.1%) and endometrium gland epithelium (7.9 ± 0.9%), followed by the T group and then the W group (Table 5). There were significant differences between all the pairs of groups. These results indicate that exposure to commercial or traditional milk led to a significant increase in the number of S-phase cells in the uterine epithelium and endometrium gland epithelium and that the effect was greater in the C group than in the T group.

¹[Estradiol + Estrone]
²[.........Water = ((69/69) - 1) × 100 = 0%
....Traditional = ((91/69) - 1) ×100 = 32%
...Commercial = ((112/69) - 1) × 100 = 62%]

 

[Travis]

But soy also has estrogenic effects that cannot be denied. In Effects of Chronic Genistein Treatment, five groups of ovarectomized Sprague-Dawley rats were fed either genestein or estradiol. These are the same types of rats used in the above experiment. The groups are summarized as follows:

Control = 0.omg/kg(day)
Low Estradiol = 0.17mg/kg(day)
High Estradiol = 0.70mg/kg(day)
Low Genestein = 5.4mg/kg(day)
High Genestein = 54mg/kg(day)

This was a long study and the rats were fed this way for three months. After this time they were decapitated and cut into pieces, but they did manage to take blood samples before they did that. The serum estradiol concentrations are listed in a nice bar graph [Table1] and raised with increasing estradiol dose. They also measured serum leutinizing hormone levels in all five groups.

The uterine weights increased in both estradiol groups and the high genestein (soy isoflavone) group. The uterine weight did not increase in the low genestein group over controls. The bar graph of Figure 2 illustrates this nicely. The percent increases over controls² were:

.............Control = 0%
..Low Estradiol = 420%
High Estradiol =497%
.Low Genestein = -4%
High Genestein = 114%

This is a good time to point out that you might not expect these radical changes in rats that haven't been ovarectimized. This shows that genestein does increase uterine weight in certain amounts. These were massive amounts of both genestein and estradiol fed to these rates. Converting the daily estradiol to micrograms we get:

Low Estradiol = 17oμg/kg(day)
High Estradiol = 700μg/kg(day)

These doses are unrealistic; but this study does demonstrate that genestein is less potent gram for gram than estradiol. The only realistic dose was the low genestein group. This works out to 1.3 kilograms³ of tofu per day (for 70kg human). This is a lot of tofu. The high genestein group represents 13 kilos of tofu per day; and both the estrogen-fed groups basically represent a daily Premarin® overdose.

Both of the estradiol groups and well as the high-genestein group exhibited mammary gland changes. The low-genestein was not affected. [Figure6]

So soy certainly can be estrogenic, but it appears that it would take massive doses; amounts that would be difficult to achieve in practice, unless Daidzein in soy turns out to be significantly more estrogenic than Genestein. This study only used concentrated genestein.

²[........ Control = ((92/92) - 1) × 100 = 0%
..Low Estradiol =((478/92) - 1) × 100 = 420%
High Estradiol =((549/92) - 1) × 100 =497%
.Low Genestein = ((88/92) - 1) × 100 = -4%
High Genestein = ((197/92) - 1) × 100 = 114%]

³[70kg × 5.4mgG/kg(day) = 378 mgG/(day) [Milligrams of Genestein per day for 70 Kg human, equivalent to low-genestein group]]
[(10²)gT/29.24mgG × 378 mgG/(day) = 1.3kgT/(day) [Kilograms of Tofu per day]]
[Genestein level in soy equated to total isoflavones and taken from table here.]

 

[Anne27]

There seems to be a lot of conflicting studies and reports on this subject. This recent study reported on "Science Daily" and conducted by researchers from the University of Ljubljana in Slovenia concluded that naturally occurring hormones in milk are found in far too low amounts to have any biological effect.

Elsevier Health Sciences. Science Daily, 3 August 2016. <www.sciencedaily.com/releases/2016/08/160803124441.htm>.

Consumption of natural estrogens in cow's milk does not affect blood levels or reproductive health
Date:
August 3, 2016
Source:
Elsevier Health Sciences
Summary:
A new study investigated cow milk's effects on blood hormone levels in adult mice and found that naturally occurring levels, and even levels as high as 100 times the average, had no effect on the mice. The study further determined that only when the mice were given 1,000 times more estrogen than average did it have any impact on reproductive health.

Estrogens found in food are thought to play a negative role in human reproductive health, but researchers are not yet sure of the exact connection between the two. One area of concern is bovine milk, which is known to contain naturally occurring estrogens. To complicate matters, estrogen levels in milk rise when a cow is pregnant, due to production in the placenta. Currently, cows are typically milked until 60 days before their expected calving, meaning milk from cows in their third trimester of pregnancy can contain up to 20 times more estrogen than milk from cows that are not pregnant.

In order to gain a better understanding about the relationship between estrogens in milk and blood estrogen levels, a team of researchers from the University of Ljubljana in Slovenia looked at the effects that different levels of milk estrogen had on adult mice. "The aim of our study was to evaluate whether the consumption of milk with known doses of estrogens (both naturally presented and added in concentrations 100 and 1,000 times higher) could affect blood hormone levels and reproductive organs in mice," explained senior co-author Tomaz Snoj, DVM, PhD, Veterinary Faculty at the Institute for Preclinical Sciences, University of Ljubljana, Ljubljana, Slovenia.

Specifically, the study examined how different concentrations of estrogens in milk affected the following parameters in mice: plasma levels of natural estrone (E1) and 17β-estradiol (E2); uterine weight in females; and testosterone levels, testes weight, and seminal vesicle weight in males. The three levels of E1 and E2 tested were concentrations similar to native milk from a pregnant cow (0.093 ng/mL for E1 and 0.065 ng/mL for E2), milk with an added 10 ng/mL of E1 and E2, and finally milk with an additional 100 ng/mL of E1 and E2.

The results of the study demonstrated that consumption of milk from a pregnant cow did not raise plasma levels of E1 and E2 in mice. It also did not affect the weight of the sex organs examined in either male or female mice. The same results were found for the milk containing an additional 10 ng/mL of E1 and E2; however, investigators did find that when the concentration was raised to 100 ng/mL, effects were seen in the mice. "We did observe elevated plasma estrogens in both sexes, increased uterus weight in females, and decreased plasma testosterone levels in males from the group that received milk with an added 100 ng/mL of E1 and E2," said senior co-author Gregor Majdic, DVM, PhD, Vice Dean, Center for Animal Genomics, Veterinary Faculty, University of Ljubljana. "However, concentrations in the third group exceeded the physiological concentration of milk estrogens by 1,000 times, so it would be extremely unlikely to find such concentrations in native cow milk."

Previous studies have shown that the gastrointestinal and hepatic systems are capable of inactivating large amounts of estrogens before they reach other parts of the body, and this fact may explain why naturally occurring estrogens in milk appeared to have little impact on the mice. "In our study," stated Dr. Snoj, "it is likely that plasma E1 and E2 did not increase in mice drinking pregnant cow's milk because the estrogens in the milk were at low enough levels to be metabolized during first liver passage and did not reach systemic circulation." Investigators caution, however, that these tests were done on mature mice and more research is needed to examine the effect estrogen from milk has on the development of the reproductive system before and during puberty.

This new research gives much needed insight into the relationship between native estrogen from cow milk and its effect on blood hormone levels. While further exploration into the issue is needed, this is a promising finding in adult mice.

"Our results suggest that estrogens in milk, even when derived from cows in the third trimester of pregnancy, do not pose a risk to reproductive health," concluded Dr. Majdic. "Even estrogens at concentrations 100 times higher than usually found in native milk did not cause any physiological effects in the present study." This is indicative that naturally occurring hormones in milk are found in far too low concentrations to exert any biological effect on consumers.

 

[Giraffe]

Prepubertal exposure to cow’s milk reduces susceptibility to carcinogen-induced mammary tumorigenesis in rats

The discussion of the results is quite weird, but the results themselves are interesting.

Rats were given either commercial milk or tap water from day 14 until day 35, from that age onwards all received tap water. At day 50 the rats were given 10 mg DMBA. In prior studies this dose "was shown to induce tumors in approximately two-thirds of the control group and thus enables assessment of both reduction and increase in tumorigenicity."

Results:

• 10-fold increased circulating E2 in milk-treated group.
• Earlier onset of puberty in milk-treated group (33.0 vs. 35.5 ).
• In the milk-treated group less rats developed tumors (46 vs. 63), and the time between DMBA administration and appearance of the first detectable tumor was longer (15.4 vs. 13.0). The number of tumors per animal was also lower (0.8 vs 1.5), but did not reach significance.

Sidenote: Both, high levels of circulating E2 and early puberty, are associated with higher risk for mammary cancer later in life.