Ronald Bailey | November 1, 2007
UroToday ("Breaking Urology News written by Urologists for Urologists") is reporting a study in the journal Fertility and Sterility that finds that eating soy products might affect semen quality. To wit:
There was an inverse association between soy food intake and sperm concentration that remained significant when evaluated with respect to age, abstinence, body mass, and caffeine, each of tobacco intake. There was no impact on sperm motility of morphology.
Access the UroToday report of the study here.
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This is not news to bodybuilders, who have avoideded soy and soy proteins for ages due to estrogenic properties
Not supprising when one considers that soy contains
estrogenic compounds.
Very true.
Also, Soy really isn't as healthy as people make it out to be. And
the treatment that soy beans go through in order to make them
palatable further reduces the health benefits of soy.
Jack | November 1, 2007, 1:12pm | #
This is not news to bodybuilders
...who already have shriveled dicks from steroid use.
soy contains estrogenic compounds.
So its not a coincidence that the most feminized segment
of society - your hard-core hippy/alternative types - eat tofu and
drink soymilk.
Then why are there so many asians on this planet?
Cause they're hot...
Ding!
That is correct. Taktrix®, would you like to go on to the bonus
round?
Heh. On my browser this post is right next to the attractive woman wearing the "I survived Roe v. Wade" T-Shirt.
"So its not a coincidence that the most feminized segment of
society - your hard-core hippy/alternative types - eat tofu and
drink soymilk."
Clearly you have not seen the manly men of National Review.
So its not a coincidence that the most feminized segment of
society - your hard-core hippy/alternative types - eat tofu and
drink soymilk.
Here's Hugh
Hewitt running in the Real Men Go To Tehran 10K Fun Run (SFW
but a little gross nevertheless).
Two porno actresses told me that pineapples, juice too, makes semen taste good. I take them at their word. Both have been in the business seven years plus. I know, they showed me the videos and DVDs.
Even knowing it makes my semen taste better, I think I'll still not drink pineapplejuice.
Clearly you have not seen the manly men of National
Review.
Nor do I care to, thanks.
Here's Hugh Hewitt running in the Real Men Go To Tehran 10K Fun
Run
No way I'm clicking on that link. What, do I look stupid?
Young asian men are plenty fertile, but the phytoestrogen takes
its toll over time.
Relates to the low rates of prostate cancer in asian societies as
well.
Here's Hugh Hewitt running in the Real Men Go To Tehran 10K
Fun Run
Oh, I look stupid. Should I be clicking on that link?
...the treatment that soy beans go through in order to make
them palatable...
What treatment? You cook the things raw in the pod and eat them. Or
you can buy the beans dried and boil them in the pressure cooker.
To make soymilk, you grind them, boil the ground beans in water,
and strain the cooking water, which is now soymilk. If you want
tofu, you can add lemon juice or magnesium sulfate (traditionally
produced in the process of refining salt from seawater) to the
soymilk and letting it coagulate. I mean, we are not exactly
talking artificial colors and flavors here.
"This is not news to bodybuilders"
or anybody who knows about nutrition. soy is estrogenic. that's why
(among other reasons) most bodybuilders and strength athletes only
use soy protein sparingly. this has been known for decades. it
figures that the conventional medical establishment is starting to
catch on (sports scientists etc. also were decades ahead on omega
oils, ketogenic diets etc.)
"...who already have shriveled dicks from steroid use."
actually, it's the testicles that shrink, not the penis.
the shrinking can be avoided if patients take chorionic
gonadotropin during cycle.
iow, it's completely avoidable.
The Government classifies estrogen as an environmental toxin
while testosterone is a controlled substance.
'nuff said
there's a reason for that.
estrogen is bioavailable, and testosterone isn't. that's why the
former can be taken orally (and the latter can't unless altered by
methylation or the adding of certain esters (which is weak) to
survive first pass metabolism, etc.).
there is TONS of estrogen in the water supply/environment because
so much has been urinatedout into the water table, and women have
been using birth control pills for decades.
environmental estrogens are bad enough (plastics, etc.) but it's
even worse due to the years of injection of estrogen by
women...
fwiw, as i stated in another post - both the DEA and AMA testified
AGAINST making testosterone and other AAS into controlled
substances. it was done "for the children" as most bad/nannystate
legislation is justified
"...who already have shriveled dicks from steroid
use."
actually, it's the testicles that shrink, not the penis.
I'm pretty sure the penises are small to begin with. Why do you
think they got into bodybuilding in the first place!
as a powerlifter and olympic style weightlifter (two strength sports that have a longgoing friendly rivalry with bodybuilding) i am contractually obligated to agree Taktix.
guys hey tofu is nice once in a while with a red curry or even
some string beans and a zesty chili paste.
fer reals.
Soy sucks.
Scientists Protest Soy Approval in Unusual Letter
Scientists' Letter
DEPARTMENT OF HEALTH and HUMAN SERVICES Public Health Service Food
and Drug Administration National Center For Toxicological Research
Jefferson, Ark. 72079-9502 Daniel M. Sheehan, Ph.D . Director,
Estrogen Base Program Division of Genetic and Reproductive
Toxicology and Daniel R. Doerge, Ph.D. Division of Biochemical
Toxicology February 18, 1999 Dockets Management Branch (HFA-305)
Food and Drug Administration Rockville, MD 20852
To whom it may concern,
We are writing in reference to Docket # 98P-0683; "Food Labeling:
Health Claims; Soy Protein and Coronary Heart Disease." We oppose
this health claim because there is abundant evidence that some of
the isoflavones found in soy, including genistein and equol, a
metabolize of daidzen, demonstrate toxicity in estrogen sensitive
tissues and in the thyroid. This is true for a number of species,
including humans.
Additionally, the adverse effects in humans occur in several
tissues and, apparently, by several distinct mechanisms. Genistein
is clearly estrogenic; it possesses the chemical structural
features necessary for estrogenic activity (; Sheehan and Medlock,
1995; Tong, et al, 1997; Miksicek, 1998) and induces estrogenic
responses in developing and adult animals and in adult
humans.
In rodents, equol is estrogenic and acts as an estrogenic endocrine
disruptor during development (Medlock, et al, 1995a,b). Faber and
Hughes (1993) showed alterations in LH regulation following this
developmental treatment with genistein. Thus, during pregnancy in
humans, isoflavones per se could be a risk factor for abnormal
brain and reproductive tract development.
Furthermore, pregnant Rhesus monkeys fed genistein had serum
estradiol levels 50- 100 percent higher than the controls in three
different areas of the maternal circulation (Harrison, et al,
1998). Given that the Rhesus monkey is the best experimental model
for humans, and that a women's own estrogens are a very significant
risk factor for breast cancer, it is unreasonable to approve the
health claim until complete safety studies of soy protein are
conducted.
Of equally grave concern is the finding that the fetuses of
genistein fed monkeys had a 70 percent higher serum estradiol level
than did the controls (Harrison, et al, 1998). Development is
recognized as the most sensitive life stage for estrogen toxicity
because of the indisputable evidence of a very wide variety of
frank malformations and serious functional deficits in experimental
animals and humans.
In the human population, DES exposure stands as a prime example of
adverse estrogenic effects during development. About 50 percent of
the female offspring and a smaller fraction of male offspring
displayed one or more malformations in the reproductive tract, as
well as a lower prevalence (about 1 in a thousand) of
malignancies.
In adults, genistein could be a risk factor for a number of
estrogen-associated diseases. Even without the evidence of elevated
serum estradiol levels in Rhesus fetuses, potency and dose
differences between DES and the soy isoflavones do not provide any
assurance that the soy protein isoflavones per se will be without
adverse effects.
First, calculations, based on the literature, show that doses of
soy protein isoflavones used in clinical trials which demonstrated
estrogenic effects were as potent as low but active doses of DES in
Rhesus monkeys (Sheehan, unpublished data). Second, we have
recently shown that estradiol shows no threshold in an extremely
large dose-response experiment (Sheehan, et al, 1999), and we
subsequently have found 31 dose-response curves for
hormone-mimicking chemicals that also fail to show a threshold
(Sheehan, 1998a).
Our conclusions are that no dose is without risk; the extent of
risk is simply a function of dose. These two features support and
extend the conclusion that it is inappropriate to allow health
claims for soy protein isolate. Additionally, isoflavones are
inhibitors of the thyroid peroxidase which makes T3 and T4.
Inhibition can be expected to generate thyroid abnormalities,
including goiter and autoimmune thyroiditis. There exists a
significant body of animal data that demonstrates goitrogenic and
even carcinogenic effects of soy products (cf., Kimura et al.,
1976). Moreover, there are significant reports of goitrogenic
effects from soy consumption in human infants (cf., Van Wyk et al.,
1959; Hydovitz, 1960; Shepard et al., 1960; Pinchers et al., 1965;
Chorazy et al., 1995) and adults (McCarrison, 1933; Ishizuki, et
al., 1991).
Recently, we have identified genistein and daidzein as the
goitrogenic isoflavonoid components of soy and defined the
mechanisms for inhibition of thyroid peroxidase (TPO)- catalyzed
thyroid hormone synthesis in vitro (Divi et al., 1997; Divi et al.,
1996). The observed suicide inactivation of TPO by isoflavones,
through covalent binding to TPO, raises the possibility of
neoantigen formation and because anti-TPO is the principal
autoantibody present in auto immune thyroid disease. This
hypothetical mechanism is consistent with the reports of Fort et
al. (1986, 1990) of a doubling of risk for autoimmune thyroiditis
in children who had received soy formulas as infants compared to
infants receiving other forms of milk.
The serum levels of isoflavones in infants receiving soy formula
that are about five times higher than in women receiving soy
supplements who show menstrual cycle disturbances, including an
increased estradiol level in the follicular phase (Setchell, et al,
1997). Assuming a dose-dependent risk, it is unreasonable to assert
that the infant findings are irrelevant to adults who may consume
smaller amounts of isoflavones.
Additionally, while there is an unambiguous biological effect on
menstrual cycle length (Cassidy, et al, 1994), it is unclear
whether the soy effects are beneficial or adverse. Furthermore, we
need to be concerned about transplacental passage of isoflavones as
the DES case has shown us that estrogens can pass the placenta. No
such studies have been conducted with genistein in humans or
primates. As all estrogens which have been studied carefully in
human populations are two-edged swords in humans (Sheehan and
Medlock, 1995; Sheehan, 1997), with both beneficial and adverse
effects resulting from the administration of the same estrogen, it
is likely that the same characteristic is shared by the
isoflavones. The animal data is also consistent with adverse
effects in humans.
Finally, initial data fi-om a robust (7,000 men) long-term (30+
years) prospective epidemiological study in Hawaii showed that
Alzheimer's disease prevalence in Hawaiian men was similar to
European-ancestry Americans and to Japanese (White, et al, 1996a).
In contrast, vascular dementia prevalence is similar in Hawaii and
Japan and both are higher than in European-ancestry
Americans.
This suggests that common ancestry or environmental factors in
Japan and Hawaii are responsible for the higher prevalence of
vascular dementia in these locations. Subsequently, this same group
showed a significant dose-dependent risk (up to 2.4 fold) for
development of vascular dementia and brain atrophy from consumption
of tofu, a soy product rich in isoflavones (White, et al,
1996b).
This finding is consistent with the environmental causation
suggested from the earlier analysis, and provides evidence that soy
(tofu) phytoestrogens causes vascular dementia. Given that
estrogens are important for maintenance of brain function in women;
that the male brain contains aromatase, the enzyme that converts
testosterone to estradiol; and that isoflavones inhibit this
enzymatic activity (Irvine, 1998), there is a mechanistic basis for
the human findings. Given the great difficulty in discerning the
relationship between exposures and long latency adverse effects in
the human population (Sheehan, 1998b), and the potential
mechanistic explanation for the epidemiological findings, this is
an important study.
It is one of the more robust, well-designed prospective
epidemiological studies generally available. We rarely have such
power in human studies, as well as a potential mechanism, and thus
the results should be interpreted in this context. Does the Asian
experience provide us with reassurance that the isoflavones are
safe? A review of several examples lead to the conclusion, - "Given
the parallels with herbal medicines with respect to attitudes,
monitoring deficiencies, and the general difficulty of detecting
toxicities with long Iatencies, I am unconvinced that the long
history of apparent safe use of soy products can provide confidence
that they are indeed without risk." (Sheehan, 1998b).
It should also be noted that the claim on p. 62978 that soy protein
foods are GRAS is in conflict with the recent return by CFSAN to
Archer Daniels Midland of a petition for GRAS status for soy
protein because of deficiencies in reporting adverse effects in the
petition. Thus GRAS status has not been granted. Linda Kahl can
provide you with details. It would seem appropriate for FDA to
speak with a single voice regarding soy protein isolate. Taken
together, the findings presented here are self-consistent and
demonstrate that genistein and other isoflavones can have adverse
effects in a variety of species, including humans. Animal studies
are the front line in evaluating toxicity, as they predict, with
good accuracy, adverse effects in humans.
For the isoflavones, we additionally have evidence of two types of
adverse effects in humans, despite the very few studies that have
addressed this subject. While isoflavones may have beneficial
effects at some ages or circumstances, this cannot be assumed to be
true at all ages. Isoflavones are like other estrogens in that they
are two-edged swords, conferring both benefits and risk (Sheehan
and Medlock, 1995; Sheehan, 1997).
The health labeling of soy protein isolate for foods needs to
considered just as would the addition of any estrogen or goitrogen
to foods, which are bad ideas. Estrogenic and goitrogenic drugs are
regulated by FDA, and are taken under a physician's care. Patients
are informed of risks, and are monitored by their physicians for
evidence of toxicity. There are no similar safeguards in place for
foods, so the public will be put at potential risk from soy
isoflavones in soy protein isolate without adequate warning and
information.
Finally, NCTR is currently conducting a long-term multigeneration
study of genistein administered in feed to rats. The analysis of
the dose range-finding studies are nearly complete now. As
preliminary data, which is still confidential, may be relevant to
your decision, I suggest you contact Dr. Barry Delclos at the
address on the letterhead, or email him.
Sincerely,
Daniel M. Sheehan
Daniel R. Doerge
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