[quote]The_Grim_Reaper wrote:
Soy has been consuemd for hundreds of years.[/quote]
And alcohol has been consumed for thousands. People have been smoking for a few thousand years too. None of that proves anything is healthy.
And you make them from what?
[quote]MookJong wrote:
The_Grim_Reaper wrote:
Soy has been consuemd for hundreds of years.
And alcohol has been consumed for thousands. People have been smoking for a few thousand years too. None of that proves anything is healthy.
I make my own soy shakes at home.
And you make them from what?[/quote]
Alcohol isn’t bad for you.I drink red wine every now and then.Alcohol doesn’t make you fat or give you liver disease.Too much does.
[quote]The_Grim_Reaper wrote:
MookJong wrote:
The_Grim_Reaper wrote:
Soy has been consuemd for hundreds of years.
And alcohol has been consumed for thousands. People have been smoking for a few thousand years too. None of that proves anything is healthy.
I make my own soy shakes at home.
And you make them from what?
Alcohol isn’t bad for you.I drink red wine every now and then.Alcohol doesn’t make you fat or give you liver disease.Too much does. [/quote]
Ok. Hmm. Alcohol isn’t bad for you because you drink it. Riiight. Any proof that red wine is any better for you than grape juice?
And Alcohol doesn’t make you fat or give you liver disease huh? But too much does? Too much of what exactly? Alcohol?
Or is it a case that once you gather “too much” of a substance, it is no longer the same substance?
You’ll claim to have found the philosopher’s stone next.
Logic isn’t one of your strongest suits, is it?
Logic huh? You might be a little mixed up.If alcohol made you fat you’d gain weight by the first or second drink. Red wine is healthy.I drink some red wine on the weekends.Oh,but this website(the website that doesn’t think using steroids is wrong) goes on about how soy is bad for you. This is hypocrisy at it’s best.
[quote]MookJong wrote:
The_Grim_Reaper wrote:
MookJong wrote:
The_Grim_Reaper wrote:
Soy has been consumed for hundreds of years.
And alcohol has been consumed for thousands. People have been smoking for a few thousand years too. None of that proves anything is healthy.
I make my own soy shakes at home.
And you make them from what?
Alcohol isn’t bad for you.I drink red wine every now and then.Alcohol doesn’t make you fat or give you liver disease.Too much does.
Ok. Hmm. Alcohol isn’t bad for you because you drink it. Riiight. Any proof that red wine is any better for you than grape juice?
And Alcohol doesn’t make you fat or give you liver disease huh? But too much does? Too much of what exactly? Alcohol?
Or is it a case that once you gather “too much” of a substance, it is no longer the same substance?
You’ll claim to have found the philosopher’s stone next.
Logic isn’t one of your strongest suits, is it?[/quote]
[quote]The_Grim_Reaper wrote:
If alcohol made you fat you’d gain weight by the first or second drink.[/quote]
Too funny.
If soft drink made you fat, you’d gain weight after 1 or 2 drinks. If doughnuts made you fat, it would only take 1 or 2.
By your “logic” NOTHING makes people fat.
I guess everyone is big boned and has hormone problems or something.
[quote]MookJong wrote:
The_Grim_Reaper wrote:
If alcohol made you fat you’d gain weight by the first or second drink.
Too funny.
If soft drink made you fat, you’d gain weight after 1 or 2 drinks. If doughnuts made you fat, it would only take 1 or 2.
By your “logic” NOTHING makes people fat.
I guess everyone is big boned and has hormone problems or something.[/quote]
actually it’s not that “nothing” can make you fat, but the overconsumption and/or abuse of anything that can make you fat; even sacred protein.
and logic is following a point to its final true outcome, not just deconstructing a thought partially to get the result you want. that’s just being cute.
from an beer, wine, and bourbon drinker.
It’s true. Most people are fat because they usually eat too much.When you see fat people eat they don’t stop at one cookie,one soda,one beer,or one piece of cake.There is more to weight loss than just calories in and calories out,but most fat people eat too much.The funny thing is most fat people eat “diet foods”.
There are “hormone problems” that can make people gain weight too. What I’m saying is too much of any food can make you gain weight.Period; and that everyone on here shouldn’t be telling me about soy when they use steroids.I don’t care if people use them,but don’t tell me about using soy when steroids are just as bad,if not worse.
[quote]MookJong wrote:
The_Grim_Reaper wrote:
If alcohol made you fat you’d gain weight by the first or second drink.
Too funny.
If soft drink made you fat, you’d gain weight after 1 or 2 drinks. If doughnuts made you fat, it would only take 1 or 2.
By your “logic” NOTHING makes people fat.[/quote]
I’m not going to argue because you’re right.
[quote]i.g. wrote:
MookJong wrote:
The_Grim_Reaper wrote:
If alcohol made you fat you’d gain weight by the first or second drink.
Too funny.
If soft drink made you fat, you’d gain weight after 1 or 2 drinks. If doughnuts made you fat, it would only take 1 or 2.
By your “logic” NOTHING makes people fat.
I guess everyone is big boned and has hormone problems or something.
actually it’s not that “nothing” can make you fat, but the overconsumption and/or abuse of anything that can make you fat; even sacred protein.
and logic is following a point to its final true outcome, not just deconstructing a thought partially to get the result you want. that’s just being cute.
from an beer, wine, and bourbon drinker.[/quote]
[quote]The_Grim_Reaper wrote:
The funny thing is most fat people eat “diet foods”[/quote]
That’s because most diet foods are highly processed junk - not because they’re good but fat people eat too much of them.
The “low fat” craze meant loads of sugar.
The “low carb” craze then meant loads of soy protein and/or trans fats.
Next thing you’ll be saying a calorie is just a calorie.
The_Grim_Reaper:
I don’t want to rain on your parade. However, I don’t think consuming Soy Protien is a wise choice!
The first article is from right here at good old T-Nation. They have been preaching the evils of soy for a long long time.
Just in case you think they are mistaken the second article is from an unrelated source.
Soy is Still Bad Protein
by Glen Neilson
We first published an article about how soy protein is estrogenic, can lower Testosterone counts, and can even kill testicular cells in January of 2000. We then published new research on the matter in February of 2001. But you know something? The national media still won’t touch the story. You can pick up the “Food” section of practically any local newspaper and see glowing reviews of the healthy attributes of soy protein, complete with yummy, Testosterone-lowering recipes.
Likewise, the other weightlifting and bodybuilding mags still tout its benefits, and a week doesn’t go by that we don’t get a letter from some irate soy fan who ends up questioning our parentage.
Given all that, we think that the topic deserves to be visited again and again until every man, woman, and child knows the truth. Hence this new article on soy. Oh, and make sure you read the letter that follows the article. It was written by two of the Food and Drug Administration’s soy experts who attempted to stop FDA approval of soy.
There’s a lot of talk today about soy. Turn on the news and its soy, read a diet book and you’ll find soy, go to your local gym and a personal trainer will recommend soy. What is it about soy that has captivated this nation? Well for starters it has many health benefits backed up by good science, it’s inexpensive, it has a good track record in Asia, and the government has allowed a seal of approval to be stamped on food items that contain 6.25 grams of soy protein.
Sounds like soy is a “can’t miss” product, but is it? In this article we’ll uncover the darker side of supposedly innocent soy and show you why you might not choose to include it in your otherwise healthy diet.
Many papers have exhorted the benefits of soy, but as the saying goes “if it sounds too good to be true, it probably is” fits soy better than anything else you might imagine.
Science has shown soy, more importantly its phyto-estrogen components, namely genistein, has the ability to attach to estrogen receptor sites and through transcription, act as female hormones such as estradiol. This, in some cases, can have benefits so it’s not strange that soy would receive some well-deserved attention. The problem with this attention is that individuals who have no need of soy, and even some to which soy could be hazardous, have started using it. Science is now beginning to see what this “benign” protein can do, though.
This review will cover the negative effects that soy protein may have on fetal development of both males and females, hormonal balance in males of a pre-mature and mature age, and efforts of weight training individuals trying to increase fat-free muscle mass. Studies will be included of human and non-human species, both immature and mature in age. Only abstracts and full-length articles from peer reviewed journals will be referenced in this paper.
Literature
Both abstracts and journals were found through the PubMed database and in the local university library. Limits were set on searches such as “human only,” “male,” “female,” “abstract only,” and others. Key words used included “soy,” “soy protein,” “genistein,” as well as “Testosterone production,” “effects on Testosterone,” and others. Finally, studies or points in favor of soy were not included, as countless papers have been written on its positive effects.
Findings
The largest concern scientists have about soy are its effects on sexual development of infants consuming soy-based formula. The data is startling, yet most concerns have fallen on deaf ears.
One study showed that when manufacturer-suggested amounts of soy formula are fed to infants, the infants ingest a daily dose of approximately 3 mg of total isoflavones (i.e. genistein and daidzein) per kg of body weight, which is maintained at a fairly constant level between 0 and 4 months of age.(3) Supplementing the diet of 4-month old infants with a single daily serving of soy-based cereal can increase their isoflavone intake by over 25%, depending on the brand chosen.
This rate of isoflavone intake is much greater than that shown to alter reproductive hormones in adult humans. The available evidence suggests that infants can digest and absorb dietary phytoestrogens in active forms and neonates are generally more susceptible than adults to perturbations of the sex-steroid milieu.
Another study assessed the effect of administering neonatal animals genistein in the amount of 4 mg per kg per day from days 2-18 of life.(1) Administration of genistein significantly retarded most measures of pubertal spermatogenesis. Plasma FSH levels in the treatment groups changed in parallel to the spermatogenic changes (reduced when pubertal spermatogenesis retarded, increased when pubertal spermatoenesis advanced).
By day 25, the changes in FSH levels largely persisted. In adulthood, the animals that were fed a soy-free diet in infancy and on, had significantly larger testes than controls fed a soy-containing diet. Of the animals that had neonatal treatment with genistein, a minority did not mate or were infertile.
In concluding this article, the authors stated “the presence or absence of soy or genistein in the diet has significant short-term (pubertal spermatogenesis) and long-term (body weight, testis size, FSH levels, and possibly mating) effects on males.”
The ugliness continues. The developing fetus is uniquely sensitive to perturbation with estrogenic chemicals. The carcinogenic effect of prenatal exposure to diethylstilbestrol (DES) is the classic example. The carcinogenic potential of genistein, a naturally occurring plant estrogen in soy, has been shown in mice treated neonatally. In a study reported in the journal, Cancer Research, the incidence of uterine adenocarcinoma in 18-month-old mice was 35% for genistein and 31% for DES (diethylstilbestrol).(6)
This data suggests that genistein is carcinogenic if exposure occurs during critical periods of differentiation. The author admonished: “Thus, the use of soy-based infant formulas in the absence of medical necessity and the marketing of soy products designed to appeal to children should be closely examined.”
Finally, as far as soy and its effects on infants, hypothyroidism has been shown in infants receiving soy formula.(2)
The next major concern is genistein’s estrogenic and anti-androgenic effects on adult male animals and humans. This effect was shown clearly in a study on adult male reproductive tracts.(8) In intact adult male mice, genistein (2.5 mg per kg of body weight per day for only 9 days) reduced testicular and serum Testosterone concentrations and pituitary LH-content. These results suggest that genistein ? in doses comparble to those that would exist in a soy-based diet ? induced typical estrogenic effects.
A second study showed plasma Testosterone and androstenedione levels were significantly lower in the animals fed a phytoestrogen-rich diet compared with animals fed a phytoestrogen-free diet.(9) These results indicated that consumption of dietary phytoestrogens over a relatively short period can significantly alter plasma androgen hormone levels.
In a study of Japanese men, total and free Testosterone concentrations were inversely correlated with soy product intake. (5)
The evidence continues. In rats that were fed a diet in which casein was replaced by soy protein isolate/isoflavones, both serum levels of Testosterone and weight of testes were significantly reduced.(7)
Finally, in a study that may correlate more strongly with weight-training athletes, diets that consist of inferior protein (soy) may increase protein breakdown in skeletal muscle.(4) Pigs were fed diets based on soybean-protein isolate or casein for 15 weeks. A transient rise in the level of cortisol was shown to occur in the postprandial phase only in the soybean group. The authors of this study concluded: “These data suggest that the inferior quality of dietary soybean protein induces hormonally-mediated upregulation of muscle protein breakdown for recruitment of circulatory amino acids in a postabsorptive state.”
In other words, soy intake induces the body to break down muscle protein in order for it to get its required amino acids.
Conclusions
At this time it’s recommended that:
? Infants not be given soy-based formula until more research is done on safety in regard to neonatal sexual development and its effects on thyroid suppression.
? Men not use soy products until more research is done on its effects on Testosterone and testicular function.
? Weight-training individuals who hope for increased muscle hypertrophy not use soy protein until more research is done on effects of decreased Testosterone, increased cortisol levels and muscle protein breakdown.
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
References
Atanassova N (2000). Comparative Effects of Neonatal Exposure of Male Rats to Potent and Weak (Environmental) Estrogens on Spermatogenesis at Puberty and the Relationship to Adult Testis Size and Fertility: Evidence for Stimulatory Effects of Low Estrogen Levels. Endocrinology Vol. 141, No. 10 3898-3907
Chorazy PA (1995). Persistent hypothyroidism in an infant receiving a soy formula: case report and review of the literature. Pediatrics Jul: 96 (1 Pt 1): 148-50
Irvine CHG (1998). Phytoestrogens in soy-based infant foods: concentrations, daily intake, and possible biological effects. Proc Soc Exp Biol Med1998 Mar; 217 (3): 247-53)
Lohrke B (2001). Activation of skeletal muscle protein breakdown following consumption of soybean protein in pigs. Br J Nutr 2001 Apr; 85 (4): 447-57
Nagata C (2000). Inverse association of soy product intake with serum androgen and estrogen concentrations in Japanese men. Nutr Cancer; 36 (1): 14-8
Newbold RR (2001). Uterine Adenocarcinoma in Mice Treated Neonatally with Genistein. Cancer Research 61, 4325-4328
Pollard M (2000). Prevention of spontaneous prostate-related cancer in Lobund-Wistar rats by soy protein isolate/isoflavone diet. Prostate 2000 Oct 1; 45 (2): 101-5
Strauss L (1998). Genistein exerts estrogen-like effects in male mouse reproductive tract. Mol Cell Endocrinol Sep 25; 144 (1-2): 83-93
Weber KS (2001). Dietary soy-phytoestrogens decrease testosterone levels and prostate weight without altering LH, prostate 5alpha-reductase or testicular steroidogenic acute regulatory peptide levels in adult male Sprague-Dawley rats. J Endocrinol Sep; 170 (3): 591-9
THIS SECOND ARTICLE IS UNRELATED TO T-NATION.
By John MacArthur
“Tofu Shrinks Brain!” No science fiction scenario, this sobering soybean revelation is for real. But how did the ?poster bean? of the ?90s go wrong? Apparently, in many ways?none of which bode well for the brain.
In a major ongoing study involving 3,734 elderly Japanese-American men, those who ate the most tofu during midlife had up to 2.4 times the risk of later developing Alzheimer?s disease. As part of the three-decade long Honolulu-Asia Aging Study, 27 foods and drinks were correlated with participants? health. Men who consumed tofu at least twice weekly had more cognitive impairment than those who rarely or never ate the soybean curd.1, 2
?The test results were about equivalent to what they would have been if they were five years older,? said lead researcher Dr. Lon R. White from the Hawaii Center for Health Research. For the guys who ate no tofu, however, they tested as though they were five years younger.
What?s more, higher midlife tofu consumption was also associated with low brain weight. Brain atrophy was assessed in 574 men using MRI results and in 290 men using autopsy information. Shrinkage occurs naturally with age, but for the men who had consumed more tofu, White said ?their brains seemed to be showing an exaggeration of the usual patterns we see in aging.?
Phytoestrogens?Soy Self Defense
Tofu and other soybean foods contain isoflavones, three-ringed molecules bearing a structural resemblance to mammalian steroidal hormones. White and his fellow researchers speculate that soy?s estrogen-like compounds (phytoestrogens) might compete with the body?s natural estrogens for estrogen receptors in brain cells.
Plants have evolved many different strategies to protect themselves from predators. Some have thorns or spines, while others smell bad, taste bad, or poison animals that eat them. Some plants took a different route, using birth control as a way to counter the critters who were wont to munch.
Plants such as soy are making oral contraceptives to defend themselves, says Claude Hughes, Ph.D., a neuroendocrinologist at Cedars-Sinai Medical Center. They evolved compounds that mimic natural estrogen. These phytoestrogens can interfere with the mammalian hormones involved in reproduction and growth?a strategy to reduce the number and size of predators.
Toxicologists Concerned
About Soy?s Health Risks
The soy industry says that White?s study only shows an association between tofu consumption and brain aging, but does not prove cause and effect. On the other hand, soy experts at the National Center for Toxicological Research, Daniel Sheehan, Ph.D., and Daniel Doerge, Ph.D., consider this tofu study very important. ?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.?
In a 1999 letter to the FDA (and on the ABC News program 20/20), the two toxicologists expressed their opposition to the agency?s health claims for soy, saying the Honolulu study ?provides evidence that soy (tofu) phytoestrogens cause 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, there is a mechanistic basis for the human findings.? 3
Although estrogen?s role in the central nervous system is not well understood, White notes that ?a growing body of information suggests that estrogens may be needed for optimal repair and replacement of neural structures eroded with aging.?
One link to the puzzle may involve calcium-binding proteins, which are associated with protection against neurodegenerative diseases. In recent animal studies at Brigham Young University?s Neuroscience Center, researchers found that consumption of phytoestrogens via a soy diet for a relatively short interval can significantly elevate phytoestrogen levels in the brain and decrease brain calcium-binding proteins.4
Concerns About Giving Soy to Infants
The most serious problem with soy may be its use in infant formulas. ?The amount of phytoestrogens that are in a day?s worth of soy infant formula equals 5 birth control pills,? says Mike Fitzpatrick, a New Zealand toxicologist. Fitzpatrick and other scientists believe that infant exposure to high amounts of phytoestrogens is associated with early puberty in girls and retarded physical maturation in boys.5
A study reported in The Lancet found that the ?daily exposure of infants to isoflavones in soy infant-formulas is 6-11 fold higher on a bodyweight basis than the dose that has hormonal effects in adults consuming soy foods.? (This dose, equivalent to two glasses of soy milk per day, was enough to change menstrual patterns in women.6 In the blood of infants tested, concentrations of isoflavones were 13,000-22,000 times higher than natural estrogen concentrations in early life.7 )
Soy Interferes with Enzymes
While soybeans are relatively high in protein compared to other legumes, they are a poor source of protein because other proteins found in soybeans act as potent enzyme inhibitors. These ?anti-nutrients? block the action of trypsin and other enzymes needed for protein digestion. Trypsin inhibitors are large, tightly folded proteins that are not completely deactivated during ordinary cooking and can reduce protein digestion. Therefore, soy consumption may lead to chronic deficiencies in amino acid uptake.8
Soy?s ability to interfere with enzymes and amino acids may have direct consequence for the brain. As White and his colleagues suggest, ?isoflavones in tofu and other soyfoods might exert their influence through interference with tyrosine kinase-dependent mechanisms required for optimal hippocampal function, structure and plasticity.?2
High amounts of protein tyrosine kinases are found in the hippocampus, a brain region involved with learning and memory. One of soy?s primary isoflavones, genistein, has been shown to inhibit tyrosine kinase in the hippocampus, where it blocked ?long-term potentiation,? a mechanism of memory formation.9
Tyrosine, Dopamine,
and Parkinson?s Disease
The brain uses the amino acids tyrosine or phenylalanine to synthesize the key neurotransmitters dopamine and norepinephrine, brain chemicals that promote alertness and activity. Dopamine is crucial to fine muscle coordination. People whose hands tremble from Parkinson?s disease have a diminished ability to synthesize dopamine. An increased incidence of depression and other mood disorders are associated with low levels of dopamine and norepinephrine. Also, the current scientific consensus on attention-deficit disorder points to a dopamine imbalance.
Soy has been shown to affect tyrosine hydroxylase activity in animals, causing the utilization rate of dopamine to be ?profoundly disturbed.? When soy lecithin supplements were given throughout perinatal development, they reduced activity in the cerebral cortex and ?altered synaptic characteristics in a manner consistent with disturbances in neural function.?10
Researchers at Sweden?s Karolinska Institute and at the National Institutes of Health are finding a connection between tyrosine hydroxylase activity, thyroid hormone receptors, and depleted dopamine levels in the brain?particularly in the substantia nigra, a region associated with the movement difficulties characteristic of Parkinson?s disease.11,12,13
Soy Affects the Brain via the Thyroid Gland
Tyrosine is crucial to the brain in another way. It?s needed for the body to make active thyroid hormones, which are a major physiological regulator of mammalian brain development. By affecting the rate of cell differentiation and gene expression, thyroid hormones regulate the growth and migration of neurons, including synaptic development and myelin formation in specific brain regions. Low blood levels of tyrosine are associated with an underactive thyroid gland.
It is well known that isoflavones in soy products can depress thyroid function, causing goiter (enlarged thyroid gland) and autoimmune thyroid disease. In the early 1960s, goiter and hypothyroidism were reported in infants fed soybean diets.14 Scientists at the National Center for Toxicological Research showed that the soy isoflavones genistein and daidzein ?inhibit thyroid peroxidase-catalyzed reactions essential to thyroid hormone synthesis.?15
Japanese researchers studied effects on the thyroid from soybeans administered to healthy subjects. They reported that consumption of as little as 30 grams (two tablespoons) of soybeans per day for only one month resulted in a significant increase in thyroid stimulating hormone (TSH), which is produced by the brain?s pituitary gland when thyroid hormones are too low. Their findings suggested that ?excessive soybean ingestion for a certain duration might suppress thyroid function and cause goiters in healthy people, especially elderly subjects.?16
Thyroid Hormones and
Fetal Brain Development
Thyroid alterations are among the most frequently encountered autoimmune conditions in children. Researchers at Cornell University Medical College showed that the ?frequency of feedings with soy-based milk formulas in early life was significantly higher in children with autoimmune thyroid disease.?17 In a previous study, they found that twice as many diabetic children had received soy formula in infancy as compared to non-diabetic children.18
Recognizing the risk, Swiss health authorities recommend ?very restrictive use? of soy for babies. In England and Australia, public health agencies tell parents to first seek advice from a doctor before giving their infants soy formula. The New Zealand Ministry of Health recommends that ?Soy formula should only be used under the direction of a health professional for specific medical indications. . . Clinicians who are treating children with a soy-based infant formula for medical conditions should be aware of the potential interaction between soy infant formula and thyroid function.?19
Thyroid hormones exert their influence during discrete windows of time during development of the infant. Inappropriate hormone levels can have a devastating effect on the developing human brain, especially during the first 12 weeks of pregnancy when the fetus depends on the mother?s thyroid hormones for brain development. After that, both maternal and fetal thyroid hormone levels affect the central nervous system.
A 1999 study published in the New England Journal of Medicine showed that pregnant women with underactive thyroids were four times more likely to have children with low IQs if the disorder were left untreated. The study found that 19 percent of the children born to mothers with thyroid deficiency had IQ scores of 85 or lower, compared with only 5 percent of those born to mothers without such problems.20
Thyroid, Brain, and Environmental Toxins
Children exposed prenatally and during infancy to common environmental toxins like dioxin and polychlorinated biphenyls (PCBs) can suffer behavioral, learning, and memory problems because these chemicals may be disrupting the normal action of thyroid hormone.21
Soybeans grown in the United States contain residues of the pesticide dieldrin, an organochlorine similar to DDT. Although both chemicals were banned in the 1970s, dieldrin still persists in soils and is absorbed through the roots. Today it is the most toxic residue found on domestic soybeans.22 In Silent Spring, Rachel Carson warned that dieldrin is nearly 50 times as poisonous as DDT. In addition to disrupting hormones, it can have long delayed neurological effects, ranging from loss of memory to mania.23 Chinese aphids were recently discovered in fields scattered across Wisconsin, so increased pesticide applications are likely.
Combinations of insecticides, weed killers, and artificial fertilizers?even at low levels?have measurable detrimental effects on thyroid and other hormones as well as on the brain.24 EPA scientists now want to upgrade the commonly used herbicide, atrazine, to a ?likely carcinogen.? In animal tests, atrazine attaches to sites on the hypothalamus, a crucial brain region involved with regulating levels of stress and sex hormones.25
Individuals newly diagnosed with Parkinson?s disease were more than twice as likely to have been exposed to insecticides in their home, compared to those without the disease.26 In September 2000, The Lancet reported that farmers and gardeners regularly exposed to pesticides may have more than five times the risk of developing mild cognitive dysfunction.
Soy formulas for infants can contain other neurotoxins: aluminum, cadmium, and fluoride. Studies found that aluminum concentrations in soy-based formulas were a 100-fold greater compared to human breast milk,27 while cadmium content was 8-15 times higher than in milk-based formulas.28 In an Australian study, the fluoride content of soy-based formulas ranged from 1.08 to 2.86 parts per million. The authors concluded that ?prolonged consumption (beyond 12 months of age) of infant formula reconstituted with optimally-fluoridated water could result in excessive amounts of fluoride being ingested.?29 A study of Connecticut children revealed that mild to moderate fluorosis was strongly associated with soy-based infant formula use.30
In May 2000, Boston Physicians for Social Responsibility released their report, ?The Toxic Threats to Child Development.? In the section on neurotoxins, they concluded, ?Studies in animals and human populations suggest that fluoride exposure, at levels that are experienced by a significant proportion of the population whose drinking water is fluoridated, may have adverse impacts on the developing brain.?31
Iodine versus Fluorine
The thyroid gland uses tyrosine and the natural element iodine to make thyroxine (T4), a thyroid hormone containing four iodine atoms. The other, much more biologically active thyroid hormone is tri-iodothyronine (T3), which has three iodine atoms. Lack of dietary iodine has long been identified as the problem in diminished thyroid hormone synthesis.
According to the International Council for the Control of Iodine Deficiency Disorders: ?Iodine deficiency has been called the world?s major cause of preventable mental retardation. Its severity can vary from mild intellectual blunting to frank cretinism, a condition that includes gross mental retardation, deaf mutism, short stature, and various other defects. . . The damage to the developing brain results in individuals poorly equipped to fight disease, learn, work effectively, or reproduce satisfactorily.?
This crucial role of iodine is another reason why the thyroid gland is especially vulnerable today. Canadian researcher Andreas Schuld has documented more than 100 studies during the last 70 years that demonstrate adverse effects of fluoride on the thyroid gland.32 Schuld says, ?Fluorine, being the strongest in the group of halogens, will seriously interfere with iodine and iodine synthesis, forcing more urinary elimination of ingested iodine as fluoride ingestion or absorption increases.? (See page 21.)
Soy Inhibits Zinc Absorption
The high phytic-acid content in soy may also have adverse effects on brain function. Phytic acid is an organic acid present in the outer portion of all seeds which blocks the uptake of essential minerals in the intestinal tract: calcium, magnesium, iron, and especially zinc. Soybeans have very high levels of a form of phytic acid that is particularly difficult to neutralize and which interferes with zinc absorption more completely than with other minerals.
The soy industry acknowledges the problem with the admission that while ?one-half cup of cooked soybeans contains one mg of zinc
. . . zinc is poorly absorbed from soyfoods.? As for iron, ?both phytate and soy protein reduce iron absorption so that the iron in soyfoods is generally poorly absorbed.?33
According to unpublished documents, researchers testing soy formula found that it caused negative zinc balance in every infant to whom it was given.34 Even when the diets were additionally supplemented with zinc, there was a strong correlation between phytate content in formula and poor growth.
Zinc and the Brain
Relatively high levels of zinc are found in the brain, especially the hippocampus. Zinc plays an important role in the transmission of the nerve impulse between brain cells. Deficiency of zinc during pregnancy and lactation has been shown to be related to many congenital abnormalities of the nervous system in offspring. In children, ?insufficient levels of zinc have been associated with lowered learning ability, apathy, lethargy, and mental retardation.?35
The USDA references a study of 372 Chinese school children with very low levels of zinc in their bodies. The children who received zinc supplements had the most improved performance?especially in perception, memory, reasoning, and psychomotor skills such as eye-hand coordination. Three earlier studies with adults also showed that changes in zinc intake affected cognitive function.36
New research has identified a specific contingent of neurons, called ?zinc-containing? neurons, which are found almost exclusively in the forebrain, where in mammals they have evolved into a ?complex and elaborate associational network that interconnects most of the cerebral cortices and limbic structures.? This suggests the importance of zinc in the normal and pathological processes of the cerebral cortex.37 Furthermore, age-related tissue zinc deficiency may contribute to brain cell death in Alzheimer?s dementia.38
Not a Good Idea
High levels of phytoestrogens and zinc-blocking phytic acid, plus additional neurotoxic compounds such as dieldrin, aluminum, fluoride and cadmium combine in soy to yield a veritable witches? brew that can have adverse effects on the brain during development and throughout life.
Unfortunately, many American are now consuming soy foods in high amounts as infant formula, soy milk and tofu-based products, usually as a substitute for nourishing animal foods. In Asia, soy is consumed in small amounts as a fermented condiment and not as a substitute for animal foods.
Asians recognize the need for ?brain foods? like eggs and fish and realize that large amounts of soy can cause thyroid problems and inhibit growth. They know that for optimum mental function, soy foods are not a good idea.
About the author
John D. MacArthur is a freelance writer who?s recently been researching neuroscience topics for www.Brain.com. Links to his 20 reports can be found at www.getwrite.com. (Email: macarthur@getwrite.com ) This report was originally published online by Brain.com in July 2000, as ?The Trouble with Tofu.? At www.brain.com, visitors can use free tests to measure brain performance. Healthcare providers can access the Cognitive Care System, a web-based service for early detection and management of cognitive impairment.
References
White LR, Petrovich H, Ross GW, Masaki KH, Association of mid-life consumption of tofu with late life cognitive impairment and dementia: the Honolulu-Asia Aging Study. Fifth International Conference on Alzheimer?s Disease, #487, 27 July 1996, Osaka, Japan.
White LR, Petrovitch H, Ross GW, Masaki KH, Hardman J, Nelson J, Davis D, Markesbery W, Brain aging and midlife tofu consumption. J Am Coll Nutr 2000 Apr;19(2):242-55.
Doerge and Sheehan, Letter to the FDA, Feb 18, 1999. (http://abcnews.go.com/onair/2020/2020_000609_soyfdaletter_feature.htm)
Lephart ED, Thompson JM, Setchell KD, Adlercreutz H, Weber KS, Phytoestrogens decrease brain calcium-binding proteins… Brain Res 2000 Mar 17;859(1):123-31.
Soy Infant Formula Could Be Harmful to Infants: Groups Want it Pulled. Nutrition Week, Dec 10, 1999;29(46):1-2; See also www.soyonlineservice.co.nz
Cassidy A, Bingham S, Setchell KD, Biological effects of a diet of soy protein rich in isoflavones on the menstrual cycle of premenopausal women. Am J Clin Nutr 1994 Sep;60(3):333-40.
Setchell KD, Zimmer-Nechemias L, Cai J, Heubi JE, Exposure of infants to phyto-oestrogens from soy-based infant formula. Lancet 1997 Jul 5;350(9070):23-27.
Fallon SA, Enig MG, Tragedy and Hype, The Third International Soy Symposium. Nexus Magazine, Vol 7, No 3, April-May 2000.
O?Dell TJ, Kandel ER, Grant SG, Long-term potentiation in the hippocampus is blocked by tyrosine kinase inhibitors. Nature 1991 Oct 10 353:6344 558-60.
Bell JM, Whitmore WL, Cowdery T, Slotkin TA, Perinatal dietary supplementation with a soy lecithin preparation: effects on development of central catecholaminergic neurotransmitter systems. Brain Res Bull 1986 Aug;17(2):189-95.
Zetterstrom RH, Williams R, Perlmann T, Olson L, Cellular expression of the immediate early transcription factors Nurr1 and NGFI-B suggests a gene regulatory role in several brain regions including the nigrostriatal dopamine system. Brain Res Mol Brain Res 1996 Sep 5;41(1-2):111-20.
Castillo SO, Baffi JS, Palkovits M, Goldstein DS, Kopin IJ, Witta J, Magnuson MA, Nikodem VM, Dopamine biosynthesis is selectively abolished in substantia nigra… Mol Cell Neurosci 1998 May;11(1-2):36-46.
Baffi JS, Palkovits M, Castillo SO, Mezey E, Nikodem VM, Differential expression of tyrosine hydroxylase in catecholaminergic neurons of neonatal wild-type and Nurr1-deficient mice. Neuroscience 1999;93(2):631-42.
Shepard TH, Soybean goiter. New Eng J Med 1960;262:1099-1103.
Divi RL, Chang HC, Doerge DR, Anti-thyroid isoflavones from soybean: isolation, characterization, mechanisms of action. Biochem Pharmacol 1997 Nov 15;54(10):1087-96.
Ishizuki Y, Hirooka Y, Murata Y, Togashi K, The effects on the thyroid gland of soybeans administered experimentally in healthy subjects. Nippon Naibunpi Gakkai Zasshi 1991 May 20;67(5):622-29.
Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F, Breast and soy-formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. J Am Coll Nutr 1990 Apr;9(2):164-67.
Fort P, Lanes R, Dahlem S, Recker B, Weyman-Daum M, Pugliese M, Lifshitz FJ, Breast feeding and insulin-dependent diabetes mellitus in children. Am Coll Nutr 1986;5(5):439-41.
Regulatory Guidance in other countries: New Zealand Ministry of Health Position Statement on Soy Formulas (Domain parked by OnlyDomains)(Adobe Acrobat PDF file: Domain parked by OnlyDomains)
Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, O?Heir CE, Mitchell ML, Hermos RJ, Waisbren SE, Faix JD, Klein RZ, Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999 Aug 19;341(8):549-55.
Hauser P, McMillin JM, Bhatara VS, Resistance to thyroid hormone: implications for neurodevelopmental research on the effects of thyroid hormone disruptors. Toxicol Ind Health 1998 Jan-Apr;14(1-2):85-101.
Groth E, Benbrook CM, Lutz K, Update: pesticides in children?s foods, an analysis of 1998 USDA PDP data on pesticide residues, Consumers Union of U.S., Inc., May, 2000 (Adobe Acrobat PDF file).
Hayes WJ, The toxicity of dieldrin to man. Bull World Health Organ 1959;20:891-92.
Porter WP, Jaeger JW, Carlson IH, Endocrine, immune and behavioral effects of aldicarb (carbamate), atrazine (triazine) and nitrate (fertilizer) mixtures at groundwater concentrations. Toxicol Ind Health 1999 Jan-Mar;15(1-2):133-50.
Watson, Traci, Common herbicide likely causes cancer. USA Today, June 29, 2000.
Nelson L, American Academy of Neurology?s 52nd annual meeting in San Diego, CA, April 29-May 6, 2000.
McGraw M, Bishop N, Jameson R, Robinson MJ, O?Hara M, Hewitt CD, Day JP, Aluminium content of milk formulae and intravenous fluids used in infants.Lancet 1986 Jan 18;1(8473):157.
Dabeka RW, McKenzie AD, Lead, cadmium, and fluoride levels in market milk and infant formulas in Canada. J Assoc Off Anal Chem 1987;70(4):754-57.
Silva M, Reynolds EC, Fluoride content of infant formulae in Australia. Aust Dent J 1996 Feb;41(1):37-42.
Pendrys DG, Katz RV, Morse DE, Risk factors for enamel fluorosis in a fluoridated population. Am J Epidemiol 1994 Sep 1;140(5):461-71.
Schettler T, Stein J, Reich F, Valenti M, In Harm?s Way: Toxic Threats to Child Development. (http://www.igc.org/psr/ihw.htm) Greater Boston Physicians for Social Responsibility, May 2000.
Studies dealing with fluoride and thyroid. (http://www.bruha.com/fluoride/html/thyroid_studies.htm)See also: Fluoride Controversy in the Townsend Letter for Doctors and Patients. (http://www.tldp.com/fluoride.htm)
Soy Nutritive Content, United Soybean Board. (Talksoy.com - Hotels & Accommodation in Amsterdam)
Pfeiffer CC, Braverman ER, Zinc, the brain and behavior. Biol Psychiatry 1982 Apr;17(4):513-32.
Personal communication with Dr. Mary G. Enig
U.S. Department of Agriculture, Agricultural Research Service, Food & Nutrition Research Briefs, July 1997. (http://www.nal.usda.gov/fnic/usda/fnrb/fnrb797.html)
Frederickson CJ, Suh SW, Silva D, Frederickson CJ, Thompson RB, Importance of zinc in the central nervous system: the zinc-containing neuron. J Nutr 2000 May;130(5S Suppl):1471S-83S.
Ho LH, Ratnaike RN, Zalewski PD, Involvement of intracellular labile zinc in suppression of DEVD-caspase activity in human neuroblastoma cells. Biochem Biophys Res Commun 2000 Feb 5;268(1):148-54.
Thankyou for warning me,but from my experience, it’s how soy is processed.I don’t consume soy every single day,but I do every now and then.
[quote]ZEB wrote:
The_Grim_Reaper:
I don’t want to rain on your parade. However, I don’t think consuming Soy Protien is a wise choice!
The first article is from right here at good old T-Nation. They have been preaching the evils of soy for a long long time.
Just in case you think they are mistaken the second article is from an unrelated source.
Soy is Still Bad Protein
by Glen Neilson
We first published an article about how soy protein is estrogenic, can lower Testosterone counts, and can even kill testicular cells in January of 2000. We then published new research on the matter in February of 2001. But you know something? The national media still won’t touch the story. You can pick up the “Food” section of practically any local newspaper and see glowing reviews of the healthy attributes of soy protein, complete with yummy, Testosterone-lowering recipes.
Likewise, the other weightlifting and bodybuilding mags still tout its benefits, and a week doesn’t go by that we don’t get a letter from some irate soy fan who ends up questioning our parentage.
Given all that, we think that the topic deserves to be visited again and again until every man, woman, and child knows the truth. Hence this new article on soy. Oh, and make sure you read the letter that follows the article. It was written by two of the Food and Drug Administration’s soy experts who attempted to stop FDA approval of soy.
There’s a lot of talk today about soy. Turn on the news and its soy, read a diet book and you’ll find soy, go to your local gym and a personal trainer will recommend soy. What is it about soy that has captivated this nation? Well for starters it has many health benefits backed up by good science, it’s inexpensive, it has a good track record in Asia, and the government has allowed a seal of approval to be stamped on food items that contain 6.25 grams of soy protein.
Sounds like soy is a “can’t miss” product, but is it? In this article we’ll uncover the darker side of supposedly innocent soy and show you why you might not choose to include it in your otherwise healthy diet.
Many papers have exhorted the benefits of soy, but as the saying goes “if it sounds too good to be true, it probably is” fits soy better than anything else you might imagine.
Science has shown soy, more importantly its phyto-estrogen components, namely genistein, has the ability to attach to estrogen receptor sites and through transcription, act as female hormones such as estradiol. This, in some cases, can have benefits so it’s not strange that soy would receive some well-deserved attention. The problem with this attention is that individuals who have no need of soy, and even some to which soy could be hazardous, have started using it. Science is now beginning to see what this “benign” protein can do, though.
This review will cover the negative effects that soy protein may have on fetal development of both males and females, hormonal balance in males of a pre-mature and mature age, and efforts of weight training individuals trying to increase fat-free muscle mass. Studies will be included of human and non-human species, both immature and mature in age. Only abstracts and full-length articles from peer reviewed journals will be referenced in this paper.
Literature
Both abstracts and journals were found through the PubMed database and in the local university library. Limits were set on searches such as “human only,” “male,” “female,” “abstract only,” and others. Key words used included “soy,” “soy protein,” “genistein,” as well as “Testosterone production,” “effects on Testosterone,” and others. Finally, studies or points in favor of soy were not included, as countless papers have been written on its positive effects.
Findings
The largest concern scientists have about soy are its effects on sexual development of infants consuming soy-based formula. The data is startling, yet most concerns have fallen on deaf ears.
One study showed that when manufacturer-suggested amounts of soy formula are fed to infants, the infants ingest a daily dose of approximately 3 mg of total isoflavones (i.e. genistein and daidzein) per kg of body weight, which is maintained at a fairly constant level between 0 and 4 months of age.(3) Supplementing the diet of 4-month old infants with a single daily serving of soy-based cereal can increase their isoflavone intake by over 25%, depending on the brand chosen.
This rate of isoflavone intake is much greater than that shown to alter reproductive hormones in adult humans. The available evidence suggests that infants can digest and absorb dietary phytoestrogens in active forms and neonates are generally more susceptible than adults to perturbations of the sex-steroid milieu.
Another study assessed the effect of administering neonatal animals genistein in the amount of 4 mg per kg per day from days 2-18 of life.(1) Administration of genistein significantly retarded most measures of pubertal spermatogenesis. Plasma FSH levels in the treatment groups changed in parallel to the spermatogenic changes (reduced when pubertal spermatogenesis retarded, increased when pubertal spermatoenesis advanced).
By day 25, the changes in FSH levels largely persisted. In adulthood, the animals that were fed a soy-free diet in infancy and on, had significantly larger testes than controls fed a soy-containing diet. Of the animals that had neonatal treatment with genistein, a minority did not mate or were infertile.
In concluding this article, the authors stated “the presence or absence of soy or genistein in the diet has significant short-term (pubertal spermatogenesis) and long-term (body weight, testis size, FSH levels, and possibly mating) effects on males.”
The ugliness continues. The developing fetus is uniquely sensitive to perturbation with estrogenic chemicals. The carcinogenic effect of prenatal exposure to diethylstilbestrol (DES) is the classic example. The carcinogenic potential of genistein, a naturally occurring plant estrogen in soy, has been shown in mice treated neonatally. In a study reported in the journal, Cancer Research, the incidence of uterine adenocarcinoma in 18-month-old mice was 35% for genistein and 31% for DES (diethylstilbestrol).(6)
This data suggests that genistein is carcinogenic if exposure occurs during critical periods of differentiation. The author admonished: “Thus, the use of soy-based infant formulas in the absence of medical necessity and the marketing of soy products designed to appeal to children should be closely examined.”
Finally, as far as soy and its effects on infants, hypothyroidism has been shown in infants receiving soy formula.(2)
The next major concern is genistein’s estrogenic and anti-androgenic effects on adult male animals and humans. This effect was shown clearly in a study on adult male reproductive tracts.(8) In intact adult male mice, genistein (2.5 mg per kg of body weight per day for only 9 days) reduced testicular and serum Testosterone concentrations and pituitary LH-content. These results suggest that genistein ? in doses comparble to those that would exist in a soy-based diet ? induced typical estrogenic effects.
A second study showed plasma Testosterone and androstenedione levels were significantly lower in the animals fed a phytoestrogen-rich diet compared with animals fed a phytoestrogen-free diet.(9) These results indicated that consumption of dietary phytoestrogens over a relatively short period can significantly alter plasma androgen hormone levels.
In a study of Japanese men, total and free Testosterone concentrations were inversely correlated with soy product intake. (5)
The evidence continues. In rats that were fed a diet in which casein was replaced by soy protein isolate/isoflavones, both serum levels of Testosterone and weight of testes were significantly reduced.(7)
Finally, in a study that may correlate more strongly with weight-training athletes, diets that consist of inferior protein (soy) may increase protein breakdown in skeletal muscle.(4) Pigs were fed diets based on soybean-protein isolate or casein for 15 weeks. A transient rise in the level of cortisol was shown to occur in the postprandial phase only in the soybean group. The authors of this study concluded: “These data suggest that the inferior quality of dietary soybean protein induces hormonally-mediated upregulation of muscle protein breakdown for recruitment of circulatory amino acids in a postabsorptive state.”
In other words, soy intake induces the body to break down muscle protein in order for it to get its required amino acids.
Conclusions
At this time it’s recommended that:
? Infants not be given soy-based formula until more research is done on safety in regard to neonatal sexual development and its effects on thyroid suppression.
? Men not use soy products until more research is done on its effects on Testosterone and testicular function.
? Weight-training individuals who hope for increased muscle hypertrophy not use soy protein until more research is done on effects of decreased Testosterone, increased cortisol levels and muscle protein breakdown.
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
References
Atanassova N (2000). Comparative Effects of Neonatal Exposure of Male Rats to Potent and Weak (Environmental) Estrogens on Spermatogenesis at Puberty and the Relationship to Adult Testis Size and Fertility: Evidence for Stimulatory Effects of Low Estrogen Levels. Endocrinology Vol. 141, No. 10 3898-3907
Chorazy PA (1995). Persistent hypothyroidism in an infant receiving a soy formula: case report and review of the literature. Pediatrics Jul: 96 (1 Pt 1): 148-50
Irvine CHG (1998). Phytoestrogens in soy-based infant foods: concentrations, daily intake, and possible biological effects. Proc Soc Exp Biol Med1998 Mar; 217 (3): 247-53)
Lohrke B (2001). Activation of skeletal muscle protein breakdown following consumption of soybean protein in pigs. Br J Nutr 2001 Apr; 85 (4): 447-57
Nagata C (2000). Inverse association of soy product intake with serum androgen and estrogen concentrations in Japanese men. Nutr Cancer; 36 (1): 14-8
Newbold RR (2001). Uterine Adenocarcinoma in Mice Treated Neonatally with Genistein. Cancer Research 61, 4325-4328
Pollard M (2000). Prevention of spontaneous prostate-related cancer in Lobund-Wistar rats by soy protein isolate/isoflavone diet. Prostate 2000 Oct 1; 45 (2): 101-5
Strauss L (1998). Genistein exerts estrogen-like effects in male mouse reproductive tract. Mol Cell Endocrinol Sep 25; 144 (1-2): 83-93
Weber KS (2001). Dietary soy-phytoestrogens decrease testosterone levels and prostate weight without altering LH, prostate 5alpha-reductase or testicular steroidogenic acute regulatory peptide levels in adult male Sprague-Dawley rats. J Endocrinol Sep; 170 (3): 591-9
THIS SECOND ARTICLE IS UNRELATED TO T-NATION.
By John MacArthur
“Tofu Shrinks Brain!” No science fiction scenario, this sobering soybean revelation is for real. But how did the ?poster bean? of the ?90s go wrong? Apparently, in many ways?none of which bode well for the brain.
In a major ongoing study involving 3,734 elderly Japanese-American men, those who ate the most tofu during midlife had up to 2.4 times the risk of later developing Alzheimer?s disease. As part of the three-decade long Honolulu-Asia Aging Study, 27 foods and drinks were correlated with participants? health. Men who consumed tofu at least twice weekly had more cognitive impairment than those who rarely or never ate the soybean curd.1, 2
?The test results were about equivalent to what they would have been if they were five years older,? said lead researcher Dr. Lon R. White from the Hawaii Center for Health Research. For the guys who ate no tofu, however, they tested as though they were five years younger.
What?s more, higher midlife tofu consumption was also associated with low brain weight. Brain atrophy was assessed in 574 men using MRI results and in 290 men using autopsy information. Shrinkage occurs naturally with age, but for the men who had consumed more tofu, White said ?their brains seemed to be showing an exaggeration of the usual patterns we see in aging.?
Phytoestrogens?Soy Self Defense
Tofu and other soybean foods contain isoflavones, three-ringed molecules bearing a structural resemblance to mammalian steroidal hormones. White and his fellow researchers speculate that soy?s estrogen-like compounds (phytoestrogens) might compete with the body?s natural estrogens for estrogen receptors in brain cells.
Plants have evolved many different strategies to protect themselves from predators. Some have thorns or spines, while others smell bad, taste bad, or poison animals that eat them. Some plants took a different route, using birth control as a way to counter the critters who were wont to munch.
Plants such as soy are making oral contraceptives to defend themselves, says Claude Hughes, Ph.D., a neuroendocrinologist at Cedars-Sinai Medical Center. They evolved compounds that mimic natural estrogen. These phytoestrogens can interfere with the mammalian hormones involved in reproduction and growth?a strategy to reduce the number and size of predators.
Toxicologists Concerned
About Soy?s Health Risks
The soy industry says that White?s study only shows an association between tofu consumption and brain aging, but does not prove cause and effect. On the other hand, soy experts at the National Center for Toxicological Research, Daniel Sheehan, Ph.D., and Daniel Doerge, Ph.D., consider this tofu study very important. ?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.?
In a 1999 letter to the FDA (and on the ABC News program 20/20), the two toxicologists expressed their opposition to the agency?s health claims for soy, saying the Honolulu study ?provides evidence that soy (tofu) phytoestrogens cause 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, there is a mechanistic basis for the human findings.? 3
Although estrogen?s role in the central nervous system is not well understood, White notes that ?a growing body of information suggests that estrogens may be needed for optimal repair and replacement of neural structures eroded with aging.?
One link to the puzzle may involve calcium-binding proteins, which are associated with protection against neurodegenerative diseases. In recent animal studies at Brigham Young University?s Neuroscience Center, researchers found that consumption of phytoestrogens via a soy diet for a relatively short interval can significantly elevate phytoestrogen levels in the brain and decrease brain calcium-binding proteins.4
Concerns About Giving Soy to Infants
The most serious problem with soy may be its use in infant formulas. ?The amount of phytoestrogens that are in a day?s worth of soy infant formula equals 5 birth control pills,? says Mike Fitzpatrick, a New Zealand toxicologist. Fitzpatrick and other scientists believe that infant exposure to high amounts of phytoestrogens is associated with early puberty in girls and retarded physical maturation in boys.5
A study reported in The Lancet found that the ?daily exposure of infants to isoflavones in soy infant-formulas is 6-11 fold higher on a bodyweight basis than the dose that has hormonal effects in adults consuming soy foods.? (This dose, equivalent to two glasses of soy milk per day, was enough to change menstrual patterns in women.6 In the blood of infants tested, concentrations of isoflavones were 13,000-22,000 times higher than natural estrogen concentrations in early life.7 )
Soy Interferes with Enzymes
While soybeans are relatively high in protein compared to other legumes, they are a poor source of protein because other proteins found in soybeans act as potent enzyme inhibitors. These ?anti-nutrients? block the action of trypsin and other enzymes needed for protein digestion. Trypsin inhibitors are large, tightly folded proteins that are not completely deactivated during ordinary cooking and can reduce protein digestion. Therefore, soy consumption may lead to chronic deficiencies in amino acid uptake.8
Soy?s ability to interfere with enzymes and amino acids may have direct consequence for the brain. As White and his colleagues suggest, ?isoflavones in tofu and other soyfoods might exert their influence through interference with tyrosine kinase-dependent mechanisms required for optimal hippocampal function, structure and plasticity.?2
High amounts of protein tyrosine kinases are found in the hippocampus, a brain region involved with learning and memory. One of soy?s primary isoflavones, genistein, has been shown to inhibit tyrosine kinase in the hippocampus, where it blocked ?long-term potentiation,? a mechanism of memory formation.9
Tyrosine, Dopamine,
and Parkinson?s Disease
The brain uses the amino acids tyrosine or phenylalanine to synthesize the key neurotransmitters dopamine and norepinephrine, brain chemicals that promote alertness and activity. Dopamine is crucial to fine muscle coordination. People whose hands tremble from Parkinson?s disease have a diminished ability to synthesize dopamine. An increased incidence of depression and other mood disorders are associated with low levels of dopamine and norepinephrine. Also, the current scientific consensus on attention-deficit disorder points to a dopamine imbalance.
Soy has been shown to affect tyrosine hydroxylase activity in animals, causing the utilization rate of dopamine to be ?profoundly disturbed.? When soy lecithin supplements were given throughout perinatal development, they reduced activity in the cerebral cortex and ?altered synaptic characteristics in a manner consistent with disturbances in neural function.?10
Researchers at Sweden?s Karolinska Institute and at the National Institutes of Health are finding a connection between tyrosine hydroxylase activity, thyroid hormone receptors, and depleted dopamine levels in the brain?particularly in the substantia nigra, a region associated with the movement difficulties characteristic of Parkinson?s disease.11,12,13
Soy Affects the Brain via the Thyroid Gland
Tyrosine is crucial to the brain in another way. It?s needed for the body to make active thyroid hormones, which are a major physiological regulator of mammalian brain development. By affecting the rate of cell differentiation and gene expression, thyroid hormones regulate the growth and migration of neurons, including synaptic development and myelin formation in specific brain regions. Low blood levels of tyrosine are associated with an underactive thyroid gland.
It is well known that isoflavones in soy products can depress thyroid function, causing goiter (enlarged thyroid gland) and autoimmune thyroid disease. In the early 1960s, goiter and hypothyroidism were reported in infants fed soybean diets.14 Scientists at the National Center for Toxicological Research showed that the soy isoflavones genistein and daidzein ?inhibit thyroid peroxidase-catalyzed reactions essential to thyroid hormone synthesis.?15
Japanese researchers studied effects on the thyroid from soybeans administered to healthy subjects. They reported that consumption of as little as 30 grams (two tablespoons) of soybeans per day for only one month resulted in a significant increase in thyroid stimulating hormone (TSH), which is produced by the brain?s pituitary gland when thyroid hormones are too low. Their findings suggested that ?excessive soybean ingestion for a certain duration might suppress thyroid function and cause goiters in healthy people, especially elderly subjects.?16
Thyroid Hormones and
Fetal Brain Development
Thyroid alterations are among the most frequently encountered autoimmune conditions in children. Researchers at Cornell University Medical College showed that the ?frequency of feedings with soy-based milk formulas in early life was significantly higher in children with autoimmune thyroid disease.?17 In a previous study, they found that twice as many diabetic children had received soy formula in infancy as compared to non-diabetic children.18
Recognizing the risk, Swiss health authorities recommend ?very restrictive use? of soy for babies. In England and Australia, public health agencies tell parents to first seek advice from a doctor before giving their infants soy formula. The New Zealand Ministry of Health recommends that ?Soy formula should only be used under the direction of a health professional for specific medical indications. . . Clinicians who are treating children with a soy-based infant formula for medical conditions should be aware of the potential interaction between soy infant formula and thyroid function.?19
Thyroid hormones exert their influence during discrete windows of time during development of the infant. Inappropriate hormone levels can have a devastating effect on the developing human brain, especially during the first 12 weeks of pregnancy when the fetus depends on the mother?s thyroid hormones for brain development. After that, both maternal and fetal thyroid hormone levels affect the central nervous system.
A 1999 study published in the New England Journal of Medicine showed that pregnant women with underactive thyroids were four times more likely to have children with low IQs if the disorder were left untreated. The study found that 19 percent of the children born to mothers with thyroid deficiency had IQ scores of 85 or lower, compared with only 5 percent of those born to mothers without such problems.20
Thyroid, Brain, and Environmental Toxins
Children exposed prenatally and during infancy to common environmental toxins like dioxin and polychlorinated biphenyls (PCBs) can suffer behavioral, learning, and memory problems because these chemicals may be disrupting the normal action of thyroid hormone.21
Soybeans grown in the United States contain residues of the pesticide dieldrin, an organochlorine similar to DDT. Although both chemicals were banned in the 1970s, dieldrin still persists in soils and is absorbed through the roots. Today it is the most toxic residue found on domestic soybeans.22 In Silent Spring, Rachel Carson warned that dieldrin is nearly 50 times as poisonous as DDT. In addition to disrupting hormones, it can have long delayed neurological effects, ranging from loss of memory to mania.23 Chinese aphids were recently discovered in fields scattered across Wisconsin, so increased pesticide applications are likely.
Combinations of insecticides, weed killers, and artificial fertilizers?even at low levels?have measurable detrimental effects on thyroid and other hormones as well as on the brain.24 EPA scientists now want to upgrade the commonly used herbicide, atrazine, to a ?likely carcinogen.? In animal tests, atrazine attaches to sites on the hypothalamus, a crucial brain region involved with regulating levels of stress and sex hormones.25
Individuals newly diagnosed with Parkinson?s disease were more than twice as likely to have been exposed to insecticides in their home, compared to those without the disease.26 In September 2000, The Lancet reported that farmers and gardeners regularly exposed to pesticides may have more than five times the risk of developing mild cognitive dysfunction.
Soy formulas for infants can contain other neurotoxins: aluminum, cadmium, and fluoride. Studies found that aluminum concentrations in soy-based formulas were a 100-fold greater compared to human breast milk,27 while cadmium content was 8-15 times higher than in milk-based formulas.28 In an Australian study, the fluoride content of soy-based formulas ranged from 1.08 to 2.86 parts per million. The authors concluded that ?prolonged consumption (beyond 12 months of age) of infant formula reconstituted with optimally-fluoridated water could result in excessive amounts of fluoride being ingested.?29 A study of Connecticut children revealed that mild to moderate fluorosis was strongly associated with soy-based infant formula use.30
In May 2000, Boston Physicians for Social Responsibility released their report, ?The Toxic Threats to Child Development.? In the section on neurotoxins, they concluded, ?Studies in animals and human populations suggest that fluoride exposure, at levels that are experienced by a significant proportion of the population whose drinking water is fluoridated, may have adverse impacts on the developing brain.?31
Iodine versus Fluorine
The thyroid gland uses tyrosine and the natural element iodine to make thyroxine (T4), a thyroid hormone containing four iodine atoms. The other, much more biologically active thyroid hormone is tri-iodothyronine (T3), which has three iodine atoms. Lack of dietary iodine has long been identified as the problem in diminished thyroid hormone synthesis.
According to the International Council for the Control of Iodine Deficiency Disorders: ?Iodine deficiency has been called the world?s major cause of preventable mental retardation. Its severity can vary from mild intellectual blunting to frank cretinism, a condition that includes gross mental retardation, deaf mutism, short stature, and various other defects. . . The damage to the developing brain results in individuals poorly equipped to fight disease, learn, work effectively, or reproduce satisfactorily.?
This crucial role of iodine is another reason why the thyroid gland is especially vulnerable today. Canadian researcher Andreas Schuld has documented more than 100 studies during the last 70 years that demonstrate adverse effects of fluoride on the thyroid gland.32 Schuld says, ?Fluorine, being the strongest in the group of halogens, will seriously interfere with iodine and iodine synthesis, forcing more urinary elimination of ingested iodine as fluoride ingestion or absorption increases.? (See page 21.)
Soy Inhibits Zinc Absorption
The high phytic-acid content in soy may also have adverse effects on brain function. Phytic acid is an organic acid present in the outer portion of all seeds which blocks the uptake of essential minerals in the intestinal tract: calcium, magnesium, iron, and especially zinc. Soybeans have very high levels of a form of phytic acid that is particularly difficult to neutralize and which interferes with zinc absorption more completely than with other minerals.
The soy industry acknowledges the problem with the admission that while ?one-half cup of cooked soybeans contains one mg of zinc
. . . zinc is poorly absorbed from soyfoods.? As for iron, ?both phytate and soy protein reduce iron absorption so that the iron in soyfoods is generally poorly absorbed.?33
According to unpublished documents, researchers testing soy formula found that it caused negative zinc balance in every infant to whom it was given.34 Even when the diets were additionally supplemented with zinc, there was a strong correlation between phytate content in formula and poor growth.
Zinc and the Brain
Relatively high levels of zinc are found in the brain, especially the hippocampus. Zinc plays an important role in the transmission of the nerve impulse between brain cells. Deficiency of zinc during pregnancy and lactation has been shown to be related to many congenital abnormalities of the nervous system in offspring. In children, ?insufficient levels of zinc have been associated with lowered learning ability, apathy, lethargy, and mental retardation.?35
The USDA references a study of 372 Chinese school children with very low levels of zinc in their bodies. The children who received zinc supplements had the most improved performance?especially in perception, memory, reasoning, and psychomotor skills such as eye-hand coordination. Three earlier studies with adults also showed that changes in zinc intake affected cognitive function.36
New research has identified a specific contingent of neurons, called ?zinc-containing? neurons, which are found almost exclusively in the forebrain, where in mammals they have evolved into a ?complex and elaborate associational network that interconnects most of the cerebral cortices and limbic structures.? This suggests the importance of zinc in the normal and pathological processes of the cerebral cortex.37 Furthermore, age-related tissue zinc deficiency may contribute to brain cell death in Alzheimer?s dementia.38
Not a Good Idea
High levels of phytoestrogens and zinc-blocking phytic acid, plus additional neurotoxic compounds such as dieldrin, aluminum, fluoride and cadmium combine in soy to yield a veritable witches? brew that can have adverse effects on the brain during development and throughout life.
Unfortunately, many American are now consuming soy foods in high amounts as infant formula, soy milk and tofu-based products, usually as a substitute for nourishing animal foods. In Asia, soy is consumed in small amounts as a fermented condiment and not as a substitute for animal foods.
Asians recognize the need for ?brain foods? like eggs and fish and realize that large amounts of soy can cause thyroid problems and inhibit growth. They know that for optimum mental function, soy foods are not a good idea.
About the author
John D. MacArthur is a freelance writer who?s recently been researching neuroscience topics for www.Brain.com. Links to his 20 reports can be found at www.getwrite.com. (Email: macarthur@getwrite.com ) This report was originally published online by Brain.com in July 2000, as ?The Trouble with Tofu.? At www.brain.com, visitors can use free tests to measure brain performance. Healthcare providers can access the Cognitive Care System, a web-based service for early detection and management of cognitive impairment.
References
White LR, Petrovich H, Ross GW, Masaki KH, Association of mid-life consumption of tofu with late life cognitive impairment and dementia: the Honolulu-Asia Aging Study. Fifth International Conference on Alzheimer?s Disease, #487, 27 July 1996, Osaka, Japan.
White LR, Petrovitch H, Ross GW, Masaki KH, Hardman J, Nelson J, Davis D, Markesbery W, Brain aging and midlife tofu consumption. J Am Coll Nutr 2000 Apr;19(2):242-55.
Doerge and Sheehan, Letter to the FDA, Feb 18, 1999. (http://abcnews.go.com/onair/2020/2020_000609_soyfdaletter_feature.htm)
Lephart ED, Thompson JM, Setchell KD, Adlercreutz H, Weber KS, Phytoestrogens decrease brain calcium-binding proteins… Brain Res 2000 Mar 17;859(1):123-31.
Soy Infant Formula Could Be Harmful to Infants: Groups Want it Pulled. Nutrition Week, Dec 10, 1999;29(46):1-2; See also www.soyonlineservice.co.nz
Cassidy A, Bingham S, Setchell KD, Biological effects of a diet of soy protein rich in isoflavones on the menstrual cycle of premenopausal women. Am J Clin Nutr 1994 Sep;60(3):333-40.
Setchell KD, Zimmer-Nechemias L, Cai J, Heubi JE, Exposure of infants to phyto-oestrogens from soy-based infant formula. Lancet 1997 Jul 5;350(9070):23-27.
Fallon SA, Enig MG, Tragedy and Hype, The Third International Soy Symposium. Nexus Magazine, Vol 7, No 3, April-May 2000.
O?Dell TJ, Kandel ER, Grant SG, Long-term potentiation in the hippocampus is blocked by tyrosine kinase inhibitors. Nature 1991 Oct 10 353:6344 558-60.
Bell JM, Whitmore WL, Cowdery T, Slotkin TA, Perinatal dietary supplementation with a soy lecithin preparation: effects on development of central catecholaminergic neurotransmitter systems. Brain Res Bull 1986 Aug;17(2):189-95.
Zetterstrom RH, Williams R, Perlmann T, Olson L, Cellular expression of the immediate early transcription factors Nurr1 and NGFI-B suggests a gene regulatory role in several brain regions including the nigrostriatal dopamine system. Brain Res Mol Brain Res 1996 Sep 5;41(1-2):111-20.
Castillo SO, Baffi JS, Palkovits M, Goldstein DS, Kopin IJ, Witta J, Magnuson MA, Nikodem VM, Dopamine biosynthesis is selectively abolished in substantia nigra… Mol Cell Neurosci 1998 May;11(1-2):36-46.
Baffi JS, Palkovits M, Castillo SO, Mezey E, Nikodem VM, Differential expression of tyrosine hydroxylase in catecholaminergic neurons of neonatal wild-type and Nurr1-deficient mice. Neuroscience 1999;93(2):631-42.
Shepard TH, Soybean goiter. New Eng J Med 1960;262:1099-1103.
Divi RL, Chang HC, Doerge DR, Anti-thyroid isoflavones from soybean: isolation, characterization, mechanisms of action. Biochem Pharmacol 1997 Nov 15;54(10):1087-96.
Ishizuki Y, Hirooka Y, Murata Y, Togashi K, The effects on the thyroid gland of soybeans administered experimentally in healthy subjects. Nippon Naibunpi Gakkai Zasshi 1991 May 20;67(5):622-29.
Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F, Breast and soy-formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. J Am Coll Nutr 1990 Apr;9(2):164-67.
Fort P, Lanes R, Dahlem S, Recker B, Weyman-Daum M, Pugliese M, Lifshitz FJ, Breast feeding and insulin-dependent diabetes mellitus in children. Am Coll Nutr 1986;5(5):439-41.
Regulatory Guidance in other countries: New Zealand Ministry of Health Position Statement on Soy Formulas (Domain parked by OnlyDomains)(Adobe Acrobat PDF file: Domain parked by OnlyDomains)
Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, O?Heir CE, Mitchell ML, Hermos RJ, Waisbren SE, Faix JD, Klein RZ, Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999 Aug 19;341(8):549-55.
Hauser P, McMillin JM, Bhatara VS, Resistance to thyroid hormone: implications for neurodevelopmental research on the effects of thyroid hormone disruptors. Toxicol Ind Health 1998 Jan-Apr;14(1-2):85-101.
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Soy Nutritive Content, United Soybean Board. (Talksoy.com - Hotels & Accommodation in Amsterdam)
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U.S. Department of Agriculture, Agricultural Research Service, Food & Nutrition Research Briefs, July 1997. (http://www.nal.usda.gov/fnic/usda/fnrb/fnrb797.html)
Frederickson CJ, Suh SW, Silva D, Frederickson CJ, Thompson RB, Importance of zinc in the central nervous system: the zinc-containing neuron. J Nutr 2000 May;130(5S Suppl):1471S-83S.
Ho LH, Ratnaike RN, Zalewski PD, Involvement of intracellular labile zinc in suppression of DEVD-caspase activity in human neuroblastoma cells. Biochem Biophys Res Commun 2000 Feb 5;268(1):148-54.
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You’re 100% right.There are even “diet foods” that contain trans fat and HFCS.I don’t believe a “calorie is just a calories”.Like I said before:I believe there is more to weight loss than just calories in and calories out.
What I’m saying is most " diet foods",in my experience,can actually make you gain weight.Go on a diet with nothing but slimfast bars,then diet with real foods.You’ll know what I’m talking about.
[quote]MookJong wrote:
The_Grim_Reaper wrote:
The funny thing is most fat people eat “diet foods”
That’s because most diet foods are highly processed junk - not because they’re good but fat people eat too much of them.
The “low fat” craze meant loads of sugar.
The “low carb” craze then meant loads of soy protein and/or trans fats.
Next thing you’ll be saying a calorie is just a calorie.
[/quote]