Why is Soy Good? - Soy Milk - Soy Dangers?

Soy Protein is now a popular weight loss alternative and is indeed an effective and healthy meal replacement. Studies have shown that soy protein is healthy and is effective at lowering cholesterol, but is best consumed in foods rich in soy. DrSoy Diet is an effective and convenient way of adding soy protein to your diet during your busy day.

Soy helps increase your muscle mass

Your muscles burn energy in the form of calories for daily maintenance and during exercise. Increased muscle mass burns more calories on a dialy basis even if you are not exercising - even if you just sit around. Soy can also improve energy levels.

Soy helps reduce the amount of fat your body stores

* You convert less calories into fat from the food that you eat
* Fewer “sugar cravings” as a result of reduced insulin fluctuations
* Binge eating due to sugar cravings often defeats the efforts of millions in their diets.

Losing fat while increasing muscle

Soy is naturally a low-calorie, low-carbohydrate food. Recent studies by physicians at Iowa State University documented 2 key properties of soy protein concluding that soy has an inherent medical properties, apart from low calorie content, that help with weight loss. The studies showed that consumption of soy protein rich in isoflavones decreases fat storage while increasing muscle mass. Isoflavone-rich soy may attenuate the increase in fat deposition and prevent loss in lean tissue during menopause. This is extremely important as lean muscle tissue even at rest burns up to 17 times more calories than the same amount of fat tissue.

Soy protein stimulates your metabolism

* Increasing the rate at which your fat cells burn stored fat
* Increasing the activity directly inside of fat cells
* Minimizing insulin fluctuations due to soy’s low-glycemic index
* Reducing sugar cravings
* Helping you feel more satisfied and less hungry until the next meal
* Increasing your energy level

Soy foods have played an important role in the traditional diets of many regions throughout the world for many centuries. Soy contains protein, calcium and isoflavones. Soy protein is extracted from soy bean.
The soy bean is one of the very few plants that provide a complete protein source (40% protein). Soy beans contain the essential amino acids that form what is known as a complete protein. The body cannot synthesize essential amino acids, they must be obtained from food.

Soy foods have become more widely available in the Western culture. Extensive research has confirmed that we need to consume less fat and more fiber. The soy bean provides high-quality protein and is relatively low in fat content. It also contains other macronutrients carbohydrates, fats and micronutrients, fiber, minerals and vitamins which make soy beans an excellent and complete source of food for human consumption. Soy is also a unique dietary source of many phytochemicals (naturally occurring compounds in plants), the most well known and thoroughly studied of them are isoflavones.

Regular consumption of soy in Southeast Asian populations is associated with the reduction in the rates of certain chronic health conditions like cardiovascular disease. Recent experimental evidence suggests that phytochemicals, i.e. isoflavones in soy are responsible for its beneficial effects which may also help in enhancing bone health. Soy foods can also be a great source of nutrition for women, children and simply a good food for all ages to enjoy both its taste and health benefits.

Why Not Soy?

During pregnancy in humans, isoflavones could be a risk factor for abnormal brain and reproductive tract in fetal development.

Phytoestrogens in Soy Depress Immune Function

An article published in the Proceedings of the National Academy of Science (May 28, 2002;99(11):7616-7621) has raised new concerns about soy. Researchers injected mice with the soy isoflavones genistein and daidzein and then looked at the thymus gland.

They found that the injections produced dose-responsive decreases in thymic weight of up to 80 percent. In other words, the more isoflavones given, the greater decrease in the weight of the thymus gland. The genistein-injected mice showed a large decrease in the number of immune cells and changes in the thymus, where immune cells mature. Genistein decreased thymocyte numbers up to 86 percent and doubled apoptosis (cell death), indicating that the mechanism of the genistein effect on loss of thymocytes is caused in part by increased apoptosis. In addition, genistein produced suppression of humoral immunity.
Genistein injected at 8 mg/kg per day produced serum genistein levels comparable to those reported in soy-fed human infants, and this dose caused significant thymic and immune changes in mice.

Said the researchers: "Critically, dietary genistein at concentrations that produced serum genistein levels substantially less than those in soy-fed infants produced marked thymic atrophy. These results raise the possibility that serum genistein concentrations found in soy-fed infants may be capable of producing thymic and immune abnormalities, as suggested by previous reports of immune impairments in soy-fed human infants."
These results explain the frequent infections, high fevers and autoimmune problems (including diabetes) that often occur in soy-fed children.
Unlike earlier reports on the negative effects of soy, this study was actually reported in a major newspaper. "A Closer Look at Soy and Babies" appeared in the Science section of the New York Times, May 21, 2002. The article quotes Dr. Paul S. Cook, head of the study, as stating that "parents whose babies did not need to drink soy formula for health reasons, like allergies, should consider using milk-based formula instead, if they do not breast feed." Mead Johnson Nutritionals, maker of soy formula, naturally defended the use of soy formula. But this article represents the first hole in the media dike and yet another warning to parents to avoid soy formula for their babies.
This review appeared in the Summer 2002 edition of Wise Traditions.

FDA Scientists Against Soy

Original Source: alkalizeforhealth.net/Lsoy2.htm

Scientists Protest Soy Approval
In Unusual Letter, FDA Experts Lay Out Concerns
Researchers Daniel Doerge and Daniel Sheehan, two of the Food and Drug Administration's experts on soy, signed a letter of protest, which points to studies that show a link between soy and health problems in certain animals. The two say they tried in vain to stop the FDA approval of soy because it could be misinterpreted as a broader general endorsement beyond benefits for the heart. The text of the letter follows.

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

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 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 from 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 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 latencies, 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 near-complete or 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
870-543-7561 Fax 870-543-7682
DSHEEHAN@NCTR.FDA.GOV
870-543-7943 Fax 870-543-7136
DDOERGE@NCTR.FDA.GOV
Enclosures
cc: Dr. Bernard Schwetz, Director, NCTR
Dr. Barry Delclos

REFERENCES

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Divi, R.L. and Doerge, D.R. Inhibition of thyroid peroxidase by dietary flavonoids. Chem. Res. Toxicol. 9, 16-23, 1996.
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