Bulletin Board Archived Bulletin Board About John Latest Ideas Symptoms Tests and Drugs Weight Loss Experiment Hyperthyroidism Hypothyroidism Supplement List Medical Science Heredity Other Diseases Thyroid Physiology Deeper Studies Nutrients and Toxics Hair Analysis Book Reports Glossary Table of Contents


    Soy beans are the basis of many foods like tofu which are being eaten more and more in this country as a good, vegetarian protein source.  However many people are suspecting that soy adversely affects the thyroid and may contribute to hypothyroidism

    Soy beans are high in copper, as most beans are, and therefore would be expected to slow the thyroid.  A cup of soy beans contains 0.7 mg of copper and 1.9 mg of zinc (according to the Nutrition Almanac). This is a zn:cu ratio of less than 3 which is definitely in the range for slowing thyroid function. 



    Thus if a person has autoimmune induced hypothyroidism, then soy may be a good food to suppress the immune system to prevent it from causing damage. 

The following study shows that both defatted soybean consumption and iodine deficiency decrease thyroid hormone production and cause an increase in thyroid gland size. However there is a very significant synergism between soybean consumption and iodine deficiency. Look at the thyroid gland weights. While iodine deficiency caused a doubling of thyroid gland weight (from 8.4 to 15.5),  iodine deficiency combined with soy intake caused the weight to nearly increase 10-fold!! (from 8.4 to 81.7).

Carcinogenesis 2000 Apr;21(4):707-13

Dramatic synergism between excess soybean intake and iodine deficiency on the development of rat thyroid hyperplasia.

Ikeda T, Nishikawa A, Imazawa T, Kimura S, Hirose M

Division of Pathology, National Institute of Health Sciences,1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan.

The effects of defatted soybean and/or iodine-deficient diet feeding were investigated in female F344 rats. Rats were divided into four groups, each consisting of 10 animals, and fed basal AIN-93G diet in which the protein was exchanged for 20% gluten (Group 1), iodine-deficient gluten (Group 2), 20% defatted soybean (Group 3) and iodine-deficient defatted soybean (Group 4). At week 10, relative thyroid gland weights (mg/100 g body wt) were significantly (P < 0.01) higher in Groups 2 (15.5 +/- 1.3) and 4 (81.7 +/- 8.6) than in Group 1 (8.4 +/- 2.0) and pituitary gland weights (mg/100 g body wt) were significantly (P < 0.01) higher in Groups 3 (9.1 +/- 0. 6) and 4 (9.7 +/- 1.5) than in Group 1 (6.5 +/- 1.5). Serum biochemical assays revealed thyroxine to be significantly (P < 0.05) lower in Groups 2 and 4 than in Group 1. On the other hand, serum thyroid-stimulating hormone (TSH) was significantly (P < 0.01) higher in Groups 3 and 4 than in Group 1. This was particularly striking for TSH (ng/ml) at week 10 in Group 4 (126 +/- 11) as compared with Groups 1 (4.36 +/- 0.30), 2 (4.84 +/- 0.80) and 3 (5. 78 +/- 0.80). Histologically, marked diffuse follicular hyperplasia of the thyroid was evident in Group 4 rats. Proliferating cell nuclear antigen labeling indices (%) were significantly higher (P < 0.05) in Groups 2 (4.8 +/- 2.5) and 4 (13.2 +/- 1.1) than in Group 1 (0.4 +/- 0.5). Ultrastructurally, severe disorganization and disarrangement of mitochondria were apparent in thyroid follicular cells of Group 4. In the anterior pituitary, dilated rough surfaced endoplasmic reticulum and increased secretory granules were remarkable in this group. Our results thus strongly suggest that dietary defatted soybean synergistically stimulates the growth of rat thyroid with iodine deficiency, partly through a pituitary-dependent pathway.

The story of the effect of soy protein on the thyroid seems complicated by other studies such as the following which states that

J Nutr 1995 Mar;125(3 Suppl):619S-623S

Soy protein, thyroid regulation and cholesterol metabolism.

Forsythe WA 3rd

School of Home Economics, University of Southern Mississippi, Hattiesburg 39406.

The effects of dietary protein on plasma cholesterol concentrations are well documented: animal proteins (casein) are hypercholesterolemic compared with plant proteins (soy protein). Although this effect of protein source on plasma cholesterol has been shown in many species, the mechanism is not completely understood. This paper reviews the relationship between dietary protein source and plasma thyroxine concentration. The basic premise is that feeding soy protein lowers plasma cholesterol concentration by causing an increase in plasma thyroxine concentrations. The metabolic changes involving cholesterol that occur when soy protein is fed are discussed. These changes are consistent with changes induced by elevating thyroxine. Data are presented from animal studies showing that feeding soy protein to laboratory animals consistently elevates plasma thyroxine concentrations. Furthermore, this elevation in plasma thyroxine concentrations precedes the change in plasma cholesterol concentrations: a necessary requirement for hypothesizing a causative effect. Possible mechanisms as to how a dietary protein source affects plasma thyroxine are also presented.
Toxicol Appl Pharmacol 2000 Nov 1;168(3):244-52

Dietary genistein inactivates rat thyroid peroxidase in vivo without an apparent hypothyroid effect.

Chang HC, Doerge DR.

Division of Biochemical Toxicology, Jefferson, Arkansas 72079, USA.

Biological effects of genistein are currently under investigation by the National Toxicology Program because of widespread and increasing soy consumption by humans and evidence for modulation of endocrine function. Rats were exposed to genistein aglycone in soy-free feed fortified at 0, 5, 100, and 500 ppm starting in utero through 20 weeks. Thyroid glands and serum were analyzed for total genistein (aglycone + conjugates) using HPLC with electrospray mass spectrometric detection. Microsomal thyroid peroxidase (TPO) activity was measured spectrophotometrically. The total genistein content in rat serum was as high as 8 microM, and significant dose-dependent increases of genistein in thyroid tissue up to 1 pmol/mg were found in male and female rats. The activity of TPO in male and female rats was found to be reduced by up to 80% in a dose-dependent manner. Male and female rats consuming a standard soy-based rodent diet (NIH 31) had TPO activity approximately 50% lower than rats consuming a soy-free diet and this loss was commensurate with measured serum levels of isoflavones. Suicide inactivation of rat, porcine, and human TPO was observed in vitro at concentrations of genistein aglycone comparable to those measured in rat thyroids. Thyroid hormone levels (T3, T4, TSH) in serum, thyroid weights, and histopathology showed no differences between treated and untreated groups. These findings suggest that, even though substantial amounts of TPO activity are lost concomitant to soy isoflavone consumption by normal rats, the remaining enzymatic activity is sufficient to maintain thyroid homeostasis in the absence of additional perturbations.
Cancer Res 2001 Jun 1;61(11):4325-8

Uterine adenocarcinoma in mice treated neonatally with genistein.

Newbold RR, Banks EP, Bullock B, Jefferson WN.

Developmental Endocrinology Section, Laboratory of Toxicology, Environmental Toxicology Program, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.

The developing fetus is uniquely sensitive to perturbation with estrogenic chemicals. The carcinogenic effect of prenatal exposure to diethylstilbestrol (DES) is the classic example. Because phytoestrogen use in nutritional and pharmaceutical applications for infants and children is increasing, we investigated the carcinogenic potential of genistein, a naturally occurring plant estrogen in soy, in an experimental animal model previously reported to result in a high incidence of uterine adenocarcinoma after neonatal DES exposure. Outbred female CD-1 mice were treated on days 1-5 with equivalent estrogenic doses of DES (0.001 mg/kg/day) or genistein (50 mg/kg/day). At 18 months, the incidence of uterine adenocarcinoma was 35% for genistein and 31% for DES. These data suggest that genistein is carcinogenic if exposure occurs during critical periods of differentiation. 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.

Food Chem Toxicol 1999 May;37(5):493-502

Reproductive effects of dietary soy in female Wistar rats.

Gallo D, Cantelmo F, Distefano M, Ferlini C, Zannoni GF, Riva A, Morazzoni P, Bombardelli E, Mancuso S, Scambia G.

Department of Obstetrics and Gynecology, Catholic University of the Sacred Heart, Rome, Italy.

This study was designed to assess the effects of administration of dietary soy on reproductive function and fertility of female Wistar rats. Four groups, each of 20 females, were used. Control animals were fed a standard cereal-based diet for rats. Treated animals were fed a standard diet supplemented with 0.7%, 1.2% or 2.4% of a soy extract. Treatment started at weaning and continued until day 7 post-partum (day of sacrifice). Growth depression was seen in the 2.4% soy group. Vaginal opening occurred earlier in females receiving soy supplemented feed when compared with controls. Analysis of vaginal smears revealed that all animals were cycling, although an increase in the mean duration of each cycle was seen in the 2.4% soy group. Uterine effects were observed in high-dose females and included increases in weight, oedema, endothelial hyperplasia and leucocytic infiltration. Vaginal modifications (i.e. inflammation, hyperkeratosis and dyskeratosis) and alterations in the distribution of follicular size in the ovaries were also observed among treated animals. These data suggest that long-term exposure to high doses of phytoestrogens can produce significant agonistic actions in several oestrogen-dependent tissues and parameters, even though in this model no clear influence on reproductive processes was observed.


From Dr. Mercola's site at

How Safe is Soy Infant Formula?

By David Goodman

New research suggests high concentrations of manganese found in soybean-based baby formula can lead to brain damage in infants and altered behaviors in adolescents.

Dr. Francis Crinella, clinical professor of pediatrics at UC-Irvine, and Trinh Tran, a graduate researcher at the UC-Davis Department of Animal Studies, have described how the soybean plant lifts up manganese in the soil and concentrates it so that its use in soy-based infant formula can result in as many as 200 times the level found in natural breast milk.

These and other experts believe that such high concentrations could pose a threat to the immature metabolic systems of babies up to 6 months of age.

The size of the market for soy-based infant formula is held closely, and none of the producers contacted by Insight would reveal sales figures. An independent expert estimates the market for all infant formula to be about $3 billion, with soy-based formula accounting for about $750 million of that, having doubled in the last 10 years.

The best-selling brand is Isomil (Ross Products Division of Abbott Laboratories), followed by Enfamil ProSobee (Mead Johnson), Nursoy (Wyeth-Ayerst) and Alsoy (Carnation).

According to Crinella and Tran, the discovery of potential harm from such products began in 1980 when a federal agency then called the Food and Nutrition Board established safe and acceptable values for manganese in adults, toddlers and infants.

Permissible levels for the three age groups ranged from 2.5 to 3 mg per day for adults, 1 to 1.5 mg per day for toddlers and 0.5 to 1 mg per day for infants under 6 months. This job now is handled by the Food and Drug Administration (FDA), which today permits 0.6 mg per day for infants, 120 times the amount found in mother's milk.

The FDA says that in the next few months it will lower the guidelines.

Ruth Welch, an FDA spokeswoman, confirms that a report will recommend a minimum of only 0.005 mg of manganese a day and no maximum for infants up to age 6 months.

Despite government assurances of safety at the recommended levels, the professional literature shows that in 1983 Phillip Collipp, a pediatric physician at Nassau County [N.Y.] Medical Center, tested infant formula for manganese in popular soy brands, including Isomil, ProSobee and Nursoy, purchased locally. He published data showing that they contained from 0.2 mg to 1 mg per quart. Later that year, Drs. Bo Lönnerdal and Carl Keen of the UC-Davis Department of Nutrition tested formula taken from pharmacy shelves worldwide.

They found higher manganese concentrations in soy formulas, ranging from 0.4 mg to 2.2 mg; the mean value of 1.2 mg vastly exceeded the infinitesimal 0.005 mg found in mother's breast milk.

After the research by Collipp, Lönnerdal and Keen, nutritional scientists worldwide reported that newborn babies, in symbiosis with their mothers during the first weeks, absorbed most of the manganese in breast milk. The tiny amounts the baby suckles a dozen times a day appear to function as a catalyst for more than 50 biochemical reactions. This suggests a newborn's digestive system is superbly attuned to absorb the infinitesimal levels of manganese in mother's milk, and that, in fact, it is essential to the development process.

At least some of this soy formula, which tested at up to 200 times the manganese of breast milk clearly has the potential to overload the infant's little body.

Lönnerdal says the baby's immature liver cannot handle the manganese load by excreting the excess. In newborns, ingested manganese rises to high levels in the blood plasma and red blood cells, then permeates the liver, kidneys and other soft tissues of the body, including the brain. He believes, however, that by the time of weaning, when the infant normally consumes solid food, it can metabolize manganese.

Crinella calculated that by the age of 8 months an infant fed soy formula daily absorbs approximately 1.1 mg of manganese above metabolic need. "A significant amount, about 8 percent, is deposited in a brain region vulnerable to threat of manganese attack," he says.

Six years ago, tragic incidents in two London hospitals, the Hospital for Sick Children and Queen Elizabeth's Hospital for Children, alerted the medical community to the vulnerability of sick babies to manganese attacks on the brain. Suffering from liver disease, the babies had received nutrient solutions containing recommended amounts of manganese through an intravenous tube. The manganese had no greater concentration than in soy formula and was considered safe by government standards, but after a few months the infant brains showed damage.

Of 57 babies receiving "safe" amounts of manganese, two fell ill with movement disorders and six suffered damage to their basal ganglia when examined by magnetic resonance imaging (MRI).

Also, Crinella has done extensive studies on the effect of manganese in adolescents. His research detected relatively high levels of manganese in the scalp hair of hyperactive children when compared with matched control subjects.

Crinella at first was puzzled by the high manganese levels in hyperactive children. The only exposure of his subjects had to be through diet, yet California has historic low levels of manganese in its soil, air and water. Because adolescents metabolize at least 97 percent of manganese ingested, the exposure had to have occurred earlier in life, possibly from manganese in baby food, or (as his research proceeded further) soy-based infant formula. Could elevated manganese be a clue to the current epidemic of adolescent violence sweeping the nation?

Crinella did a study with rats and manganese supplementation and the results were clear-cut: Rats given 0.05 mg. of manganese daily for 18 days in the amount comparable with the manganese in breast milk did as well as the control group given no manganese. Rats given supplemental manganese five times higher at 0.25 mg daily suffered a precipitous decline in basal-ganglia dopamine of 48 percent. The rats dosed daily with the highest amount, 0.50 mg, had a plunge in dopamine by a staggering 63 percent.

"The brain undergoes a tremendous proliferation of neutrons, dentrites and synapses during the first months of life," Crinella says. "The brain especially is vulnerable in early life precisely because such rampant growth is taking place, and at that time intrusions by potentially toxic substances like manganese perturbing the emerging neural organization can exert long-term effects. Manganese ingested during a period of rapid brain growth and deposited in the critical basal ganglia region may affect behavior during puberty when powerful stresses are un- leashed on the dopamine neurons, and altered behavioral patterns appear."

These altered behavioral patterns during late childhood and early adolescence, according to Crinella, may be diagnosed as hyperactivity with attentional deficit - or perhaps as "manganese-toxicity syndrome."

Everett Hodges, founder of the Violence Research Foundation, thinks Crinella's case is overwhelming. "Criminals ages 16 and 17 years old today, some of them born to poor mothers between 1983 and 1984, could have received from the government soy formula with enough manganese to disrupt growing brains, and this may be why adolescents have difficulty restraining aggressive impulses now."

Dr. Stanley van den Noort, a member of the foundation's board, is former dean of the UC-Irvine College of Medicine. He says, "I think the data presented at the conference are convincing that manganese is a neurotoxin. Newborn infants exposed to high levels of manganese may be predisposed to neurological problems. We should exercise strong caution in the use of soy-based formula around the world."

Naomi Baumslag, clinical professor of pediatrics at Georgetown University Medical College and president of the Woman's Public Health Network, tells Insight, "Only 50 percent of newborns today suckle at the mother's breast even once. After six months, the number has fallen to only one mother in five. Often mothers for the sake of convenience plunk soy bottles into the infant's mouth. Why do so many mothers in the United States imagine they have given birth to a baby soybean instead of a human child?"

Baumslag goes further: "There is a great deal of scientific evidence that soy formula can be damaging to newborns, quite aside from the manganese." She says a tablespoon of soy formula can be dangerous both for what it does not have and for what it has.

That spoonful may be deficient in linoleic and oleic essential fatty acids, DHA-brain-growth factor, epidermal growth factor, lactoferrin, casomorphin and immune factors such as IgA, neutrophils, macrophages, T-cells, B-cells and interferon - all provided by the mother in breast milk to defend her baby.

On the other hand, Baumslag says, that spoonful does contain phytates, protease factors, soy lectins, enormous amounts of phytoproteins, and genistein and daidzen, both moderate estrogen mimics in humans.

"Why deprive the newborn infants of perfectly good breast milk - a nutritionally superior food in every way for the baby - and feed them soy beans?" Baumslag asks.

Insight Magazine


This is a new one for me with soy formula. I was not aware of its elevated manganese levels. I have known of the increased aluminum levels in soy.

The other significant issue are the estrogens in soy. A soy-fed baby receives the equivalent of five birth control pills' worth of estrogen every day. These babies' isoflavone levels were found to be from 13,000 to 22,000 times higher than in non-soy fed infants.

Responses to Manganese in Soy

We had two good follow-up emails from the the recent article we had about elevated Manganese levels in soy article.

The first is from David Vaughan ( who is one of the top nutritionists in Seattle and the second is from Andreas Schuld (, a well-known expert on fluoride.

David Vaughan:

The worst offender of manganese in baby food, however, is baby food with turkey meat. It has a whopping 30mg of Mn in 100gms.

Next worst is creamed peaches, which has 15.68mg.

I have been screaming about MN/soy as a problem for years. So little valid research has been done that it is a tough argument to make. One ends up talking about such archaic problems as "Manganic Madness" and the like. A piece of research was done showing high MN in hair of violent and criminally insane prisoners.

In the Northwest part of Washington State there is a huge problem with MN in the well water. EVERYONE who drinks well water from that region has or will have very serious health problems.

There are no known chelators specific to MN Filtering it from water is very expensive and problematic. Because it is the main fuel for the mitochondria this MN overload is a very sticky problem. My view is that it is the higher valence MN (biounavailable) that causes the body to shunt the normal use of bioavailable MN thus causing a toxic buildup for which we have no solution (yet). Big problem.


Fluoride/Manganese Association

Andrease Schuld had some excellent comments as to the importance of the manganese as relates to its interaction with fluoride.

First of all, as the soy formula article from last week states, manganese levels in soy formula are 200 times that of breast milk.

Add to that, the fact that fluoride can increase manganese absorption, and you now have an even more lopsided and dangerous situation. The soy formula has massive manganese levels and the fluoridated water that may be used to reconstitute the powder version or concentrate version of the soy formula causes even greater manganese absorption in the infant.

As Andreas points out, the scientific literature clearly shows that increased manganese levels can cause several problems, such as replacing magnesium in many enzymes that the body makes.

Be sure to vist Andreas's website at

Andreas Schuld:

There are many interactions between fluoride and manganese, especially as it relates to signal transduction in disease. However, as this requires some understanding of pathways etc., it might be too complex to get into at this point. This is, again, particularly important as it relates to thyroid hormone function.

Kanwar, Singh et al (1981) exposed rats to various fluoride levels in drinking water and found that fluoride caused a significant fall of manganese levels in the liver and kidney, while it increased manganese levels in bone.

Kanwar KC, Singh M - "Zinc, copper and manganese levels in various tissues following fluoride administration" Experientia 37(12):1328-9 (1981)]

also in:

Singh M, Kanwar KC - "Effect of fluoride on copper, manganese and zinc in bone and kidney" Bull Environ Contam Toxicol 26(3):428-31 (1981)

When rats were fed green and black tea extracts (high in Fluoride and Aluminum), it was found that the manganese and copper absorption was increased, while zinc, calcium and iron absorption was decreased. In all tea extracts used, the manganese absorption was increased, resulting in increased manganese in the tibia.

[Zeyuan D, Bingying T, Xiaolin L, Jinming H, Yifeng C - "Effect of green tea and black tea on the metabolisms of mineral elements in old rats." Biol Trace Elem Res 65(1):75-86 (1998)]

This is quite important, as tea has very high levels of fluoride, aluminum and manganese. The content of manganese was 1440 micrograms/g in the case of oolong tea, 670 micrograms/g in green tea, and 535 micrograms/g in black tea.

[Matsushima F, Meshitsuka S, Nose T - "Contents of aluminum and manganese in tea leaves and tea infusions" Nippon Eiseigaku Zasshi 48(4):864-72 (1993)]

Manganese absorption also depends a great deal on zinc.

When zinc deficient, manganese levels in brain are altered.

From 10-27-01:

Soy Can Lead to Kidney Stones

New research indicates that soybeans and soy-based foods, a staple in the diets of many health-conscious consumers, may promote kidney stones in those prone to the painful condition.

The researchers measured nearly a dozen varieties of soybeans for oxalate, a compound that can bind with calcium in the kidney to form kidney stones.

They also tested 13 types of soy-based foods, finding enough oxalate in each to potentially cause problems for people with a history of kidney stones, according to Linda Massey, Ph.D., at Washington State University in Spokane.

The amount of oxalate in the commercial products easily eclipsed the American Dietetic Association's 10 milligram-per-serving recommendation for patients with kidney stones, with some foods reaching up to 50 times higher than the suggested limit, she noted.

"Under these guidelines, no soybean or soy-[based] food tested could be recommended for consumption by patients with a personal history of kidney stones," she said.

No one had previously examined soy foods for oxalate, thus the researchers are the first to identify oxalate in store-bought products like tofu, soy cheese and soy drinks. Other foods, such as spinach and rhubarb, also contain significant oxalate levels, but are not as widely consumed for their presumed health benefits, Massey said.

During their testing, the researchers found the highest oxalate levels in textured soy protein, which contains up to 638 milligrams of oxalate per 85-gram serving.

Soy cheese had the lowest oxalate content, at 16 milligrams per serving. Spinach, measured during previous research, has approximately 543 milligrams per one-cup (2 oz. fresh) serving.

Soy, a natural source of protein, fiber and healthy oils, is used to enhance a myriad of foods, ranging from hamburgers to ice cream. It can be ground into flour and used in a variety of grain products, or formed into chunks and ground like meat.

Soy is also being studied for its potential to lower cholesterol, reduce bone loss and prevent breast cancer. The U.S. Food and Drug Administration recently approved a new label on foods containing at least 6.25 grams of soy protein per serving that boasts of a reduced risk of cardiovascular disease.

Oxalate, however, cannot be metabolized by the body and is excreted only through urine, Massey said. The compound has no nutritional value, but binds to calcium to form a mass (kidney stones) that can block the urinary system, she said.

Further research is needed to find types of soybeans with less oxalate, or to develop a processing method to remove the compound before it reaches consumers, she added.

No one knows precisely why kidney stones occur in particular individuals.

But Massey said high levels of oxalate in the urine increase the risk and those with a family history of the ailment are more likely to suffer from the condition; individuals with a low probability of kidney stones are unlikely to be affected by oxalate in soy-based foods.

More than one million people were diagnosed with kidney stones in the United States in 1996, the most recent available data, according to the National Institutes of Health.

Stones can range in size from the diameter of a grain of rice to the width of a golf ball. An estimated 10 percent of the U.S. population, mostly men, will develop a kidney stone at some point in their lives, according to the NIH.

Journal of Agricultural and Food Chemistry September 2001


Yet one more nail in the coffin of non-fermented soy which I do not believe is designed to be eaten. This study suggests that the over one million patients with kidney stones should not consume soy.

If you are still brainwashed by the edible oil industry's incredibly effective media spin on soy, then please review the soy index page link below which has hundreds of pages describing the reason's you will not want to regularly consume non-fermented soy products.

Soy protein powders and soy formula are the worst offenders and I don't believe that they should be consumed by anyone

Even Cheetahs Can't Tolerate Soybeans

By Dr. Sue Ann Bowling

This article is provided as a public service by the Geophysical Institute, University of Alaska Fairbanks, in cooperation with the UAF research community. Dr. Sue Ann Bowling is an Associate Professor of Physics at the Institute.

Pity the poor cheetahs! These speedy spotted cats managed to survive one population crisis, which left them the most inbred wild animal known. Then human inroads on their habitat and hunting for their fur shoved them toward a second population crisis, which seemed headed off by captive breeding. Now it appears that the zoo diet in North America is simultaneously killing them off with liver disease and preventing them from breeding effectively.

In 1985, 29 American zoo cheetahs died and only 18 were born, and 7 of the 18 died before adulthood. Only about 10% of North American adult female cheetahs have been producing live cubs in the last 5 years, compared with 60 to 80 % in other countries.

Since North American cheetahs mostly eat a commercial feline diet based on horsemeat and soy, while the cheetahs living and breeding more successfully elsewhere are being fed whole carcasses, a group of researchers in Ohio decided to look at the zoo cheetah's food. They found that the soybean part of the diet (the same textured soy protein and soy flakes used increasingly as a meat extender in human diets) contained natural plant estrogens, chemicals akin to mammalian female hormones and having some of the same effects.

When these chemicals were injected into immature female mice, they caused damage to the mice's uteruses.

Experiments were carried out at the zoo as well as in the lab. When four cheetahs in the Cincinnati Zoo were switched to a diet based on chicken meat without soy, their liver function improved. Right now we don't know whether they will breed again or whether permanent damage has occurred.

What does this mean in terms of other soy consumers? Cheetahs are likely to be exceptionally sensitive to problems of any kind because they are so inbred. On the other hand, soy made up a relatively small percentage of the cheetahs' diet, and apparently all cats are rather poor at getting rid of extra estrogens. Our pets might face some problems.

A quick scan of supermarket dog and cat food labels indicates that about half of the commercial dry pet foods have soy as the main protein source, with soy appearing as the first ingredient after corn or (in some very high protein products such as kitten food) as the first ingredient. As a dog breeder I would hesitate to maintain my breeding stock on a commercial diet that used soy as the primary protein source, or listed soy as one of the top three ingredients. But other questions need to be answered, as well.

How about the human consumption of soy?

Alaska Science Forum January 18, 1988


This article is nearly 15 years old and way back then the warnings for soy consumption were being raised.

Fermented soy products are the only ones you should even consider using. Most all children should avoid soy due to its hormonal influences. This is particularly true of soy formula and soy milk for children.