New book in Dutch

Eet vet word slank

Eet vet word slank gepubliceerd januari 2013

In dit boek lees je o.a.: * heel veel informatie ter bevordering van je gezondheid; * hoe je door de juiste vetten te eten en te drinken kan afvallen; * hoe de overheid en de voedingsindustrie ons, uit financieel belang, verkeerd voorlichten; * dat je van bewerkte vetten ziek kan worden.

Trick and Treat:
How 'healthy eating' is making us ill
Trick and Treat cover

"A great book that shatters so many of the nutritional fantasies and fads of the last twenty years. Read it and prolong your life."
Clarissa Dickson Wright

Natural Health & Weight Loss cover

"NH&WL may be the best non-technical book on diet ever written"
Joel Kauffman, PhD, Professor Emeritus, University of the Sciences, Philadelphia, PA

Soy Online Service

SOY & DES (Diethylstilbestrol)


Diethylstilbestrol is a synthetic estrogen that caused cancerous birth defects in the daughters of women who took it while pregnant. The defects did not become apparent until those young women reached maturity. Subsequent events showed that male reproductive function was also impaired. DES is so potent and harmful that it is banned as a residue of growth promoters in beef liver at one part in two billion. The UK Food Surveillance program knew that a Government laboratory, the Central Veterinary laboratory, had established by 1980 that soy food for human consumption had an estrogenic equivalence of more than 16 parts per billion of DES. The abstract of that work by Drane et al is posted at the foot of this page. Also posted here are numerous warnings by other scientists of the equivalent danger from soy foods.

Soy Information Service believes that regulators all over the world have ignored these warnings for political reasons; the "Precautionary Principle" dictated that that consumers be protected from these hazards by decrees that isoflavones be removed from soy products for human consumption. That they did not do so may be behind the alarming increase in UK birth defects  and hormonal cancers  and to the decrease in sperm quality and quantity.  Further evidence that exposure of a pregnant woman to estrogenic toxins can be devastating for her child in later life can be found Here.

Where's the Proof? Read on.


Follow this link to an Endocrine Disruptors and Man-made Chemicals Timeline which provides information, historical use and discovery of the harmful effects chemicals like DES can have on people.  Research as far back as 1952 showed "...that DES actually increases the number of miscarriages, premature births, and deaths among infants".


What to have for Breakfast?

A slice of "sheila bread" (Burgen's Soy and Linseed) is at the cancer-risk level that caused diethylstilbestrol to be banned from meat as a growth promoter'.


"Estrogenic Activity of Burgen Bread to Female Rats"

Ashby J., and Tinwell H.

Journal of Human and Experimental Toxicology (1998) (17) pp 394-399.

In this research a four day dose of soy & linseed bread caused the uterus weights of female rats to DOUBLE . AND one slice (34 gr) of Burgen bread had estrogenic equivalence of 0.5 ppb of Diethylstilbestrol


There is concern that environmental exposure of humans to synthetic oestrogens may be responsible for the reported declines in human sperm quality and increases in the incidence of human reproductive organ cancers. This has led to extensive international efforts to devise/refine assays for the identification of synthetic oestrogens such as diethylstilboestrol (DES) and nonylphenol (NP) and to institute appropriate regulatory measures to control their release into the environment. A major complication to these endeavours is the extensive dietary exposure of humans to plant oestrogens (phytoestrogens), the potential hazards/benefits of which remain uncertain.

Burgen brown bread was recently introduced into the United Kingdom with the implication that it can ease post-menopausal symptoms in women. It is enriched with an unspecified quantity of soya flour and linseed, both of which contain phytoestrogens. The advertisements and the wrapper state that Burgen bread is high in natural plant oestrogens and a variety of anecdotal endorsements are offered including that it is capable of putting the ‘waltz back into Matilda'. The telephone help-line provided adds to the clinical area of the product. We report here the estrogenic activity of Burgen bread in the immature rat uterotrophic assay, one of the most well established methods of assessing the estrogenic potential of chemicals. The test relies on the ability of oestrogens such as DES and NP to induce precocious growth of the uterus of sexually immature (weanling) animals and provides information on the potential hormonal activity of chemicals to estrogen-responsive tissues of humans.

Access of weanling female AP rats to Burgen bread as their sole food for 4 days led to a doubling or uterus weights on the fifth day. The positive control agent DES (in arachis oil (AO)) increased uterus weights fourfold in that encountered in sexually mature young rats. Normal laboratory rat diet (RMI). AO, and similar access to Hovis brown bread, were without activity in the assay. The synthetic environmental oestrogen NP (as its maximum activity close level in AO) gave a uterotrophic response of similar magnitude in that given by Burgen bread. Comparison of these data indicates that one slice of Burgen bread (~34 g) is of equal oestrogenic activity to the rat uterus as the daily administration of ~0.5 m g of the hormonal drug DES or 30 mg of the industrial chemical NP.


Organisation versus Activation:  The Role of Endocrine-disrupting Contaminants (EDCs) during Embryonic Development in Wildlife.

Guillette L. J. Jr, Crain D. A., Rooney A. A., Pickford D. B.

Environmental Health Perspectives 103 (7) 1995, 157-164.


Many environmental contaminants disrupt the vertebrate endocrine system.  Although they may be no more sensitive to endocrine-disrupting contaminants (EDCs) than other vertebrates, reptiles are good sentinels of exposure to EDCs due to the lability in their sex determination.  This is exemplified by a study of alligators at Lake Apopka, Florida, showing that EDCs have altered the balance of reproductive hormones resulting in reproductive dysfunction.  Such alterations may be activationally or organizationally induced.  Much research emphasizes the former, but a complete understanding of the influence of EDCs in nature can be generated only after consideration of both activational and organizational alterations.  THe organizational model suggests that a small quantity of an EDC, administered during a specific period of embryonic development, can permanently modify the organization of the reproductive, immune, and nervous systems.   Additionally, this model helps explain evolutionary adaptations to naturally occurring estrogenic compounds, such as phytoestrogens.


In rodents, exposure to estrogenic compounds during in utero development or immediately after birth results in pathological changes of the reporductive tract, as well as functional differences at puberty and throughout adulthood.  Similar estrogenic effects have also been demonstrated on the immune and neuroendocrine systems.

Many of the observed DES-induced modifications to the reproductive system are morphologically subtle but result in major functional changes.

Although changes in receptor type and abundance can be considered subtle, developmental abnormalities of this type may be the basis for infertility or reproductive cancers.

Similar to the reproductive effects caused by DES, immune modification resulting from neonatal DES exposure occurs during a critical period.  Whereas adult exposure to estrogens temporarily inhibits many aspects of the immune system, neonatal exposure to DES causes a persistent impairment of several immune parameters, including reduced delayed hypersensitivity reponse, decreased in vitro mitogen response, and depressed graft versus host reaction.

The mechanisms of action of estrogens on the immune system appear to involve both lymphoid and nonlymphoid tissues.  Estrogen receptors are present at low levels in lymphoid cells and near uterine levels in thymic epithelium.  EDCs may alter estrogen receptor levels in immune tissues, similar to receptor changes of the reprodutive system.

A complication when examining the immune or reproductive systems is the interwoven nature of their function.

Endocrine irregularities associated with this T-lymphocyte deficiency include delays in puberty in females, alterations in normal adenohypophysis formation, and abnormal circulating levels of gonadal hormones.

Interestingly, it is also important to note that many organizational modifications do not become apparent until later in life.


"Estrogens in the Environment: Naturally-Occurring Non-Steroidal Estrogens of  Dietary Origin"

Setchell   K.D.R 1985

"While the potency of DES far exceeds that of either the endogenous estrogens, or the phytoestrogens, the amounts of the latter consumed are significantly greater. The effects of plant estrogens in man should be of some concern, since it has been suggested that soya might be as beneficial as a growth promoter as DES is in animals. For example, the concentrations of phytoestrogens insoy (calculated to match 0.5 ppb of DES) are well within the concentration range of consumed soya products" 


Uterine adenocarcinoma in mice treated neonatally with genistein.

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

Cancer Research 61: 4325-4328 2001.

For commentary, follow the link below

Original abstract :

Uterine Adenocarcinoma in Mice Treated Neonatally with Genistein

Retha R. Newbold1, Elizabeth Padilla Banks, Bill Bullock and Wendy N. Jefferson

Cancer Research 61, 4325-4328, June 1 2001

Developmental Endocrinology Section, Laboratory of Toxicology, Environmental Toxicology Program, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 [R. R. N., E. P. B., W. N. J.], and Department of Pathology, Wake Forest University School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157 [B. B.]

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.


"Dietary Estrogens :Probable Cause of Infertility and Liver Disease in Captive Cheetahs"

KDR Setchell et al. 

Gastroenterology, 1987 pp 225-233

Click this link to read the abstract.

"Despite concerns over the deleterious effects of is apparent that the contribution of plant estrogens is rarely considered.   This is surprising since the levels of phytoestrogens in foods is substantially higher than the estrogen levels in animal tissues.....Our observations in cheetahs further support serious consideration of the potential implications of dietary estrogens in humans" 


"The Case for Expanded Phytoestrogen Research"

Sheehan, D.M.

 P.S.E.B.M. 1992, 208 pp 3-5. 

"Phytoestrogens have some of the same capabilities to induce developmental toxicity as do other estrogens... given the DES tragedy, it would be foolish to ignore the possibility that phytoestrgens constitute a developmental hazard"


Genotoxicity of Estrogens

Metzler M, Kulling SE, Pfeiffer E and Jacobs E. 

Z Lebensm Unters Forsch A 1998, 206: 367-73. 

Click this link to read the abstract.

"it is likely that the genotoxicity of the estrogens acts in concert with their hormonal activity to give rise to their carcinogenic has long been known that estrogenic activity is not limited to steroidal hormones.  In 1938, the stilbene estrogen diethylstilbestrol was synthesised and found to match or even exceed E2 in therms of hormonal activity."


The Wingspread Commentary

Follow this link to the Wingspread Statement

"Daughters born to mothers who took DES now suffer increased rates of clear-cell cancer, various genital tract abnormalities, abnormal pregnancies and some changes in immume response.  Both sons and daughters experience congenital abnormalities of their reproductive systemand reduced fertility".


Isoflavone content of soya-based laboratory animal diets.

Murphy PA, Farmakalidis E, Johnson LD

Food Chem Toxicol 1982 Jun 20:3 315-7

"The soy phytoestrogens have a number of pharmocological activities, including the ability to promote tumor growth...just as the naturally occurring mammalian estrogens do."
" The concentrations of  soy phytoestrogens, calculated to match  0.5ppb DES, are well within the concentration range of most soy products examined".


Long-Term Adverse Effects After Developmental Exposure to Genistein

Retha R Newbold et al.

Third International Soy Symposium, Nov 3, 1999.

Click this link to see the full abstract.

"Mice were followed to evaluate the potential risk for histological abnormalities, including uterine tumors later in life. Many of the long-term effects observed after DES treatment, including uterine adenocarcinoma, were observed after development exposure to genistein."


Excerpts from the report "The Toxicity of Soybeans and Related Products"

Allan Aspell and Associates: Scientific Consultants

Author M. G. Fitzpatrick PhD March 31 1994.

DES is a synthetic, non-steroidal estrogen which was used as a growth stimulant in cattle and sheep.  DES daughters, born to mothers who used DES during pregnancy, have a much higher probability of cervicovaginal abnormalities, such as incomplete cervical collar and vaginal adenosis (a condition characterised by the presence of non-malignant glandular tissue in the vagina) (Kincl, 1990).  Ultimately, this has had an effect on the fertility of DES daughters.  Women with gross cervical abnormalities have a threefold increase in the incidence of miscarriage compared with other women.  DES daughters also have greater difficulty conceiving than their peers (Apfel and Fisher, 1984).  There is also a strong association between clear cell adenocarcinoma, a rare form of malignant vaginal cancer, and fetal exposure to DES (Apfel and Fisher, 1984).  DES sons were also affected; the incidence of genitourinary abnormalities and infertility is higher in exposed males (Kincl, 1990).  Follow up studies on physical changes in DES sons have not received detailed attention; such studies are difficult since there is no single condition, such as adenosis in the female, that typifies exposure to DES (Apfel and Fisher, 1984).

The significant effects of DES on the fetus, and that DES syndrome can also be caused by other exogenous estrogens (Amdur et al 1993) has stigmatised the use of estrogens in humans (Kirk et al 1978); modern medical practice is to avoid their use during pregnancy (Apfel and Fisher, 1984).

Fetal cells are generally less sensitive to endogenous estrogens than those of the mother; exceptions are tissues of the vagina, uterus and breast of female fetuses, and the prostate tissue of male fetuses (Apfel and Fisher, 1984).  The fetus may be especially sensitive to exogenous estrogens; this is the case with DES.  DES exposure probably sensitised the fetus to all estrogens, hence, increasing the vulnerability to the carcinogenic effects of estrogens later on in life (Apfel and fisher 1984).  DES cancer may develop 20 years to 25 years after transplacental exposure, highlighting the often delayed effects that prenatal exposure to estrogens can have.


From "Cellular and Mollecular Mechanisms of Hormonal Carcinogenisis..Environmental Influences"

ISBN 0-471-02202-0

Chapter 6 'Mechanisms of Estrogen-Associated Carcinogenesis'

by Dr J.Carl

Bennett and Dr Takeki Tsutsui

Of US NIEHS at Research Triangle Park, NC 27709; and the Dept ofPharmocology, Nippon School of Dentistry, Tokyo 102, Japan.

" There is stong evidence from several systems to support the hypothesis that estrogens are epigenic carcinogens, acting via a promoting effect related to stimulation of proliferation of estrogen-responsive cells..........Tumors are induced by both D E S and 17B estradiol.....both induce transformation of hamster cells that is indistinguishable from that induced by other chemical carcinogens...sarcomas are also induced by subcutaneous injection of Syrian hamsters."


Oestrogenic Activity of Soya-Bean Products

 H. M. Drane, D. S. Patterson, B. A. Roberts and N. Saba

Central Veterinary Laboratory, Weybridge, Surrey, KT15 3NB England


 Normal rat cake containing soya meal was found to be oestrogenic.   Sixteen samples of soya meal were examined in the mouse uterine bioassay and all were found to have oestrogenic activity.  Ethyl-acetate extracts of the meals also had oestrogenic activity.  Genistein and daidzein were present in the extracts.


Little attention seems to have been paid to soya meal as a possible source of oestrogenicity although daidzein and genistein were isolated from soya beans nearly 50 years ago (Walz, 1931).

Various reproductive disturbances in animals have been traced to the ingestion of oestrogenic feeds.

 The conception rate was lowered in sheep fed 8-16 mg DES/day and conception was prevented altogether in sheep given 32 mg DES/day (Morley, Bennett & Axelsen, 1963).  The present results suggest that comparable levels of oestrogenic activity might be provided by diets containing soya products; in those whole soya meals in which quantifiable amounts of oestrogenic activity were present, levels equivalent to 8-37 ng DES/g soya were detected.


Sample No.

Maximum total dose †(g whole soya meal/mouse)

Uterine weight(geometric mean; mg)

DES equivalent (ng/g soya)









Note: *** P < 0.001)

In human foods 24 ppb and 16 ppb of DES equivalence was measured.


Incidence of squamous neoplasia of the cervix and vagina in women exposed prenatally to diethylstilbestrol (United States). 

Hatch EE.  Herbst AL.  Hoover RN.  Noller KL.  Adam E.  Kaufman RH. Palmer JR.  Titus-Ernstoff L.  Hyer M.  Hartge P.  Robboy SJ.  Cancer Causes & Control. 12(9):837-845, 2001 Nov.

Women exposed prenatally to diethylstibestrol (DES) have an excess risk of clear-cell adenocarcinoma of the vagina and cervix

The findings support an association between in-utero DES exposure and high-grade squamous neoplasia

Full abstract Here


More on Diethylstilbestrol can be found here:






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