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

Immune System Effects of Phytoestrogens

Reports in the scientific literature of the potential effects of soy on immune system function have been numerous over the last five years.   In particular the ability of the soy phytoestrogen genistein to inhibit tyrosine kinases is well documented. The slant of much of the research into this aspect of soy has been toward the possible role of genistein in fighting cancer, but Soy Online Service believes the potential for soy cause immune system disorders has been overlooked.

Just how might genistein affect immune system function?   Genistein has been described as a potent immunosuppressant

Soy Online Service often receives reports of the association of another auto-immune disease with soy consumption, both in adults and in children who had been fed soy formulas as infants. That disease is alopecia. Read the experience of such a victim here



Excessive soy consumption has been linked to migraine pain. Read more about this here.

An article published in Scientific American (2002) suggests soy infant formula may impair the developing immune system.  Read More Here

The literature is replete with numerous studies showing deleterious effects on multiple organ systems - including the immune system.  For example this letter from the American Journal of Clinical Nutrition.


Early exposure to genistein exerts long-lasting effects on the endocrine and immune systems in rats.
Klein SL, Wisniewski AB, Marson AL, Glass GE, Gearhart JP.
Mol Med 2002 Nov;8(11):742-9

Discussion: These data illustrate that exposure to genistein during pregnancy and lactation exerts long-lasting effects on the endocrine and immune systems in adulthood. Whether exposure to phytoestrogens during early development affects responses to infectious or autoimmune diseases, as well as cancers, later in life requires investigation.

Full Abstract Here


The phytoestrogen genistein induces thymic and immune changes: A human health concern?
Srikanth Yellayi*, Afia Naaz*, Melissa A. Szewczykowski*, Tomomi Sato*, Jeffrey A. Woods, Jongsoo Chang§, Mariangela Segreĥ, Clint D. Allred§, William G. Helferich§,, and Paul S. Cooke* Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 11, 7616-7621, May 28, 2002

Use of soy-based infant formulas and soy/isoflavone supplements has aroused concern because of potential estrogenic effects of the soy isoflavones genistein and daidzein.

...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.

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.

Full Abstract Here



Breast feeding and insulin-dependent diabetes mellitus in children
Fort P. Lanes R. Dahlem S. Recker B. Weyman-Daum M. Pugliese M. Lifshitz F.
Journal of the American College of Nutrition. 5(5):439-41, 1986.
We have evaluated the hypothesis of a protective effect of human milk on the development of insulin dependent diabetes mellitus (IDDM). We studied the feeding histories of 95 diabetic children and compared them with controls consisting of their non-diabetic siblings and a pair matched group of nondiabetic peers of the same age, sex, geographical location, and social background. The incidence of breast feeding in diabetic children was 18%. This was similar to the control group. The duration of breast feedings was also similar among all three groups. There was no difference in the age of introduction of solid food between diabetic and nondiabetic children. Twice as many diabetic children, however, received soy containing formula in infancy as compared to control children. The mean age of onset of IDDM was not related to the type of feeding during infancy. The incidence of positive thyroid antibodies was two and one half times higher in formula-fed diabetic children than in breast-fed ones. In our studies we were unable to document any relationship between the history of breast feeding and subsequent development of IDDM in children.
Breast and soy-formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children.
Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F.
Department of Pediatrics, North Shore University Hospital-Cornell University Medical College, Manhasset, New York 11030.
Am Coll Nutr 1990 Apr;9(2):164-7
It has been suggested that feeding practices in infancy may affect the development of various autoimmune diseases later in life. Since thyroid alterations are among the most frequently encountered autoimmune conditions in children, we studied whether breast and soy-containing formula feedings in early life were associated with the subsequent development of autoimmune thyroid disease. A detailed history of feeding practices was obtained in 59 children with autoimmune thyroid disease, their 76 healthy siblings, and 54 healthy nonrelated control children. There was no difference in the frequency and duration of breast feeding in early life among the three groups of children. However, the frequency of feedings with soy-based milk formulas in early life was significantly higher in children with autoimmune thyroid disease (prevalence 31%) as compared with their siblings (prevalence 12%; chi 2 = 7.22 with continuity factor; p less than 0.01), and healthy nonrelated control children (prevalence 13%, chi 2 = 5.03 with continuity factor; p less than 0.02). Therefore, this retrospective analysis documents the association of soy formula feedings in infancy and autoimmune thyroid disease.
Odd chromosome movement and inaccurate chromosome distribution in mitosis and meiosis after treatment with protein kinase inhibitors.
Nicklas RB, Krawitz LE, Ward SC
J Cell Sci 1993 Apr 104 ( Pt 4) 961-73
Errors in chromosome orientation in mitosis and meiosis are inevitable, but normally they are quickly corrected. We find that such errors usually are not corrected in cells treated with protein kinase inhibitors. Highly inaccurate chromosome distribution is the result. When grasshopper spermatocytes were treated with the kinase inhibitor 6-dimethylaminopurine (DMAP), 84% of maloriented chromosomes failed to reorient; in anaphase, both partner chromosomes were distributed to the same daughter cell. These chromosomes were observed for a total of over 60 h, and not a single reorientation was seen. In contrast, in untreated cells, maloriented chromosomes invariably reoriented, and quickly: in 10 min, on average. A second protein kinase inhibitor, genistein, had exactly the same effect as DMAP. DMAP affected PtK1 cells in mitosis as it did spermatocytes in meiosis: improper chromosome orientations persisted, leading to frequent errors in distribution. We micromanipulated chromosomes in spermatocytes treated with DMAP to learn why maloriented chromosomes often fail to reorient. Reorientation requires the loss of improper microtubule attachments and the acquisition of new, properly directed kinetochore microtubules. Micromanipulation experiments disclose that neither the loss of old nor the acquisition of new microtubules is sufficiently affected by DMAP to account for the indefinite persistence of malorientations. Drug treatment causes a novel form of chromosome movement in which one kinetochore moves toward another kinetochore. Two kinetochores in the same chromosome or in different chromosomes can participate, producing varied, dance-like movements executed by one or two chromosomes. These kinetochore-kinetochore interactions evidently are at the expense of kinetochore-spindle interactions. We propose that malorientations persist in treated cells because the kinetochores have numerous, short microtubules with a free end that can be captured by a second kinetochore. Kinetochores capture each other's kinetochore microtubules, leaving too few sites available for the efficient capture of spindle microtubules. Since the efficient capture of spindle microtubules is essential for the correction of errors, failure of capture allows malorientations to persist. Whether the effects of DMAP actually are due to protein kinase inhibition remains to be seen. In any case, DMAP reveals interactions of one kinetochore with another, which, though ordinarily suppressed, have implications for normal mitosis.
Flavonoids as DNA topoisomerase antagonists and poisons: structure-activity relationships.
Constantinou A, Mehta R, Runyan C, Rao K, Vaughan A, Moon R
J Nat Prod 1995 Feb 58:2 217-25
Selected flavonoids were tested for their ability to inhibit the catalytic activity of DNA topoisomerase (topo) I and II. Myricetin, quercetin, fisetin, and morin were found to inhibit both enzymes, while phloretin, kaempferol, and 4',6,7-trihydroxyisoflavone inhibited topo II without inhibiting topo I. Flavonoids demonstrating potent topo I and II inhibition required hydroxyl group substitution at the C-3, C-7, C-3', and C-4' positions and also required a keto group at C-4. Additional B-ring hydroxylation enhanced flavonoid topo I inhibitory action. A C-2, C-3 double bond was also required, but when the A ring is opened, the requirement for the double bond was eliminated. Genistein has been previously reported to stabilize the covalent topo II-DNA cleavage complex and thus function as a topo II poison. All flavonoids were tested for their ability to stabilize the cleavage complex between topo I or topo II and DNA. None of the agents stabilized the topo I-DNA cleavage complex, but prunetin, quercetin, kaempferol, and apigenin stabilized the topo II DNA-complex. Competition experiments have shown that genistein-induced topo II-mediated DNA cleavage can be inhibited by myricetin, suggesting that both types of inhibitors (antagonists and poisons) interact with the same functional domain of their target enzyme. These results are of use for the selection of flavonoids that can inhibit specific topoisomerases at specific stages of the topoisomerization reaction.
Genistein as an inducer of tumor cell differentiation: possible mechanisms of action.
Constantinou A, Huberman E
Proc Soc Exp Biol Med 1995 Jan 208:1 109-15
Decreased activity of either topoisomerases or tyrosine kinases has been implicated in the differentiation of a number of cell types. It is therefore conceivable that genistein, because of its reported ability to inhibit these activities in vitro, may be an inducer of cellular differentiation. We investigated this possibility in human promyelocytic HL-60 and erythroid K-562 leukemia cells and in human SK-MEL-131 melanoma cells. Our results indicated that genistein, in a dose-dependent manner, inhibited cell multiplication and induced cell differentiation. The maturing HL-60 cells acquired granulocytic and monocytic markers. The differentiating K-562 cells stained positively with benzidine, which indicates the production of hemoglobin, an erythroid marker. Following genistein treatment, maturing SK-MEL-131 melanoma cells formed dendrite-like structures and exhibited increased tyrosinase activity and melanin content. Experiments were designed to identify the molecular mechanism of genistein's action. Data from our laboratory suggest that this isoflavone triggers the pathway that leads to cellular differentiation by stabilizing protein-linked DNA strand breakage. Other possible mechanisms reported in the literature are discussed.
Genistein induces apoptosis in immature human thymocytes by inhibiting topoisomerase-II.
McCabe MJ Jr, Orrenius S
Biochem Biophys Res Commun 1993 Jul 30 194:2 944-50
The toxicity of genistein, an inhibitor of tyrosine kinases and topoisomerase-II, on human thymocytes was investigated. Genistein induced marked chromatin fragmentation indicative of apoptosis in human thymocyte cultures. Genistein-induced thymocyte apoptosis is unlikely due to an inhibition of basal tyrosine kinase activity, since another tyrosine kinase inhibitor, herbimycin A, does not induce thymocyte apoptosis, whereas other topoisomerase-II inhibitors do. The thymocyte subpopulation most sensitive to genistein-induced apoptosis exhibited a CD3-CD4+CD8+ phenotype. This subpopulation of thymocytes is also sensitive to glucocorticoid-induced apoptosis; however, differences between genistein- and glucocorticoid-induced apoptosis were noted. In particular, unlike glucocorticoid-induced apoptosis, genistein-induced apoptosis does not involve changes in [Ca2+]i and cannot be blocked by activation of protein kinase C.
p53, mutations, and apoptosis in genistein-exposed human lymphoblastoid cells.
Morris SM, Chen JJ, Domon OE, McGarrity LJ, Bishop ME, Manjanatha MG, Casciano DA
Mutat Res 1998 Aug 31 405:1 41-56
The phytoestrogen, genistein, is a naturally occurring isoflavone found in soy products. On a biochemical basis, genistein is a competitive inhibitor of tyrosine kinases and the DNA synthesis-related enzyme, topoisomerase-II (topo-II). Exposure of mammalian cells to genistein results in DNA damage that is similar to that induced by the topo-II inhibitor and chromosomal mutagen, m-amsa. In order to determine the potential genotoxicity of genistein, human lymphoblastoid cells which differ in the functional status of the tumor suppressor gene, p53, were exposed to genistein and the induction of micronuclei quantified by
microscopic analysis. In addition, the mutant fraction at the thymidine kinase (tk) locus (both the normal-growth and slow-growth phenotypes) was determined by resistance to trifluorothymidine (TFT) and at the hypoxanthine phosphoribosyl transferase (hprt) locus by resistance to 6-thioguanine (6-TG). Flow cytometric analysis of the percentage of viable, apoptotic and degenerating cells was utilized to determine the rate and kinetics of cell death after genistein exposure. The detection of micronuclei in both cell lines indicated that genistein-induced damage had occurred in both AHH-1 tk+/- and L3. Linear regression analysis detected a significant increase in the number of 6-TG-resistant clones in both AHH-1 tk+/- (p53+/-) and L3 (p53+/+). A comparison of slopes revealed no difference between the lines. In contrast, a significant, concentration-dependent increase in the number of TFT-resistant clones with the slow-growth phenotype was detected in AHH-1 tk+/- (mutant p53), but not in L3 (wild-type p53). Cell death occurred primarily by apoptosis in both cell lines; however, a concentration-dependent decrease in the percentage of viable cells was detected immediately after exposure in L3, but not until 32 h after exposure in AHH-1 tk+/-. A comparison of the slopes of the concentration-response curves for the percentage of viable cells revealed no difference between the cell lines in the effect of genistein on cell viability. Our results may be interpreted that genistein is a chromosomal mutagen and that p53 functional status affects the recovery of chromosomal mutants, possibly by signalling cells into the apoptosis pathways.


Induction of mouse thymocyte apoptosis by inhibitors of tyrosine kinases is associated with dephosphorylation of nuclear proteins.
Azuma Y, Onishi Y, Sato Y, Kizaki H
Cell Immunol 1993 Nov 152:1 271-8
Incubation of mouse thymocytes with the protein tyrosine kinase inhibitors herbimycin A and methyl-2,5-dihydroxycinnamate induced a decreased and altered profile of nuclear phosphotyrosine proteins in parallel with an increase in internucleosomal DNA fragmentation and cell death dose-dependently. No change in the profile of cytoplasmic phosphotyrosine proteins was observed. DNA fragmentation was dependent on the synthesis of RNA and protein, suggesting that the inhibition of tyrosine phosphorylation of the nuclear proteins induces apoptosis. DNA fragmentation was enhanced by simultaneous incubation with
phorbol esters capable of activating protein kinase C. Genistein, another inhibitor of protein tyrosine kinase, induced DNA fragmentation more rapidly than herbimycin A, but there was no predominant alteration of phosphotyrosine proteins in early incubation, suggesting that genistein may induce apoptosis by a mechanism other than direct inhibition of protein tyrosinekinase activity.


p53, mutations, and apoptosis in genistein-exposed human lymphoblastoid cells.

Morris SM, Chen JJ, Domon OE, McGarrity LJ, Bishop ME, Manjanatha MG, Casciano DA.Mutat Res 1998 Aug 31;405(1):41-56

Our results may be interpreted that genistein is a chromosomal mutagen ...

Full Abstract Here




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