Soybeans Linked To Brain
Atrophy & Cell Death
From Ian Goddard <>
As a vegetarian, I present the following with great regret. Soy products like tofu have provided the staple alternative to eating murdered animals. Unfortunately the study reported here: has found a significant link between eating tofu and brain aging and atrophy! My first reaction was to hope that the study was flawed. Unfortunately, a quick study of published research at the National Library of Medicine indicates that there is a STRONG physiological basis for the findings in that study. It seems that a main phytochemical in soybeans, genistein, reduces DNA synthesis in the brain, and reduced DNA synthesis promotes apoptosis, which is also known as "programmed cell death." Multiple studies I found indicate that drug-induced reduction of DNA synthesis is routinely assoicated with reduced cell proliferation and death. DNA synthesis is a critical part of the life cycle of a cell:
It appears that the ability of genistein to reduce DNA synthesis may be why it is a promising anti-cancer agent, for research suggests genistein can kill cancer cells and other drugs that reduce DNA synthesis kill cancer cells. Unfortunately, genistein's cytotoxic properties appear to be nonspecific, ie, it doesn't only kill cancer cells. In the first abstract below, it was found that genistein "induced significant testicular cell death." Ouch! The second study finds that genistein reduced DNA synthesis in the brain. To get the full picture of what I've stated here, I recommend using the National Library of Medicine's search engine: It is easily the most powerful tool on the Internet, accessing most of the published medical research since around 1965.
Too much tofu induces brain aging,, study shows:
Soy-phytochemical genistein "induced significant testicular cell death."
Biol Cell 1999 Sep;91(7):515-23
Cytotoxic potential of the phytochemical genistein isoflavone (4',5',7-trihydroxyisoflavone) and certain environmental chemical compounds on testicular cells.
Kumi-Diaka J, Nguyen V, Butler A
Florida Atlantic University, Department of Biology, College of Liberal Arts & Sciences, Davie 33314, USA.
[Medline record in process]
The effects of genistein (Gn), sodium azide (naz), and dexamethasone (dxm) on testicular cells TM3, TM4 and GC-1 spg were studied in vitro. First, a series of experiments were performed to assess the response of the cells to the exposure of Gn, naz, dxm, a combination of Gn with naz and Gn with dxm. Trypan blue exclusion assay was used to determine the percentage of viability, and LDH-cytotoxicity test was used to assess the degree of treatment-induced cytotoxicity on each cell type. A second series of experiments were performed to study cytomorphology and determine the type and percentage of treatment-induced cell death (apoptosis and necrosis) on each cell line, using fluorescent dye technique to detect apoptotic and necrotic cells, and tunnel assay to confirm apoptosis. The results from the data obtained demonstrated: i) that incubation of testis cells with each of the agents (Gn, dxm, naz) alone and in two combinations (Gn-dxm, and Gn-naz) induced significant testicular cell death; ii) that both genistein and dexamethasone mostly and significantly induced apoptotic cell death while sodium azide induced necrotic cell death; iii) that addition of dexamethasone to genistein demonstrated synergism in apoptosis on testis cells; and iv) that combination of naz with Gn demonstrated synergism in necrosis on testis cells even though Gn alone did not induce significant necrosis. It is concluded that the synergistic actions of genistein and dxm, and of genistein + sodium azide in induction of apoptosis and/or necrosis may be of clinical and pathophysiological research interest considering the chemopreventive and chemotherapeutic potential of genistein; and the clinico-pharmacological application of dexamethasone and sodium azide.
"Genistein decreased the DNA synthesis within less than 30 min."
Exp Neurol 1999 Sep;159(1):164-76
Early effects of protein kinase modulators on DNA synthesis in rat cerebral cortex.
Yakisich JS, Siden A, Vargas VI, Eneroth P, Cruz M
Applied Biochemistry, Clinical Research Center, Karolinska Institute, Novum, Huddinge University Hospital, Huddinge, S-141 86, Sweden.
By using tissue miniunits, protein kinase modulators, and topoisomerase inhibitors in short-term incubation (0-90 min) we studied (1) the role of protein phosphorylation in the immediate control of DNA replication in the developing rat cerebral cortex and (2) the mechanism of action for genistein- mediated DNA synthesis inhibition. Genistein decreased the DNA synthesis within less than 30 min. None of the other protein kinase inhibitors examined (herbimycin A, staurosporine, calphostin-C) or the protein phosphatase inhibitor sodium orthovanadate inhibited DNA synthesis and they did not affect the genistein-mediated inhibition. The selective topoisomerase inhibitors camptothecin and etoposide decreased the DNA synthesis to an extent similar to that of genistein and within less than 30 min. In addition, the effects of these substances on topoisomerase I and II were studied. Etoposide and genistein but not herbimycin A, staurosporine, or calphostin-C strongly inhibited the activity of topoisomerase II. Our results (1) strongly suggest that the net rate of DNA replication during the S phase of the cell cycle is independent of protein phosphorylation and (2) indicate that the early inhibitory effect of genistein on DNA synthesis is mediated by topoisomerase II inhibition rather than protein tyrosine kinase inhibition. Copyright 1999 Academic Press.
Reduce DNA synthesis associated with aging
Acta Neuropathol (Berl) 1999 Jan;97(1):71-81
Age-related changes of DNA repair and mitochondrial DNA synthesis in the mouse brain.
Schmitz C, Axmacher B, Zunker U, Korr H
Department of Anatomy and Cell Biology, RWTH University of Aachen, Germany. cschmitz@alpha.imib.rwth-aachen,de
Using quantitative autoradiography, both nuclear DNA repair - measured as nuclear unscheduled DNA synthesis (UDS) - and mitochondrial (mt) DNA synthesis were evaluated in situ for several types of cells in the brains of untreated mice of various age. It was found that distinct types of neuronal cells showed a decline of both UDS and mtDNA synthesis with age, whereas - except for glial cells of the cerebral cortex - no glial or endothelial cells showed age-related alterations of UDS. Together with various data reported in the literature, these patterns of a cell type-specific decrease of UDS and mtDNA synthesis with age in the mouse brain lead to an improved understanding of the complex interrelationships between the molecular events associated with the phenomenon of aging as well as to a new idea regarding the cause of the specific distribution pattern of those cells in the human brain that are affected by the formation of paired helical filaments in Alzheimer's disease.
To get the full picture of what I stated above, I recommend using the National Library of Medicine's search engine: The key words you choose make all the difference!


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