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- 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: http://starbulletin.com/1999/11/19/news/story4.html
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: http://www.geocities.com/CollegePark/Lab/1580/cycle2.gif
http://www.geocities.com/CollegePark/Lab/1580/cycle.html
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- 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: http://www.ncbi.nlm.nih.gov/PubMed It is easily the most powerful
tool on the Internet, accessing most of the published medical research
since around 1965.
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- Too much tofu induces brain aging,, study shows: http://starbulletin.com/1999/11/19/news/story4.html
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- _____
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- Soy-phytochemical genistein "induced significant
testicular cell death."
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- Biol Cell 1999 Sep;91(7):515-23
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- Cytotoxic potential of the phytochemical genistein isoflavone
(4',5',7-trihydroxyisoflavone) and certain environmental chemical compounds
on testicular cells.
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- Kumi-Diaka J, Nguyen V, Butler A
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- Florida Atlantic University, Department of Biology, College
of Liberal Arts & Sciences, Davie 33314, USA.
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- [Medline record in process]
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- 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.
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- Link
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- _____
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- "Genistein decreased the DNA synthesis within less
than 30 min."
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- Exp Neurol 1999 Sep;159(1):164-76
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- Early effects of protein kinase modulators on DNA synthesis
in rat cerebral cortex.
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- Yakisich JS, Siden A, Vargas VI, Eneroth P, Cruz M
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- Applied Biochemistry, Clinical Research Center, Karolinska
Institute, Novum, Huddinge University Hospital, Huddinge, S-141 86, Sweden.
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- 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.
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- Link
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- _____
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- Reduce DNA synthesis associated with aging
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- Acta Neuropathol (Berl) 1999 Jan;97(1):71-81
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- Age-related changes of DNA repair and mitochondrial DNA
synthesis in the mouse brain.
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- Schmitz C, Axmacher B, Zunker U, Korr H
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- Department of Anatomy and Cell Biology, RWTH University
of Aachen, Germany. cschmitz@alpha.imib.rwth-aachen,de
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- 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.
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- Link
_____
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- To get the full picture of what I stated above, I recommend
using the National Library of Medicine's search engine: http://www.ncbi.nlm.nih.gov/PubMed
The key words you choose make all the difference!
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- GODDARD'S JOURNAL: http://www.erols.com/igoddard/journal.htm
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