Why Raloxifene and Tamoxifen may Reduce Breast Cancer Risk
(My Interpretation of the Results of STAR (Study of Tamoxifen and Raloxifene) 0f
2006)
Copyright 2006, James Michael
Howard,
It is my hypothesis that low DHEA may trigger breast cancer
(Annals of Internal
Medicine 2005; 142:
471-472). I think all tissues depend on
DHEA so low DHEA causes changes in “vulnerable” cells. This effect depends upon two cellular
changes. I think low DHEA initiates
reductions in support of genes of cell adhesion within “precancerous” cells
which ultimately separates these cells. That
is, the overall, low DHEA reduces support of cell maintenance and the
differentiated state. Once separated
from the surrounding cellular (tissue) milieu, these cells exhibit increased
cell surface area which increases their ability to absorb DHEA more rapidly
than surrounding cells. So, even in a
low state of DHEA, these cells may increase their supply of DHEA. I suggest this causes a sub fraction of the cells
already separated from the others to trigger genes of growth because of the
increased DHEA. (According to my
explanation of growth and development, the large amounts of DHEA early in
development stimulate cell divisions.
This produces a cell mass. The
size of the cell mass and the reduced cell surface area contribute to
differential availability of DHEA so activation of genes increases while cell
duplication decreases. As DHEA
availability decreases, the ratio of cell differentiation to cell division
decreases.) When these cells experience
an increase in DHEA because of increased absorption, their genes of cell
division are activated. These are
“oncogenes.” Conversely, as we age, our
DHEA begins to naturally decline, reaching very low levels in old age. This is why cancer increases in old age, but
it grows less rapidly.
It is also
my hypothesis that all tissues rely on DHEA for optimal DNA transcription and
replication. All tissues compete for
available DHEA; this effect may produce differentiation of tissues (above) as
well as affect the entire body plan. So,
once initiated, cancer absorbs DHEA at the expense of other tissues. (I suggest this is the cause of “cachexia” of
cancer, that is, the cancer robs the body of available DHEA and is very
noticeable in cancer of old age when DHEA is low.) My point here is that, once initiated, cancer
relies on an increased source of DHEA.
If available DHEA can be reduced, cancer will be adversely affected
because cancer relies on DHEA more than differentiated tissues. I think many anticancer chemotherapeutics
work by reducing available DHEA. This
may explain why chemotherapy is so damaging; reducing DHEA affects all tissues. Hopefully, the cancer dies before other tissues,
which rely on less DHEA. (Because cancer
uses DHEA at the expense of other tissues, cancer reduces overall DHEA. Therefore, my explanation of cancer and low
DHEA also explains why some cancers stimulate the onset of different kinds of
cancer. When cancer reduces DHEA, it can
cause the initiation of other cancers by reducing DHEA. Also, since some chemotherapy, and other
anticancer therapies, may reduce DHEA, I suggest this is why some of these
treatments have also been demonstrated to cause other types of cancers.)
I think raloxifene
and tamoxifen work by reducing DHEA.
Both raloxifene and tamoxifen reduce prolactin. Prolactin is a direct stimulator of DHEA
production; if one reduces prolactin, one reduces DHEA. Raloxifene and tamoxifen do not affect
prolactin identically, so one would expect differences. The STAR report found that both reduced the
risk of invasive breast cancer by approximately 50%. If breast cancer is started by low DHEA and
depends on DHEA once formed, then reducing prolactin should reduce the ability
of the cancer to function. These two
chemicals both reduce the extension of cancer.
It is also
my hypothesis that low DHEA may increase blood clots (http://www.anthropogeny.com/Thrombosis%20May%20Be%20Caused%20by%20Low%20DHEA.htm
). Both tamoxifen and raloxifene
increase blood clots. Obviously, I think
this effect is due to reduction of DHEA by both. Since raloxifene and tamoxifen exert effects
differently, the results should differ. Raloxifene
simply affects the levels of DHEA differently than tamoxifen.