FAQFAQ   SearchSearch   MemberlistMemberlist   UsergroupsUsergroups 
 ProfileProfile   PreferencesPreferences   Log in to check your private messagesLog in to check your private messages   Log inLog in 
Forum index » Medicine forums » patology
Raloxigene, Tamoxifen, DHEA, Breast Cancer, and the STAR Report
Post new topic   Reply to topic Page 1 of 1 [1 Post] View previous topic :: View next topic
Author Message
James Michael Howard
medicine forum addict

Joined: 30 Apr 2005
Posts: 78

PostPosted: Tue Apr 18, 2006 5:04 pm    Post subject: Raloxigene, Tamoxifen, DHEA, Breast Cancer, and the STAR Report Reply with quote

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, Fayetteville, Arkansas, U.S.A.

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
). 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.
Back to top

Back to top
Display posts from previous:   
Post new topic   Reply to topic Page 1 of 1 [1 Post] View previous topic :: View next topic
The time now is Tue Feb 19, 2019 9:01 am | All times are GMT
Forum index » Medicine forums » patology
Jump to:  

Similar Topics
Topic Author Forum Replies Last Post
No new posts Report Finds Drug Errors Hurt 1.5 Million BreastImplantAwareness.or lyme 0 Thu Jul 20, 2006 6:51 pm
No new posts Report Finds Drug Errors Hurt 1.5 Million BreastImplantAwareness.or nursing 0 Thu Jul 20, 2006 6:50 pm
No new posts Diet supplements don't benefit cancer patients: journal J cancer 0 Wed Jul 19, 2006 10:01 am
No new posts Seaweed extract may help halt cervical cancer virus Roman Bystrianyk cancer 0 Wed Jul 19, 2006 1:34 am
No new posts Proteins, linked to pancreatic cancer spread, found J cancer 2 Tue Jul 18, 2006 5:00 pm

Copyright © 2004-2005 DeniX Solutions SRL
Other DeniX Solutions sites: email marketing campaigns , electronics forum, Science forum, Unix/Linux blog, Unix/Linux documentation, Unix/Linux forums

Powered by phpBB © 2001, 2005 phpBB Group
[ Time: 0.0135s ][ Queries: 16 (0.0032s) ][ GZIP on - Debug on ]