Breast Cancer Increases: ...(response to Phillip Bigelow)

James Howard (
Thu, 21 Nov 1996 14:04:42 GMT

Breast Cancer Increases: ...(response to Phillip Bigelow)

Well, I would rather consider my theory of human evolution, but I will respond
to Mr. Bigelow. As Mr. Bigelow has correctly pointed out, I have placed a
number of posts in this newsgroup concerning my theory of testosterone and human
evolution. Part of my theory is that testosterone periodically increases, and a
number of my posts were designed to demonstrate this is occurring now. The
current increase in breast cancer is one example. Mr. Bigelow has not responded
to the content of my theory, in of any of these posts.

My post, "Breast Cancer Increases: sign of increasing testosterone," includes
a copy of a letter I just sent to my local newspaper. I have been "posting"
my theory to this newspaper for some time. Again, rather than concern
himself with my theory of human evolution, Mr. Bigelow concerns himself
with another matter, entirely. In my letter to the newspaper, for sake of
history, I wrote:

"I sent my hypothesis of high testosterone and low DHEA in breast cancer to
the Journal of the American Medical Association, Feb 4, '94. It was rejected.
Later, in 1994, two reports connected high testosterone and low DHEA in
breast cancer in women: "Abnormal Production of Androgens in Women with
Breast Cancer," Anticancer Res. 1994; 14: 2113 and "Hormonal Profiles in
Women with Breast Cancer," Obstet. Gynecol. Clin. North Am. 1994; 21:

This is Mr. Bigelow's reason for responding to me. Mr. Bigelow says:

"A sincere suggestion:
Post a copy of your submitted AMA research draft on a website (NOT a
modified draft sanitized for the web, but the *exact* draft that you sent the
AMA journal). That way, we can all see exactly what you wrote, and
compare it to the later published work by others. You do have a copy of
your old submitted draft,...... don't you?......"

Since Mr. Bigelow has shown no interest in my theory of human evolution, I
guess I will respond to his interest in the letter I sent to the "Journal of the
American Medical Association." Please note that Mr. Bigelow has changed
the content here, either accidentally, or on purpose. I clearly state that I
sent my "hypothesis" to JAMA; Mr. Bigelow changes this to "research draft."
Here is the letter; it is not altered or "sanitized." It is very short; JAMA
has a restriction on word number and reference number for "letters to the
editor." It is dated February 4, 1994.

"Re: Breast Cancer Increases in the U.S.

Dear Editor:

(Please consider the following as a "Letter to the Editor." It contains 379
words and two references.)

I suggest the rise in breast cancer results from the same mechanism that
produces the 'secular trend.' The increases in breast cancer directly parallel
the secular trend. I think the secular trend is produced by increases in
testosterone. Testosterone increases size, sexuality, aggression, and, I
suggest, hastens puberty in both males and females (hallmarks of the trend).
In a well-fed society, these individuals will increase in percentage
exponentially. I suggest it is this increased testosterone in these women that
increases breast cancer.

My work suggests transcription and replication of DNA require the hormone,
dehydroepiandrosterone (DHEA). That is, all gene activity competes for
DHEA. Testosterone causes use of DHEA for testosterone-target tissues. I
suggest aging results when DHEA naturally begins to decline around 28
years (aging is loss of support of transcription of DNA). Therefore,
increased use of DHEA by testosterone tissues advances the decline of
available DHEA, i.e., testosterone advances aging and the following
mechanism explains why aging causes cancer.

I suggest activation of genes of cell division require larger amounts of DHEA
than genes of differentiation. Therefore, as growth occurs, DHEA decreases
in availability, genes of differentiation then begin to use DHEA, and cell
division declines. This is how differentiation competes with, and inhibits,
cell division. As aging begins, I suggest loss of DHEA begins the opposite
process. That is, genes of advanced differentiation are closed down in
reverse order. For oncogenes to become activated, I suggest transcription
reversal must include loss of transcription of genes controlling cell adhesion.
Loss of cell adhesion is characteristic of oncogene function. I suggest loss
of cell adhesion triggers oncogene activity, because it increase the surface
area of the cell for DHEA absorption. "This" increased DHEA would then be
able to activate oncogenes.

It is known that breast tumors, but not normal breast tissue, concentrate
DHEA (J. Steroid Biochem. 26: 151, 1987). Measurable levels of DHEA are
reduced in women with breast cancer, and this reduction in DHEA occurs as
early as nine years prior to diagnosis (Geriatrics 37: 157, 1982). While there
isn't space here to explain the connection of this mechanism with known
breast cancer risk factors, one is very clear. Early menstruation, or rather
early puberty, could be explained by rapid maturation produced by
testosterone's effect in the midbrain."

Mr. Bigelow finishes his response to my post with material I do not think
merits a response.

James Howard