Breast Cancer, the Secular Trend, Testosterone, and DHEA: Originality

James Howard (
Sat, 23 Nov 1996 20:22:30 GMT

Breast Cancer, the Secular Trend, Testosterone, and DHEA: Originality

Phillip Bigelow has taken it upon himself to respond to the originality of my
posts regarding the secular trend, breast cancer increases, increasing
testosterone, and decreased DHEA. One can either respond to my material
or attack my integrity. Mr. Bigelow decided to attack my integrity. I will do
my best to respond to his posts.. To summarize the posts and the
information, therein: I posted "Breast Cancer Increases: sign of increasing
testosterone," Nov 17, 1996. This post consisted mainly of a "letter to the
editor" to my local newspaper, sent Nov. 17, 1996. I posted it here, because
it is another example of increasing testosterone; I have posted a number of
signs of increasing testosterone here. The letter was a response to an article
in the newspaper about a link between increased bone mineral density and
increased breast cancer in women. To shorten my letter, I mentioned that
May 16, 1993, the newspaper published my hypothesis that testosterone is
rising and is the cause of the secular trend, and that March 14, 1994, they
published my hypothesis that increases in testosterone cause the secular
trend, this increase in testosterone and low levels of DHEA may cause
breast cancer, and this may account for the current rise in breast cancer. (In
my post here of Nov. 17, 1996, I said March 7, 1994, for the publication date
of one of my letters; I sent it to the paper that day, they published it March
14, 1994.)

My letter to the editor explained the connection of high testosterone and
bone mineral density and the connection of high testosterone and low DHEA
in breast cancer. In that letter to the editor I said: "I sent my hypothesis of
high testosterone and low DHEA 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: 751."

My letter closed with this summation of my past letters and the current
reason for writing: "One known risk factor in breast cancer in women is early
menstruation (puberty). This early onset of puberty may also be attributed to
the increase in testosterone. My work suggests testosterone is rising in the
U.S. I think this increase is the cause of the 'secular trend,' i.e., the
increase in size, and earlier puberty, in children. This is why breast cancer
may be increasing. I suggest the connection of increased bone density and
increased breast cancer in women is due to this increase in testosterone."

Nov. 20, 1996, Mr. Bigelow requested I post my letter of Feb. 4, 1994, to
JAMA. I posted it here, Nov. 21, 1996. Later, Nov 21, 1996, I also posted a
follow-up, "Breast Cancer Increases: additional information." It said:

"I just found the following citation. It further supports my contention that
the increase in breast cancer is the result of increases in testosterone.

Berrino F, et al., "Serum Sex Hormone Levels after Menopause and
Subsequent Breast Cancer," Journal of the National Cancer Institute 1996;
88: 291

'Conclusions and Implications: This prospective study provides further
evidence in support of the already established association between elevated
estrogen levels and breast cancer. Even more importantly, it provides new
evidence that high serum testosterone levels precede breast cancer
occurrence.' "

Nov. 21, 1996, Mr. Bigelow responded to suggest I have "a bad case of 'sour
grapes.' "

Nov. 22, 1996, Mr. Bigelow responded to my "...additional information." with

"I think that, until you can show us that your 'work' in this area was
conducted and published in a scientific journal *prior* to this and the other
authors work you have mentioned earlier, I think it would be more accurate
to have put it this way: 'I agree with the previous work of others.' "

Nov. 23, 1996, James Howard responds:

I have attempted publication in scientific journals; all were rejected. I,
therefore, felt the need to document the originality of my thesis and
published the only place possible. I have published my idea; it is on public
record. I can prove it was submitted to JAMA in February, 1994, I have a
letter from a U.S. Congressman, acknowledging receiving a copy of said
"letter to the editor," to my newspaper of March 14, 1994, and I have proof
the same hypothesis was received by the Journal of the National Cancer
Institute, April 19, 1994. This is my idea. It is original. It would be very
supportive of my claim to have it published in a scientific jounal,
nevertheless, it is my idea.

More importantly, the two citations, mentioned in my letter to the editor of
Nov. 17, were published some time after I first published my idea in March
14, 1994. Secreto and Zumoff, "Abnormal Production of Androgens in
Women with Breast Cancer," Anticancer Res. 1994; 14: 2113, was in the
Sept.-Oct issue. Zumoff, "Hormonal Profiles in Women with Breast Cancer,"
Obstet. Gynecol. Clin. North Am. 1994; 21: 751, was in the December issue.
(These are quoted at the end of this document.) So, these two publications,
which mentioned increased testosterone and low DHEA in breast cancer,
were published months after my idea was published. Furthermore, neither
of these citations makes the connection of increased testosterone, and low
DHEA, with the secular trend, or increasing breast cancer. In fact, Secreto
and Zumoff reported specifically about a syndrome in women, characterized
by high testosterone. My theory of the cause of breast cancer, and why it is
increasing, concerns the population of women at large, not a single
syndrome. In fact, Secreto and Zumoff proposed a mechanism involving
testosterone, entirely different from mine. They do not mention the
connection of DHEA with their mechanism, at all, nor the secular trend or the
increase in breast cancer. Later in 1994, Zumoff published again. Both of
these articles appear to be summations of other reports in the literature.

Before I wrote this, I did a medline search to see if anyone had connected
the secular trend with breast cancer. I found eight, from 1983 to 1995.
None of these mentioned androgens at all; no mention of DHEA or
testosterone. Most mentioned the secular trend, because it is characterized
by early maturation, and breast cancer is higher in women who mature early.
I could find no studies including just the secular trend and testosterone, nor
any studies of the secular trend and DHEA.

I started my work on DHEA in 1984, and I publish it where I can. Anyone
interested, can read some other applications of my work at on the web.
James Howard
(Secreto and Zumoff and Secreto citations follow.)

Secreto G and Zumoff B "Abnormal Production of Androgens in Women
with Breast Cancer" Anticancer Res 1994; 14: 2113 [Sept.-Oct., 1994]

"Two long and broad streams of medical literature, from the 1950's to date,
have established the existence of two unrelated abnormalities of androgen
production in women with breast cancer. One is the genetically determined
presence of subnormal production of adrenal androgens (i.e. DHEA and
DHEAS) in women with premenopausal breast cancer and their sisters, who
are at increased risk for breast cancer. The other is excessive production of
testosterone, of ovarian origin, in subsets of women with either
premenopausal or postmenopausal breast cancer and women with atypical
breast-duct hyperplasia, who are at increased risk for breast cancer; along
with the hypertestosteronism, there is frequently chronic anovulation in the
premenopausal patients. The combination of ovarian hypertestosteronism
and chronic anovulation is characteristic of the polycystic ovary syndrome
and is also frequently seen in women with abdominal ("android") obesity;
both PCOS and abdominal obesity are known to be characterized by high
risk for postmenopausal cancer. The elevated testosterone levels and the
increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and
abdominal obesity could favor the development of breast cancer in several
ways, all of which have been demonstrated experimentally: binding of
testosterone to cancer cells bearing testosterone receptors, with direct
stimulation; intratissular aromatization of testosterone to estradiol, with
stimulation of estrogen-sensitive cells; stimulation of the production of
epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of
EGF on cancer cells; stimulation of aromatase by insulin and IGF-I; direct
mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II; and
stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to
estradiol. Since PCOS is probably largely genetically determined, and
abdominal obesity may also be, the hypertestosteronism of these conditions
may represent a second genetically determined hormonal risk factor for
breast cancer."

Zumoff B "Hormonal Profiles in Women with Breast Cancer" Obstet
Gynecol Clin North Am 1994; 21: 751 [December, 1994]

"The literature findings on endogenous hormonal profiles in women with
breast cancer are reviewed in detail. It is concluded that four sets of findings
are valid: (1) diminished adrenal androgen production, probably genetic, in
women with premenopausal breast cancer; (2) ovarian dysfunction (luteal
inadequacy plus increased testosterone production) in breast cancer at all
ages; (3) increased 16 alpha-hydroxylation of estradiol in breast cancer at all
ages; and (4) evidence that prolactin is a permissive risk factor for breast
cancer, and that the pregnancy-induced decrease in prolactin levels may
account for the protective effect of early pregnancy against breast cancer."

--end of post