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While I am neither an MD nor a cancer specialist, I do have
considerable experience in assessing occupational and environmental
carcinogens from previous work in occupational and environmental
health.
What initiates prostate cancer is not known conclusively. However,
here is what the summary of the World Cancer Research Fund report has
to say about causes of prostate cancer, bearing in mind that this
review concentrates on nutrition, physical activity and lifestyle
factors. I posted a link to this report previously.
************
"The Panel judges as follows:
Foods containing lycopene, as well as selenium or foods containing
it, probably protect against prostate cancer.
Foods containing calcium are a probable cause of this cancer. It is
unlikely that beta-carotene (whether from foods or supplements) has a
substantial effect on the risk of this cancer.
There is limited evidence suggesting that pulses (legumes) including
soya and soya products, foods containing vitamin E, and alpha-
tocopherol supplements are protective; and that processed meat, and
milk and dairy products are a cause of this cancer.
In final summary, the strongest evidence, corresponding to judgements
of "convincing" and "probable", shows that foods containing lycopene,
as well as selenium or foods containing it, probably protect against
prostate cancer, and that foods containing calcium are a probable
cause of this cancer. It is unlikely that beta-carotene (whether from
foods or supplements) has a substantial effect on the risk of this
cancer."
************
They also note that: "There are no other established causes of
prostate cancer."
The careful assessments of this very large team of elite cancer
specialists and scientists has produced a state of the art report on
current knowledge of cancer causes and preventative factors in
nutrition and physical activity.
Now here comes the interesting bit. Here is what they say about
testosterone (TS):
"Growth factors, particularly IGF, as well as androgens have also
been implicated in the development of prostate cancers.
Serum levels of IGF-1 can be associated with prostate cancer
independently of PSA levels. High levels of testosterone promote cell
differentiation, which could protect against the development of this
cancer. Therefore, declining levels of this hormone in older age may
contribute to the development of this cancer."
The key to understanding this paradox -- if androgens are also
clearly promoters -- is that when men are young, high TS levels
probably protect cells from mutation in prostate gland. However, when
a cancer has been initiated, say, by any of the above factors, TS
then becomes a good promoter of *cancer cell* differentiation. The
less TS you have in old age, the slower the growth of a slow-growing
cancer.
Which is not to say that you can't have your cake and eat it too by
watching diet and nutrition and hoping you don't have cancer in the
first place, in which case TS may be protective. Got it? Except you
can't know without invasive tests. PSA is not entirely reliable.
BTW, why caclium seems to be implicated in prostate cancer may be
related to an imbalance of calcium intake and vitamin D3. This is
discussed in the report. Vitamin D3 status seems to be protective of
prostate cancer and too much calcium inhibits vitamin D3 formation.
Estrogens do not get a mention in the report in relation to prostate.
Oh well, back to the Brazil nuts and tomatoes.
Paul Rogers
Gympie, Australia
--- In Supertraining@
<bioforce.inc@
>
>
> Paul Rogers wrote:
>
> > Ken,
> >
> > I think you assume too much if you consider that
> > prostate cancer is
> > primarily caused or promoted by estradiol or
> > estrogens in general.
>
> Ralph Giarnella wrote:
>
> Before I try to answer this post it is important that
> I issue a disclaimer.
> I am and Internist and Gastroenterologist. I am not a
> Urologist or Oncologist. I do not treat Prostate
> cancer and by no means do I know enough about prostate
> cancer to discuss it.
>
> Having said that I went to an Oncology Textbook
> (cancer treatment textbook) and read the Chapter on
> Prostate Cancer.
>
> <<Abeloff: Clinical Oncology, 3rd ed.
> Copyright © 2004 Churchill Livingstone, An Imprint of
> Elsevier
> Chapter 87 Prostate Cancer>>
>
> Below are what I think are relevant excerpts for this
> discussion. All texts enclosed by << ...>> are from
> the above textbook.
>
> First of all the chilling facts of the incidence of
> prostate cancer in apparently healthy mean.
>
> <<INTRODUCTION
> One challenge for prostate cancer screening is the
> prevalence of the disease in the United States:
> Autopsy series have revealed small prostate cancers in
> as many as 29% of men between ages 30 and 40 years and
> 64% of men between ages 60 and 70 years.[4]
>
> These are not men who died from prostate cancer,
> rather they are prostate cancer which were found
> incidentally. This not new information, since I was
> taught this in Medical School 40 years ago.
>
> Nowhere in the chapter is there reference to estrogens
> or estradiol with regards to increasing the risk for
> prostate cancer. On the contrary in some situations
> Estrogen is used to treat prostate cancer.
>
> John Casler writes:
>
> Hi Ralph,
>
> I too claim no "insight" into the DIRECT hormonal relationship
between
> Prostate problems, and Testosterone, but wonder at the evidence, or
the
> interpretation of it.
>
> If the aromatized DHT was "THE" culprit, it seems strange that it
occurs at
> a time in one's life where the levels are the lowest, compared to
the ages
> of say 18 when they are the highest.
>
> It would seem then, that it is likely a more complex inter-
relationship of
> sensitivities, balances, exposures, genetic markers or keys, and
such.
>
> While it cannot be denied that DHT is an anabolic enabler to what
might seem
> a "more" sensitive cellular proliferation of cancer cells, it might
not be
> "THE" cause. Much like gasoline certainly will make a fire flare
up, but it
> may not be the cause of the fire.
>
> I would assume that at some point in the exploration to understand
diabetes,
> that some thought it was generally caused by too little insulin,
which we
> now know is not always the case.
>
> As we also know, the relationship, profile, and production of the
endogenous
> hormones changes as we age. Many are exploring that "relationship"
as well
> as the related elements like cellular sensitivities to various
hormonal
> levels. Much evidence for many diseases of aging seem to stem from
the
> various reactive adjustments to these variations, and the
inflammation that
> seems to accompany them.
>
> Any thoughts?
>
>
> Regards,
>
> John Casler
> TRI-VECTOR 3-D Force Systems
> Century City, CA
>
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