They are on the wrong track. Yes, there are all kinds of molecules
that can be called "growth factors" that are normal, and yes, they can
help cancer growth to some degree, but the key question is, "what is
the underlying cause?"
And that has been known for a while: arachidonic acid metabolites,
which are inhibited to some degree by things like vitamin E, fruits and
vegetables, fish oil, etc. However, these items are not without risks
of their own (I've posted plenty of studies here over the years making
that point). Instead, just avoid any major source of polyunsaturated
fatty acids (and keeping all unsaturated fatty acids in your diet low
is a good idea, as Asian demographic evidence demonstrates), and the
cancer will have its fuel supply cut off. There's a good chance you
would never get cancer to begin with on such a diet. All this other
stuff they talk about is beyond the root cause, and so is
"epiphenomenal," meaning that if you cut out the root cause, you don't
have to worry about the other things, some of which are normal and
won't cause any problems.
The evidence is very clear, for example:
Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13182-7.
Inhibition of arachidonate 5-lipoxygenase triggers massive apoptosis in
human prostate cancer cells.
Ghosh J, Myers CE.
University of Virginia Cancer Center, Charlottesville, VA 22908, USA.
Diets high in fat are associated with an increased risk of prostate
cancer, although the molecular mechanism is still unknown. We have
previously reported that arachidonic acid, an omega-6 fatty acid common
in the Western diet, stimulates proliferation of prostate cancer cells
through production of the 5-lipoxygenase metabolite, 5-HETE
(5-hydroxyeicosatetraenoic acid). We now show that 5-HETE is also a
potent survival factor for human prostate cancer cells. These cells
constitutively produce 5-HETE in serum-free medium with no added
stimulus. Exogenous arachidonate markedly increases the production of
5-HETE. Inhibition of 5-lipoxygenase by MK886 completely blocks 5-HETE
production and induces massive apoptosis in both hormone-responsive
(LNCaP) and -nonresponsive (PC3) human prostate cancer cells. This cell
death is very rapid: cells treated with MK886 showed mitochondrial
permeability transition between 30 and 60 min, externalization of
phosphatidylserine within 2 hr, and degradation of DNA to nucleosomal
subunits beginning within 2-4 hr posttreatment. Cell death was
effectively blocked by the thiol antioxidant, N-acetyl-L-cysteine, but
not by androgen, a powerful survival factor for prostate cancer cells.
Apoptosis was specific for 5-lipoxygenase-programmed cell death was not
observed with inhibitors of 12-lipoxygenase, cyclooxygenase, or
cytochrome P450 pathways of arachidonic acid metabolism. Exogenous
5-HETE protects these cells from apoptosis induced by 5-lipoxygenase
inhibitors, confirming a critical role of 5-lipoxygenase activity in
the survival of these cells. These findings provide a possible
molecular mechanism by which dietary fat may influence the progression
of prostate cancer.
Biochem Biophys Res Commun. 2004 Mar 12;315(3):624-35.
Rapid induction of apoptosis in prostate cancer cells by selenium:
reversal by metabolites of arachidonate 5-lipoxygenase.
Ghosh J.
Department of Urology, Vattikuti Urology Institute, Henry Ford Health
System, Detroit, MI 48202, USA. [email hidden]
Recent clinical trials have documented that selenium significantly
reduces the incidence of clinical prostate cancer. However, nothing is
clearly known about the underlying molecular mechanisms by which
selenium exerts its anti-cancer effect. This report provides evidence
that selenium at micro-molar concentrations induces rapid apoptotic
death in human prostate cancer cells, but not in normal prostate
epithelial cells. Apoptosis involves activation of caspase 3 which
plays a critical role in the cell death process. Interestingly, the
apoptosis-inducing effect of selenium in prostate cancer cells is
substantially alleviated by the 5-lipoxygenase metabolites, 5(S)-HETE
and its dehydrogenated derivative 5-oxoETE, but not by metabolites of
12-lipoxygenase (12(S)-HETE) or 15-lipoxygenase (15(S)-HETE). Apoptosis
is also prevented by their precursor, arachidonic acid, an omega-6,
polyunsaturated fatty acid, presumably by metabolic conversion through
the 5-lipoxygenase pathway. These results indicate that selenium's
anticancer effect may involve induction of apoptosis specifically in
prostate cancer cells sparing normal prostate epithelial cells, and
that 5-lipoxygenase may be a molecular target of selenium's anticancer
action. The present report warrants that care should be taken about
high intake of dietary fat containing arachidonic acid or its precursor
fatty acids when selenium is used for the management of prostate
cancer, and suggests that a combination of selenium and 5-lipoxygenase
inhibitors may be a more effective regimen for prostate cancer control.
Nippon Rinsho. 2005 Oct;63(10):1839-48.
[Relationship between cyclooxygenase (COX)-2 and malignant tumors]
[Article in Japanese]
Yoshimura R, Matsuyama M, Tsuchida K, Takemoto Y, Nakatani T.
Department of Urology, Osaka City University Graduate School of
Medicine.
Recently, epidemiologic studies and animal experiments have
demonstrated that nonsteroidal anti-inflammatory drugs(NSAIDs) reduce
the incidence of colorectal carcinoma. Cyclooxygenase(COX) is the
principal target of NSAIDs. COX is the first oxidase in the process of
prostaglandins(PGs) production from arachidonic acid(AA). PGs and COX
enzyme may be involved in the initiation and/or the promotion of
carcinogenesis because the major action of NSAIDs is the inhibition of
COX. In this review, we demonstrated the expression of COX-2 in
urological cancer(renal cell carcinoma, bladder tumor, prostate cancer,
and testicular tumor) tissues as well as the effects of COX inhibitors.
Histol Histopathol. 2005 Jul;20(3):969-75.
New aspects on the role of lipoxygenases in cancer progression.
Catalano A, Procopio A.
Department of Molecular Pathology and Innovative Therapies, Polytechnic
University of Marche, Via Ranieri, 60131 Ancona, Italy. [email hidden]
The Lipoxygenases (LOXs) are a class of enzymes that convert
arachidonic, linoleic, and other polyunsaturated fatty acid into
biologically active metabolites involved in the inflammatory and immune
responses. Recent evidences indicate that LOXs and the signaling
pathways that are involved in their activation are also important for
carcinogenesis and tumor progression. LOXs should therefore receive as
much attention from cancer researchers as it has already from
immunologists. In this article, we will review some evidence that the
LOXs pathways affect several aspects of lung, pancreatic and prostate
cancer progression. Moreover, we discuss how this new perspective on
the roles of LOXs and their metabolites can have important implications
to cancer therapy.
And you can find many others at pubmed.com. Note that they sometimes
say "fat" when there is no way saturated fatty acids can be
metabolitzed into the molecules that cause cancer. Whether they know
this or not is impossible to say without contacting each one of them.
In fact, saturated fatty acids block metabolization, which is why
animals fed only 100% saturated fatty acids are said to be "essential
fatty acid deficient," that is, the saturated fatty acids will block
this and the animals may get some dry skin and not grow at the same
rate as those given ample amounts of PUFAs. However, no experiment has
controlled for omega 9 PUFAs, and thus the claim that omega 6 PUFAs
(which are the fuel for cancer) are "essential" has never been
demonstrated in a properly controlled experiment. After reviewing the
evidence, I came to the conclusion that omega 6 and 3 PUFAs are very
dangerous and are not "essential." I have avoided any major source of
these molecules for about 4 years now and have seen only benefits, yet
the literature states that I should have experienced "deficiency
symptoms" within about 3 weeks. Now you too know, and you can avoid
cancer if you wish (unless you get massive radiation doses or something
like that).
