2011-12-31

#cancer #prostate prevention factors #health

11.13 ... 12.31: web.health/
cancer#prostate/prevention factors:

intro:

. I was recently introduced to a fund drive
for awareness of prostate cancer .
. it wasn't clear to me how funds could cure cancer;
but the drive certainly does promote awareness;
and, awareness begets prevention ...
however, I was stumped by the question
"(what prevents prostate cancer?);
and, they weren't offering any clues,
so I directed my available resources at research .
12.1:
. my first strategy for assessing prostate risk
is to look at several cultures with low risk;
the most significant result of that has been: [12.28:
# paleo is not easy:
. even if you could afford grass-fed, chances are
your fats are contaminated with xenoestrogens .]
# soy & grain not required:
. the controversial soy & grain plan
is not required for prostate care:
soy has been the apparent source of Japanese health
but has not been needed by the Inuit .
. moreover, soy confuses 2 preventive factors:
# weakly estrogenic Isoflavones,
# legume diet's hormone-balancing benefits:
the pro-biotic, soluble fiber,
and the fiber's drip-feeding of glucose & protein
all work to reduce prostate risk
(even peanuts benefit from being legumes!).
12.23:
. other strategies include trying to integrate the teachings
of the Zone diet (an advanced paleo diet),
and cancer reports with battle strategies,
all of which have unique contributions to the war on cancer .


12.31: summary:

. the working theory of this paper is that
the primary cause of prostate cancer
is estrogen's dominance over progesterone;
however, the major contributer to all cancers,
is a high-glycemic diet or a high-stress lifestyle
because they raise insulin (cancer growth factor):
most of your dietary protein and carb' should be
drip-fed to you by legumes,
and have few insulin resistors, such as fructose .
. T (testosterone) levels have been implicated,
but T levels only magnify the damage done by
estrogen dominance that means progesterone dysfunction,
that in turn means high DHT, a powerful growth factor .
. even when you have birth defects from pollution,
lifestyles choices may prevent the cancer from
spreading into a very painful bone invasion .

it waits for old age:

. cancer is a very unusual disease before age 50,
but, prostate's rates increase exponentially thereafter:
eg, england, 1992:
8 per thousand in men aged 50 to 56 years (4 deaths)
68 per thousand in men aged 60 to 64 years (37 deaths),
260 per thousand in men aged 70 to 74 years (166 deaths),
406 per thousand in men aged 75 to 79 years. [12.28:
--. I think there has been some acceleration mixed in;
because, the xenoestrogen load has gotten very thick
only recently:
. sperm counts were halved between 1940 and 1990,
due to the effect of pollution acting as estrogens on the testis;
dioxin is a very potent sperm`count reducer .]

12.1:  why it waits for old age:

. why does cancer wait for old age?
is it because of natural hormone changes
that could be surpressed with effective (unpatented)
bio-identical, non-oral hormone replacement therapy ?
or is it a delayed action, like when
skin cancer happens 30years after a serious sun burn ?
. well, if you look at 30 + 10..20 = 40..50
-- 40..50 is when most people also have
hormone imbalances too;
perhaps people who would get burned under the sun
are actually having their first experience of that
30 years before their age of hormonal decline .

. most prostate cancer comes after the age of 60;
because, aging naturally increases over-expression of
the enzymes 5-LOX, COX-2, and their end-products
that can promote metastasis of prostate cancer cells;
mostly what aging does though,
is change our sex hormones:
the hormone system was once so strong,
no amount of foolishness could upset the balance;
after age 50, the opposite is true:
even with a wise lifestyle, T (testosterone) is too low,
estrogen is out-yelling progesterone signals,
and DHT is then stealing even more T
as a result of progesterone dysfunction .
. this is the sort of stress that brings out the
vulnerabilities created by birth defects .

there is usually hope for prevention:

. only 9% of all prostate cancers are genetic;
http://www.cancer.gov/cancertopics/pdq/prevention/prostate/healthprofessional/page3
eg, 15% of cases will have a father or brother with prostate cancer;
so, prevention is within our grasp:
there are 2 active fronts in the war on prostate cancer:
prenatal care awareness, and lifestyle choices .

prevention# birth defects: imprinting:

. estrogenic pollutants cause subtle birth defects
that create a tendency to get prostate cancer
by altering fetal cell differentiation .
. 75% of prostate c'cases have reduced sperm counts,
indicating xenoestrogens were involved .

. a pregnancy diet has many subtle pitfalls:
pollutants, food additives, natural food anti-nutrients,
plasticizers such as BPA, recreational drugs, and stress;
all of these conditions can expose the fetus to
higher than normal levels of estrogenics .
. many mothers are often excessively exposed to
birth control pills (estrogens, progestins),
lead, benzopyrenes, ozone, dioxins, PCBs, food additives .
. some migrant mothers are exposed to pesticides:
DDT, DDE, methoxychlor, chlordecone, parathion,
malathion, pyrethroids, paraquat .
. some teen mothers are exposed to drugs:
tetrahydrocannabinol, cocaine and opiates.

high-dosed estrogenics in the 2nd or 3rd trimester:

. when a pregnancy diet is resulting in
prenatal exposure to DDE (anti-androgenic),
PCB, or any other estrogenic,
that will raise serum IGF-I levels later on,
and that, in turn, raises the risk of
next-generation prostate cancer .

an example of how prenatal diet works:
. when the pregnant rat's diet was 20% corn oil,
this caused the next generation to have
20% rates of prostate cancer;
whereas, a diet of 5% energy from corn oil,
caused no cancers in the pups .
. this is a relevant example, too, because
a woman could try slimming while pregnant,
and, poly'oils such as corn oil are one way to do that .

high-glycemic or high-insulin diets:
. in the USA, hiafric (african-ancestry) males
have twice the risk of prostate cancer;
one explanation is from having mothers with
a unique hormone profile:

hiAfric vs hiEuric usa women with no morning sickness:
free E#2: 30% -- 1.66 vs 1.28 (Estradiol, an estrogen)
total E#2: 37% -- 189 vs 138
SHBG-bc: 22% -- 5.7 vs 4.7
T: 48%  -- 114.4 vs 77.3 (high testosterone, sign of PCOS).

. of usa women with no morning sickness
those of african-ancestry had 30% higher estrogen
than women of euro-ancestry . [12.31:
. one clue to why
is that hiafrics also had 40% higher T levels;
and both of these symptoms together are
the signature of PCOS (PolyCystic Ovary Syndrome)
caused by insulin resistance and obesity;
also, half with PCOS also have visceral or liver fat,
a sign that high fructose or alcohol
is being the primary cause of the insulin resistance );
moreover, there is a strong genetic component,
which is consistent with the theory that
hieurics are genetically more tolerant of high-glycemics
than most other races, including hiafrics;
yet, nearly everyone is now on a high-glycemic diet .
. PCOS does respond to a low-glycemic diet,
with correction of estrogen dominance
(and the associated progesterone dysfuction).
. the prostate is the embryological twin of the uterus,
so it is of interest to men that women with PCOS
are more likely to get endometrial (uterus lining) cancer
due to lack of progesterone resulting in
prolonged stimulation of uterine cells by estrogen .]

helpful defects:

. men with under-developed testes rarely get prostate cancer,
and men who cannot produce DHT
have no risk of prostate cancer .
("under-developed" is in contrast to "atrophied":
a third of prostate-cancer-cases have atrophied testicles).
[12.31: interesting coincidences:
. DHT is caused by progesterone dysfunction,
usually from diet-caused estrogen dominance;
DHT is a more powerful growtht factor than T,
while T has anti-estrogenic, anti-cancer properties
-- unless of course it's turned into DHT
by a progesterone dysfunction ! ]

prevention# water pollution:

. rising rates of prostate cancer are related to
increasing doses of endocrine disruptors in the water supply:
PCBs, pesticides, plasticizers (BPA), and birth control pills .
. in all of the 87 countries studied,
prostate cancer in 2007 was proportional to oral contraceptive use;
estrogen in birth-control pills is excreted into the water,
and there is evidence that low levels of estrogens in males
may cause prostate cancer.
. insecticide chlordecone (Kepone) in Martinique and Guadeloupe,
significantly increased the risk of prostate cancer
(half of all cancers in that area are in prostate).
birth-control pills:
. a country's rate of prostate cancer is related to
its rate of oral contraceptive use by females;
the estrogen in birth-control pills is excreted in the urine
and gets into the environment, particularly into water,
and scientific evidence suggests that low levels may cause cancer,
including prostate cancer.

prevention# personal choices# causes(+) of prostate cancer:

+ xenoestrogens (polycarbonates, pesticides;
none of our products are tested for hormone disruption .
. bisphenol A leaches from polycarbonate plastic,
and from linings of many canned foods
esp'ly when food has been heated first and contains oil .
. buy organic food to avoid pesticides,
especially for your green leafies ),

+ inflammation (genetic damage:
In response to injury, local inflammatory cells
 (neutrophil granulocytes and macrophages)
secrete a number of cytokines into the bloodstream,
most notable of which are:
# interleukins: IL-1, IL-6 and IL-8;
# Tumor necrosis factor (TNF, cachexin or cachectin
formerly known as TNF-α):
. TNF is a cytokine involved in systemic inflammation
stimulating the acute phase reaction.
Acute-phase proteins are those whose plasma concentrations
increase (positive acute-phase proteins)
or decrease (negative acute-phase proteins)
in response to inflammation ),

+ arachidonic acid (omega-6 poly'oil, egg yolks, organ meats:
excess arachidonic acid can provoke
the dangerous 5-lipoxygenase (5-LOX) pathway;
resulting in prostate cancer proliferation stimulators,
such as 5-HETE (5-hydroxyeicosatetraeonic acid);
and, 5-LOX breakdown products (such as
leukotriene B4, 5-HETE, and hydroxylated fatty acids)
cause tissue destruction, chronic inflammation,
and resistance to apoptosis attempts .
. another product leukotriene B4,
is a potent pro-inflammatory agent .
.{5-LOX, 5-HETE} are overexpressed in Prostate Cancer;
and, prostate cancer cases are proportional to
a region's use of high-arachidonic foods .
. 5-LOX allows cancer to benefit from
epidermal growth factor (EGF);
conversely, complete inhibition of 5-LOX induces
apoptosis in even advanced human prostate cancers
-- both the androgen-{dependent, independent} stages .
. both COX-1 & -2 (cyclo-oxygen-ase-1 and -2)
also participate in the misuse of arachidonic acid.
COX-1 causes the production of thromboxane A2,
promoting abnormal arterial blood clotting (thrombosis);
and, COX-2 is causing cancer cell propagation,
while its breakdown product (prostaglandin E2)
promotes chronic inflammation ),

+ high protein (100g per day instead of 50g: high IGF-1;
high levels of insulin-like growth factor 1 (IGF-1),
result in a 4.3-fold increased risk of prostate cancer ),

+ high-glycemic (refined-carb) diet (less IGF-1 binding;
. glycemic index has an effect on IGF binders:
At 4 h, the {high, low}-GI meals made these changes in
IGF-binder-{1,3} levels (ng/mL):
binder { #1, #3 }:
hi-GI: -13, -110 -- less binders,
lo-GI: -55, +251 -- more binders .

Thus, the low-GI meal produced a greater decrease in IGFBP-1
and produced an increase, rather than a decrease, in IGFBP-3.
. so in total, the low-GI diet didn't promote freeing of IGF-1,
and offered additional binder#3 (reliable apoptosis);
whereas, the high-GI diet did free some bound IGF,
and removed some binder#3 .
. high-glycemics also stimulate production of arachidonic acid
[because the definition of a high-glycemic
means the body has to raise an insulinemic storage response
that turns the glucose into saturated fats (a cancer promoter)]),

+ estrogen dominance (progesterone dysfunction = more DHT;
estrogen can also dominate T:
ie, a falling testosterone to estradiol ratio may have
a great deal to do with getting prostate cancer:
prostate cancer is the male version of
endometrial cancer:
(the inner lining of the uterus;
risk factors are obesity, excessive estrogen exposure;
ie, unopposed, not balanced by a source of progesterone,
and a proper sensitivity to progesterone).
. when not balanced by healthy levels of progesterone,
estrogen (estradiol) activates the oncogene Bcl-2
that prevents sick cells from self-destructing ),

+ metabolic syndrome (obesity, estrogen dominance, diabetes, DHT)

+ androsterone glucuronide (index of 5α-reductase activity;
5α-reductase facilitates conversion of T to DHT
that promotes prostate cancer growth,
as well as benign prostatic hyperplasia,
and male pattern baldness ),

+ 3α,17b-androstanediol glucuronide (index of 5α-reductase activity),

+ omega-6 (non-fish poly'oils -- converts to arachidonic acid;
. when the preganancy diet has high omega-6,
pups have more prostate cancer,
and more AH (atypical hyperplasia):
20% corn oil: 73% AH, 20% cancer
5% corn oil:  20% AH, 0% cancer ),

+ sat'fats (Saturated FattyAcid, insulin resistor),

+ animal fat (contaminated with xenoestrogens:
PCBs, dioxins, furans),

+ red meat (grain-fed meat is heavy in
omega6 oil & sat'fats & arachidonic acid;
some of meat's risk could also be due to pervasive
under-the-table addition of estrogens),

+ egg yolks (risk of cancer becoming lethal:
. among confirmed cases of cancer,
Men who consumed 2.5 or more eggs per week
had an 81% increased risk of lethal prostate cancer
compared to men who consumed less than 0.5 eggs per week)

+ grilled red meat (PhIP-DNA adducts:
PhIP (2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine)
is the major heterocyclic amine generated from
cooking meats at high temperatures;
induces prostate cancer in rats;
. while the link to grilled red meats was strong(P = 0.001)
grilled white meat's association
could have been chance(P = 0.15)),

+ cured meat,

+ working hard not smart (occupational hazards:
chlorinated pesticides, methyl bromide fumigant),

+ virus (caspace blocker: inhibits apoptosis:
 . just as apoptosis is used to defend against viruses,
 viruses carry caspase inhibitors to block apoptosis .
 . HPV (a sexually transmitted virus) turns off p53,
 the tumor suppressor protein gene),

+ DNA damage (mutation of turmour supressor gene p53:
. this gene is very easy to mutate,
and mutations of it are found in half of all cancers ),

+ caspase inhibitors ( inhibits apoptosis:
. the class of *-{fluoro, chloro}-methyl ketones;
medicinally used for stopping cell deaths during
heart attack, stroke, Alzheimer's, and motor neurone disease),

 + Survivin overexpression (caspace blocker: inhibits apoptosis:
. plays a central role in cell division, and also
promotes cell growth by stabilizing microtubules during mitosis.
Over-expression causes resistance to chemotherapies,
such as what you might apply yourself using se-methyselenocysteine),

+ Bel-2 gene overexpression (inhibits apoptosis),

+ NF-kappaB protein overexpression (inhibits apoptosis;
NF-kB( nuclear transcription factor)
is the immune system's rapid-action first responder),

+ dairy (small unexplained risk:
Men with the highest intake of dairy products
(RR =1.11 [95% CI = 1.00 to 1.22], P = .047)
were more likely to develop prostate cancer .
. prostate cancer - dairy product Ptrend = .029
The pooled relative risks of advanced prostate cancer
were 1.33 (95% CI = 1.00 to 1.78; P = .055)
for the highest versus lowest intake categories of dairy products,
[12.31: one theory:
. men who drank milk a lot were using it as an antiacid;
what they had was a diabetic nervous inflammation .]),

+ calcium (conroversial, see cadmium section;
Men with the highest intake of calcium
(RR = 1.39 [95% CI = 1.09 to 1.77], P = .018)
and dairy products
(RR =1.11 [95% CI = 1.00 to 1.22], P = .047)
were more likely to develop prostate cancer;
prostate cancer - calcium Ptrend = .014 .
The pooled relative risks of advanced prostate cancer
were 1.46 (95% CI = 0.65 to 3.25; P > .2)
for the highest vs lowest intake categories of calcium),

+ folic acid supp(but Multivitamin Use not a risk);

+ Synthetic Alpha Tocopherol supps(depletes gamma tocopherol:
 men taking synthetic alpha tocopherol
had a 17% greater incidence of prostate cancer)

prevention# personal choices# prostate risk reducers(-):

- Zone diet(50..60g protein, 60 .. 90g carb, T balance:
. when carb intake vastly exceeded protein,
there was more estrogen in the system .
44protein, 35carb, 21fat = high protein (%calories)
10protein, 70carb, 20fat = high carb .
. cytochrome P-450-dependent oxidation is the E2 (estradiol) reducer .
. microsomal delta^4-5alpha-reductase is the T reducer .
. the high protein diet metabolizes some drugs faster,
thus decreasing the clearance time of the drug.
. it is common for things that enhance E2 reducer
to also decrease T reducer activity;
[ hence anything that increases estrogen metabolism
may be a likely candidate for decreasing T metabolism .]
. a high protein diet
increased the E2 reducer by about 14-15%;
but no change in reducing T to DHT or androsterone;
. changing to the high carb diet
increased the T oxidation rate from 30% to 40%,
resulting in more (T -> androsterone) conversion;
and E2 became higher as there was less reducer .
--
. xenoestrogens also increase estrogen reduction;
those include many carcinogens affecting prostate:
dioxin, hexachlorobenzene, dibenzofurans,
and polyhalogenated biphenyls .

- Omega-3 fish oil (EPA/DHA,
inhibits COX-2, 5-LOX, and NF-kB;
reduces inflammation-mediated growth of prostate cancers ).

- CLA (encourages necrosis of cancer cells;
but, beware high doses of CLA pills:
. pills are 44% t10c12 CLA isomer
that may cause insulin resistance and liver hypertrophy .
. both the c9,t11 and t10,c12 CLA isomers appear to be
active inhibitors of carcinogenesis in animal models.
. in ruminant products (milk and meat of cows),
the CLA is 80% c9t11 (cis-9,trans-11) isomer;
whereas the synthetic CLA (shown to reduce mouse fat)
has a mix of:
40% c9t11 -- main ruminant product increases lean mass;
44% t10c12 -- main pill ingredient reduces mouse fat;
however, the equivalent dose in humans would be
56 g (0.70 g CLA/kg) -- that's a lot of
pro-oxidant poly'oil and insulin resistance),

- gamma tocopherol (the form of vit'E found in food:
down-regulates control molecules known as cyclins,
which trap cancer cells in the midst of their reproduction cycle;
in prostate cancer cells, gamma-E's stimulation of PPAR-gamma
(affecting genes that control cancer cell changes)
resulted in a complete cessation of cancer cell growth,
reduced the development of new blood vessel formation,
and induced apoptosis by blocking synthesis of cell membrane growth .
. gamma-E, but not alpha-E, exhibited potent reduction of
2 powerful pro-inflammatory factors in rats:
# COX-2's PGE2
# arachidonic's 5-LOX's leukotriene B4 .

- alpha & gamma vit'E (combinations of alpha-E and gamma-E
optimally reduce arachidonic end products )

- selenium (inhibiting 5-LOX, see also cadmium section .
. Selenium causes a dose-dependent increase in
cellular thioredoxin activity.
. transgenic mice that overexpress thioredoxin,
are more resistant to inflammation, and live 35% longer
apparently due to anti-oxidant activity .
. for cancer prevention this may be good,
but beware megadosing if you have advanced cancers,
(unless combining it with chemotherapy)
because several types of cancer (including prostate)
are thriving on their overexpression of thioredoxin,
the production of which is proportional to selenium intake .

- methylated selenium (se-MSC, MSeA: apoptosis promoter:
. MSeA-induced apoptosis was accompanied by
the activation of multiple caspases (caspase-3, -7, -8, and -9),
. MSeA has killed some prostate cancers,
but not the cancers producing nuclear survivin
(an inhibitor of both caspase-3 and caspase-7).
. Se-MSC (a commercially available form of methylated Se)
induces apoptosis through caspase-3 activation
in HumanLeukemia-60 cells  ),

selenium is not a cancer cure:

. having selenium in your food or water (ie,
being in a region with a good supply of selenium)
tends to lower the risk of prostate cancer .
. but once you get prostate cancer,
you have a 75% chance of carrying a gene for
manganese superoxide dismutase (SOD2)
that means
higher selenium intake leads to poorer outcomes .
By contrast, the 25 percent of men with a
different variant of the same gene
and who had high selenium levels
were at 40% lower risk of aggressive disease.
. likewise for other late anti-cancer efforts:
selenium with vit'E and soy did not stop
high-grade prostatic intraepithelial neoplasia (HGPIN)
from proceeding to prostate cancer .
... uh, but form counts:
 . the Nutritional Prevention of Cancer clinical trial
 showed that selenium in the form [se-methyselenocysteine]
 did reduce the risk of cancer;
  a later study (Selenium and Vitamin E Cancer Prevention Trial)
 did not show a benefit because of using bad forms:
 # selenium's [Se-Methionine] form,
 # vitamin E's all-racemic synthetic alpha-tocopheryl acetate .
  . subsequent in vitro studies found that
 lung cancer cells processed se-methyselenocysteine
 differently than Se-Methionine,
 and were killed more often by se-methyselenocysteine
 than by Se-Methionine .
-- in animals, use of se-methyselenocysteine
results in apoptosis of some cancers
in a dose-dependent manner
(why being non-toxic is exciting news).

- vitamin E & selenium  (combination:
. selenium potentiates vitamin E-induced inhibition of
[androgen-sensitive human prostate cancer cells] in vitro).

- β-cryptoxanthin & selenium
(the prevention more pronounced in ex-smokers
than in current smokers, and unclear in never-smokers),

- folic acid from food (but not supplements)

- zinc (from supplements, not diet; but see cadmium:
. risk of advanced prostate cancer was decreased .
. inhibits 5-alpha-reductase [same as progesterone does]
and may inhibit prostate's uptake of cadmium .
. zinc-deficient rats significantly lowered
testosterone, estradiol and LH;
lowered rates of: testosterone ->DHT -> 3a-diol;
and, raised livers conversion of testosterone to estradiol .

- sun tan (Calcitriol) or vitamin D (1,25(OH)2D3) (inhibits NFκB;
Calcitriol encourages apoptosis,
and limits blood supply to the tumor .
These may be the roles that vitamin D plays in prostate cancer,
near the beginning and end stages.
Exposure to sunlight in early years to midlife
may reduce the risk of prostate cancer.
Vitamin D levels up to 27 years prior to prostate cancer diagnosis
do not seem to affect risk of prostate cancer.)
. Vitamin D up-regulates IκBα levels
by increasing mRNA stability
and decreasing IκBα phosphorylation.
The increase in IκBα levels downgrades NFκB activity.
Since NFκB is a major transcription factor of inflammatory mediators,
these findings suggest that the less-calcaemic analog, 1,24(OH)2D2
may be effective as an anti-inflammatory therapeutic agent .)

- cruciferous veg' (cauliflower, broccoli;
an esp'ly helpful veg because of it's effect on
sexual hormone metabolism .
. cruciferous trigger a high production of
glutathione S-transferase -- this is deactivated
in every case of cancer .)

- flax lignans (controversial),

- soy isoflavones (controversial, NF-kB inhibitor:
Genistein prevents NF-kB’s movement into the nucleus;
Genistein promotes apoptosis as a result of down-regulation of NF-kB
. genistein is working in 3ways,
it inhibits the DHT conversion enzyme; and it prevents fat from
either promoting the enzyme or promoting the cancer growth
[. depending on your risk of prostate
you may want to consider the use of soy,
but it's a medication with significant side affects .]
. safer medicines include cruciferous vegetables,
and the high-bean Zone diet ),

- T (testosterone, balancing:
. while T's conversion to DHT should be minimized
low T increases the risk of prostate cancer .
[. keep in mind how the same lifestyles that cause low T,
can also cause prostate issues:
. the hormone imbalances of aging that affect prostate
are also causing a 10% T drop every decade after 30,
and there can be increases in SBHG (T-binder).
. specific causes of low T:
stress -> hypercortisolism,
malnutrition -> stress,
obesity -> hypercortisolism, sleep apnea,
hyperthyroidism -> lower bioavailable T;
excessive heat -> autoimmune damage;
medications, tobacco and alcohol, Morphine,
anabolic steroids .]
. low T and prostate cancer linked by estrogen excess:
. obesity's fat is turning T into estrogen (estradiol);
liver failure is a "(fairly common cause) of estrogen excess;
[. some common liver diseases are caused by
omega-6 oils and fructose -- main fast foods ingredients,
along with glucose, and sat'fats or hydrogenated fats .
. estrogen's dominance over progesterone
is what turns T into the powerful DHT .]
11.18: news.health/bhrt/testosterone supplementation:
. lef.org said you should use supp's to correct a low T state;
but only if you don't have prostate cancer currently;
that had me retorting "(great . how do you know?).
. one practical way to interpret that is:
if you are able to lower your lifestyle risks for cancer,
and can test for your exposure to xenoestrogens,
then if your lifestyle still hasn't normalized your T,
you might consider asking for a patch .
. there might also look for clues to your fetal risk:
the genetic shifts that can increase prostate cancer risk
when your mother was exposed to certain conditions .
[12.31:
. keep in mind the reason why T feeds a cancer:
those who have prostate cancer are also
those who are converting their T into estrogen,
and that estrogen is what fuels the cancer;
so, any physician who changes your testosterone,
needs to also be managing your whole lifestyle .])

- progesterone (your natural DHT inhibitor;
inhibitors can shrink the volume of the prostate;
and reduce the risk of prostate cancer by 25%.
--[. older men often have progesterone dysfunction
due to estrogen dominance from being overweight .]

- legume (see legume section)

- yellow-orange vegetables,

- tomatoes cooked with mono'oil
(lycopene lowers 5-LOX activity),

- non-fruit veg'
(perhaps because it displaced more destructive carb's;
 other studies found dark green leafies helped too .)

- cereal (grains; likely whole grains;
international epi'study: strong preventive .
. no clues as to why from an epidemiological;
theories include:
# mere displacement:
. the only people who used a lot of cereal
were those who are vegetarian in poverty,
and missed out on most high risks:
milk, meat, eggs, vegetable oils, obesity;
# estrogen load reduction:
. grains include phytoestrogens,
and some are very weak,
so they can be estrogen blockers .
# implied legumes:
. heavy grain users are likely to
combine their grains with legumes
(another prostate star food). ),

- aspirin (daily = 49% reduced risk of an enlarged prostate;
48% less likely to have an elevated PSA;
Aspirin inhibits the COX-1 enzymes,
which are also involved in the arachidonic acid inflammatory pathway;

- caffeine (induces apoptosis:
. modulates or induces p53 gene expression;
reduces mitochondrial membrane potentials
and induces apoptosis in a dose-dependent manner ),

- green tea (inhibits COX-2, and NF-kB;
epigallocatechin-3-gallate selectively inhibits COX-2
and polyphenols inhibit oxidized LDL-induced NF-kB activation
EGCG caused apoptosis of prostate cancer in vitro).

- black tea (COX2 inhibitor, induced apoptosis;
theaflavin-{3-monogallate, 3′-monogallate} mixture
induced apoptosis and strong COX2 inhibitor;
its EGCG ((−)-epigallocatechin gallate)
is a mild COX2 inhibitor ),

- coffee (less likely it spreads to the bone;
60% less risk with at least six cups per day,
30% less risk with 3 cups .
. phenolic acids are potent antioxidants;
they affect glucose metabolism and levels of sex hormones
. the same applies to caffeine,
but it may supress some routes to apoptosis ).

- grape seed extract (ATM-Chk2 activation induces apoptosis;
the main active ingredient is Gallic acid;
but this action is inhibited by caffeine .
ATM (ataxia telangiectasia mutated):
. ATM is recruited and activated by DNA double-strand breaks
and initiate activation of the DNA damage checkpoint,
leading to cell cycle arrest, DNA repair or apoptosis.
Several of these targets are tumor suppressors,
including p53, CHK2 and H2AX ),

- European Milk Thistle (Isosilybin A, induces apoptosis:
. Isosilybin A is targeting Akt, NF-κB,
and androgen receptor signaling
. lef.org`Certified European Milk Thistle ),

- curcumin (lowers 5-LOX activity, inhibits COX-2,
known to promote prostate cancer proliferation).

- boswellia plant Extracts (selectively inhibit 5-LOX),

- ashwagandha (Withania somnifera, NF-kB inhibitor:
Withaferin A (WFA) is a steroidal lactone
isolated from Indian Ginseng (Ashwagandha),
which is an inhibitor of NFκB activity,
and traditionally used as an anti-inflammatory ),

- pomegranate extracts (inhibits NF-kB),

- Ginger (inhibits NF-kB;
contains Gingerol, zerumbone,
promotes apoptosis of prostate cancer),

[lef.org's summary of nutraceuticals: and what they do:

( less omega-6 is not mentioned in this figure. )
( also omitted is soy isoflavones (often implies high omega-6)).
# low meat & egg: -arachidonic acid;
# low-insulin diet: -arachidonic acid
# cold-water fishoil: -arachidonic acid;
# sesame lignans: -arachidonic acid;
# aspirin: -cox-1;
# green tea: -cox-2;
# curcumin: -(cox-2, 5-LOX);
lower arachidonic acid:  -(cox-1, cox-2, 5-LOX);
lower cox-1: -thromboxane a2: -(platelet aggregation)
lower cox-2: -prostaglandin e2;
lower 5-LOX: -(leukotriene b4, 5hete);
lower prostaglandin e2: -(inflammation, atherosclerosis, arthritis)
lower leukotriene b4: -(inflammation, atherosclerosis, arthritis);
lower 5hete: +apoptosis: -cancer cells .]

12.2: the Inuit way:

[12.24: intro:

. the purpose of bringing up the Inuit case,
is to separate the factors that go into a meat diet;
it's not just the meat; rather,
it's being exposed to estrogenic pollution in the fat,
which reduces your progesterone function
and that means losing T into DHT production .
. another main problem with today's meat
is not being grass-fed like wild game is:
meat now has more omega-6 oil,
and less omega-3 .]

Inuit are protected against prostate cancer:
. cancer is rare among Inuit,
and this is attributed to their traditional diet,
which is rich in omega-3's and selenium .
--
. much more relevant to prostate cancer
was the Inuit getting most of their energy from
mono'oils rather than high-glycemic carb's
(refined grains, sugars, corn syrup),
and esp'ly their not mixing a high-glycemic diet
with a high-fat diet (that would cause high insulin).

. Inuit's had a very special ketogenic diet;
not only was it very low-carb,
but coming from fish-like wild game,
they were also getting most energy from
a special mixture of lipids:
( more mono'oils & less sat'fat
, high-omega3
, low-omega6 but high-CLA
) . this diet also contained certain sat'fats
that could cause some arterial plaque;
but, prostate cancer was very rare;
and Inuit's often lived long enough to find out .
so,  from that we know,
if you could escape all birth defects,
and a lifetime of xenoestrogen exposures,
then a high fat diet per se
isn't going to cause prostate cancer .

11.18: chemistry of of Inuit's grass-fed way:

. grass-fed vs grain-fed meat has more
total CLA (C18:2) isomers,
and trans vaccenic acid (TVA) (C18:1 t11),
a precursor to CLA .

. some sat'fats are neutral like mono'oils:
the cholesterol-elevating sat'fats are
myristic (C14:0) and palmitic (C16:0) .
stearic fat (C18:0) has a neutral effect on
LDL, HDL, and total cholesterol;
Lauric acid (C12:0) improves the
HDL per total cholesterol ratio .
. grass-fed elevates glutathione (GT),
superoxide dismutase (SOD),
and precursors for Vitamin A and E .

. while grain-fed has more mono'oils than grass-fed,
primarily oleic acid (C18:1 cis-9), [olive oil has some n-9 ]
it also has more total fat, and more of the wrong sat'fats .
. grass-fed provides more omega-3 (n-3),
CLA(C18:2 c-9, t-11), a potent anti-carcinogen,
and TVA (C18:1 t11), convertable to CLA .

CLAs originate from two sources in nature:
# the rumen's action on poly'oils
(bacterial isomerization by Butyrivibrio fibrisolvens
and/or biohydrogenation)
-- if Grain consumption hasn't decreased rumen pH
# human's fat and mammary gland's
desaturation of trans-fatty acids .

. there are 2 essential fatty acids,
# Linoleic (C18:2n-6) -- root of omega-6's --
# α-Linolenic (C18:3n-3) -- root of omega-3's --
. these distinct omega families can
interfere with each other's metabolism,
reducing their incorporation into tissue lipids
and altering their overall biological effects .

the usa NIH` RDI (recom'd daily intakes)
vs the Institute of Medicine's DRI (dietary reference intake):

650 mg of EPA and DHA,
αLA(omega-3): 2.22 g/day vs 1.1 ..1.6 g
LA(omega-6): 4.44 g/day vs 12 ..17 g
-- a healthy omega-6 limit is
less than 4 times the omega-3 intake;
whereas, the typical grain-fed meat and grain-oil diet
tends to have 11 to 30 times more
which increases the rate of inflammatory disorders .

. the average omega-6 : -3 ratios for meat depends on the feed:
grass-fed: 1.53  -- range 1.44 .. 3.72
grain-fed: 7.65 -- range 3.0 ... 13.6
-- range depends on using entire animal or just muscle .

omega-6 (*n-6) production line:
. linoleic (c18:2n-6)
GLA (gamma linolenic, c18:3n-6)
DGLA (dihomo-gamma linolenic, c20:3n-6)
arachadonic (c20:4n-6) -- cancer promoter
adrenic (c22:4n-6)
docosapentaenoic (c22:5n-6).

omega-3 (*n-3) production line:
. alpha-linolenic (c18:3n-3)
stearidonic (c18:4n-3)
eicosatetraenoic (c20:4n-3)
EPA, eicosapentaenoic (c20:5n-3)
DPA, docosapentaenoic (c22:5n-3)
DHA, docosahexaenoic (c22:6-3).
-- conversion of αLA to DHA is below 5% .

CLA (Conjugated linoleic acid) production line:
. TVA (11t-C18:1) (potential CLA)
CLA  (9c11t-C18:2)(cis-9, trans-11)(rumenic acid),
-- rate of conversion is 19 .. 30% in humans .
. this cis-9,trans-11 CLA isomer enhances growth
in young rodents, perhaps by improving
feed efficiency (making food more usable).

12.2: the Inuit advantage could be low-carb:

how did Inuit's diet affect their testosterone, or DHT?
. the testosterone is related to prostate by several rates:
production, excretion, inactivation(with bindings),
conversion to DHT (related to
benign prostate enlargement)
or conversion to androsterone .
. a very low carb diet is good at preserving T,
flushing estrogen, and minimizing DHT;
higher carbs may produce more T,
but wide fluctuations in T from meal-time surges
are what cause the body to look for ways to
reduce or excrete T;
and, reduction to {DHT, estrogen} is not good .
. a high carb diet increases the ability of the liver to
reduce testosterone to androsterone .

. low carb'ing increases excretion of T;
--. this is when the carbs are so low
that the diet is ketogenic,
and the kidneys toss T along with ketones .
. a ketogenic diet is where the lack of carbs
and the abundance of dietary fat
is causing the body to generate ketones for brain fuel .
. most people can generate ketones by
keeping their daily carb count under 20g .

high-protein diet lowers T:

. the high protein study (men 23-43 years, 150 pounds)
compared 2 diets having the same amount
of calories and fats,
while (protein, carb) was varying in:
{ (44%, 35%), (10%, 70%) }.

. the high protein diet for 2450 kcals/day was
44% protein (270 g) [(2450 kcals/d times .44) (divide by 4)]
-- 5 x zone level for protein;
35% carb (215 g) [(2450 x.35 /4]
-- 2 x zone level for carb;
21% fat (58 g)[(2450 x .21) /9]
-- . one odd thing about this study was the calories;
was it the low carb that lowered T,
or the fact that it was over-using insulin?

. the high-carb diet for 2450 kcals/d was:
10% protein(62 g) -- near zone level for protein;
70% carb (429 g) -- 4 x zone level for carb;
20% fat(55 g).
--or .91g protein/kg vs the RDA of .8g/kg BW.
. while the T is increasing on this diet
the SHBG (T inactivator) is increasing more than T is .

overfeeding causes lower T levels & high estrogen:

. abdominal fat and high fasting insulin
predicts lower T levels .
. high fasting insulin levels raise the risk of
prostate cancer being lethal .

The steroid precursor DHEA-S
and the metabolite: androsterone glucuronide
were also lowered by abdominal fat,
whereas the androgen metabolite:
androstane-3α,17β-diol glucuronide
was raised by higher levels of
total and regional fat measures
before and after overfeeding .

. it seems that T levels also go down with
small chronic increases in body fat .
Perhaps this is due to an inverse relationship
between T and insulin
and/or the aromatase enzyme.
It is clear that with excessive body fat,
aromatase activity in fat cells increases,
thus more of T is converted into an estrogen,
estradiol (E2) -- [. not good news for prostate .]

Some research has shown insulin to
regulate T in a positive fashion
but the research was injecting insulin
rather than increasing it with glucose
and they found it only worked in the obese,
and only because obesity causes low T .
--- this likely is due to
obesity causing insulin resistance,
and insulin sensitivity being needed for
T production (ie, more insulin is not better
unless your problem is being deaf to less) .
. T activity was increased by
sat'fats and mono'oils but not poly'oils .
. the Inuits had healthy T levels .

okinawan way (soy users):

. the okinawans have a low rate of prostate cancer
(4 in 100,000 per year, 1996)
and their longest living genetic variants
have a particular insulin-pathway gene
that is associated with improved
energy usage and insulin sensitivity;
but as to whether their advantage is genetic or dietary,
they noted that those who move away
(changing both diet and culture)
tend to get modern diseases like most others,
but those who stay home while changing their diet
(still keeping in touch with family & social ways)
tend to stay healthy despite a modern diet
-- this was seen in 1st generation USA hispanics too .

greater stature associated with prostate cancer risk:

. for each 10 cm increase in height,
there is a 6...12 % increase in risk of prostate cancer,
and a 5... 19 % increase in risk of getting
more advanced and/or aggressive cancers .
[. this is likely due to the fact that
stature is strongly associated with the liberal use of
diets that are high in both protein and glycemic index .
. this pattern of dieting is usually carried through life-long,
and increases the severity of an elder's metabolic resistance .]

. the easiest way to reduce estrogenic pollution
is by avoiding animal fat,
because our modern farm animals typically eat
high on the food chain,
getting some of their protein from meat by-products .
. farm products also have the wrong mix of fat;
because, the animals are grain-fed not grass-fed;
moreover, the best animal fat grows in the arctic,
where the bitter cold raises levels of
the rare long-chain omega-3 oils,
which reduce inflammation levels
that are an important contributer to most cancers .
. see the Omega Zone or The Anti-Inflammation Zone
books for the power of omega 3 .

the Mediterranean diet way:

. natives of Italy and Greece who consume a traditional
Mediterranean diet of fish, olive oil,
fresh fruits (esp'ly tomatoes),
and vegetables (including peas, lentils, and beans)
have a lower incidence of prostate cancer .
--
. this reminded me of how the okinawan diet had been
twisted by academics to fit in with usa economics
(politicians feel dependent on grain growers,
so they had us reading about okinawans on whole grains ...
in fact, ok's ate sweet potatoes, and their rice was refined
but it was used only during festivals, like their pork ).
. it was recently news to me
(from an author of the omega diet)
that while greece's mediterranian diet is
not noted for much egg use,
it just so happens
that Greeks raise a very health pastured egg,
using fertile fields for chickens to catch bugs in !
(how do Greeks not get bulldozed by globalization?
they must be trading within a localized bartering system
-- avoids taxes too ...)
. some suggest we follow the Greeks
in replacing our grains with fish;
but what about the estrogenic dioxins and PCB's?
. the japanese did rely on fish a lot,
but that was just practicing a policy of
moderation in all poisons:
a little of fish, and a little of soy .
. and,
was that fish really the healthiest part of their diet?
Dr. Darmadi's paper shows that legumes
are the most significant anti-aging food .
. yams are interesting like legumes
in being a source of soluble fiber
without high glycemic loads -- unlike grains .

11.16: parts of Mediterranean diet providing longevity:

# olive oil -- 9% reduction in risk --
# high consumption of vegetables,
[esp'ly] legumes; [or other sources of
non-sugary soluble fiber, like yams?]
# low consumption of meat and meat products
-- replacing red meat with legumes
(using more peas, beans and lentils)
cut the risk of cancer by 12 % .
# moderate consumption of ethanol .

11.16: irrelevant parts of Mediterranean:

# raising seafood and cereals
--[seafood has mercury, pcbs, dioxins, low-quality protein;
however, if you do use a lot of omeg-6 oils from nuts,
you may want to balance them with distilled fish oil .]
# lowering dairy products
. whey protein isolate has anti-cancer properties,
( it's the casein, as in cheese,
that is dairy's cancer-promoting part;
however, there's also the issue of
GMO-induced inflammation
(depending on your local dictatorship ...)).
. whey can even be a Zone-favorable protein,
at least when pureed with beans to slow its assimilation,
and when protein levels follow the
{Zone diet, RDA} .

legumes protect prostate without being soy:

#
multi-ethnic cohort of 82,483 men excluding soy products:
highest legume use had a 10% lower risk of total prostate cancer
and a 28% lower risk of nonlocalized or high-grade prostate cancer
compared to those who consumed the least amount of non-soy legumes .
#
6-year prospective study of 14,000 Seventh Day Adventist usa men
the highest (beans, lentils, or split peas)
had a significantly lower risk of prostate cancer .
#
58,000 men in the Netherlands:
the highest legumes had a 29% lower risk of prostate cancer
than those with the lowest intakes .
#
1,500+ usa men with prostate cancer
and healthy men matched for age and ethnicity,
the highest legume had a 38% lower risk of prostate cancer
than those with the lowest intakes .

avoid dioxins:

intro/sources:

. dioxins are in most animal fats,
and some cooking ingredients:
( PEG, Polyethylene ...eth(eg, laureth), Polyethylene Glycol,
oxynol, polysorbate 60 and 80 ).

intro/the problem:

. human and animal sperm counts have dropped
50% between 1938 and 1990;
because, 1.4-dioxane is an 'estrogen mimic';
dioxins create 3 generations of damage including
estrogen-linked cancers (breast, prostate, endometrial),
hormonal/fertility disruption, and immune suppression .

intro/Agent orange (dioxins) risk:

. 13,000 Vietnam veterans enrolled in the
VA Northern California Health Care System
were stratified into two groups:
those {exposed, not exposed} to  Agent Orange (1962 - 1971).
. by 2006, twice as many Agent Orangers
were identified with prostate cancer,
and were nearly four times more likely
to present with metastatic disease.
more aggressive cancers:
Agent Oranger's  have a 48% higher risk of
prostate cancer recurrence following surgery,
and when the disease comes back, it seems more aggressive .

intro/dioxins esp'ly estrogenic in the absence of estrogen:

Dioxin induces an estrogen-like, estrogen receptor-dependent
gene expression response in the rodent' uterus.
. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)
is a ubiquitous environmental contaminant
that elicits a broad range of toxicities
in a tissue-, sex-, age-, and species-specific manner,
including alterations in estrogen signaling.
TCDD has a dual nature,
being an antiestrogen in the presence of estrogen,
and an estrogen in its absence:
the antiestrogenic properties may be a contributing factor
in compromised reproduction, breast cancer incidence,
and earlier onset of menopause,
while in children it could have the effect of
an earlier onset of puberty .

meat:

. meat should have no estrogens
if cattle ranchers play by the rules;
but they will still be concentrating xenoestrogens:
fat-soluble PCB's and the very potent dioxins .
. if farm animals are being fed meat-byproducts,
then they sit high on the food chain,
and dioxin concentrations will be heavy .
. many farm feeds use oils containing dioxins
to enhance machine handling of the feed .
. there are many sources of dioxins to watch for:
motor oil, vehicle exhaust, burning garbage,
and burning pvc plastics during house fires;
dioxins settle into their food and water .

fish:

. dioxins are an especially big problem for fish;
always use 3rd-party tested fish oil for your omega-3's
(IFOSprogram.com publishes Dioxin and Furan levels)
. LEF.org adds an effective rosemary freshener
to provide an oil with very low peroxide levels too
(their latest purity testing results are here).

beans & fat-free animal protein

. the healthiest protein for avoiding all cancers
is a zone-favorable combination of
beans for drip-fed carb's and proteins
with another 25g of animal protein*
for optimal protein utilization
. one of the healthiest things about soy, in fact,
is that it happens to be a bean;
however, soy also has a lot of inflammatory
-- inflammatory -- omega-6 oils,
so these either need to be removed
or balanced with a lot of fish oil
and other protein sources, as the Japanese do .
*:
( traditionally humans eat quite a few insects;
eg, for every cup of dried beans in a Zone diet,
you should have 25g of dried insects ).

. when considering dioxin-loaded, grain-fed product
the animal protein should be either fat-free
or low on the food chain
(crickets and grasshoppers are very-low in fat,
but they are known to eat meat by-products).

protein options (vegan-animal, fiber-isolate):

. if you're trying to avoid too much bean fiber,
you might be thinking about non-allergenic
rice or pea protein isolates (organic or non-gmo);
but, keep in mind that food processing
often involves adding a bit of cadmium:
food processors line their equipment with cadmium;
because, cadmium is tougher than zinc plating;
but, cadmium raises prostate risk .
[12.31: also,
the more processed a food is,
the more it tends to get sausaged:
throwing in quality you wouldn't approve of,
if you only had some way of knowing about .
. so until they offer cadmium levels on the label,
beware non-organic, processed foods .
(and make sure your country's Organic code
includes protections from excessive heavy metals,
and even from naturally-occuring poisons, like arsenic
(but praise the selenium!)) ]

. eggs can be a humane way of balancing beans
-- and more appetizing than insects --
but the yolks have multiple risk factors:
#1: arachidonic acid:
. they have inflammatory arachidonic oil,
even more so because hens are fed grains
instead of grass and beans or insects .
#2: dioxins:
. there are strong economic incentives to cut corners
in ways that add dioxins to chicken feed .

. the usual (caged) egg powder is very cheap,
but certified-humane eggs are harder to get:
eggology ships nation-wide, but frozen, not dried;
and there are currently some dead ends online .
. hiddenvilla.com may have liquid in local stores,
but, Eggland's Best Cage Free eggs
have not been seen in Tucson .
. if you can find something to do with the yolks,
then Vitalfarms has humane eggs nationally
(found in Tucson, at least).
. after realizing hens could be fed fish by-products
that could be contaminated with PCBs,
you might want to give those yolks away
to a well-exercised dog or cat .

cadmium -- even the leanest meats have hazards:

. cadmium raises prostate risk .
Cadmium affects the prostate by interfering with
zinc enzymes and cellular energy production.
Displacement of zinc by cadmium results in
impaired protein synthesis
which affects joint smoothness
[thereby increasing inflammation?]

eat low on the food chain:

. cadmium is higher in animals fed organ meats;
it can get in lean meats in high doses
when animals are fed grains grown with
sewer sludge fertilizer or irrigation water .
. cadmium is used for treating poultry parasites .

beware air polution and processed food:

. cars and incinerators emit cadmium .
Fossil fuels, such as coal and oil,
release cadmium fumes into the air;
soil or water may be a dump for  nickel-cadmium batteries
(careful with those inner-city gardens! use hydroponics).

get plenty of essential minerals:

. the body's cadmium detoxifier (binder)
is also binding and wasting zinc, and copper .
. legumes contain relatively high amounts of zinc;
but, prostate risk was reduced by taking a supplement .
. chronic prostate infections are a source of scars
-- a risk factor for cancers --
and, these infections are less likely with more dietary zinc
(legumes have a balance of copper too, for heart protection)
(make sure copper is organically bound
or not mixed with vitamin C).

. calcium competes with cadmium for
intestinal absorption, reducing cadmium intake;
conversely, high doses of cadmium in the blood
can replace zinc and calcium
causing them to be left standing in blood unused,
contributing to kidney stones and calcified arteries .
. iron, too, protects against cadmium absorption,
but excessive iron can cause heart disease .

. selenium prevents cadmium's testicular tumors;
moreover,
selenium deficiency can cause many cancers;
and, such deficiency is quite likely
when eating low on the food chain .
. farmers supplement their animals with sodium selenate;
but, the (expensive) se-msc form is safer at high doses
which may be useful for thyroiditis .
. cadmium binds to selenium;
this could impede selenium's ability to protect you .
. the surest way to get the intended amount
is taking more than you need of a non-toxic form;
and then what is not bound by cadmium or useful
will harmlessly be excreted .
Manganese -- plentiful in seaweed and seafood --
when combined with zinc and copper
exerts a protective effect against low levels of
cadmium toxicity;
moreover,
manganese is essential for production of
an anti-cancer enzyme, superoxide dismutase (MnSOD),
that works by suppressing oxidative damage caused by
the reactive oxygen species, superoxide (O2-),
converting it to peroxide (H2O2) and oxygen .
MnSOD also controls spreading of cancer
by its influence on cell migration
and on adhesion to the extracellular matrix .
. seaweed is a great source of manganese for MnSOD,
and is responsible for the Japanese'
low rate of breast cancer .

. dietary ways of removing cadmium include
methionine(high-quality protein), vitamin C,
and some B-vitamins (inositol and choline);
but B-6 may enhance cadmium absorption
or in some other way increases cadmium toxicity .

cancer.gov's site may need an update on cadmium:

"( The earliest studies of this agent
documented an apparent association [cancer,cadmium];
better-designed studies have failed to note an association ).
--[
. but the only references they give for that
have not proven cadmium doesn't promote cancer:

# Geochemical prospection of cadmium in a
high incidence area of prostate cancer, ...
    Sci Total Environ 116 (3): 243-51, 1992:
"( Anomalous amounts of Cd were found in stream sediments.
This anomaly does not correspond to
human activity, [ie, capitalist mining]
but rather to high regional amounts of
cadmium in the substrate. [natural sources]
Thus, the contents of Cd in soils ...
and the concentration in underground waters
should be considered as a risk factor in this area.)
--[ . this ref proves only that
mining is not the cause of all cadmium cancers .]

# Methodological aspects of the epidemiological association
    between cadmium and cancer in humans.
Lyon, France: International Agency for Research on Cancer, 1992, pp 425-434:
"( main epidemiological evidence of an association
between cadmium exposure and human cancer
comes from studies on occupational groups
such as smelter and nickel-cadmium battery workers.
Lung and prostate are the sites more frequently reported to be
at increased risk of cancer,
but the various epidemiological studies do not enable
any definite conclusion to be reached. )
--[. but the main epidemiological evidence
is not our main evidence that
cadmium causes prostate cancer .
. we have conclusive animal studies .]

if all else fails, the cures are getting better:

12.26: news.health/cancer#prostate/
ART (Advanced Robotic Technique) prostatectomy:
prostate cancer care uses robotics:
ART (Advanced Robotic Technique) prostatectomy
is a term that encompasses the robotic surgical techniques developed by
Dr. Ash Tewari and his team in the course of over
2500 robotic procedures performed over the past six years.
Dr. Tewari continues to perform over 50 prostate cancer surgeries monthly;
The ART™ technique refines the robotic approach
to attain the best prostate cancer treatment results.
The benefits include:
    High rates of early post surgical continence.
    High rates of sexual function recovery
    Avoidance of thermal cauterization to control bleeding during
nerve sparing surgery and thus better preserve nerve health .