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Medical Forum / Diseases and Disorders / Prostate Cancer / September 2006

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A new study: Lifestyle changes may help in prostate cancer

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Juhana Harju - 18 Aug 2006 14:40 GMT
Dietary changes and stress management may attenuate prostate cancer
progression according to a new study.

--------------------------------------------------------------------------------------

Integr Cancer Ther. 2006 Sep;5(3):206-13. Related Articles, Links

Potential attenuation of disease progression in recurrent prostate cancer
with plant-based diet and stress reduction.

Saxe GA, Major JM, Nguyen JY, Freeman KM, Downs TM, Salem CE.

Department of Family and Preventive Medicine, Moores UCSD Cancer Center,
University of California, San Diego, La Jolla, California. gsaxe@ucsd.edu.

A rising level of prostate-specific antigen (PSA), after primary surgery or
radiation therapy, is the hallmark of recurrent prostate cancer and is often
the earliest sign of extraprostatic spread in patients who are otherwise
asymptomatic. While hormonal therapy may slightly extend survival in a
minority of patients, it is not curative and produces side effects including
hot flashes, decreased libido, and loss of bone mass. Alternatively, dietary
modification may offer an important tool for clinical management.
Epidemiologic studies have associated the Western diet not only with
prostate cancer incidence but also with a greater risk of disease
progression after treatment. Conversely, many elements of plant-based diets
have been associated with reduced risk of progression. However, dietary
modification can be stressful and difficult to implement. We therefore
conducted a 6-month pilot clinical trial to investigate whether adoption of
a plant-based diet, reinforced by stress management training, could
attenuate the rate of further PSA rise. Urologists at the University of
California, San Diego, and San Diego Veterans Affairs Medical Centers
recruited 14 patients with recurrent prostate cancer. A pre-post design was
employed in which each patient served as his own control. Rates of PSA rise
were ascertained for each patient for the following periods: from the time
of posttreatment recurrence up to the start of the study (prestudy) and from
the time immediately preceding the intervention (baseline) to the end of the
intervention (0-6 months). There was a significant decrease in the rate of
PSA rise from prestudy to 0 to 6 months (P < .01). Four of 10 evaluable
patients experienced an absolute reduction in their PSA levels over the
entire 6-month study. Nine of 10 had a reduction in their rates of PSA rise
and an improvement of their PSA doubling times. Median PSA doubling time
increased from 11.9 months (prestudy) to 112.3 months (intervention). These
results provide preliminary evidence that adoption of a plant-based diet, in
combination with stress reduction, may attenuate disease progression and
have therapeutic potential for clinical management of recurrent prostate
cancer. PMID: 16880425

http://tinyurl.com/h4b9a

The full study as a pdf-file:

http://ict.sagepub.com/cgi/reprint/5/3/206

Signature

Juhana

"All facts are theory-laden"
- Paul Feyerabend

NICK - 18 Aug 2006 21:14 GMT
Veggie wrote:

> Alternatively, dietary  modification may offer an important tool for clinical management.

  ___may___

> may attenuate disease progression and  have therapeutic potential for clinical
> management of recurrent prostate cancer. PMID: 16880425

___may___

Absolutely no proof one way or the other.
ron - 18 Aug 2006 21:42 GMT
>  Absolutely no proof one way or the other.

Amen!  You wonder how some of this stuff gets published, or why it gets
published.  There are many factors and biochemical steps involved in
PSA production, from the number of prostate cells (cancerous and
benign), to gene expression, protein production, amino acid
availability, etc.  This paper makes no effort to separate the change
in PSA production due to the number of cells present before and after
treatment (the factor we're interested in), versus all of the other
factors / steps that can alter the amount of PSA produced.  As an
extreme example to illustrate my point, suppose these "lifestyle"
changes.severely reduced the prostatic concentration of one of the
amino acids needed to build PSA.  Then the PSA level could go to (near)
zero and remain there.  Great, no PSA and a super-long doubling time,
but unfortuneately the number of prostatic cells has not been
decreased.  I think lifestyle changes may have an effect on PCa growth,
but this paper does nothing to test this approach in a scientifically,
meaningful manner (and let's not even get into the number of subjects
and duration of the study)...Best wishes and good health, ron
Alex - 18 Aug 2006 23:08 GMT
>>  Absolutely no proof one way or the other.
>
[quoted text clipped - 15 lines]
> meaningful manner (and let's not even get into the number of subjects
> and duration of the study)...Best wishes and good health, ron

Perhaps one reason it gets published is that the study is trying to explore
a complex, not-easilyrelationship between cancer and other factors that
affect the body:  food, stress and the way these easily-controlled variables
affect the body's neurological system, which in turn affects body chemistry,
hormones and other mechanisms which impact PCa.
The very first studies of PSA probably were as imprecise in their findings
and questionable in their approach as this study. As the topic was more
fully explored and more accurately understood, the studies got better and
yielded more applicable results.
It is certainly reasonable to be skeptical of this or any other study. But
it is also reasonable to look at the impact of diet and so on, given the
wide variations in the incidences of PCa by region (Japan vs. the U.S., for
example.)
Stress may seem more of a reach. But the fact that a third of patients
typically respond to a placebo in ways that are medically meaurable (changes
in blood pressure, brain center activity, blood chemistry, etc.) indicates
that what we think/feel/believe/expect does impact the way our body
functions.

Alex
Juhana Harju - 19 Aug 2006 07:44 GMT
: But it is also reasonable to look at the impact of diet and so
: on, given the wide variations in the incidences of PCa by region
: (Japan vs. the U.S., for example.)

Yes, the variations in PCa by region are huge. Some of this variation might
be explained by the fact that PCa is more often diagnosed in developed
Western countries but this does not explain the vast difference in incidence
between U.S. and Japan.

http://jncicancerspectrum.oxfordjournals.org/cgi/statContent/cspectfstat;99

--
Juhana

"All facts are theory-laden"
- Paul Feyerabend
JohnHace - 19 Aug 2006 16:31 GMT
> : But it is also reasonable to look at the impact of diet and so
> : on, given the wide variations in the incidences of PCa by region
[quoted text clipped - 6 lines]
>
> http://jncicancerspectrum.oxfordjournals.org/cgi/statContent/cspectfstat;99

I really feel diet is important. It stands to reason that we have an
immune system that is fighting like hell to kill the cancer within us.
If we nourish that system it can only help it do its job.

On the other hand, I always wonder when the Japan vs U.S.numbers are
raised, could it be a racial difference. We know African-American men
are more prone to PC. Are there any comparisons of Japanese-American
men versus Japanese-Japanese (for lack of a better term) men?

The numbers in the above mentioned chart seem to indicate Asians in
Asia do much better than Asians in America. Am I reading it correctly?

John
I.P. Freely - 19 Aug 2006 17:36 GMT
> I really feel diet is important.

If so, why can't medical or mathematical science find a link? They've
repeatedly found solid links between such pairs as smoking and cancer,
obesity and cancer, sat fats and cardiovascular disease (CVD), smoking
and CVD, obesity and diabetes, obesity and CVD, dirt biking and clavicle
fractures, and rednecks (qwitcherbitchin' . . . I is one) and NASCAR,
but they can't find a diet-cancer link.

I.P.
rosbif - 19 Aug 2006 18:20 GMT
>> I really feel diet is important.
>
[quoted text clipped - 6 lines]
>
>I.P.

That could hinge on the problem arising from analysing diet which is
often a vast broad-based mix of variables (foods and trace
ingredients).  Perhaps the optimised PCa-avoidance regime, if there
were such a thing, would be formed of a slant towards a particular
food-type or range of foods rather than a balanced mix of everything.
Much easier to take the hypothesis that a single thing, like smoking,
causes cancer and to test for it.
Steve Kramer - 19 Aug 2006 20:17 GMT
> On the other hand, I always wonder when the Japan vs U.S.numbers are
> raised, could it be a racial difference. We know African-American men
[quoted text clipped - 3 lines]
> The numbers in the above mentioned chart seem to indicate Asians in
> Asia do much better than Asians in America. Am I reading it correctly?

It's an age-old inquiry.  Why some and not others?  Some think it's sun
and/or Vit D.  Some think it's fish and rice vs meat and potatoes.  Some
think it's Omega 3 and Omega 6.  It's fat, free radicals, oxidants, and too
little sex -- or maybe too much.

Nobody knows why.  And since some Asians DO get it and some Blacks DO NOT,
then it hardly matters why.  Should doctors screen Blacks earlier?
Probably.  Should Asians living in Asia screen at all?  Probably.  Should
you stand in the sun all your life?  No.  Should you be distain red meat all
your life?  Not if your sole concern is PCa.

What we do know, finally, is that it involves one of two DNA strands and
there is no apparent distinction between races, localities or healthstyles.
If we can fix those, none will die of PCa.
pc55 - 02 Sep 2006 17:30 GMT
I have been following PC research as it relates to omega-3, green tea,
vitamin D, etc. for two years.  Having had immediate treatment failure,
I am heavily into nutratherapy.  However, there is a 1999 study by
Post, et al, that may shed some light on the reason for varying PC
rates around the world.

Post postulated that the increase in PC rates in men under age 60 was
not entirely due to PSA testing.  He looked at rates in SE Netherlands
& East Anglia (UK) in the pre-PSA era.  He found that the incidence of
PC increased about 50% between 1971 & 1989.  The 5-year survival rate
in Holland actually declined from 65% (1975-9) to 48% (1985-9),
indicating a higher rate of aggressive cancer in this younger
population.

I only have the BJC extract, so I don't know if Post offered an
explanation, but the striking thing about this study is that the older
men would have lived more of their lives in an era when food was
scarce.  The Depression hit Europe very hard; the WWII years were worse
(& the Dutch had the German occupation); the post war years were also
tough - again, more so for the Dutch (also, in England, the last
remnants of rationing were lifted years after the war); the 1950's was
not a decade of affluent for most British/Dutch men.  It is therefore
possible that a restricted diet explains the protective effect.

In other words, the good statistics from elsewhere may be due to
calorie restriction & perhaps to a limited intake of more expensive
foods, such as meat - & not to soy (which is not a large component of
the Asian diet), or any other food component.  [One study has found
that green tea reduces risk only if more than a dozen cups are taken
daily.]

The "protective" foods, such as soy, tea, fish, therefore need to be
viewed in the context of a low-calorie diet, and may be much less
important.

In China, PC rates are increasing as more men become "affluent".  This
translates to a greater intake of pork, but also a shift from lard to
omega-6-rich vegetable oil.  Japanese rates are also on the rise.

While cancer happens at the cellular level & involves pure chance, I
view the process as a form of Russian Roulette (with many chambers)
where some men have more bullets in their revolvers.  Changing the diet
may well reduce risk, but how do you sell the kind of diet that a
Londoner might have had in 1948, let alone a Chinese peasant under Mao?

Curing or restraining active PC requires a more aggressive approach
than simply modifying the diet.  If soy, tea, omega-3, etc. are
therapeutic, the doses may bear little relationship to diets around the
world, & may not be achievable through food alone.  Also, men with
local invasive cancer need to tackle metastasis, which is not an issue
for men who are successfully nipping PC in the bud.

Incidentally, the statistics from African countries reinforce, both,
the damaging effect of Vitamin D deprivation in North America, and the
possible influence of diet in Africa (rates vary tremendously across
the continent (while still being much much lower than that of US
blacks.))

-PC55

> > On the other hand, I always wonder when the Japan vs U.S.numbers are
> > raised, could it be a racial difference. We know African-American men
[quoted text clipped - 18 lines]
> there is no apparent distinction between races, localities or healthstyles.
> If we can fix those, none will die of PCa.
I.P. Freely - 02 Sep 2006 19:16 GMT
I almost deleted the crosspost path, but this topic applies well to both
forums, so with apologies to J, here goes.

To me, the real question is whether any lifestyle changes are worth the
effort to change and require significant sacrifices, given their dubious
benefit in most cases. I love my lifestyle, and although PC may cut it
short, I'll be damned if I'm voluntarily giving it up to the beast in
the very slim chance it may extend my heartbeat by a month or a year out
of a decade. Glassman and I have chosen different paths (diets, for that
OTHER forum who don't know us) to that end, but we're shoulder to
shoulder on the same path in principle.

I.P.
NICK - 04 Sep 2006 23:40 GMT
> Incidentally, the statistics from African countries reinforce, both,
> the damaging effect of Vitamin D deprivation in North America, and the
> possible influence of diet in Africa (rates vary tremendously across
> the continent (while still being much much lower than that of US
> blacks.))

Read somewhere over the weekend that the Vitamin D "deprivation"
is caused by the lack of absorption by the darker skin.

Amd there's a danger that Caucasians may be doing the same with
the "super" SPF values used these days.
pc55 - 05 Sep 2006 18:54 GMT
>  Read somewhere over the weekend that the Vitamin D "deprivation"
>  is caused by the lack of absorption by the darker skin.
>
>  Amd there's a danger that Caucasians may be doing the same with
>  the "super" SPF values used these days.

The advice given on Vitamin D these days is a mess.

Technically, vitamin D is not a vitamin, since the body can manufacture
all it needs, although it rarely does in winter months.  Also, unlike
true vitamins, you can't get what you need from natural food.  To
complicate matters: this "vitamin" is a steroid hormone.

Vitamin D3 (cholecalciferol) is manufactured when the skin is exposed
to sunlight.  The skin contains a form of cholesterol,
7-dehydrocholesterol, which absorbs short-wave ultraviolet radiation
[UVB], to generate cholecalciferol.  (Most sunscreens are good at
blocking UVB).  UVB exposure can lead to sunburn; excessive exposure
may result in skin cancer.

The more damaging long-wave form (UVA) can cause subcutaneous DNA
damage, and ultimately cancer.  Many sunscreens offer inadequate UVA
protection.

Ironically, sunscreens empower prople to spend longer periods in the
sun - avoiding sunburn but incurring DNA damage (the Law of Unintended
Consequences strikes again!)

Sun exposure has not been known to produce toxic amounts of Vitamin D.

Melanin blocks UV rays - the more you have the more you block.
Presumably, Africans in Africa developed a balance of cancer protection
& vitamin D production.  This balance is lost in North America &
Europe.

The fact that ancient people who settled in northern lattitudes evolved
a way of losing melanin in periods of weak sunlight exposure attests to
the survival importance of D.  The fact that they also retained the
ability to produce melanin attests to the survival danger of unfiltered
UV.

Almost all Americans are D-deficient, with African-Americans more so.

Giovannucci, et al, 2006, found that a vitamin D increment of 25 nmol/L
was associated with a reduced risk of total cancer incidence (risk =
0.83), total cancer mortality (risk = 0.71) and digestive system cancer
mortality (risk = 0.55).  The supplementation needed to achieve
protection was estimated to be at least 1500 IU/day.

The recommended daily allowance [RDA] for men is 200 IU, rising to 400
IU after age 50, and 600 IU at age 70.  Many experts believe the RDA to
be too low.  A supplementation level of 1,000 IU is sometimes
suggested.  Men should be aware that sustained very high intakes of
Vitamin D can result in toxicity.  However, this is not at all likely
below a 2,000 IU per day level.  A more realistic safe limit may be
5,000 IU.  [A young, near-naked, white-skinned male will produce 20,000
IUs during the first 20 minutes of summer sun exposure.]

A vitamin D-deficiency connection with prostate cancer, was only
postulated in 1990, by Schwartz, et al.

Cholecalciferol is not biologically active and must be converted to the
active hormonal form.  The first step of the conversion occurs in the
liver, where cholecalciferol is turned into the pro-hormone, calcidiol.
The production of calcidiol is loosely controlled.  Since the
half-life of calcidiol in the blood can be several weeks, this is where
a possibility of massive over-supplementation, over an extended period
of time, might lead to toxic levels.

The second vitamin D conversion step occurs in the kidneys, where
calcidiol becomes the active secosteroid hormone, calcitriol. Levels of
calcitriol circulating in the blood are highly regulated.  Blood levels
of calcitriol are small, compared to calcidiol - perhaps a thousand
times smaller.  In contrast with calcidiol, the half-life of calcitriol
is measured in hours.  Calcitriol is a hormone, because the
parathyroids cease to stimulate its production when calcium blood
levels have been regulated.

The primary purpose of calcitriol is to assist in the absorption of
calcium and phosphate.  Calcitriol levels therefore rise and fall as
the parathyroid glands exert their stabilizing influence.

The epithelial cells of the prostate have vitamin D receptors that have
a particular affinity for calcitriol.  Calcitriol is important in the
development of the prostate and plays an important part in controlling
cell division.  Calcitriol has been shown to be able to regulate the
growth and differentiation of prostate cancer cells and even induce
programmed cell death.

Although the kidneys are the primary source of calcitriol, prostate
cells are also able to convert calcidiol into calcitriol, for local
use.  Since calcitriol levels fluctuate, a sufficient level of
circulating calcidiol is required to ensure that the prostate has the
calcitriol it needs.

The fact that prostate cells can convert calcidiol to calcitriol,
indicates the importance of a steady supply of calcitriol to the
prostate.  As prostate cancer cells evolve, multiple regulatory systems
fail.  Loss of the conversion capability is common.  Maintaining a
healthy level of calcidiol is then, by itself, not sufficient.  At this
stage, it is important that the kidneys produce calcitriol on a regular
basis.  This does not occur when the diet contains excessive levels of
calcium.  This perhaps explains the association between high calcium
intake & advanced disease.

Calcitriol is not available as a supplement.  It is a powerful hormone,
and supplementation would totally disrupt the system that governs
calcium levels in blood and bone.  Although some laboratory studies
have used physiological levels of calcitriol, many others have used
levels that are simply impracticable in the body.  With such doses, the
patient would inevitably experience hypercalciuria or hypercalcemia.
Because of this, there has been much research into producing a
lookalike that lacks the calcemic properties of calcitriol.  {As of
2002, according to Mehta, almost 400 analogs had been synthesized.}

Vitamin D3 is, by definition, an animal product.  Virtually all of the
vitamin D added to food is synthetic vitamin D3, which is
animal-derived.  The vegetarian alternative is vitamin D2, which can be
processed by the body.

Ergocalciferol is the plant form of vitamin D.  The yeast form is
ergosterol, which can be converted to ergocalciferol.  Ergocalciferol
can be converted to calcidiol.

Synthetic Vitamin D3 is is the form that is added to milk and fortified
cereals.  It is generally made by exposing 7-dehydrocholesterol from
animal skins to ultraviolet radiation.  An alternative process starts
with cholesterol, obtainable from the lanolin in sheep's wool, to
create the 7-dehydrocholesterol.  Regardless, the final product is pure
vitamin D3.

A pint of unprocessed milk may contain up to 35 IU of vitamin D.  An
additional 200 IU of synthetic vitamin D is added.  However, milk
intake is associated with an increased risk of advanced PC.  This may
be due to the calcium intake, or to growth factors (bovine IGF-I is
identical to human IGF-I & dairy cattle receiving growth hormones to
boost milk yield, produce more IGF-I.)

{Personal note: I prefer not to take fish oil supplements.  I do take a
good omega-3 supplement, but cod liver oil is not a good way to obtain
high levels of D3.  The synthetic D3 is pure & exactly what the body
produces.  Unfortunately, you have to search for it.  Another problem
with fish oil, apart from the amount of oil you might ingest, is that
vitamin D is coupled with vitamin A.  The latter is an issue for men
with PC.)
Matti Narkia - 20 Aug 2006 02:22 GMT
>> : But it is also reasonable to look at the impact of diet and so
>> : on, given the wide variations in the incidences of PCa by region
[quoted text clipped - 15 lines]
>are more prone to PC. Are there any comparisons of Japanese-American
>men versus Japanese-Japanese (for lack of a better term) men?

Low vitamin D level is one of the risk factors for PCa.
African-American men need about 3-6 times longer to get the same
amount of vitamin D from the sun than light skinned people.

Fish is the most important dietary source of vitamin D. I think that
Japanese eat a lot more fish than Americans. Because of that they
probably also have better omega-6/omega-3 ratio than Americans, and in
general Japanese diet is healthier than typical American diet.
Japanese also consume more soy than Americans, and soy phytoestrogens
are thought to help in preventing PCa.

Japanese-American men perhaps have higher PCa incidence than
Japanese-Japanese, but Japanese-Japanese may typically have more
advanced PCa than Japanese-Americans. Both of these phenomenons may be
partially, but not completely, explained by better PCa detection
system in North America.

References:

Marks LS, Kojima M, Demarzo A, Heber D, Bostwick DG, Qian J, Dorey FJ,
Veltri RW, Mohler JL, Partin AW.
Prostate cancer in native Japanese and Japanese-American men: effects
of dietary differences on prostatic tissue.
Urology. 2004 Oct;64(4):765-71.
PMID: 15491717 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15491717
>

Veltri RW, Park J, Miller MC, Marks L, Kojima M, van Rootselaar C,
Khan MA, Partin AW.
Stromal-epithelial measurements of prostate cancer in native Japanese
and Japanese-American men.
Prostate Cancer Prostatic Dis. 2004;7(3):232-7.
PMID: 15303120 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15303120
>

Fukagai T, Shimada M, Yoshida H, Namiki T, Carlile RG.
Clinical-pathological comparison of clinical prostate cancer between
Japanese Americans in Hawaii and Japanese living in Japan.
Int J Androl. 2000;23 Suppl 2:43-4.
PMID: 10849493 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=10849493
>

Shibata A, Whittemore AS, Imai K, Kolonel LN, Wu AH, John EM, Stamey
TA, Paffenbarger RS.
Serum levels of prostate-specific antigen among Japanese-American and
native Japanese men.
J Natl Cancer Inst. 1997 Nov 19;89(22):1716-20.
PMID: 9390541 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=9390541
>

Shiraishi T, Atsumi S, Yatani R.
Comparative study of prostatic carcinoma bone metastasis among
Japanese in Japan and Japanese Americans and whites in Hawaii.
Adv Exp Med Biol. 1992;324:7-16.
PMID: 1283503 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=R
etrieve&dopt=abstractplus&list_uids=1283503
>

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