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Well, since we've started a thread here on the "General Health and Longevity" forum dedicated to Colon Cancer Prevention, I figured we might as well have one for prostate cancer too, particularly since CR practitioners are overwhelmingly male, and because among US men, prostate cancer is the most common cancer and second leading cancer killer based on CDC Statistics.

 

Plus, there is a new study [1] showing how good my favorite diet (vegan) is for prostate cancer prevention. The study followed ~26,000 men (obviously) who are participating in the famous Adventist Health Study-2, and recruited between 2002 and 2007. It found that men eating a vegan diet were 35% less likely to develop prostate cancer (HR: 0.65; 95% CI: 0.49, 0.85) relative to omnivores during the mean follow-up period of 7.8 year, even after adjusting for age, race, family history of prostate cancer, education, screening for prostate cancer, calorie intake, and BMI. The last is significant because it shows that it wasn't just a result of the vegans being thinner than the omnivores that protected them from prostate cancer.

 

Interestingly, and distinctively from other studies of this population where health benefits relative to omnivores have been observed among all the categories of vegetarians, the benefits observed here for prostate cancer avoidance were entirely restricted to the vegan diet group. Below is the summary table of relative risks for the different diet groups, broken down by race. Looking at data for white men I've highlighted. None of the other vegetarian categories have even a hint of reduction in prostate cancer risk relative to omnivores, not even the pesky pesco-vegetarians ;)xyz - only the vegans:

 

4FKK9EV.png

 

So if you want to avoid the most common form of cancer among men in the US, and the second leading cause of cancer death, go vegan!

 

--Dean

 

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

[1] Am J Clin Nutr. 2015 Nov 11. pii: ajcn106450. [Epub ahead of print]

Are strict vegetarians protected against prostate cancer?

Tantamango-Bartley Y(1), Knutsen SF(2), Knutsen R(2), Jacobsen BK(3), Fan J(2),
Beeson WL(2), Sabate J(2), Hadley D(4), Jaceldo-Siegl K(2), Penniecook J(2),
Herring P(2), Butler T(2), Bennett H(2), Fraser G(2).


BACKGROUND: According to the American Cancer Society, prostate cancer accounts
for ∼27% of all incident cancer cases among men and is the second most common
(noncutaneous) cancer among men. The relation between diet and prostate cancer is
still unclear. Because people do not consume individual foods but rather foods in
combination, the assessment of dietary patterns may offer valuable information
when determining associations between diet and prostate cancer risk.
OBJECTIVE: This study aimed to examine the association between dietary patterns
(nonvegetarian, lacto-ovo-vegetarian, pesco-vegetarian, vegan, and
semi-vegetarian) and prostate cancer incidence among 26,346 male participants of
the Adventist Health Study-2.
DESIGN: In this prospective cohort study, cancer cases were identified by
matching to cancer registries. Cox proportional hazards regression analysis was
performed to estimate HRs by using age as the time variable.
RESULTS: In total, 1079 incident prostate cancer cases were identified. Around 8%
of the study population reported adherence to the vegan diet. Vegan diets showed
a statistically significant protective association with prostate cancer risk (HR:
0.65; 95% CI: 0.49, 0.85). After stratifying by race, the statistically
significant association with a vegan diet remained only for the whites (HR: 0.63;
95% CI: 0.46, 0.86), but the multivariate HR for black vegans showed a similar
but nonsignificant point estimate (HR: 0.69; 95% CI: 0.41, 1.18).
CONCLUSION: Vegan diets may confer a lower risk of prostate cancer. This lower
estimated risk is seen in both white and black vegan subjects, although in the
latter, the CI is wider and includes the null.

© 2016 American Society for Nutrition.

PMID: 26561618

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Thanks Dean.  A great idea for a new thread.  And I especially like the use of a capitalized subject line when the matter involves a specific important topic which is likely to be of lasting interest.

 

HOWEVER (!!!) Take a look at the data here:

 

http://www.worldlifeexpectancy.com/cause-of-death/prostate-cancer/by-country/

 

You will see that in the UK and Australia the prostate cancer mortality rate is about 20 per 100,000.

 

In the US and Canada it is about 15 per 100,000.

 

In China and Japan it is about 3 per 100,000.

 

And in other miscellaneous countries which probably suffer more from poor data collection than from prostate cancer, it is supposedly a lot lower than 3.

 

Also note that in many caribbean countries death rates from prostate cancer are veritably huge.  The country with the highest rate is Guyana where the rate is over 100 per 100,000.

 

Quite obviously there are some conclusions that can be drawn from these data.  One of which is that there are factors causing or preventing death from prostate cancer that are enormously more important than veganism!  (SORRY!)  Another may be that these differences are so huge that, surely, the solution to this disease can be figured out by a very careful search for causes among these numbers.  This in fact is a little project I have been working on from time to time in the past couple of years.  And it is clear the issue is not genetics. 

 

Another point that needs to be made about these data, though, is that if you look at several sources for the death rates of this disease in any given country, different sources claim quite different rates.  The Australians claim the rate in Australia to be 28, whereas these data show it as about 20.  There is a similarly large difference in the case of the US also, and having been in contact with the purveyors at both ends of these seemingly contradictory data, they have been unable to explain it, except to suggest that when you use different techniques to calculate age-adjusted rates you come out with different results.  But these differences in rates are certainly a cause for concern regarding accuracy.  And it is not as if the differences are *all* 30% lower, or *all* 45% higher.  Under some listings different countries appear at the top of the list.

 

I have looked at these data quite carefully recently over several months.  One very curious aspect of these mortality figures seems to be that, in addition to the Caribbean and east Asia as being at extremes, MUSLIM countries also seem to have very little mortality from prostate cancer.  So there are hints galore as to what this disease is about.  And I would like to solve this puzzle!  I will certainly enjoy TRYING to solve it!

 

(But I am also working on some more urgent projects too, so I am not working on this full time.)

 

And I want you to know that I wrote and edited this post standing up.  It seems to be not very difficult.  So easy in fact that it is difficult to believe working standing up could really burn off as much as 350 extra calories daily.

 

Rodney.

 

"The unverified conventional wisdom is almost invariably mistaken."

Edited by nicholson

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Thanks Dean.  A great idea for a new thread.  And I especially like the use of a capitalized subject line when the matter involves a specific important topic which is likely to be of lasting interest.

 

HOWEVER (!!!) Take a look at the data here:

 

http://www.worldlifeexpectancy.com/cause-of-death/prostate-cancer/by-country/

 

...

 

Also note that in many caribbean countries death rates from prostate cancer are veritably huge.  The country with the highest rate is Guyana where the rate is over 100 per 100,000.

 

Quite obviously there are some conclusions that can be drawn from these data.  One of which is that there are factors causing or preventing death from prostate cancer that are enormously more important than veganism!  (SORRY!)  Another may be that these differences are so huge that, surely, the solution to this disease can be figured out by a very careful search for causes among these numbers.  This in fact is a little project I have been working on from time to time in the past couple of years.  And it is clear the issue is not genetics. 

 

...

 

I have looked at these data quite carefully recently over several months.  One very curious aspect of these mortality figures seems to be that, in addition to the Caribbean and east Asia as being at extremes, MUSLIM countries also seem to have very little mortality from prostate cancer.  So there are hints galore as to what this disease is about.  And I would like to solve this puzzle!  I will certainly enjoy TRYING to solve it!

 

(But I am also working on some more urgent projects too, so I am not working on this full time.)

 

Rodney,

 

Yes - prostate cancer risk varies widely between countries. But interpreting this type of epidemiological data correctly is notoriously difficult, and even more difficult is convincing others that your interpretation of the data is correct. Just ask Ancel Keys (Seven Country Study of diet and heart disease link) or T. Colin Campbell (China-Cornell-Oxford project of link between diet and disease among provinces of China). As Michael Rae has pointed out many times in the past, epidemiological evidence is the weakest of evidence there is. Good for making hypotheses, but very difficult to draw conclusions.

 

Here are several hypotheses to explain the variation in prostate cancer rates between countries, as explicated in several videos by Dr. Greger:

 

Milk Consumption & Prostate Cancer

 

Here is a graph from this study [1] from this Greger video, showing countries where men drink a lot of milk have a much higher rate of prostate countries where milk consumption is low. Obviously vegans don't drink milk...

 

WbGIVgM.png

 

 

Soy, Flaxseeds & Isoflavones vs. Prostate Cancer

 

In this video, Dr. Greger suggests some of the variation between in the rate of prostate cancer across different countries (e.g. 120x lower rates in men from Shanghai than men from the US!) may result from differences in the amount of weak estrogens in men's diet from foods such as soy and flaxseeds, citing [2] as epidemiological support for such a hypothesis.

 

 

Tumeric and Prostate Cancer

 

In this video, Dr. Greger investigates the cancer prevention efficacy of turmeric, using several lines of evidence, and looks at several cancer types. In his discussion of prostate cancer rates, he cites [3], which observed that men from India have 23x less prostate cancer than men from the US. Study [3] postulates that the difference may in part be due to the high intake of turmeric in the curry dishes so common in India.

 

 

In short, there is no shortage of potential explanations for the variation in prostate cancer risks across countries. The key is get beyond epidemiological correlations to figure out which hypotheses are actually valid based on more controlled studies, the best of which are obviously randomized, double-blind clinical trials...

 

 

And I want you to know that I wrote and edited this post standing up.  It seems to be not very difficult.  So easy in fact that it is difficult to believe working standing up could really burn off as much as 350 extra calories daily.

 

Very nice! I too find working at a standing desk to be quite easy. But typing and fine mouse control while on a treadmill desk I find much more difficult. In contrast, such detailed work is quite easy while pedalling at my bike desk since I'm seated and therefore much more stable than when walking on a treadmill desk.

 

--Dean

 

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

[1] Int J Cancer. 2002 Mar 10;98(2):262-7.

Incidence and mortality of testicular and prostatic cancers in relation to world

dietary practices.

 

Ganmaa D(1), Li XM, Wang J, Qin LQ, Wang PY, Sato A.

 

Author information:

(1)Department of Environmental Health, Medical University of Yamanashi, Tamaho,

Yamanashi, Japan.

 

The incidence and mortality rates of testicular and prostatic cancers in 42

countries were correlated with the dietary practices in these countries using the

cancer rates (1988-92) provided by the International Agency for Research on

Cancer (IARC) and the food supply data (1961-90) provided by the Food and

Agriculture Organization (FAO). Among the food items we examined, cheese was most

closely correlated with the incidence of testicular cancer at ages 20-39,

followed by animal fats and milk. The correlation coefficient ® was highest (r

= 0.804) when calculated for cheese consumed during the period 1961-65 (maternal

or prepubertal consumption). Stepwise-multiple-regression analysis revealed that

milk + cheese (1961-65) made a significant contribution to the incidence of

testicular cancer (standardized regression coefficient [R] = 0.654). Concerning

prostatic cancer, milk (1961-90) was most closely correlated (r = 0.711) with its

incidence, followed by meat and coffee. Stepwise-multiple-regression analysis

identified milk + cheese as a factor contributing to the incidence of prostatic

cancer (R = 0.525). The food that was most closely correlated with the mortality

rate of prostatic cancer was milk (r = 0.766), followed by coffee, cheese and

animal fats. Stepwise-multiple-regression analysis revealed that milk + cheese

was a factor contributing to mortality from prostatic cancer (R = 0.580). The

results of our study suggest a role of milk and dairy products in the development

and growth of testicular and prostatic cancers. The close correlation between

cheese and testicular cancer and between milk and prostatic cancer suggests that

further mechanistic studies should be undertaken concerning the development of

male genital organ cancers.

 

Copyright 2001 Wiley-Liss, Inc.

 

PMID: 11857417

 

-----------

[2] Prostate. 1997 Jul 1;32(2):122-8.

Lignans and isoflavonoids in plasma and prostatic fluid in men: samples from

Portugal, Hong Kong, and the United Kingdom.

 

Morton MS(1), Chan PS, Cheng C, Blacklock N, Matos-Ferreira A, Abranches-Monteiro

L, Correia R, Lloyd S, Griffiths K.

 

Author information:

(1)Department of Mass Spectrometry, Tenovus Cancer Research Centre, University of

Wales College of Medicine, Cardiff, United Kingdom.

 

BACKGROUND: Chinese men have lower incidences of prostate cancer compared to men

from Europe and North America. Asians consume large quantities of soya, a rich

source of isoflavanoids phyto-oestrogens and have high plasma and urinary levels

of these compounds. The mammalian lignans, enterolactone and enterodiol, are

another group of weak plant oestrogens and are derived from seeds, cereals and

grains. Vegetarians have high plasma and urinary concentrations of lignans.

METHODS: The concentrations lignans and isoflavonic phyto-oestrogens were

determined by gas chromatography-mass spectrometry (GC-MS) in plasma and

prostatic fluid from Portuguese, Chinese and British men consuming their

traditional diets.

RESULTS: In prostatic fluid the mean concentrations of enterolactone were 31, 162

and 20.3 ng/ml for Hong Kong, Portugal and Britain respectively. Very high levels

of enterolactone (> 600 ng/ml) were observed in the prostatic fluid of some of

the men from Portugal. High concentrations of equol (3270 ng/ml) and daidzein

(532 ng/ml) were found in a sample of prostatic fluid from Hong Kong. Higher mean

levels of daidzein were observed in prostatic fluid from Hong Kong at 70 ng/ml,

compared to 4.6 and 11.3 ng/ml in samples from Portugal and Britain respectively.

Mean levels of daidzein were higher in the plasma samples from Hong Kong (31.3

ng/ml) compared to those from Portugal (1.3 ng/ml) and Britain (8.2 ng/ml). In

general, the mean plasma concentrations of enterolactone from the three centres

were similar, at 6.2, 3.9 and 3.9 ng/ml in samples from Hong Kong Portugal and

Britain respectively.

CONCLUSIONS: Higher concentrations of the isoflavanoid phyto-oestrogens, daidzein

and equol, were found in the plasma and prostatic fluid of men from Hong Kong

compared to those from Britain and Portugal. However, the levels of the lignan,

enterolactone, were very much higher in prostatic fluid of Portuguese men.

Isoflavanoids and lignans have many interesting properties and may, in part, be

responsible for lower incidences of prostate cancer in men from Asia and also

some Mediterranean countries. The isoflavanoids from soya, which are present in

high concentrations in the prostatic fluid of Asian men, may be protective

against prostate disease.

 

PMID: 9215400

 

-----------

[3] Nutr Hosp. 2009 May-Jun;24(3):273-81.

Plant-derived health: the effects of turmeric and curcuminoids.

 

Bengmark S(1), Mesa MD, Gil A.

 

Author information:

(1)Institute of Hepatology, University College London Medical School, London.

 

Plants contain numerous polyphenols, which have been shown to reduce inflammation

and hereby to increase resistance to disease. Examples of such polyphenols are

isothiocyanates in cabbage and broccoli, epigallocatechin in green tee, capsaicin

in chili peppers, chalones, rutin and naringenin in apples, resveratrol in red

wine and fresh peanuts and curcumin/curcuminoids in turmeric. Most diseases are

maintained by a sustained discreet but obvious increased systemic inflammation.

Many studies suggest that the effect of treatment can be improved by a

combination of restriction in intake of proinflammatory molecules such as

advanced glycation end products (AGE), advanced lipoperoxidation end products

(ALE), and rich supply of antiinflammatory molecules such as plant polyphenols.

To the polyphenols with a bulk of experimental documentation belong the

curcuminoid family and especially its main ingredient, curcumin. This review

summarizes the present knowledge about these turmericderived ingredients, which

have proven to be strong antioxidants and inhibitors of cyclooxigenase-2 (COX-2),

lipoxygenase (LOX) and nuclear factor kappa B (NF-kappaB) but also AGE. A

plethora of clinical effects are reported in various experimental diseases, but

clinical studies in humans are few. It is suggested that supply of polyphenols

and particularly curcuminoids might be value as complement to pharmaceutical

treatment, but also prebiotic treatment, in conditions proven to be rather

therapy-resistant such as Crohn's, long-stayed patients in intensive care units,

but also in conditions such as cancer, liver cirrhosis, chronic renal disease,

chronic obstructive lung disease, diabetes and Alzheimer's disease.

 

PMID: 19721899

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Thanks Dean.  All good stuff and I agree of course with almost everything you say.

 

I realize that figuring out the causes/preventions of prostate cancer is not a simple task.  If it were, we would already know the answer(s) and all the males at CRsociety would already be implementing the solution.  

 

As for carefully controlled clinical trials, obviously that is not within my capability, and anyway one needs to derive a strong hint from somewhere as to what the explanation might be in order to justify devoting the considerable resources required to run a new trial. 

 

There are many suggested possible partial causes.  Milk you mentioned, and linolenic acid is another according to the Health Professionals Followup Study, I recall.  And not just milk, but calcium intake from vegetables seemed to have been implicated in Singapore where dairy product intake is negligible.  And of course smoking is on the list, as usual, as well as an increase in BMI since age 50 and, curiously, exercise (see below).  In addition, industrialized countries generally have much higher rates than poorer nations - another big hint of some sort.  My point, though, is that these causes do not seem able to account for the truly huge variations in risk from one country/region to another.  This suggests to me that there may be one factor, or perhaps a very small number of combined factors, that can very nearly eliminate the risk of death from this disease, about which we presently have no knowledge despite the fact the epidemiological stuff seems to be positively screaming at us with hints.  

 

You mention curcumin consumption in India as possibly explaining the very low risk of this disease in that country.  But it seems unlikely it could account for much of the low rate in India, as other countries with astonishingly low risk not far away are not renowned for their preference for curry powder with every meal.   Similarly with veganism:  From the data you posted it seems that if someone susceptible to the disease were to convert to veganism, the substantial majority of the risk remains (35% risk reduction still leaves the other 65%).  And while smoking seems to be associated with prostate cancer, the Japanese, noted for very high rates of smoking, have much lower prostate cancer mortality than many countries that smoke much less.  It seems there may be some very specific (mysterious?) factor involved that confers protection against this disease.  And perhaps there is a couple of unrelated, maybe strange dietary habits, factors in the Caribbean, having the opposite effect.  It is a puzzle, and certainly not an easy one, but some people enjoy playing with puzzles even if they find solutions only occasionally!

 

Incidentally, when I mentioned earlier that: "it is not genetics" I was thinking about the low rates in Asia.  But there definitely does appear to be an issue among those with african ancestry.  The higher rates in some of the Caribbean islands and in southern US states, as well as in the middle region of Africa itself, seem quite well correlated with the percentage of the population with african roots.   

 

More ideas for candidates for a possible the key factor causing the astonishingly low rates of death from this disease in Asia would certainly be appreciated.  And a possible muslim connection is tantalizing also.  What do muslims around the world and the non-muslims in south and east Asia have in common?  (I don't think it is curry powder!)

 

Rodney.

 

Regarding exercise: see this from PMID:  9134247   ............

 

"In a multivariate model, age, cigarette smoking (relative risk [RR] = 2.9 for currently smoking 20 or more cigarettes per day compared with never smoking; P trend = 0.009), greater body mass index (BMI) (wt/ht2) (RR = 1.7 for BMI > 27.8 kg/m2 compared with < 23.6; P trend = 0.1), and greater level of physical activity (RR = 1.9 for high activity level cf inactive; P trend = 0.05) were independent predictors of prostate cancer."  Oooops.

==================

"The unverified conventional wisdom is almost invariably mistaken."

Edited by nicholson

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The first post in this thread focused on the advantage of a vegan diet over omnivore or vegetarian diets for prostate cancer risk, but it didn't talk about the mechanism. Here are a couple studies that might explain this vegan advantage.

 

Prostate cancer seems to be one of the cancers most sensitive to elevated IGF-1, per this study [1], but especially this meta-analysis [2] of 42 studies of the relationship between IGF-1 and prostate cancer risk.

 

The pooled odds ratios (95% confidence intervals) per standard deviation increase in peptide were: IGF-I, OR = 1.21 (1.07, 1.36)...

 

Our meta-analysis confirms that raised circulating lGF-I is positively associated with prostate cancer risk.

 

In both men [3] and women [4], a vegan diet is associated with lower IGF-1, relative to omnivorous and vegetarian diets.

 

So whether or not low IGF-1 will extend lifespan in humans may be controversial, it looks pretty clear that it will decrease one's risk of prostate cancer. For men who don't smoke and are therefore at a very low risk of lung cancer, and who eat a healthy diet and are therefore at a low risk of colorectal cancer, prostate cancer is by far the most likely cancer we'll get, and the most likely cancer we'll die from.

 

A vegan diet is one way to reduce IGF-1.

 

--Dean

 

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

[1] J Natl Cancer Inst. 2000 Dec 6;92(23):1910-7.

Plasma insulin-like growth factor-I, insulin-like growth factor-binding proteins,
and prostate cancer risk: a prospective study.

Stattin P(1), Bylund A, Rinaldi S, Biessy C, Déchaud H, Stenman UH, Egevad L,
Riboli E, Hallmans G, Kaaks R.

Author information:
(1)Department of Urology and Andrology, Umeå University Hospital, Sweden.
par.stattin@urologi.umu.se

Comment in
J Natl Cancer Inst. 2001 Apr 18;93(8):649-51.

BACKGROUND: Recent studies have suggested that men with elevated plasma levels of
insulin-like growth factor-I (IGF-I) may have an increased risk of prostate
cancer. Furthermore, IGF-binding proteins (IGFBPs) and insulin can modulate the
activity of IGF-I. In this study, we sought to determine the role of IGF-I as
well as IGFBPs-1, -2, and -3 and insulin as possible etiologic factors for
prostate cancer.
METHODS: We conducted a nested case-control study within the Northern Sweden
Health and Disease Cohort Study. We measured levels of IGF-I, IGFBP-1, IGFBP-2,
IGFBP-3, and insulin in plasma samples from 149 men who had a diagnosis of
prostate cancer between 1 month and 10 years after blood collection and among 298
control men. All statistical tests are two-sided.
RESULTS: Case subjects had statistically significantly higher mean levels of
IGF-I than control subjects (229 ng/mL; 95% confidence interval [CI] = 218-240
ng/mL] versus 214 ng/mL [95% CI = 208-221 ng/mL]; P =.02) and IGFBP-3 (2611 ng/mL
[95% CI = 2518-2704 ng/mL] versus 2498 ng/mL [95% CI = 2437-2560 ng/mL]; P =.04).
Conditional logistic regression analyses showed increases in prostate cancer risk
with rising levels of IGF-I (P:(for trend) =.02) and IGFBP-3 (P(for trend) =.03).
In case subjects younger than 59 years at the time of blood collection, the risk
associated with increased IGF-I was higher (P:(for trend) =.01), whereas the risk
associated with increased IGFBP-3 was lower (P(for trend) =.44) than the
corresponding risks in the full cohort. Prostate cancer risk was not associated
with levels of IGFBP-1, IGFBP-2, or insulin.
CONCLUSIONS: Prostate cancer risk is increased in men with elevated plasma IGF-I.
This association was particularly strong in younger men in this study, suggesting
that circulating IGF-I may be specifically involved in the early pathogenesis of
prostate cancer.

PMID: 11106682

 

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

[2] Int J Cancer. 2009 May 15;124(10):2416-29. doi: 10.1002/ijc.24202.

Circulating insulin-like growth factor peptides and prostate cancer risk: a
systematic review and meta-analysis.

Rowlands MA(1), Gunnell D, Harris R, Vatten LJ, Holly JM, Martin RM.

Author information:
(1)Department of Social Medicine, University of Bristol, Bristol, United Kingdom.
mari-anne.rowlands@bristol.ac.uk

Insulin-like growth factors (IGF-I, IGF-II) and their binding proteins
(IGFBP-1-6) play a key role in cell proliferation, differentiation and apoptosis,
suggesting possible involvement in carcinogenesis. Several epidemiological
studies show associations of IGFs with prostate cancer. We searched the published
literature for all studies relating levels of IGFs or IGFBPs with prostate
cancer. We performed random effects meta-analysis to calculate summary odds
ratios. The number of studies (prostate cancer cases) included in each
meta-analysis were 42 (7,481) IGF-I; 10 (923) IGF-II; 3 (485) IGFBP-1; 5 (577)
IGFBP-2; 29 (6,541) IGFBP-3 and 11 (3,545) IGF-1:IGFBP-3 ratio. The pooled odds
ratios (95% confidence intervals) per standard deviation increase in peptide
were: IGF-I, OR = 1.21 (1.07, 1.36);
IGF-II, OR = 1.17 (0.93, 1.47); IGFBP-1, OR
= 1.21 (0.62, 2.33); IGFBP-2, OR = 1.18 (0.90, 1.54); IGFBP-3, OR = 0.88 (0.79,
0.98); IGFI:IGFBP-3 ratio, OR = 1.10 (0.97, 1.24). For all exposures, there was
substantial heterogeneity (all I(2) > 75%), partly explained by study design: the
magnitude of associations was smaller in prospective vs. retrospective studies,
and for IGFBP-3, the inverse association with prostate cancer risk was seen in
retrospective but not prospective studies. There was weak evidence that
associations of IGF-I and IGFBP-3 with prostate cancer were stronger for advanced
disease. Our meta-analysis confirms that raised circulating lGF-I is positively
associated with prostate cancer risk. Associations between IGFBP-3 and prostate
cancer were inconsistent, and there was little evidence for a role of IGF-II,
IGFBP-1 or IGFBP-2 in prostate cancer risk.

© 2008 Wiley-Liss, Inc.

PMCID: PMC2743036
PMID: 19142965

 

---------

[3] Br J Cancer. 2000 Jul;83(1):95-7.

Hormones and diet: low insulin-like growth factor-I but normal bioavailable
androgens in vegan men.

Allen NE(1), Appleby PN, Davey GK, Key TJ.

Author information:
(1)Cancer Epidemiology Unit, Imperial Cancer Research Fund, Radcliffe Infirmary,
Oxford, UK.

Mean serum insulin-like growth factor-I was 9% lower in 233 vegan men than in 226
meat-eaters and 237 vegetarians (P = 0.002).
Vegans had higher testosterone
levels than vegetarians and meat-eaters, but this was offset by higher sex
hormone binding globulin, and there were no differences between diet groups in
free testosterone, androstanediol glucuronide or luteinizing hormone.

PMCID: PMC2374537
PMID: 10883675

 

-----------

[4] Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1441-8.

The associations of diet with serum insulin-like growth factor I and its main
binding proteins in 292 women meat-eaters, vegetarians, and vegans.

Allen NE(1), Appleby PN, Davey GK, Kaaks R, Rinaldi S, Key TJ.

Author information:
(1)Cancer Research United Kingdom Epidemiology Unit, University of Oxford, Oxford
OX2 6HE, United Kingdom. naomi.allen@cancer.org.uk

The lower rates of some cancers in Asian countries than in Western countries may
be partly because of diet, although the mechanisms are unknown. The aim of this
cross-sectional study was to determine whether a plant-based (vegan) diet is
associated with a lower circulating level of insulin-like growth factor I (IGF-I)
compared with a meat-eating or lacto-ovo-vegetarian diet among 292 British women,
ages 20-70 years. The mean serum IGF-I concentration was 13% lower in 92 vegan
women compared with 99 meat-eaters and 101 vegetarians (P = 0.0006). The mean
concentrations of both serum IGF-binding protein (IGFBP)-1 and IGFBP-2 were
20-40% higher in vegan women compared with meat-eaters and vegetarians (P = 0.005
and P = 0.0008 for IGFBP-1 and IGFBP-2, respectively). There were no significant
differences in IGFBP-3, C-peptide, or sex hormone-binding globulin concentrations
between the diet groups. Intake of protein rich in essential amino acids was
positively associated with serum IGF-I (Pearson partial correlation coefficient;
r = 0.27; P < 0.0001) and explained most of the differences in IGF-I
concentration between the diet groups. These data suggest that a plant-based diet
is associated with lower circulating levels of total IGF-I and higher levels of
IGFBP-1 and IGFBP-2.

PMID: 12433724

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I'm going to resuscitate this interesting thread.

 

Since I seem to be pretty healthy, lean and  statistically at a low mortality risk, my current hobby is to lower those statistical odds and prevent, as much as possible and within reason, the oncoming of the big C (and other known killers of course). Of course Karma (or fate, or bad luck) is at work, so I might die today or tomorrow anyway. The concept that I believe we all share here is: do all we can to decrease the degree of probability of death.

 

Any further opinions since the latest post from Dean?

 

The first study on the adventists has the drawback of little numerosity from vegans (n=15). Whereas other arguments in favour of veganism are pretty reasonable (such as, lower IGF-1).

 

One very interesting recent development is the focus on the mTOR pathway, whose amplification favours cell proliferation, including cancer cells whose 'intelligence', or genetic blueprint, is proliferation at all costs (even the killing of the host organism).

 

PI3K-AKT-mTOR signaling in prostate cancer progression and androgen deprivation therapy resistance

 

Even though the above article is strictly related to the PC form resistant to chemical castration (androgen deprivation) it explains the mechanistic relationships of the signaling cascade.

 

We know well that the PI3-K-AKT signal is triggered by Insulin and IGF1, but PI3-K-AKT is only effective in that it inhibits TSC2, which prevents Rheb to activate.

Rheb activation is one necessary condition to mTOR activation, the other is the Leucine-Amminoacids signal, that is the generic presence of enough leucine and amminoacids in the cell, otherwise mTOR won't bind to the lysosome body, where it can start its activity.

 

From the above, it ensues that any dietary scheme which moderates Insulin-IGF-1 and prevents a potential excess of leucine and amminoacids is likely to prevent amplification of mTOR signaling in the whole body and especially in the prostate.

 

A vegan diet, as well as a vegetarian or omnivore diet which carefully moderates proteins and carbs can serve the purpose. More rigorously, we might even say that we we either moderate strictly carbs OR protein, since mTOR needs both signals to be activated: (Insulin+IGF-1)→PIK3→Akt AND (Leu+Amminos)→RAgGTpases

 

Of course there are other factors which intervene in different dietary schemes. For example, a diversified, well researched vegan diet is more likely to provide protective phytochemicals. Which doesn't rule out other dietary schemes though, providing they are specifically targeted.

 

Another factor may be the competition of phytoestrogens with natural estrogens (the latter apparently a factor which favours PCa) . In such a way soy products, which are usually consumed in high amounts by vegans (and Asian populations) would decrease PCa risk. Phytoestrogens also may exhibit different mechanism decreasing PCa risk and some seem to be more efficient than others.

Phytoestrogens and risk of prostate cancer: a meta-analysis of observational studies

post-7347-0-00547600-1490440725_thumb.jpg

 

The risk of PCa decreased significantly in association with high consumption of genistein (OR 0.83, 95 % CI 0.72–0.95) and daidzein (OR 0.82, 95 % CI 0.70–0.97), but high consumption of lignans (OR 0.87, 95 % CI 0.69–1.09) and isoflavones (OR 0.93, 95 % CI 0.84–1.04) were not significantly associated with the risk of PCa. 
This meta-analysis demonstrated that consumption of phytoestrogens was associated with a reduction in PCa risk of 20 % in men when the highest reported intake was compared with the lowest reported intake. The results of our separate analysis based on the type of phytoestrogens showed inverse associations for the consumption of genistein and daidzein and with increased serum concentrations of enterolactone. However, no significant associations were observed for isoflavone intake, lignan intake, or serum level of genistein, daidzein, and equol.

 

So, like Nicholson suspects, there are apparently many factors governing the prevention of PCa (some already suggested by Dean).

 

At the end, what would be a reasonable dietary scheme which decreases PCa risk? I'm starting a 'shopping list', I'd like other people to add to it or to suggest modifications so that we come up with a best shared strategy. 

 

  • Moderate IGF-1 by methionine moderation
  • Moderate mTOR by  moderation of Leucine and amminos intake
  • Moderate  insulin by moderating carbs and general protein intake
  • Eat curcumin
  • Eat products containint genistein and daidzein

 

 

 

Isoflavones such as genistein and daidzein are found in a number of plants including lupinfava beanssoybeanskudzu, and psoralea being the primary food source,[2][3] also in the medicinal plantsFlemingia vestita[4] and F. macrophylla,[5][6] and coffee.[7] It can also be found in Maackia amurensis cell cultures.[8]
Daidzein and other isoflavone compounds, such as genistein, are present in a number of plants and herbs like Kwao Krua (Pueraria mirifica) and Kudzu (Pueraria lobata). It can also be found in Maackia amurensis cell cultures.[2]
Edited by mccoy

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I already have an update on the list: milk consumption appears to be a strong factor increasing PCa, always in the framework of mTOR overactivation

 

post-7347-0-81023100-1490441349_thumb.jpeg

 

The Impact of Cow's Milk-mediated mTORC1-signaling in the Initiation and Progression of Prostate Cancer

Bodo C Melnik; Swen M John; Pedro Carrera-Bastos; Loren Cordain

Disclosures

Nutr Metab. 2012;9(74) 

 

 

 

Boostering effects of cow's milk consumption on prostate cancer-associated high mTORC1 signaling. Milk and dairy protein consumption increase serum insulin and IGF-1 concentrations and provide abundant leucine for mTORC1 activation. Milk-derived estrogens and androgen-precursors from pregnant* cows augment LAT-mediated leucine uptake promoting further mTORC1 activation. Milk signaling shares common pathways of PCa with hyperactivated mTORC1 signaling due to cancer-associated alterations of Akt, PI3K, PTEN and Rheb (labeled in red).

 

  • Moderate IGF-1 by methionine moderation
  • Moderate mTOR by  moderation of Leucine and amminos intake
  • Moderate  insulin by moderating carbs and general protein intake
  • Moderate milk and dairy products
  • Eat curcumin
  • Eat products containing genistein and daidzein

I myself am in the process of moderating dairy products. Not eliminating them for now, but dairy restriction appears to be a must in this PCa risk-decreasing scheme

Edited by mccoy

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To me the most interesting was the study Dean posted - PMID: 11857417. Here's the full text:

 

http://onlinelibrary.wiley.com/doi/10.1002/ijc.10185/full

 

What I found of particular interest were the following numbers from Table III regarding what food items were most correlated with prostate cancer:

 

1)Fish consumption confers only slightly higher risk of PC

 

2)Fruit consumption confers a HIGHER risk of PC compared to Fish 

 

3)Tomatoes confer very slightly HIGHER risk of incidence of PC than Fish, though are slightly protective against PC *mortality*

 

4)Tea was weakly protective against incidence of PC, but very slightly higher risk of PC mortality

 

5)Coffee very, very strongly boosted the risk of incidence of PC and mortality from PC - actually much higher than even alcohol, comparable to meat (in incidence) but even worse than meat in mortality from PC, worse than even cheese in incidence of PC - only milk was worse than coffee. 

 

So there you have it - a bunch of paradoxes and counter to what we have read before, where coffee and tomatoes were protective against PC - yet here, even fruit is bad. I guess if you're really trying to die of PC, you should drink some coffee with milk.

 

But this is one study. How convincing is it? Here is a metastudy that involved a lot of studies in PC, both incidence and mortality: 

 

PMID: 24584929

 

Coffee consumption and prostate cancer risk: an updated meta-analysis.

 

"CONCLUSIONS:

Our meta-analysis suggests that high (e.g., highest ≥ 4 or 5 cups/day) coffee consumption may not only be associated with a reduced risk of overall prostate cancer, but also inversely associated with fatal and high-grade prostate cancer."

 

So drink up your coffee. Or not.

 

Nutrition science strikes again. And another reason to be cautious about acting on one study and making life changes based on some study or another. Shrug.

Edited by TomBAvoider

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Tombavoider, as we all know, the epidemiological studies may conceal some hidden 'problems' with data.

 

For example, the IJC, 2001 article, figure 1, increase of occurrence of testicular cancer with increased consumption of cheese. That relationship seems invalid to me, simply because the cheese quantities are too little to reflect an average dietary behaviour of the specific populaces. For example, in Italy on the average we eat more, far more than 20 grams of cheese per day.

The French sure eat much more than 30 g/day. Also, with the same amount of 20 g/d, we have Italy with 6/100000 cancer incidence, and Switzerland with 22/100000 cancer incidence. Clearly, there are different subsets in the population plus confounding factors and the average does not explain the incidence, although the correlation coefficient is apparently OK.

 

Do we all believe that cheese is such a powerful carcinogenic that 20 g/day are enough to cause a 22/100000 incidence of cancer, 10 times more than those who consume no cheese? IARC would have probably classified it in the 'known carcinogens' group, together with seasoned meats and red meat.

 

More reasons for my skepticism: 23 grams of Swiss emmental cheese contain 6 g of protein, 0.7 g Leucine and 0.2 g Methionine. No carbs. 4 g of saturated fats. There is no way such amount may upregulate mTOR or contribute significantly to its upregulation. There is no mechanistic explanation, unless Swiss cheese contains cancer enhancing toxins.

 

Maybe the study should have considered number of people eating above a certain threshold of cheese, such as # people eating > 100 g/d

 

I believe that's the real meaning of the correlation, and the bottom line is that, while consumption of modest amounts of cheese is probably harmless, regular consumption of large amounts increases on the average the likelyhood of testicular cancer.

Edited by mccoy

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Though they have an important role and place in nutritional science, observational studies are susceptible to while host of methodological problems including confounding and other biases. This even more than for RCTs repeatability is key as is taking even apparently well conducted studies in the context of the overall scenery of current evidence before making any conclusions.

 

OTOH, I would not dismiss the possibility of adverse effect given the wide array of not only ( and yet scarcely) known and also unknown potential mediating risk factors.

 

Mycotoxins are one interesting known category of potential concern, with increasing interest and attention to the impact in our food supply: http://www.wageningenacademic.com/doi/pdf/10.3920/WMJ2008.x041

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Interesting article mechanism, if memory serves me right mycotoxins may also be present in nuts, grains cocoa and other food especially if organic. Best not to think about it... but most probably the human being  developed some resistance to acute effects.

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Again re. the IJC, 2001 article the correlation coefficient between PCa incidence and fruit consumption is pretty low, about 0.3, which to all practical effects means that the correlation is so weak that it is not significant. To all practical purposes, those data would suggest that there is no correlation (neither harm nor protective effects).

 

In lack of details (type and quantity of fruit ingested) those data are probably meaningless.

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Again re. the IJC, 2001, the data on milk (probably cow's milk in lieu of details)  appear more robust, which average quantities which are realistic.

We also have a mechanistic explanation here, so at this point I would be worried (in a PCa prevention context) to drink more than half glass a day, none to be safe. As a matter fo fact, I'm already using soymilk as a substitute in the very few occasions I drink pure milk, with the double benefit of avoiding potential mTOR amplification and ingesting protective phytoestrogens like genistein. 

Edited by mccoy

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From Al's Pater updating on literature, green tea appears to be possibly preventive aginst PCa but in pretty large doses, > 7 cups a day.

 

Unless we are big tea enthustiasts, this may not be the best preventional strategy. Whereas green tea catechins (extracts?) would turn out to be great preventors. I didn't read the whole article yet.

 

 

 

Green tea and the risk of prostate cancer: A systematic review and meta-analysis.
Guo Y, Zhi F, Chen P, Zhao K, Xiang H, Mao Q, Wang X, Zhang X.
Medicine (Baltimore). 2017 Mar;96(13):e6426. doi: 10.1097/MD.0000000000006426. Review.
PMID: 28353571 Free Article
Abstract
Prostate cancer (PCa) now remains the 2nd most frequently diagnosed cancer. In recent years, chemoprevention for PCa becomes a possible concept. Especially, many phytochemicals rich foods are suggested to lower the risk of cancer. Among these foods, green tea is considered as effective prevention for various cancers. However, clinical trials and previous meta-analyses on the relationship between green tea consumption and the risk of PCa have produced inconsistent outcomes. This study aims to determine the dose-response association of green tea intake with PCa risk and the preventive effect of green tea catechins on PCa risk. Seven observational studies and 3 randomized controlled trials were retrieved from Cochrane Library, PubMed, Sciencedirect Online, and hand searching. The STATA (version 12.0) was applied to analyze the data. The relative risks (RRs) and 95% confidence intervals were pooled by fixed or random effect modeling. Dose-response relations were evaluated with categories of green tea intake. Although there was no statistical significance in the comparison of the highest versus lowest category, there was a trend of reduced incidence of PCa with each 1 cup/day increase of green tea (P = 0.08). Our dose-response meta-analysis further demonstrated that higher green tea consumption was linearly associated with a reduced risk of PCa with more than 7 cups/day. In addition, green tea catechins were effective for preventing PCa with an RR of 0.38 (P = 0.02). In conclusion, our dose-response meta-analysis evaluated the association of green tea intake with PCa risk systematically and quantitatively. And this is the first meta-analysis of green tea catechins consumption and PCa incidence. Our novel data demonstrated that higher green tea consumption was linearly reduced PCa risk with more than 7 cups/day and green tea catechins were effective for preventing PCa. However, further studies are required to substantiate these conclusions.

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I was not aware of this, but it appears that curcumin is a known downregulator of both mTORC1 and mTORC2. Hence its beneficial effect in conditions of cancer and specifically PCa.

 

In a sense, it's even more effective than rapamycin, which inhibits only mTORC1 (unless dosages are massive).

 

PMCID: PMC3638063
NIHMSID: NIHMS432492

Hitting the Golden TORget: Curcumin’s Effects on mTOR Signaling

Edited by mccoy

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Good find, mccoy. However, from everything I understand, curcumin is very poorly absorbed from supplements/diet, so bioavailability is a question when it comes to dosing. You can't assume that just because you take curcumin supps, or consume turmeric, you are getting any appreciable amounts of it into your system.

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Good find, mccoy. However, from everything I understand, curcumin is very poorly absorbed from supplements/diet, so bioavailability is a question when it comes to dosing. You can't assume that just because you take curcumin supps, or consume turmeric, you are getting any appreciable amounts of it into your system.

 

TomB, that seems to be a basic issue in the use of curcumin and , as a matter of fact, in the latest article linked it is cited that presently there is much ongoing research on the pharmacocynetiks of such compound which after ingestion is subject to many metabolic vicissitudes.

 

I guess that for now we must be happy with some semi-empirical methods suggested by literature, like use of piperine and alternate use of high temperature.

I also remember that Dr. Mercola advertises some curcumin supplements with augmented bioavailability.

 

While using curcumin from natural sources like turmeric it would be probably impossible to reach a consistent and precise dosage, due to the known variability in the content of macro and micronutrients of natural foods

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Yesterday, (Easter) I fixed myself a powerful anti-PCa lunch:

 

A steamed 1-pound cauliflower heavily laced with turmeric powder (curcumin), black pepper (piperin), fresh hot chile (capsaicin) and arugula (myrosine), plus arrabiata sauce (lycopene and more capsaicin for good measure). Liberally sprinkled with EVOOO. I must have gone a bit over the board with the anti-PCa ingredients because nausea soon occurred and I felt like I ate a 6-pounds cauliflower.

Next time around I'm going to fix a less powerful mix.

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Interesting interview with dr Rudi Moerck and Dr Mercola on BPH and PCa.

Some of preventive measures advised:

 

Healthy diet

Beta-carotenoids

Lycopene

exercise

Regular sex (once a week or more ideal)

Vitamin D 

 

Saw Palmetto (Serenoa repens) oil supercritically extracted (with CO2) 320 mg together with pumpkin oil seed.

This is the classic formulation of commercial supplementation, which I just bought at the pharmacy, at a reasonable price of 18 US$ per package, which lasts one month. As a preventive measure, according to the pharmacist 4 times a year is all right.

This is told to decrease the DHT blood concentration

 

Edited by mccoy

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Again on coffee, after the metastudy cited by Tombavoider, a recent article listed in Alpater's citations. If caffeine is eally so effective against PCa, then it might be worthy to drink those 4 cups and more per day of Italian espresso. A couple of remarks though:

 

  1. The questionnaire method in this case may be reliable: Italians remember pretty well how many cups of coffee they drink daily and barring CVD problems, they tend to keep it constant
  2. Caffeine is contained in tea and cacao as well. It should be part of the total caffeine, about 160 mg per day
  3. The cancer cell lines have been treated with caffeine (pure caffeine?) so source of caffeine should not be relevant.
  4. What happens if we are already taking many other cancer reducing compounds like curcumin, lycopene, sulforaphane, catechines?
  5. Is the anti-PCa property of green tea related to catechins or caffeine or both (but cagffeine killed the cancer lines in the molisani cohort)?
  6. Any negative effects of caffeine consumption which may counteract the benefits?
Reduction by coffee consumption of prostate cancer risk: Evidence from the Moli-sani cohort and cellular models.
Pounis G, Tabolacci C, Costanzo S, Cordella M, Bonaccio M, Rago L, D'Arcangelo D, Filippo Di Castelnuovo A, de Gaetano G, Donati MB, Iacoviello L, Facchiano F; Moli-sani study investigators..
Int J Cancer. 2017 Apr 24. doi: 10.1002/ijc.30720. [Epub ahead of print]
PMID: 28436066
Abstract
Meta-analytic data on the effect of coffee in prostate cancer risk are controversial. Caffeine as a bioactive compound of coffee has not yet been studied in deep in vitro. Our study aimed at evaluating in a population cohort the effect of Italian-style coffee consumption on prostate cancer risk and at investigating in vitro the potential antiproliferative and antimetastatic activity of caffeine on prostate cancer cell lines. 6,989 men of the Moli-sani cohort aged ≥50 years were followed for a mean of 4.24 ± 1.35 years and 100 new prostate cancer cases were identified. The European Prospective Investigation into Cancer and Nutrition-Food Frequency Questionnaire was used for the dietary assessment and the evaluation of Italian-style coffee consumption. Two human prostate cancer cell lines, PC-3 and DU145, were tested with increasing concentrations of caffeine, and their proliferative/metastatic features were evaluated. The newly diagnosed prostate cancer participants presented lower coffee consumption (60.1 ± 51.3 g/day) compared to the disease-free population (74.0 ± 51.7 g/day) (p < 0.05). Multiadjusted analysis showed that the subjects at highest consumption (>3 cups/day) had 53% lower prostate cancer risk as compared to participants at the lowest consumption (0-2 cups/day) (p = 0.02). Both human prostate cancer cell lines treated with caffeine showed a significant reduction in their proliferative and metastatic behaviors (p < 0.05). In conclusion, reduction by Italian-style coffee consumption of prostate cancer risk (>3 cups/day) was observed in epidemiological level. Caffeine appeared to exert both antiproliferative and antimetastatic activity on two prostate cancer cell lines, thus providing a cellular confirmation for the cohort study results.
KEYWORDS:
antineoplastic activity; caffeine; coffee; prostate cancer

 

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Flaxseed appears to be another ingredient to add to the shop list of anti Pca ingredients. Source:various references from Dr. Greger's book:how not to die

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https://www.sciencedaily.com/releases/2017/06/170606112750.htm

 

Foods that fight prostrate cancer red grapes, tumeric, and apple peels.

 

According to study, resveratrol is one of the most promising active ingredients. If red wine counts:

 

Resveratrol is found in the skin of red grapes. Malbec has a thick skin and contains much resveratrol. Vine grapes grown in cooler climates have higher resveratrol levels than those from warmer climes (such as California and Spain). The varieties with most resveratrol in the wine include malbec, petite sirah, st. laurent and pinot noir. <http://www.frenchscout.com/polyphenols>

 

No wonder Bourgogne(100% Pinot noir) is one of my favorite.

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