| | Mike, I made 2 points, but if an onlooker were only able to read your side of the debate -- then they would come away thinking that no substantial points were made by me (because of your hasty 'wrap-up' of the situation).
Congratulations, Mike, you have now pissed me off. And -- though I'll likely forgive you (and probably very soon, too) -- I'm going to 'punish' you (and any unwary onlookers) -- with a 2000+-word rebuttal.
Perhaps you require evidence for the 2 points I made (so that you can make an informed decision regarding dismissing them). Well, here are my points, along with supportive evidence for them ...
Point #1 -- US medicine is superior
Supportive evidence ...
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Cancer survival rates and GDP expenditure on health: a comparison of England and Wales and the USA, Denmark, Netherlands, Finland, France, Germany, Italy, Spain and Switzerland in the 1990s. Public Health. 2000 Sep;114(5):336-9.
The three lowest proportional GDP health expenditures over the period 1980-1990 were Denmark, England and Wales, and Spain. The USA had the highest proportional GDP expenditure, followed by France, Germany, and The Netherlands. Overall the USA had the best cancer survival rates in the 14 sites reviewed, followed by Switzerland, The Netherlands, and Germany.
The least successful were Spain, England and Wales, and Italy. In respect to the high incidence cancers, colorectal, lung, and female breast cancers, England and Wales survival rates were the poorest of all ten countries, followed by Denmark and Spain.
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This point -- about the superiority of US medicine -- is conjectured (by myself) to now be beyond debate.
Point #2 -- US nutrition is inferior
Supportive evidence ...
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International trends and patterns of prostate cancer incidence and mortality. Int J Cancer. 2000 Jan 1;85(1):60-7.
Large increases in both incidence and mortality rates of prostate cancer were seen for all countries. For incidence, increases were more pronounced in the United States, Canada, Australia, France and the Asian countries, while the increases in medium-risk countries were moderate. Increases in incidence ranged from 25%-114%, 24%-55% and 15%-104% in high-, medium- and low-risk countries, respectively.
Mortality rates rose more rapidly in Asian countries than in high-risk countries. Substantial differences in incidence and mortality across countries were evident, with U.S. blacks having rates that were 50-60 times higher than the rates in Shanghai, China.
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So ... prostate cancer rates (in a US subgroup) 50-60 were times higher? Next question: Is that disparity "nutrition"-mediated (as opposed to "genetic")? Well, let's see ...
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Prostate cancer in native Japanese and Japanese-American men: effects of dietary differences on prostatic tissue. Urology. 2004 Oct;64(4):765-71.
OBJECTIVES: To investigate the relationship between diet and prostate cancer (CaP) among native Japanese (NJ) and second-generation or third-generation Japanese-American (J-A) men--focusing on the effects of animal fat and soy on prostatic tissues.
Nuclear morphometry showed that the chromatin in each of the four groups (normal versus CaP, NJ versus J-A) was different (area under the curve 85% to 94%, P <0.01), despite fundamental genetic homogeneity.
CONCLUSIONS: NJ and J-A men, products of similar genetics but differing environments, were shown to have differences in body composition that could influence CaP evolution.
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So ... diet affects (biomarkers of) prostate cancer susceptibility. Is it just a single diet factor (so that the actual nutritional quality of the diets could be about the same -- but one diet would offer the "protective" factor, and the other not), or are there many dietary factors affecting prostate cancer risk? Well, let's see ...
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Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk. J Natl Cancer Inst. 2006 Feb 15;98(4):245-54.
Among smokers, the age-adjusted rate of advanced prostate cancer was 492 per 100,000 person-years in those who did not take supplemental vitamin E, 153 per 100,000 person-years in those who took more than 400 IU/day of supplemental vitamin E, and 157 per 100,000 person-years in those who took supplemental vitamin E for 10 or more years.
Among men with low dietary beta-carotene intake, the age-adjusted rate of prostate cancer was 1122 per 100,000 person-years in those who did not take supplemental beta-carotene, and 623 per 100,000 person-years in those who took at least 2000 microg/day of supplemental beta-carotene.
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So ... supplementing -- to the Standard American Diet (the SAD diet) -- vitamin E to smokers appears to help. And supplementing beta-carotene to those who don't eat yellow-orange fruits and veggies appears to help. Tally of nutrients influencing prostate cancer risk: 2
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A prospective study of lycopene and tomato product intake and risk of prostate cancer. Cancer Epidemiol Biomarkers Prev. 2006 Jan;15(1):92-8.
Among men with a family history of prostate cancer, risks were decreased in relation to increased consumption of lycopene (P(trend)=0.04) and specific tomato-based foods commonly eaten with fat (spaghetti, P(trend)=0.12; pizza, P(trend)=0.15; lasagna, P(trend)=0.02).
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So ... if you have a family history of prostate cancer, lycopene (from tomatoes) appears to help. Tally of nutrients influencing prostate cancer risk: 3
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Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-6:omega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating Radical Prostatectomy. Neoplasia. 2006 Feb;8(2):112-24.
Evidence indicates that a diet rich in omega (omega)-6 polyunsaturated fatty acids (PUFAs) [e.g., linoleic acid (LA)] increases prostate cancer (PCa) risk, whereas a diet rich in omega-3 decreases risk.
Thus, EPA and DHA (major components of fish oil) could potentially be promising dietary intervention agents in PCa prevention aimed at 15-LO-1 and COX-2 as molecular targets.
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So ... if you eat a lot of omega-6 fatty acids (vegetable oils, corn-fed beef, etc), then you probably need more omega-3s. Tally of nutrients influencing prostate cancer risk: 4
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Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. J Natl Cancer Inst. 2006 Apr 5;98(7):451-9.
BACKGROUND: Vitamin D has potent anticancer properties, especially against digestive-system cancers.
CONCLUSIONS: Low levels of vitamin D may be associated with increased cancer incidence and mortality in men, particularly for digestive-system cancers. The vitamin D supplementation necessary to achieve a 25(OH)D increment of 25 nmol/L may be at least 1500 IU/day.
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So ... if you're black, or if you're not tan year-round -- then you should probably be supplementing vitamin D (see below why you shouldn't rely on milk for your D). Tally of nutrients influencing prostate cancer risk: 5
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Update on prostate cancer chemoprevention. Pharmacotherapy. 2006 Mar;26(3):353-9.
BACKGROUND: Prostate cancer is the most common type of cancer and the second leading cause of cancer-related deaths in American men.
Lycopene (as beta-carotene) and selenium supplementation have been associated with a reduced risk of prostate cancer in nested case-control studies, but only in subgroups of men with low baseline plasma lycopene (or beta-carotene) and selenium levels respectively.
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So .. if you're low in selenium -- then you're at risk for prostate cancer. Tally of nutrients influencing prostate cancer risk: 6
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A prospective study of calcium intake and incident and fatal prostate cancer. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):203-10.
Higher calcium intake was not appreciably associated with total or nonadvanced prostate cancer but was associated with a higher risk of advanced and fatal prostate cancer [for fatal prostate cancer, compared with men whose long-term calcium intake was 500-749 mg/d (excluding supplement use of <5 years); those with intakes of 1,500-1,999 mg/d had a RR, 1.87; 95% CI, 1.17-3.01; and those with > or = 2,000 mg/d had a RR, 2.43; 95% CI, 1.32-4.48; P(trend) = 0.003].
Dietary calcium and supplementary calcium were independently associated with an increased risk. For high-grade prostate cancer (Gleason > or = 7), an association was observed for high versus low calcium intake (RR, 1.89; 95% CI, 1.32-2.71; P(trend) = 0.005), but a nonsignificant, inverse association was observed for organ-confined, low-grade prostate cancer (RR, 0.79; 95% CI, 0.50-1.25; P(trend) = 0.09).
Our findings suggest that calcium intakes exceeding 1,500 mg/d may be associated with a decrease in differentiation in prostate cancer and ultimately with a higher risk of advanced and fatal prostate cancer but not with well-differentiated, organ-confined cancers.
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So ... in places like the US (where we have a National Dairy Council -- and where we fortify things with calcium), you could be getting too much calcium -- and be at risk for advanced and fatal prostate cancer. Tally of nutrients influencing prostate cancer risk: 7
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Comparison of the concentration of trace metals (Ni, Zn, Co, Cu and Se), Fe, vitamins A, C and E, and lipid peroxidation in patients with prostate cancer. Clin Chem Lab Med. 2006;44(2):175-9.
The anticarcinogenic and antioxidant properties of vitamins A, C, E and pro- or antioxidant properties of trace metals have recently attracted increased attention.
Our findings, together with the results of previous animal studies, suggest that the administration of vitamins A, C, and E, and Se and Zn may be beneficial in the prevention and treatment of human prostate cancer.
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So ... we can add vitamins A and C (zinc is a wild-card; trust me on that) to the list. Tally of nutrients influencing prostate cancer risk: 9
And how about broader, whole food, choices?
[Here in the US, we all ...] Got milk? ...
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Milk consumption in relation to incidence of prostate, breast, colon, and rectal cancers: is there an independent effect? Nutr Cancer. 2005;53(1):65-72.
Data on milk consumption for 9 time periods (1964-1994) and incidence rates of prostate, female breast, colon, and rectal cancers, mostly around 1993-1997, in 38 countries were obtained from the Food and Agriculture Organization and World Health Organization, respectively.
Milk consumption was strongly correlated with incidence rates of prostate cancer (r = 0.65-0.69; all P < 0.0001) and breast cancer (r = 0.64-0.74; all P < 0.0001) in all the nine time periods examined.
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Got veggies? ...
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Intakes of selected nutrients, foods, and phytochemicals and prostate cancer risk in western New York. Nutr Cancer. 2005;53(1):33-41.
Compared with men in the lowest quartile of intake, reduced risks were observed for men in the highest quartile of intake of vitamin C (OR = 0.49; 95% CI = 0.33-0.74), beta-carotene (OR = 0.53; 95% CI = 0.36-0.79), alpha-carotene (OR = 0.67; 95% CI = 0.47-0.97), lutein (OR = 0.55; 95% CI = 0.37-0.81), lycopene (OR = 0.62; 95% CI = 0.42-0.92), total lignan precursors (OR = 0.66; 95% CI = 0.47-0.94), quercetin (OR = 0.64; 95% CI = 0.44-0.92), and total vegetables (OR = 0.53; 95% CI = 0.36-0.79), but weak increased risks were observed for snacks and sweets (OR = 1.46; 95% CI = 0.95-2.23).
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Got vegetable oil/vegetable shortening? ...
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Comparisons of prostate cancer mortality rates with dietary practices in the United States. Urol Oncol. 2005 Nov-Dec;23(6):390-8.
The largest positive correlation coefficients were associated with the consumption of: total meat (red meat, poultry and fish) (R = 0.83, T between 0 and 1); added fats and oils (R = 0.83, T = 21); ice cream (R = 0.83, T = 20); margarine (R = 0.81, T = 4); salad/cooking oil (R = 0.82, T between 3 and 4) and; vegetable shortening (R = 0.81, T between 1 and 2) where R is the correlation coefficient and T is the time in years between consumption and mortality.
In conclusion, this study found strong positive correlations between prostate cancer mortality and the consumption of: total meat; added fats and oils, ice cream, salad/cooking oils, margarine, and vegetable shortening.
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Got bacon? ...
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Meat consumption among Black and White men and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):211-6.
No measure of meat consumption was associated with risk of prostate cancer among White men.
Among Black men, total red meat intake (processed plus unprocessed red meat) was associated with higher risk of prostate cancer (RR, 2.0; 95% CI, 1.0-4.2 for highest versus lowest quartile; P(trend) = 0.05); this increase in risk was mainly due to risk associated with consumption of cooked processed meats (sausages, bacon, and hot dogs; RR, 2.7; 95% CI, 1.3-5.3 for highest versus lowest quartile; P(trend) = 0.008).
This study suggests that high consumption of cooked processed meats may contribute to prostate cancer risk among Black men in the United States.
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Got pomegranate? ...
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Prostate cancer prevention through pomegranate fruit. Cell Cycle. 2006 Feb;5(4):371-3. Epub 2006 Feb 15.
In a recent study, we showed that pomegranate fruit extract (PFE), through modulations in the cyclin kinase inhibitor-cyclin-dependent kinase machinery, resulted in inhibition of cell growth followed by apoptosis of highly aggressive human prostate carcinoma PC3 cells.
These events were associated with alterations in the levels of Bax and Bcl-2 shifting the Bax:Bcl-2 ratio in favor of apoptosis. Further, we showed that oral administration of a human acceptable dose of PFE to athymic nude mice implanted with CWR22Rnu1 cells resulted in significant inhibition of tumor growth with concomitant reduction in secretion of prostate-specific antigen (PSA) in the serum.
The outcome of this study could have a direct practical implication and translational relevance to CaP patients, because it suggests that pomegranate consumption may retard CaP progression, which may prolong the survival and quality of life of the patients.
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Got cruciferi? ...
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3,3'-Diindolylmethane downregulates pro-survival pathway in hormone independent prostate cancer. Biochem Biophys Res Commun. 2006 Feb 10;340(2):718-25. Epub 2005 Dec 20.
We have been studying the anticancer properties of compounds present in cruciferous vegetables such as indole-3-carbinol (I3C). Diindolylmethane (DIM) is a dimer of I3C that is formed under acidic conditions and unlike I3C is more stable with higher anti-cancer effects. In the present report, we demonstrate that DIM is a potent anti-proliferative agent compared to I3C in the hormone independent DU 145 CaP cells.
The anti-prostate cancer effect is mediated by the inhibition of the Akt signal transduction pathway as DIM, in sharp contrast to I3C, induces the downregulation of Akt, p-Akt, and PI3 kinase.
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And don't forget to either cook your tomatoes, or have them within a paste or sauce with some fat in it ...
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Diet after diagnosis and the risk of prostate cancer progression, recurrence, and death (United States). Cancer Causes Control. 2006 Mar;17(2):199-208.
RESULTS: Men in the highest versus lowest quartile of post-diagnostic fish consumption had a multivariate hazard ratio (HR) of progression of 0.73 (95% CI 0.52-1.02); the comparable HR for tomato sauce was 0.56 (95% CI 0.38-0.82). We observed inverse linear relationships for fish and tomato sauce and risk of progression (HR = 0.83, p-value = 0.006 and HR = 0.80, p-value = 0.04 for a two serving/week increase of fish and tomato sauce, respectively).
Milk and fresh tomato consumption were associated with small elevations in risk.
CONCLUSIONS: These data suggest that diet after diagnosis may influence the clinical course of prostate cancer, and fish and tomato sauce may offer some protection against disease progression.
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That's what you get for PISSING me off.
;-)
Ed
(Edited by Ed Thompson on 5/06, 10:22pm)
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