Markus Vinzent's Blog

Thursday, 27 October 2011

Higher Chances of Surviving Ovarian Cancer through the right Diet: 8 Suggestions

0. The pre-diagnose diet, but also the post-diagnose diet has significant impact on survival rates in cancer, and, as focussed here, on ovarian cancer:
Here one of the latest overviews:
Beyond the role of diet in modifying risk for cancer recurrence, several reports have evaluated diet as a risk factor for mortality. In fact, prediagnosis diet may influence mortality even more than it impacts recurrence of cancer. For example, a 46% reduction in overall mortality (P=0.05) and a 44% reduction in cancer recurrence (P=0.08) was shown in relation to higher vegetable intake among subjects diagnosed with oral cancer. Similarly, a 43% reduction in overall mortality was shown in the Life After Cancer Epidemiology (LACE) study of breast cancer survivors in relation to intake of a prudent, vegetable- and whole-grain–rich diet (hazard ratio=0.57, 95% confidence interval [CI] 0.36 to 0.90). Whereas the Wheat Bran Fiber trial and Polyp Prevention Trial showed no significant reduction in adenoma recurrence with dietary interventions except among those reporting strict adherence to the high-vegetable and -fruit diet of the polyp prevention trial (20). An analysis of prediagnosis diet among colorectal cancer survivors suggested those with the highest Western diet score had a hazard ratio for disease-free survival of 3.25 (95% CI 2.04 to 5.19) and of 2.85 (95% CI 1.75 to 4.63) for recurrence-free survival. These studies reinforce the need to promote a cancer-preventive diet throughout life to improve post-treatment survival.
(Cynthia A. Thomson, David S. Alberts, Diet and Survival after Ovarian Cancer ..., Journal of the American Dietetic Association Volume 110, Issue 3, March 2010, Pages 366-368)
1. Lots of Vegetable, especially from the family Cruciferae (eg, mustards) and the genus Brassica (eg, broccoli, brussels sprouts, cabbage, and cauliflower, but not Chinese cabbage), no salted fish
From the results of this cohort study, it was suggested that high intakes of dried or salted fish and Chinese cabbage were potential risk factors of ovarian cancer death. In contrast, however, a high intake of soy bean curd (tofu) might have preventive effects against the risk.
(JACC Study Group, F. Sakauchi, M.M. Khan, M. Mori, T. Kubo, Y. Fujino, S. Suzuki, S. Tokudome and A. Tamakoshi, Dietary habits and risk of ovarian cancer death in a large-scale cohort study (JACC study) in Japan. Nutr Cancer,  57  (2007), pp. 138–145).
Longer survival was associated with total fruits and vegetables (HR 0.61, 95% CI 0.38 to 0.98, P for trend=0.10) and vegetables separately (HR 0.66, 95% CI 0.43 to 1.01, P for trend <0.05). Subgroup analyses showed only yellow and cruciferous vegetables to significantly favor survival. Conversely, a survival disadvantage was shown for meats, not generally recommended (HR 2.28, 95% CI 1.34 to 3.89, P for trend <0.01), and specifically the red and cured/processed meats subgroups. An increased HR was also observed for the milk (all types) subgroup (HR 2.15, 95% CI 1.20 to 3.84, P for trend <0.05).
(Therese A. Dolecek, Bridget J. McCarthy, Charlotte E. Joslin, Caryn E. Peterson, Seijeoung Kim, Sally A. Freels, Faith G. Davis, Prediagnosis Food Patterns Are Associated with Length of Survival from Epithelial Ovarian Cancer, Journal of the American Dietetic Association Volume 110, Issue 3, March 2010, Pages 369-382 - the most recent and best survey on the topic)

2. Vitamin E
Our data suggest that, by suppressing telomerase activity, Vitamin E may be an important protective agent against ovarian cancer cell growth as well as a potentially effective therapeutic adjuvant.
(Y. Bermudez, S. Ahmadi, N.E. Lowell and P.A. Kruk, Vitamin E suppresses telomerase activity in ovarian cancer cells. Cancer Detect Prev,  31  (2007), pp. 119–128)
How to get Vitamin E: Nuts and nut oils, like almonds and hazelnuts, Green leafy vegetables, like lettuce, spinach, turnip, beet, collard, and dandelion greens, Tomato products, Pumpkin, Sweet potato (0.26 mg/100 g so it corresponds to 5.8 kg of potatoes per day of the recommended intake for adults), Rockfish, Mangoes, Asparagus, Broccoli, Papayas, Avocados
3. Each cup of tee per day (green or black) lowers the risk of ovarian carcinom by 18% das (although don't think that drinking 6 and more cups eliminates the risk):
During an average follow-up of 15.1 years, 301 incident cases of invasive epithelial ovarian cancer were ascertained. Tea consumption was inversely associated with the risk of ovarian cancer after controlling for potential confounders (P for trend, .03). Compared with women who never or seldom (less than monthly) consumed tea, the multivariate hazard ratios for those who consumed less than 1 cup per day, 1 cup per day, and 2 or more cups per day were 0.82 (95% confidence interval [CI], 0.62-1.08), 0.76 (95% CI, 0.56-1.04), and 0.54 (95% CI, 0.31-0.91), respectively. Each additional cup of tea per day was associated with an 18% lower risk of ovarian cancer (multivariate hazard ratio, 0.82; 95% CI, 0.68-0.99).
(S.C. Larsson and A. Wolk, Tea consumption and ovarian cancer risk in a population-based cohort. Arch Intern Med,  165  (2005), pp. 2683–2686)
4. Not too many eggs, but avoid saturated fats:
Among 523,217 women, 2,132 incident epithelial ovarian cancer cases were identified. Study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models, and then pooled using a random effects model. Total fat intake was not associated with ovarian cancer risk (pooled multivariate RR = 1.08, 95% CI 0.86–1.34 comparing ≥45 to 30–<35% of calories). No association was observed for monounsaturated, polyunsaturated, trans-unsaturated, animal and vegetable fat, cholesterol and egg intakes with ovarian cancer risk. A weakly positive, but non-linear association, was observed for saturated fat intake (pooled multivariate RR = 1.29, 95% CI: 1.01–1.66 comparing highest versus lowest decile). Results for histologic subtypes were similar. Overall, fat, cholesterol and egg intakes were not associated with ovarian cancer risk. The positive association for saturated fat intake at very high intakes merits further investigation.
(J.M. Genkinger et al., A pooled analysis of 12 cohort studies of dietary fat, cholesterol, and egg intake and ovarian cancer. Cancer Causes Control,  17  (2006), pp. 273–285)
5. Low-fat milk is ok and a reasonable amount of milk products, but avoid full fat milk:
Eighteen case-control and 3 prospective cohort studies were eligible for inclusion in the meta-analysis. The findings of case-control studies were heterogeneous, and, except for whole milk (RRsummary for highest vs. lowest category = 1.27, 95% confidence interval [CI] = 0.97–1.68), do not provide evidence of positive associations between dairy food and lactose intakes with risk of ovarian cancer. In contrast, the 3 cohort studies are consistent and show significant positive associations between intakes of total dairy foods, low-fat milk, and lactose and risk of ovarian cancer. The RRsummary for a daily increase of 10 g in lactose intake (the approximate amount in 1 glass of milk) was 1.13 (95% CI = 1.05–1.22) for cohort studies. In conclusion, prospective cohort studies, but not case-control studies, support the hypothesis that high intakes of dairy foods and lactose may increase the risk of ovarian cancer.
(S.C. Larsson, N. Orsini and A. Wolk, Milk, milk products, and lactose intake and ovarian cancer risk: A meta-analysis of epidemiological studies. Int J Cancer,  118  (2006), pp. 431–441)
 increased consumption of animal-derived food may have adverse effects on the development of hormone-dependent cancers. Among dietary risk factors, we are most concerned with milk and dairy products, because the milk we drink today is produced from pregnant cows, in which estrogen and progesterone levels are markedly elevated.
(D. Ganmaa and A. Sato, The possible role of female sex hormones in milk from pregnant cows in the development of breast, ovarian and corpus uteri cancers. Med Hypotheses,  65  (2005), pp. 1028–1037)
6. Switch from coffee to tee:
Coffee and caffeine consumption has been associated with ovarian cancer risk in several epidemiological studies. CYP1A2 is a key enzyme in the metabolism of coffee and in the activation of heterocyclic aromatic compounds that may be carcinogenic. Data from a preliminary investigation conducted in Hawaii of 164 epithelial ovarian cancer cases and 194 controls were used to examine the hypothesis that coffee and caffeine intake increases the risk of ovarian cancer and that these relations are modified by the CYP1A2 high-inducibility A/A genotype. A personal interview and blood specimen were collected in the subjects' homes. A significant positive trend (p = 0.02) in the odds ratios (ORs) was found with increasing intake of caffeine but not with tea or soda. Regular coffee drinkers were at significantly increased risk (OR = 1.8, 95% confidence interval, CI = 1.1-2.8) of ovarian cancer compared with women who did not drink regular coffee. Women with any CYP1A2 C allele were at similar risk of ovarian cancer (OR = 1.1, 95% CI = 0.7-1.7) compared with women with the A/A genotype. The associations of caffeine and coffee intake with risk were stronger among women with the A/A genotype than among women with any C allele. Somewhat stronger relations of coffee and caffeine intake to risk were found among women with cruciferous vegetable consumption above the median and among cases with mucinous histology. These preliminary data suggest a modest positive association of caffeine and coffee consumption with the OR for ovarian cancer that may be modified by CYP1A2 genotype and exposures, such as cruciferous vegetable consumption, that influence CYP1A2 expression.
(M.T. Goodman, K.H. Tung, K. McDuffie, L.R. Wilkens and T.A. Donlon, Association of caffeine intake and CYP1A2 genotype with ovarian cancer. Nutr Cancer,  46  (2003), pp. 23–29)

7. Moderate consumption of meat, especially read meat, better rare than well-done:
Despite these associations with meat, existing studies suggest that vegetarians do not have reduced risk of breast, bowel or prostate cancer, but there are no quantitative estimates of amounts of meat consumed by meat eaters in these cohort studies. ... individuals with the fast-acetylating genotype who eat high amounts of meat may be at increased risk of large-bowel cancer. ... the type, amount, and cooking method of meat or protein associated with increased risk are not certain. ... interaction between meat, NSP and vegetable intakes on the risk of cancer has not been studied comprehensively. ... Current Department of Health (1998) recommendations are that meat consumption should not rise, and that consumers at the top end of the distribution should consider a reduction in intakes.
(S.A. Bingham, High-meat diets and cancer risk. Proc Nutr Soc,  58  (1999), pp. 243–248.)
502 controls. The dietary assessment included several questions about usual cooking methods for meats and doneness preference for beef. High intake of red meat was associated with increased risks for both stomach and esophageal cancers. Overall, broiling or frying of beef, chicken or pork was not associated with the risk of these tumors. Barbecuing/grilling, reported as the usual cooking method for a small number of study participants, was associated with an elevated risk of stomach and esophageal cancers. after excluding those who reported usually barbecuing/grilling, a source of both PAHc and HCAs, we evaluated doneness level as a surrogate for HCA exposure. Compared to a preference for rare/medium rare beef, odds ratios were 2.4 for medium, 2.4 for medium well and 3.2 for well done, a significant positive trend. Doneness level was not associated with a significant trend in risk of esophageal cancer.
(M.H. Ward, R. Sinha, E.F. Heineman, N. Rothman, R. Markin, D.D. Weisenburger, P. Correa and S.H. Zahm, Risk of adenocarcinoma of the stomach and esophagus with meat cooking method and doneness preference. Int J Cancer,  71  (1997), pp. 14–19.)
8. Moderate consumption of alcohol is fine, but combine with 'dietary folate' (highest in Cereals, Chicken, Beans):
Alcohol has been hypothesized to promote ovarian carcinogenesis by its potential to increase circulating levels of estrogen and other hormones; through its oxidation byproduct, acetaldehyde, which may act as a cocarcinogen; and by depletion of folate and other nutrients. Case-control and cohort studies have reported conflicting results relating alcohol intake to ovarian cancer risk. We conducted a pooled analysis of the primary data from ten prospective cohort studies. The analysis included 529 638 women among whom 2001 incident epithelial ovarian cases were documented. After study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models, and then were pooled using a random effects model; no associations were observed for intakes of total alcohol (pooled multivariate RR = 1.12, 95% CI 0.86-1.44 comparing ≥ 30 to 0 g day-1 of alcohol) or alcohol from wine, beer or spirits and ovarian cancer risk. The association with alcohol consumption was not modified by oral contraceptive use, hormone replacement therapy, parity, menopausal status, folate intake, body mass index, or smoking. Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. This pooled analysis does not support an association between moderate alcohol intake and ovarian cancer risk. (British Journal of Cancer Volume 94, Issue 5, 13 March 2006, Pages 757-762)
A high dietary folate intake may play a role in reducing the risk of ovarian cancer, especially among women who consume alcohol.
(S.C. Larsson, E. Giovannucci and A. Wolk, Dietary folate intake and incidence of ovarian cancer: The Swedish Mammography Cohort. J Natl Cancer Inst,  96  (2004), pp. 396–402.)
Our findings from one of the largest data sets of ovarian cancer collected to date, as well as the overall epidemiologic evidence, do not support a role of folate and alcohol in ovarian carcinogenesis
(C. Pelucchi, M. Mereghetti, R. Talamini, E. Negri, M. Montella, V. Ramazzotti, S. Franceschi and C. La Vecchia, Dietary folate, alcohol consumption, and risk of ovarian cancer in an Italian case-control study. Cancer Epidemiol Biomarkers Prev,  14  (2005), pp. 2056–2058)


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