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Associations between Dietary Patterns and Bile Acids-Results from a Cross-Sectional Study in Vegans and Omnivores.
Trefflich, I, Marschall, HU, Giuseppe, RD, Ståhlman, M, Michalsen, A, Lampen, A, Abraham, K, Weikert, C
Nutrients. 2019;12(1)
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Colorectal cancer is associated with higher intakes of meat and lower consumption of fibre. Fibre may alter cholesterol and bile acid production and high bile acids may cause changes in the cells of the colon. Vegan diets high in fibre and low in fat may affect bile acid production and this observational study of 72 people aimed to compare bile acids in the faeces and blood of vegans and omnivores. The results showed that vegans had higher fibre and lower fat intakes, compared to omnivores, and although bile acids in the faeces were lower in vegans, blood levels were higher. Fat intake was associated with increased bile acids in the faeces whereas fibre intake was associated with lower levels. Coffee, fish, margarine, fried potatoes, bread, and processed meat were all associated with increased bile acids in the faeces and muesli was associated with lower levels. It was concluded that high fibre, low-fat intakes characteristic of vegan diets, are associated with lower bile acids in the faeces and this could impact colorectal cancer incidence. This study could be used by healthcare professionals to recommend a vegan diet high in fibre and low in saturated fat to individuals with colorectal cancer or those who are at an increased risk.
Abstract
Bile acids play an active role in fat metabolism and, in high-fat diets, elevated concentrations of fecal bile acids may be related to an increased risk of colorectal cancer. This study investigated concentrations of fecal and serum bile acids in 36 vegans and 36 omnivores. The reduced rank regression was used to identify dietary patterns associated with fecal bile acids. Dietary patterns were derived with secondary and conjugated fecal bile acids as response variables and 53 food groups as predictors. Vegans had higher fiber (p < 0.01) and lower fat (p = 0.0024) intake than omnivores. In serum, primary and glycine-conjugated bile acids were higher in vegans than in omnivores (p ≤ 0.01). All fecal bile acids were significantly lower in vegans compared to omnivores (p < 0.01). Processed meat, fried potatoes, fish, margarine, and coffee contributed most positively, whereas muesli most negatively to a dietary pattern that was directly associated with all fecal bile acids. According to the pattern, fat intake was positively and fiber intake was inversely correlated with bile acids. The findings contribute to the evidence that, in particular, animal products and fat may play a part in higher levels of fecal bile acids.
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The effects of Berberis vulgaris consumption on plasma levels of IGF-1, IGFBPs, PPAR-γ and the expression of angiogenic genes in women with benign breast disease: a randomized controlled clinical trial.
Pirouzpanah, S, Asemani, S, Shayanfar, A, Baradaran, B, Montazeri, V
BMC complementary and alternative medicine. 2019;19(1):324
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Individuals diagnosed with benign breast disease (BBD) are at an increased risk of developing breast cancer. A hormone known as insulin-like growth factor-1 (IGF-1) has been reported to correlate with the development of BBD into breast cancer. Berberis vulgaris (BV) is a herbal plant, which may have anti-cancer properties. Previous studies have reported alterations in proteins involved in tumour growth upon regular consumption, but none have looked at IGF-1 in individuals with BBD. This randomised double-blind trial aimed to study the effects of BV on IGF-1 and other proteins involved in tumour growth in 85 women recently diagnosed with BBD over an 8-week period. The results showed that compliance to BV treatment was high. IGF-1 significantly decreased within both groups. When compared to each other, there was a 16% drop in IGF-1 in the BV group compared to the placebo group. Several proteins and growth factors were also altered by BV treatment in favour of reducing breast cancer risk. The authors concluded that BV juice may reduce the risk of BBD turning into breast cancer. Clinicians could use this study to recommend regular consumption of BV to individuals with BBD as part of a wellness regime to reduce their risk of developing breast cancer.
Abstract
BACKGROUND The present study was designed to investigate the effects of Berberis vulgaris (BV) juice consumption on plasma levels of insulin-like growth factor (IGF-1), IGF-binding proteins (IGFBPs), and the expression of PPAR-γ, VEGF and HIF in women with benign breast disease. METHODS This parallel design randomized, double-blind controlled clinical trial was conducted on 85 eligible patients diagnosed with benign breast disease. They were assigned randomly into either BV juice group (n = 44, BV juice: 480 ml/day) or placebo group (n = 41, BV placebo juice: 480 ml/day) for 8 weeks intervention. Participants, caregivers and those who assessed laboratory analyses were blinded to the assignments. Plasma levels of biomarkers were measured at baseline and after 8 weeks by ELISA. Quantitative real-time PCR was used to measure the fold change in the expression of each interested gene. RESULTS The compliance of participants was 95.2% and 40 available subjects analyzed in each group at last. Relative treatment (RT) effects for BV juice caused 16% fall in IGF-1 concentration and 37% reduction in the ratio of IGF-1/1GFBP1. Absolute treatment effect expressed 111 ng/ml increased mean differences of IGFBP-3 between BV group and placebo. Plasma level of PPAR-γ increased in both groups but it was not significant. Fold changes in the expressions of PPAR-γ, VEGF and HIF showed down-regulation in the intervention group compared to placebos (P < 0.05). CONCLUSIONS The BV juice intervention over 8 weeks was accompanied by acceptable efficacy and decreased plasma IGF-1, and IGF-1/IGFBP-1 ratio partly could be assigned to enhanced IGFBP-1 level in women with BBD. The intervention caused reductions in the expression levels of PPAR, VEGF, and HIF which are remarkable genomic changes to potentially prevent breast tumorigenesis. TRIAL REGISTRATION IRCT2012110511335N2. Registered 10 July 2013 (retrospectively registered).
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The Effect of Nutrition Intervention with Oral Nutritional Supplements on Pancreatic and Bile Duct Cancer Patients Undergoing Chemotherapy.
Kim, SH, Lee, SM, Jeung, HC, Lee, IJ, Park, JS, Song, M, Lee, DK, Lee, SM
Nutrients. 2019;11(5)
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Despite the advantages of chemotherapy, it can cause cancer-related malnutrition leading to both reduced quality of life and reduced survival rate. Oral nutritional supplements (ONSs) provide balanced nutrients, calories, and protein to complement insufficient oral intake, and ONS provision during treatment may improve nutritional status. The aim of this study was to investigate the impact of ONS on nutritional status in patients undergoing chemotherapy for pancreatic and bile duct cancer. Patients were randomly allocated to the ONS group (15) and non-ONS group (19) and dietary intake and body weight were assessed at weeks 1, 2, 4 and 8. Body composition and quality of life was assessed at baseline and week 8. This study found the supply of ONS helped promote health by increasing body fat mass, improving quality of life and decreasing fatigue symptoms in pancreatic and bile duct cancer patients. These results were more pronounced in patients in the first cycle of chemotherapy. Based on these results, the authors conclude ONS may improve nutritional status by increasing fat mass and/or maintaining the body composition of patients undergoing chemotherapy.
Abstract
Chemotherapy may negatively affect nutritional status and quality of life (QOL) in pancreatic cancer patients. Our aim was to investigate the beneficial effects of oral nutrition supplements (ONS) on pancreatic and bile duct cancer patients undergoing chemotherapy. Among patients with progressive pancreatic and bile duct cancer receiving chemotherapy, the ONS group (n = 15) received two packs of ONS daily for 8 weeks while the non-ONS group (n = 19) did not. Anthropometric measures, dietary intake, nutritional status, and quality of life were assessed. ONS significantly increased daily intakes of energy, carbohydrates, proteins, and lipids at 8 weeks compared to the baseline. After 8 weeks, fat mass significantly increased in the ONS group. For patients in their first cycle of chemotherapy, body weight, fat-free mass, skeletal muscle mass, body cell mass, and fat mass increased in the ONS group but decreased in the non-ONS group. Fat mass increased in second or higher cycle only in the ONS group. Patient-generated subjective global assessments (PG-SGA) and fatigue scores in the Quality of Life Questionnaire Core 30 (QLQ-C30) improved in the ONS group. ONS might improve nutritional status by increasing fat mass and/or maintaining the body composition of pancreatic and bile duct cancer patients with chemotherapy, especially those in the first cycle, and alleviate fatigue symptoms.
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Dietary Inflammatory Index, Dietary Non-Enzymatic Antioxidant Capacity, and Colorectal and Breast Cancer Risk (MCC-Spain Study).
Obón-Santacana, M, Romaguera, D, Gracia-Lavedan, E, Molinuevo, A, Molina-Montes, E, Shivappa, N, Hebert, JR, Tardón, A, Castaño-Vinyals, G, Moratalla, F, et al
Nutrients. 2019;11(6)
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This study aims to correlate the risk factors of inflammation and antioxidant capacity in cases of colon and breast cancer, using data from a large Spanish case-controlled study (1852 colon cancer subjects, 1567 breast cancer subjects and a total 4933 controls). The role of diet in colon cancer is widely accepted, however it is more controversial with breast cancer where genetic mutations and other lifestyle factors are cited as primary risk factors. What unites these cancers is the inter-related presence of both inflammation and oxidative stress. The dietary inflammatory index (DII®) and non-enzymatic antioxidant capacity (NEAC) were used to evaluate inflammation and oxidative stress using 30 nutrient parameters and 6 inflammatory blood markers. The results showed that colon cancer subjects typically ate a more pro-inflammatory diet compared to controls, with a higher odds ratio of men to women, and tended to be older, heavier and less physically active. The breast cancer subjects also had higher inflammatory scores versus controls but demographically were younger, premenopausal, frequently with a first-degree family link to breast cancer, and including a higher percentage of smokers. For both cancers, inflammation significantly and statistically increased risk factors. Adding in oxidative stress results showed a statistically higher risk of developing colon cancer whilst in breast cancer subjects the risk was increased but non-statistically valid. They did report that meat-eaters had a relative 9% increased risk of Breast cancer. Overall the study concluded that dietary components of inflammation and oxidative stress increased risk of colon cancer but were not statistically valid for breast cancer.
Abstract
Inflammation and antioxidant capacity have been associated with colorectal and breast cancer. We computed the dietary inflammatory index (DII®), and the total dietary non-enzymatic antioxidant capacity (NEAC) and associated them with colorectal and breast cancer risk in the population-based multi case-control study in Spain (MCC-Spain). We included 1852 colorectal cancer and 1567 breast cancer cases, and 3447 and 1486 population controls, respectively. DII score and NEAC were derived using data from a semi-quantitative validated food frequency questionnaire. Unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI) for energy-adjusted DII (E-DII), and a score combining E-DII and NEAC. E-DII was associated with colorectal cancer risk (OR = 1.93, highest quartile versus lowest, 95%CI:1.60-2.32; p-trend: <0.001); this increase was observed for both colon and rectal cancer. Less pronounced increased risks were observed for breast cancer (OR = 1.22, highest quartile versus lowest, 95%CI:0.99-1.52, p-trend: >0.10). The combined score of high E-DII scores and low antioxidant values were associated with colorectal cancer risk (OR = 1.48, highest quartile versus lowest, 95%CI: 1.26-1.74; p-trend: <0.001), but not breast cancer. This study provides evidence that a pro-inflammatory diet is associated with increased colorectal cancer risk while findings for breast cancer were less consistent.
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Association of Folate and Vitamins Involved in the 1-Carbon Cycle with Polymorphisms in the Methylenetetrahydrofolate Reductase Gene (MTHFR) and Global DNA Methylation in Patients with Colorectal Cancer.
Ferrari, A, Torrezan, GT, Carraro, DM, Aguiar Junior, S
Nutrients. 2019;11(6)
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This 2012 cross-sectional observational study examines the role of epigenetic gene expression and methylation in 189 patients with colorectal adenocarcinoma, including 128 with MTHFR polymorphisms. The mean age was 61 years and there was a 50/50 gender split. The focus nutrients were folate, vitamins B2, B6, B12, choline, betaine, and methionine, all of which are known to be essential nutrients for DNA synthesis and more specifically have a key role in the 1-carbon cycle, and S-adenosylmethionine (SAM). The study is based on prospective data collection from food frequency and clinical evaluation questionnaires, and blood work. There does not appear to have been any control group or blinding of processes (at least not reported in the study). The results showed that serum folate levels were positively correlated with the equivalent total dietary folate intake and global DNA methylation. No significant differences were found between serum folate levels in relation to the different genotypes of MTHFR polymorphisms such as C677T. A weak association was found between the A1298C polymorphism and lower levels of methylation. No significant findings were reported for the vitamins used in the study. The study concludes that folate intake, serum folate levels, global DNA methylation and age were predictors of clinicopathological staging.
Abstract
Folate, vitamin B2, vitamin B6, vitamin B12, choline, and betaine are nutrients involved in the 1-carbon cycle that can alter the levels of DNA methylation and influence genesis and/or tumor progression. Thus, the objective of this study was to evaluate the association of folate and vitamins involved in the 1-carbon cycle and MTHFR polymorphisms in global DNA methylation in patients with colorectal cancer gene. The study included 189 patients with colorectal adenocarcinoma answering a clinical evaluation questionnaire and the Food Frequency Questionnaire (FFQ) validated for patients with colon and rectal cancer. Blood samples were collected for evaluation of MTHFR gene polymorphisms in global DNA methylation in blood and in tumor. The values for serum folate were positively correlated with the equivalent total dietary folate (total DFE) (rho = 0.51, p = 0.03) and global DNA methylation (rho = 0.20, p = 0.03). Individuals aged over 61 years (p = 0.01) in clinicopathological staging III and IV (p = 0.01) and with + heterozygous mutated homozygous genotypes for the MTHFR A1298C gene had higher levels of global DNA methylation (p = 0.04). The association between dietary intake of folate, serum folate, and tumor stage were predictive of global DNA methylation in patients' blood. The levels of serum folate, the dietary folate and the status of DNA methylation can influence clinicopathological staging.
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Effect of ω-3 polyunsaturated fatty acid-supplemented parenteral nutrition on inflammatory and immune function in postoperative patients with gastrointestinal malignancy: A meta-analysis of randomized control trials in China.
Zhao, Y, Wang, C
Medicine. 2018;97(16):e0472
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Omega-3 polyunsaturated fatty acids (PUFAs) can have a beneficial effect on inflammation and immune function. This meta-analysis looked at the effectiveness of omega-3 PUFAs on inflammatory and immune function in patients with stomach or colorectal cancers, following surgery. 16 Chinese randomised controlled trials with over 1000 patients carried out between 2000 and 2017 were included in the analysis. The researchers found that the numbers of immune cells in the omega-3 group were significantly higher than those in the control group. The levels of antibodies in people given omega-3 were significantly higher than those in the control group. Inflammatory markers in the omega-3 group were significantly lower. Those given omega-3 were 64% less likely to experience post-surgical infections. The result of this meta-analysis confirmed that supplementing gastrointestinal cancer patients with omega-3 improves post-surgery indicators of immune function, reduces inflammation, and reduces infections related to surgery. The authors recommend that omega-3 should be added to the nutrition formula given to gastrointestinal cancer patients following surgery.
Abstract
BACKGROUND There are no consensus regarding the efficacy of omega-3polyunsaturated fatty acids (PUFAs) on inflammatory and immune function in postoperative patients with gastrointestinal malignancy. METHODS The literatures published randomized control trials (RCT) were searched in PubMed, Embase, Scopus, Cochrane Library, CNKI, Weipu, and Wanfang Databases. The immune efficacy outcomes of ω-3 polyunsaturated fatty acid-supplemented parenteral nutrition in patients with gastrointestinal malignancy were compared. RESULTS Sixteen RCTs involving 1008 patients (506 in the omega-3 group, 502 in the control group) were enrolled into the analysis. The results of meta-analysis: the cell immunity: The proportions of CD3, CD4, CD4/CD8 in the omega-3 group were significantly higher than those in the control group (CD3: WMD = 4.48; 95% CI, 3.34-5.62; P < .00001; I = 0%; CD4: WMD = 5.55; 95% CI, 4.75-6.34; P < .00001; I = 0%; CD4/CD8: WMD = .28; 95% CI, 0.13-0.44; P = .0004; I = 81%). In the humoral immunity: The levels of IgA, IgM and IgG in the omega-3 group were significantly higher than those in the control group (IgA: WMD = 0.31; 95% CI, 0.25-0.37; P < .00001; I = 0%; IgM: WMD = 0.12; 95% CI, 0.06-1.81; P < .00001; I = 0%; IgG: WMD = 1.19; 95% CI, 0.80-1.58; P < .00001; I = 0%). The count of lymphocyte in the omega-3 group was significantly higher than that in the control group (WMD = 0.22; 95% CI, 0.12-0.33; P < .0001; I = 40%). In the postoperative inflammatory cytokine: The levels of interleukin-6, tumor necrosis factor (TNF)-α and C-reactive protein in the omega-3 group were significantly lower than those in the control group (IL-6: WMD = -3.09; 95% CI, -3.91 to 2.27; P < .00001; I = 45%; TNF-α: WMD = -1.65; 95% CI, -2.05 to 1.25; P < .00001; I = 28%; CRP: WMD = -4.28; 95% CI, -5.26 to 3.30; P < .00001; I = 37%). The rate of postoperative infective complications in the omega-3 group was significantly lower than that in the control group (OR = 0.36; 95% CI, 0.20-0.66; P = .0008; I = 0%). CONCLUSION This meta-kanalysis confirmed that early intervention with Omega -3 fatty acid emulsion in gastrointestinal cancer can not only improve the postoperative indicators of immune function, reduce inflammatory reaction, and improve the postoperative curative effect but also improve the immune suppression induced by conventional PN or tumor. Therefore, postoperative patients with gastrointestinal cancer should add omega-3 unsaturated fatty acids in their PN formula. Further high-quality RCTs are needed to verify its efficacy.
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Fasting blood glucose, glycaemic control and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer.
Murtola, TJ, Vihervuori, VJ, Lahtela, J, Talala, K, Taari, K, Tammela, TL, Auvinen, A
British journal of cancer. 2018;118(9):1248-1254
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Studies have shown that people with diabetes mellitus have lower risk of developing prostate cancer compared with non-diabetics. Glucose metabolism (the process by which simple sugars found in food are processed and used to produce energy) may have an independent role in prostate cancer development and progression. The aim of this study was to investigate the associations between fasting blood glucose and glycaemic control and prostate cancer risk. The study recruited 80,144 men who were randomly assigned either to be screened with PSA at four-year intervals (the screening arm, 31,866 men) or to control arm with no intervention and followed through national registries (48,278 men). Results indicate an association between fasting blood glucose level and elevated prostate cancer risk. This association was more noticeable in the screening arm, and concerned both poorly and well-differentiated cancers. Furthermore, compared to the normoglycemic men, overall prostate cancer risk was elevated in diabetic, but not in pre-diabetic men. Authors conclude that diabetic fasting blood glucose level is associated with elevated prostate cancer risk in a population-based cohort of Finnish men.
Abstract
BACKGROUND Diabetic men have lowered overall risk of prostate cancer (PCa), but the role of hyperglycaemia is unclear. In this cohort study, we estimated PCa risk among men with diabetic fasting blood glucose level. METHODS Participants of the Finnish Randomized Study of Screening for Prostate Cancer (FinRSPC) were linked to laboratory database for information on glucose measurements since 1978. The data were available for 17,860 men. Based on the average yearly level, the men were categorised as normoglycaemic, prediabetic, or diabetic. Median follow-up was 14.7 years. Multivariable-adjusted Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for prostate cancer overall and separately by Gleason grade and metastatic stage. RESULTS In total 1,663 PCa cases were diagnosed. Compared to normoglycaemic men, those men with diabetic blood glucose level had increased risk of PCa (HR 1.52; 95% CI 1.31-1.75). The risk increase was observed for all tumour grades, and persisted for a decade afterwards. Antidiabetic drug use removed the risk association. Limitations include absence of information on lifestyle factors and limited information on BMI. CONCLUSIONS Untreated diabetic fasting blood glucose level may be a prostate cancer risk factor.
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Adipose tissue inflammation in breast cancer survivors: effects of a 16-week combined aerobic and resistance exercise training intervention.
Dieli-Conwright, CM, Parmentier, JH, Sami, N, Lee, K, Spicer, D, Mack, WJ, Sattler, F, Mittelman, SD
Breast cancer research and treatment. 2018;168(1):147-157
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Obese breast cancer patients have double the mortality compared to non-obese patients. This is thought to be mediated by low grade inflammation of the adipose (fat) tissue. The main type of immune cells involved in the process are called adipose tissue macrophages (ATMs), of which there are two types: M1 and M2 ATMs, with the M2 ATMs having a mostly anti-inflammatory effect, whilst the M1 ATMs are more pro-inflammatory and are thought to promote cancer growth and recurrence. This 16-week randomised pilot study assessed whether exercise can positively influence adipose tissue inflammation in breast cancer survivors. Participants were randomised to either an exercise (EX) group, who had three supervised exercise sessions per week with a combination of aerobic and resistance exercise, or a control (CON) group. Outcome measures included body composition, blood biomarkers for systemic inflammation and adipose tissue biopsies which were analysed for tissue inflammatory markers, including M1 and M2 ATMs. The EX group had significant improvements in body weight and composition, as well as in metabolic blood parameters (including those for lipid and glucose metabolism) and inflammatory markers, whilst the CON group experienced a worsening of these parameters. The EX participants also had a decrease in the pro-inflammatory M1 ATMs and an increase in the anti-inflammatory M2 ATMs. The authors state that the results were not only statistically, but also clinically significant. The authors conclude that moderate-to-vigorous intensity resistance and aerobic exercise can improve adipose tissue inflammation in obese breast cancer survivors.
Abstract
PURPOSE Obesity is a leading modifiable contributor to breast cancer mortality due to its association with increased recurrence and decreased overall survival rate. Obesity stimulates cancer progression through chronic, low-grade inflammation in white adipose tissue, leading to accumulation of adipose tissue macrophages (ATMs), in particular, the pro-inflammatory M1 phenotype macrophage. Exercise has been shown to reduce M1 ATMs and increase the more anti-inflammatory M2 ATMs in obese adults. The purpose of this study was to determine whether a 16-week exercise intervention would positively alter ATM phenotype in obese postmenopausal breast cancer survivors. METHODS Twenty obese postmenopausal breast cancer survivors were randomized to a 16-week aerobic and resistance exercise (EX) intervention or delayed intervention control (CON). The EX group participated in 16 weeks of supervised exercise sessions 3 times/week. Participants provided fasting blood, dual-energy X-ray absorptiometry (DXA), and superficial subcutaneous abdominal adipose tissue biopsies at baseline and following the 16-week study period. RESULTS EX participants experienced significant improvements in body composition, cardiometabolic biomarkers, and systemic inflammation (all p < 0.03 vs. CON). Adipose tissue from EX participants showed a significant decrease in ATM M1 (p < 0.001), an increase in ATM M2 (p < 0.001), increased adipose tissue secretion of anti-inflammatory cytokines such as adiponectin, and decreased secretion of the pro-inflammatory cytokines IL-6 and TNF- α (all p < 0.055). CONCLUSIONS A 16-week aerobic and resistance exercise intervention attenuates adipose tissue inflammation in obese postmenopausal breast cancer survivors. Future large randomized trials are warranted to investigate the impact of exercise-induced reductions in adipose tissue inflammation and breast cancer recurrence.
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Presurgical weight loss affects tumour traits and circulating biomarkers in men with prostate cancer.
Demark-Wahnefried, W, Rais-Bahrami, S, Desmond, RA, Gordetsky, JB, Hunter, GR, Yang, ES, Azrad, M, Frugé, AD, Tsuruta, Y, Norian, LA, et al
British journal of cancer. 2017;117(9):1303-1313
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Obesity is a risk factor for 13 different cancers and a recent meta-analysis has shown increased weight to be associated with biochemical recurrence in men with prostate cancer. However, few studies have explored whether presurgical intentional weight loss results in improved prostate cancer outcomes. The aim of this trial was to explore the efficacy of weight loss among overweight and obese men with prostate cancer. Forty participants were randomised to either the presurgical weight loss intervention group or control arm, and changes in weight, body composition, quality of life, tumour biology and biomarkers were recorded. This study found that intentional weight loss caused mixed effects on tumour proliferation and gene expression. Based on these results, the authors recommend that more research is needed before effectively recommending presurgical weight loss among overweight men with prostate cancer.
Abstract
BACKGROUND Obesity is associated with aggressive prostate cancer. To explore whether weight loss favourably affects tumour biology and other outcomes, we undertook a presurgical trial among overweight and obese men with prostate cancer. METHODS This single-blinded, two-arm randomised controlled trial explored outcomes of a presurgical weight loss intervention (WLI) that promoted ∼1 kg per week loss via caloric restriction and increased physical activity (PA). Forty overweight/obese men with clinically confirmed prostate cancer were randomised to the WLI presurgery or to a control arm; changes in weight, body composition, quality-of-life, circulating biomarkers, gene expression, and immunohistochemical markers in tumour and benign prostatic tissue were evaluated. RESULTS The study period averaged 50 days. Mean (s.d.) change scores for the WLI vs control arms were as follows: weight: -4.7 (3.1) kg vs -2.2 (4.4) kg (P=0.0508); caloric intake: -500 (636) vs -159 (600) kcal per day (P=0.0034); PA: +0.9 (3.1) vs +1.7 (4.6) MET-hours per day (NS); vitality: +5.3 (7.l4) vs -1.8 (8.1) (P=0.0491); testosterone: +55.1 (86.0) vs -48.3 (203.7) ng dl-1 (P=0.0418); sex hormone-binding globulin: +14.0 (14.6) vs +1.8 (7.6) nmol l-1 (P=0.0023); and leptin: -2.16 (2.6) vs -0.03 (3.75) (P=0.0355). Follow-up Ki67 was significantly higher in WLI vs control arms; median (interquartile range): 5.0 (2.5,10.0) vs 0.0 (0.0,2.5) (P=0.0061) and several genes were upregulated, for example, CTSL, GSK3B, MED12, and LAMC2. CONCLUSIONS Intentional weight loss shows mixed effects on circulating biomarkers, tumour gene expression, and proliferative markers. More study is needed before recommending weight loss, in particular rapid weight loss, among men with prostate cancer.
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Weight Status and Alcohol Intake Modify the Association between Vitamin D and Breast Cancer Risk.
Deschasaux, M, Souberbielle, JC, Latino-Martel, P, Sutton, A, Charnaux, N, Druesne-Pecollo, N, Galan, P, Hercberg, S, Le Clerc, S, Kesse-Guyot, E, et al
The Journal of nutrition. 2016;146(3):576-85
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Experimental studies suggest that vitamin D may contribute to the prevention of breast cancer. However, population studies have been inconclusive, and it is possible that any relationship is dependent on other factors such as genetics or lifestyle. The objective of this study was to explore associations between blood vitamin D levels and breast cancer risk, along with 2 potential modifiers: body mass index (BMI; in kg/m(2)) and alcohol intake. The nested case-control study involved 233 women with breast cancer and 466 healthy controls. Overall, no association was found between vitamin D levels and breast cancer risk. However, a higher blood vitamin D concentration was associated with a decreased risk of breast cancer for women with a BMI under 22.4, whereas it was associated with an increased risk for women with a BMI 22.4 or over. A blood vitamin D concentration ≥ 10 ng/mL was associated with a decreased risk of breast cancer for women with alcohol intakes ≥ 7.1 g/day, whereas no association was observed for women with alcohol intakes < 7.1g/day. The authors concluded that BMI and alcohol intake modified the association between vitamin D and breast cancer risk. These lifestyle factors could explain the inconclusive results of previous studies.
Abstract
BACKGROUND Mechanistic hypotheses suggest that vitamin D may contribute to the prevention of breast cancer. However, epidemiologic evidence is inconsistent, suggesting a potential effect modification by individual factors. OBJECTIVE Our objective was to perform exploratory analyses on the prospective associations between the plasma 25-hydroxyvitamin D [25(OH)D] concentration, polymorphisms of genes encoding for the vitamin D receptor (VDR) and vitamin D-binding protein (also known as gc-globulin or group-specific component, GC), and breast cancer risk, along with 2 potential modifiers: body mass index (BMI; in kg/m(2)) and alcohol intake. METHODS A nested case-control study was set up in the SUpplémentation en VItamines et Minéraux Anti-oXydants (SU.VI.MAX) cohort (1994-2007), involving 233 women with breast cancer and 466 matched controls (mean ± SD age: 49 ± 6 y). The plasma total 25(OH)D concentration and gene polymorphisms were assessed on samples obtained at baseline. Conditional logistic regression models were computed. RESULTS A higher plasma 25(OH)D concentration was associated with a decreased risk of breast cancer for women with a BMI < the median of 22.4 [OR quartile (Q)4 compared with Q1: 0.46; 95% CI: 0.23, 0.89; P-trend = 0.01, P-interaction = 0.002], whereas it was associated with an increased risk for women with a BMI ≥ the median (OR Q4 compared with Q1: 2.45; 95% CI: 1.13, 5.28; P-trend = 0.02, P-interaction = 0.002). A plasma 25(OH)D concentration ≥ 10 ng/mL was associated with a decreased risk of breast cancer for women with alcohol intakes ≥ the median of 7.1 g/d (OR ≥10 compared with <10 ng/mL: 0.50; 95% CI: 0.26, 0.95; P = 0.03, P-interaction = 0.03). The genetic analyses were consistent with the results observed with plasma 25(OH)D. CONCLUSION In this prospective study, BMI and alcohol intake modified the association between vitamin D [plasma 25(OH)D and vitamin D-related gene polymorphisms] and breast cancer risk. These effect modifications suggest explanations for discrepancies in results of previous studies. This trial was registered at clinicaltrials.gov as NCT00272428.