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Social support, adherence to Mediterranean diet and physical activity in adults: results from a community-based cross-sectional study.
Laiou, E, Rapti, I, Markozannes, G, Cianferotti, L, Fleig, L, Warner, LM, Ribas, L, Ngo, J, Salvatore, S, Trichopoulou, A, et al
Journal of nutritional science. 2020;:e53
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Abstract
There is a growing recognition that social support can potentially exert consistent or opposing effects in influencing health behaviours. The present paper presents a cross-sectional study, including 2,064 adults from Italy, Spain and Greece, who were participants in a multi-centre randomised controlled trial (C4H study), aiming to examine whether social support is correlated with adherence to a healthy Mediterranean diet and physical activity. Social support data were available for 1,572 participants. The majority of the sample reported emotional support availability (84·5 %), financial support availability (72·6 %) and having one or more close friends (78·2 %). Mediterranean diet adherence was significantly associated with emotional support (P = 0·009) and social network support (P = 0·021). No statistically significant associations were found between participant physical activity and the social support aspects studied. In conclusion, emotional and social network support may be associated with increased adherence to the Mediterranean diet. However, further research is needed to evaluate the role of social support in adherence to healthy Mediterranean diet.
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Psychological mechanisms in a digital intervention to improve physical activity: A multicentre randomized controlled trial.
Schwarzer, R, Warner, L, Fleig, L, Gholami, M, Salvatore, S, Cianferotti, L, Ntzani, E, Roman-Viñas, B, Trichopoulou, A, Brandi, ML
British journal of health psychology. 2018;(2):296-310
Abstract
OBJECTIVES The randomized controlled trial examined factors that might be responsible for individual differences in physical activity change among men and women who participated in a lifestyle intervention. The main purpose of the analyses regarded the role of psychological mechanisms involving motivation, planning, self-monitoring, and habit strength. DESIGN A two-arm digital intervention was conducted in Italy, Spain, and Greece to improve physical activity levels, with follow-ups at 3 and 6 months after baseline assessment. METHODS Participants were 1,564 adults at baseline, n = 638 at 6-month follow-up. Linear mixed models examined the intervention effects, and a two-group longitudinal structural equation model explored which psychological constructs (motivation, planning, self-monitoring, habit strength) were associated with changes in physical activity. RESULTS In addition to an overall increase in self-reported activity, there were interactions between time and sex and between time and experimental groups, and a triple interaction between time, sex, and experimental groups, indicating that men reported an increase in activity independent of groups, whereas women in the active control group did not benefit from the intervention. Planning, self-monitoring, and habit strength mediated sequentially between initial motivation and follow-up physical activity. CONCLUSIONS Although the intervention produced overall improvements in physical activity, the time-by-treatment interaction emerged only for women. The mechanism included a sequence leading from motivation via planning, self-monitoring, and habit strength towards physical activity. Statement of contribution What is already known on this subject? Digital lifestyle interventions can be effective in terms of physical activity performance gains. Men are on average more physically active than women. Long-term adherence rates to digital interventions are usually low. What does this study add? Giving users of an online platform more interactive options did not make a difference. Women gained more than men from adaptive, dynamic online platform content. Individual characteristics (motivation, planning, self-monitoring, habit) were more important than online treatment features.
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DNA methylome analysis identifies accelerated epigenetic ageing associated with postmenopausal breast cancer susceptibility.
Ambatipudi, S, Horvath, S, Perrier, F, Cuenin, C, Hernandez-Vargas, H, Le Calvez-Kelm, F, Durand, G, Byrnes, G, Ferrari, P, Bouaoun, L, et al
European journal of cancer (Oxford, England : 1990). 2017;:299-307
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Abstract
AIM OF THE STUDY A vast majority of human malignancies are associated with ageing, and age is a strong predictor of cancer risk. Recently, DNA methylation-based marker of ageing, known as 'epigenetic clock', has been linked with cancer risk factors. This study aimed to evaluate whether the epigenetic clock is associated with breast cancer risk susceptibility and to identify potential epigenetics-based biomarkers for risk stratification. METHODS Here, we profiled DNA methylation changes in a nested case-control study embedded in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (n = 960) using the Illumina HumanMethylation 450K BeadChip arrays and used the Horvath age estimation method to calculate epigenetic age for these samples. Intrinsic epigenetic age acceleration (IEAA) was estimated as the residuals by regressing epigenetic age on chronological age. RESULTS We observed an association between IEAA and breast cancer risk (OR, 1.04; 95% CI, 1.007-1.076, P = 0.016). One unit increase in IEAA was associated with a 4% increased odds of developing breast cancer (OR, 1.04; 95% CI, 1.007-1.076). Stratified analysis based on menopausal status revealed that IEAA was associated with development of postmenopausal breast cancers (OR, 1.07; 95% CI, 1.020-1.11, P = 0.003). In addition, methylome-wide analyses revealed that a higher mean DNA methylation at cytosine-phosphate-guanine (CpG) islands was associated with increased risk of breast cancer development (OR per 1 SD = 1.20; 95 %CI: 1.03-1.40, P = 0.02) whereas mean methylation levels at non-island CpGs were indistinguishable between cancer cases and controls. CONCLUSION Epigenetic age acceleration and CpG island methylation have a weak, but statistically significant, association with breast cancer susceptibility.
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The Impact of Husbands' Prostate Cancer Diagnosis and Participation in a Behavioral Lifestyle Intervention on Spouses' Lives and Relationships With Their Partners.
Rossen, S, Hansen-Nord, NS, Kayser, L, Borre, M, Borre, M, Larsen, RG, Trichopoulou, A, Boffetta, P, Tjønneland, A, Hansen, RD
Cancer nursing. 2016;(2):E1-9
Abstract
BACKGROUND A prostate cancer diagnosis affects the patient and his spouse. Partners of cancer patients are often the first to respond to the demands related to their husband's illness and thus are likely to be the most supportive individuals available to the patients. It is therefore important to examine how spouses react and handle their husband's prostate cancer diagnosis. OBJECTIVE The aim of this study was to explore how the prostate cancer diagnosis and the participation in their partners' behavioral lifestyle intervention program influenced the spouses' life, their relationship with their partner, and how they handle the situation. METHODS Interviews were recorded with 8 spouses of potential low-risk prostate cancer patients on active surveillance as part of a clinical self-management lifestyle trial. RESULTS We identified 3 phases that the spouses went through: feeling insecure about their situation, coping strategies to deal with these insecurities, and feeling reassured. CONCLUSIONS The framework of a clinical trial should include mobilizing spousal empowerment so that they can take on an active and meaningful role in relation to their husband's disease. The observations here substantiate that the framework of active surveillance in combination with a lifestyle intervention in 1 specific prostate cancer clinical trial can mobilize spousal empowerment. IMPLICATIONS FOR PRACTICE Creating well-designed clinical patient programs that actively involve the spouse appears to promote empowerment (meaning, self-efficacy, positive impact, and self-determination) in spouses. Spousal participation in clinical patient programs can give spouses relief from anxieties while recognizing them as a vital support for their husband.
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Association of CRP genetic variants with blood concentrations of C-reactive protein and colorectal cancer risk.
Nimptsch, K, Aleksandrova, K, Boeing, H, Janke, J, Lee, YA, Jenab, M, Bueno-de-Mesquita, HB, Jansen, EH, Tsilidis, KK, Trichopoulou, A, et al
International journal of cancer. 2015;(5):1181-92
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Abstract
High blood concentrations of C-reactive protein (CRP) have been associated with elevated risk of colorectal cancer in several prospective studies including the European Prospective Investigation into Cancer and Nutrition (EPIC), but it is unknown whether these observations reflect a causal relationship. We aimed to investigate whether CRP genetic variants associated with lifelong higher CRP concentrations translate into higher colorectal cancer risk. We conducted a prospective nested case-control study within EPIC including 727 cases diagnosed between 1992 and 2003 and 727 matched controls selected according to an incidence-density sampling protocol. Baseline CRP concentrations were measured in plasma samples by a high sensitivity assay. Tagging single nucleotide polymorphisms (SNPs) in the CRP gene (rs1205, rs1800947, rs1130864, rs2808630, rs3093077) were identified via HapMap. The causal effect of CRP on colorectal cancer risk was examined in a Mendelian Randomization approach utilizing multiple CRP genetic variants as instrumental variables. The SNPs rs1205, rs1800947, rs1130864 and rs3093077 were significantly associated with CRP concentrations and were incorporated in a CRP allele score which was associated with 13% higher CRP concentrations per allele count (95% confidence interval 8-19%). Using the CRP-score as instrumental variable, genetically twofold higher CRP concentrations were associated with higher risk of colorectal cancer (odds ratio 1.74, 95% confidence interval 1.06-2.85). Similar observations were made using alternative definitions of instrumental variables. Our findings give support to the hypothesis that elevated circulating CRP may play a direct role in the etiology of colorectal cancer.
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Inflammatory and metabolic biomarkers and risk of liver and biliary tract cancer.
Aleksandrova, K, Boeing, H, Nöthlings, U, Jenab, M, Fedirko, V, Kaaks, R, Lukanova, A, Trichopoulou, A, Trichopoulos, D, Boffetta, P, et al
Hepatology (Baltimore, Md.). 2014;(3):858-71
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UNLABELLED Obesity and associated metabolic disorders have been implicated in liver carcinogenesis; however, there are little data on the role of obesity-related biomarkers on liver cancer risk. We studied prospectively the association of inflammatory and metabolic biomarkers with risks of hepatocellular carcinoma (HCC), intrahepatic bile duct (IBD), and gallbladder and biliary tract cancers outside of the liver (GBTC) in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition. Over an average of 7.7 years, 296 participants developed HCC (n=125), GBTC (n=137), or IBD (n=34). Using risk-set sampling, controls were selected in a 2:1 ratio and matched for recruitment center, age, sex, fasting status, and time of blood collection. Baseline serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), C-peptide, total high-molecular-weight (HMW) adiponectin, leptin, fetuin-a, and glutamatdehydrogenase (GLDH) were measured, and incidence rate ratios (IRRs) and 95% confidence intervals (CIs) were estimated using conditional logistic regression. After adjustment for lifestyle factors, diabetes, hepatitis infection, and adiposity measures, higher concentrations of CRP, IL-6, C-peptide, and non-HMW adiponectin were associated with higher risk of HCC (IRR per doubling of concentrations=1.22; 95% CI=1.02-1.46; P=0.03; 1.90; 95% CI=1.30-2.77; P=0.001; 2.25; 95% CI=1.43-3.54; P=0.0005; and 2.09; 95% CI=1.19-3.67; P=0.01, respectively). CRP was associated also with risk of GBTC (IRR=1.22; 95% CI=1.05-1.42; P=0.01). GLDH was associated with risks of HCC (IRR=1.62; 95% CI=1.25-2.11; P=0.0003) and IBD (IRR=10.5; 95% CI=2.20-50.90; P=0.003). The continuous net reclassification index was 0.63 for CRP, IL-6, C-peptide, and non-HMW adiponectin and 0.46 for GLDH, indicating good predictive ability of these biomarkers. CONCLUSION Elevated levels of biomarkers of inflammation and hyperinsulinemia are associated with a higher risk of HCC, independent of obesity and established liver cancer risk factors.
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Serum levels of IGF-I, IGFBP-3 and colorectal cancer risk: results from the EPIC cohort, plus a meta-analysis of prospective studies.
Rinaldi, S, Cleveland, R, Norat, T, Biessy, C, Rohrmann, S, Linseisen, J, Boeing, H, Pischon, T, Panico, S, Agnoli, C, et al
International journal of cancer. 2010;126(7):1702-15
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Plain language summary
Insulin-like growth factor-I (IGF-1) plays an important role in growth and development as a function of available energy and essential nutrients from body reserves and diet. The aim of the study was to examine the relationships of colorectal cancers with serum levels of IGF-I, and with 2 measures of IGF-binding protein (IGFBP)-3. The study also examined whether relative risks associated to IGF-I levels were modified by anthropometric and dietary factors. A meta-analysis was performed where the study results were combined with the results from previously published prospective studies. For the study, 1,121 case sets with IGF-1 and total IGFBP-3 measurements were observed. For each case participant with colon or rectum cancer, 1 control participant was selected randomly. Control were matched to cases depending on a set criteria. The study found no association between colorectal cancer risk and serum levels of IGF-1 or IGFBP-3. However, the results from the meta-analysis showed only a very mild significant positive association. Overall, findings from the study together with those from the prospective cohort studies indicate a modest role for elevated circulating IGF-I levels in the development of colorectal cancer.
Abstract
Several prospective studies have shown a moderate positive association between increasing circulating insulin-like growth factor-I (IGF-I) levels and colorectal cancer risk. However, the associations were often statistically nonsignificant, and the relationship of cancer risk with IGF-I's major binding protein, IGFBP-3, showed major discrepancies between studies. We investigated the association of colorectal cancer risk with serum IGF-I, total and intact IGFBP-3, in a case-control study nested within the EPIC cohort (1,121 cases of colorectal cancer and 1,121 matched controls). Conditional logistic regression was used to adjust for possible confounders. Our present study results were combined in a meta-analysis with those from 9 previous prospective studies to examine the overall evidence for a relationship of prediagnostic serum IGF-I with colorectal cancer risk. In the EPIC study, serum concentrations of IGF-I and IGFBP-3 showed no associations with risk of colorectal cancer overall. Only in subgroup analyses did our study show moderate positive associations of IGF-I levels with risk, either among younger participants only (and only for colon cancer) or among participants whose milk intakes were in the lowest tertile of the population distribution (RR for an increase of 100 ng/ml = 1.43 [95% CI = 1.13-1.93]). Nevertheless, in the meta-analysis a modest positive association remained between serum IGF-I and colorectal cancer risk overall (RR = 1.07 [1.01-1.14] for 1 standard deviation increase in IGF-I). Overall, data from our present study and previous prospective studies combined indicate a relatively modest association of colorectal cancer risk with serum IGF-I.