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Dietary Advanced Glycation End-products (AGE) and Risk of Breast Cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO).
Omofuma, OO, Turner, DP, Peterson, LL, Merchant, AT, Zhang, J, Steck, SE
Cancer prevention research (Philadelphia, Pa.). 2020;(7):601-610
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Abstract
Advanced glycation end-products (AGEs) are implicated in the pathogenesis of several chronic diseases including cancer. AGEs are produced endogenously but can also be consumed from foods. AGE formation in food is accelerated during cooking at high temperatures. Certain high fat or highly processed foods have high AGE values. The objective of the study was to assign and quantify Nϵ-carboxymethyl-lysine (CML)-AGE content in food and investigate the association between dietary AGE intake and breast cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. The study included women enrolled in the intervention arm who were cancer-free at baseline and completed a baseline questionnaire and food frequency questionnaire (DQX). CML-AGE values were assigned and quantified to foods in the DQX using a published AGE database. Cox proportional hazards models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI) of breast cancer among all women, and stratified by race/ethnicity, invasiveness of disease, and hormone receptor status. After a median 11.5 years of follow-up, 1,592 women were diagnosed with breast cancer. Higher CML-AGE intake was associated with increased risk of breast cancer among all women (HRQ5VSQ1, 1.30; 95% CI, 1.04-1.62; P trend = 0.04) and in non-Hispanic white women (HRT3VST1, 1.21; 95% CI, 1.02-1.44). Increased CML-AGE intake was associated with increased risk of in situ (HRT3VST1, 1.49; 95% CI, 1.11-2.01) and hormone receptor-positive (HRT3VST1, 1.24; 95% CI, 1.01-1.53) breast cancers. In conclusion, high intake of dietary AGE may contribute to increased breast cancer.
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Inflammatory potential of diet and risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
Zheng, J, Merchant, AT, Wirth, MD, Zhang, J, Antwi, SO, Shoaibi, A, Shivappa, N, Stolzenberg-Solomon, RZ, Hebert, JR, Steck, SE
International journal of cancer. 2018;(12):2461-2470
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Abstract
Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet. We aimed to examine the association between the inflammatory potential of diet, assessed with the Dietary Inflammatory Index (DII®), and pancreatic cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial prospective cohort. Our study included 101,449 participants aged 52-78 years at baseline who completed both baseline questionnaire and a diet history questionnaire. Energy-adjusted DII (E-DII) scores were computed based on food and supplement intake. Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with participants in the lowest E-DII quintile (most anti-inflammatory scores) as referent. After a median 8.5 years of follow-up, 328 pancreatic cancer cases were identified. E-DII scores were not associated with pancreatic cancer risk in the multivariable model (HRQ5vsQ1 = 0.94; 95% CI = 0.66-1.35; p-trend = 0.43). Time significantly modified the association (p-interaction = 0.01). During follow up <4 years, there was suggestive evidence of an inverse association between E-DII and pancreatic cancer (HRQ5vsQ1 = 0.60; 95% CI = 0.35-1.02; p-trend = 0.20) while there was a significant positive trend in the follow up ≥4 years (HRQ5vsQ1 = 1.31; 95% CI = 0.83-2.08; p-trend = 0.03). Similar results were observed for E-DII from food only. Our study does not support an association between inflammatory potential of diet and pancreatic cancer risk; however, heterogeneous results were obtained with different follow-up times. These divergent associations may result from the influences of undetected disease in the short-term.
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Longitudinal changes in the dietary inflammatory index: an assessment of the inflammatory potential of diet over time in postmenopausal women.
Tabung, FK, Steck, SE, Zhang, J, Ma, Y, Liese, AD, Tylavsky, FA, Vitolins, MZ, Ockene, JK, Hebert, JR
European journal of clinical nutrition. 2016;(12):1374-1380
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Abstract
BACKGROUND/OBJECTIVES The dietary inflammatory index (DII) measured at one time point is associated with risk of several chronic diseases, but disease risk may change with longitudinal changes in DII scores. Data are lacking regarding changes in DII scores over time; therefore, we assessed changes in the DII in the Women's Health Initiative (WHI). SUBJECTS/METHODS DII scores were calculated using data from repeated food frequency questionnaires in the WHI Observational Study (OS; n=76 671) at baseline and year 3, and the WHI Dietary Modification trial (DM; n=48482) at three time points. Lower DII scores represent more anti-inflammatory diets. We used generalized estimating equations to compare mean changes in DII over time, adjusting for multiple comparisons, and multivariable-adjusted linear regression analyses to determine predictors of DII change. RESULTS In the OS, mean DII decreased modestly from -1.14 at baseline to -1.50 at year 3. In the DM, DII was -1.32 in year 1, -1.60 in year 3 and -1.48 in year 6 in the intervention arm and was -0.65 in year 1, -0.94 in year 3 and -0.96 in year 6 in the control arm. These changes were modified by body mass index, education and race/ethnicity. A prediction model explained 22% of the variance in the change in DII scores in the OS. CONCLUSIONS In this prospective investigation of postmenopausal women, reported dietary inflammatory potential decreased modestly over time. Largest reductions were observed in normal-weight, highly educated women. Future research is warranted to examine whether reductions in DII are associated with decreased chronic disease risk.
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Theory-based behavioral intervention increases self-reported physical activity in South African men: a cluster-randomized controlled trial.
Jemmott, JB, Jemmott, LS, Ngwane, Z, Zhang, J, Heeren, GA, Icard, LD, O'Leary, A, Mtose, X, Teitelman, A, Carty, C
Preventive medicine. 2014;:114-20
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Abstract
OBJECTIVE To determine whether a health-promotion intervention increases South African men's adherence to physical-activity guidelines. METHOD We utilized a cluster-randomized controlled trial design. Eligible clusters, residential neighborhoods near East London, South Africa, were matched in pairs. Within randomly selected pairs, neighborhoods were randomized to theory-based, culturally congruent health-promotion intervention encouraging physical activity or attention-matched HIV/STI risk-reduction control intervention. Men residing in the neighborhoods and reporting coitus in the previous 3 months were eligible. Primary outcome was self-reported individual-level adherence to physical-activity guidelines averaged over 6-month and 12-month post-intervention assessments. Data were collected in 2007-2010. Data collectors, but not facilitators or participants, were blind to group assignment. RESULTS Primary outcome intention-to-treat analysis included 22 of 22 clusters and 537 of 572 men in the health-promotion intervention and 22 of 22 clusters and 569 of 609 men in the attention-control intervention. Model-estimated probability of meeting physical-activity guidelines was 51.0% in the health-promotion intervention and 44.7% in attention-matched control (OR=1.34; 95% CI, 1.09-1.63), adjusting for baseline prevalence and clustering from 44 neighborhoods. CONCLUSION A theory-based culturally congruent intervention increased South African men's self-reported physical activity, a key contributor to deaths from non-communicable diseases in South Africa. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT01490359.
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Effect of apolipoprotein E genotype and diet on apolipoprotein E lipidation and amyloid peptides: randomized clinical trial.
Hanson, AJ, Bayer-Carter, JL, Green, PS, Montine, TJ, Wilkinson, CW, Baker, LD, Watson, GS, Bonner, LM, Callaghan, M, Leverenz, JB, et al
JAMA neurology. 2013;(8):972-80
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Abstract
IMPORTANCE Sporadic Alzheimer disease (AD) is caused in part by decreased clearance of the β-amyloid (Aβ) peptide breakdown products. Lipid-depleted (LD) apolipoproteins are less effective at binding and clearing Aβ, and LD Aβ peptides are more toxic to neurons. However, not much is known about the lipid states of these proteins in human cerebrospinal fluid. OBJECTIVE To characterize the lipidation states of Aβ peptides and apolipoprotein E in the cerebrospinal fluid in adults with respect to cognitive diagnosis and APOE ε4 allele carrier status and after a dietary intervention. DESIGN Randomized clinical trial. SETTING Veterans Affairs Medical Center clinical research unit. PARTICIPANTS Twenty older adults with normal cognition (mean [SD] age, 69 [7] years) and 27 with amnestic mild cognitive impairment (67 [6] years). INTERVENTIONS Randomization to a diet high in saturated fat content and with a high glycemic index (High diet; 45% of energy from fat [>25% saturated fat], 35%-40% from carbohydrates with a mean glycemic index >70, and 15%-20% from protein) or a diet low in saturated fat content and with a low glycemic index (Low diet; 25% of energy from fat [<7% saturated fat], 55%-60% from carbohydrates with a mean glycemic index <55, and 15%-20% from protein). MAIN OUTCOMES AND MEASURES Lipid-depleted Aβ42 and Aβ40 and apolipoprotein E in cerebrospinal fluid. RESULTS Baseline levels of LD Aβ were greater for adults with mild cognitive impairment compared with adults with normal cognition (LD Aβ42, P = .05; LD Aβ40, P = .01). These findings were magnified in adults with mild cognitive impairment and the ε4 allele, who had higher LD apolipoprotein E levels irrespective of cognitive diagnosis (P < .001). The Low diet tended to decrease LD Aβ levels, whereas the High diet increased these fractions (LD Aβ42, P = .01; LD Aβ40, P = .15). Changes in LD Aβ levels with the Low diet negatively correlated with changes in cerebrospinal fluid levels of insulin (LD Aβ42 and insulin, r = -0.68 [P = .01]; LD Aβ40 and insulin, r = -0.78 [P = .002]). CONCLUSIONS AND RELEVANCE The lipidation states of apolipoproteins and Aβ peptides in the brain differ depending on APOE genotype and cognitive diagnosis. Concentrations can be modulated by diet. These findings may provide insight into the mechanisms through which apolipoprotein E4 and unhealthy diets impart risk for developing AD.