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Utility of self-rated adherence for monitoring dietary and physical activity compliance and assessment of participant feedback of the Healthy Diet and Lifestyle Study pilot.
O'Reilly, H, Panizza, CE, Lim, U, Yonemori, KM, Wilkens, LR, Shvetsov, YB, Harvie, MN, Shepherd, J, Zhu, FM, Le Marchand, L, et al
Pilot and feasibility studies. 2021;(1):48
Abstract
BACKGROUND We examined the utility of self-rated adherence to dietary and physical activity (PA) prescriptions as a method to monitor intervention compliance and facilitate goal setting during the Healthy Diet and Lifestyle Study (HDLS). In addition, we assessed participants' feedback of HDLS. HDLS is a randomized pilot intervention that compared the effect of intermittent energy restriction combined with a Mediterranean diet (IER + MED) to a Dietary Approaches to Stop Hypertension (DASH) diet, with matching PA regimens, for reducing visceral adipose tissue area (VAT). METHODS Analyses included the 59 (98%) participants who completed at least 1 week of HDLS. Dietary and PA adherence scores were collected 8 times across 12 weeks, using a 0-10 scale (0 = not at all, 4 = somewhat, and 10 = following the plan very well). Adherence scores for each participant were averaged and assigned to high and low adherence categories using the group median (7.3 for diet, 7.1 for PA). Mean changes in VAT and weight from baseline to 12 weeks are reported by adherence level, overall and by randomization arm. Participants' feedback at completion and 6 months post-intervention were examined. RESULTS Mean ± SE, dietary adherence was 6.0 ± 0.2 and 8.2 ± 0.1, for the low and high adherence groups, respectively. For PA adherence, mean scores were 5.9 ± 0.2 and 8.5 ± 0.2, respectively. Compared to participants with low dietary adherence, those with high adherence lost significantly more VAT (22.9 ± 3.7 cm2 vs. 11.7 ± 3.9 cm2 [95% CI, - 22.1 to - 0.3]) and weight at week 12 (5.4 ± 0.8 kg vs. 3.5 ± 0.6 kg [95% CI, - 3.8 to - 0.0]). For PA, compared to participants with low adherence, those with high adherence lost significantly more VAT (22.3 ± 3.7 cm2 vs. 11.6 ± 3.6 cm2 [95% CI, - 20.7 to - 0.8]). Participants' qualitative feedback of HDLS was positive and the most common response, on how to improve the study, was to provide cooking classes. CONCLUSIONS Results support the use of self-rated adherence as an effective method to monitor dietary and PA compliance and facilitate participant goal setting. Study strategies were found to be effective with promoting compliance to intervention prescriptions. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT03639350 . Registered 21st August 2018-retrospectively registered.
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Effects of Intermittent Energy Restriction Combined with a Mediterranean Diet on Reducing Visceral Adiposity: A Randomized Active Comparator Pilot Study.
Panizza, CE, Lim, U, Yonemori, KM, Cassel, KD, Wilkens, LR, Harvie, MN, Maskarinec, G, Delp, EJ, Lampe, JW, Shepherd, JA, et al
Nutrients. 2019;11(6)
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Excess adiposity is known to contribute to many metabolic diseases. Intermittent energy restriction (IER) has emerged as a favourable method of calorie reduction, and combining IER with the Mediterranean diet has shown promising results for reducing body fat and improving insulin resistance. The aim of this pilot study was to explore efficacy of an IER and Mediterranean diet in adiposity reduction in 60 Japanese Americans. Participants were randomised to either consume the IER + Mediterranean diet (22) or a control anti-hypertension diet (26) for 12 weeks. At baseline and 12-weeks, visceral adipose tissue and total fat mass were measured. Phone check-ins were completed weekly for the 12-weeks and both groups had equivalent dietetic support. This study found significant reductions in total fat mass in the IER + Mediterranean group compared with the control group, and found diet adherence to be high. Based on these results, the authors conclude the IER and Mediterranean diet combined can lower total adiposity and potentially improve liver function among Japanese Americans.
Abstract
Intermittent energy restriction combined with a Mediterranean diet (IER+MED) has shown promise to reduce body fat and insulin resistance. In the Multiethnic Cohort Adiposity Phenotype Study, Japanese Americans had the highest visceral adipose tissue (VAT) when adjusting for total adiposity. We conducted this pilot study to demonstrate feasibility and explore efficacy of following IER+MED for 12 weeks to reduce VAT among East Asians in Hawaii. Sixty volunteers (aged 35-55, BMI 25-40 kg/m2, VAT ≥ 90 cm2 for men and ≥ 80 cm2 for women) were randomized to IER+MED (two consecutive days with 70% energy restriction and 5 days euenergetic MED) or an active comparator (euenergetic Dietary Approaches to Stop Hypertension (DASH) diet). Participants and clinic staff (except dietitians) were blinded to group assignments. IER+MED had significantly larger reductions in DXA-measured VAT and total fat mass (-22.6 ± 3.6 cm2 and -3.3 ± 0.4 kg, respectively) vs. DASH (-10.7 ± 3.5 cm2 and -1.6 ± 0.4 kg) (p = 0.02 and p = 0.005). However, after adjusting for total fat mass, change in VAT was not statistically different between groups; whereas, improvement in alanine transaminase remained significantly greater for IER+MED vs. DASH (-16.2 ± 3.8 U/L vs. -4.0 ± 3.6 U/L, respectively, p = 0.02). Attrition rate was 10%, and participants adhered well to study prescriptions with no reported major adverse effect. Results demonstrate IER+MED is acceptable, lowers visceral and total adiposity among East Asian Americans, and may improve liver function more effectively than a healthful diet pattern. ClinicalTrials.gov Identifier: NCT03639350.
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Genome-wide physical activity interactions in adiposity - A meta-analysis of 200,452 adults.
Graff, M, Scott, RA, Justice, AE, Young, KL, Feitosa, MF, Barata, L, Winkler, TW, Chu, AY, Mahajan, A, Hadley, D, et al
PLoS genetics. 2017;(4):e1006528
Abstract
Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery.
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Effects of smoking on the genetic risk of obesity: the population architecture using genomics and epidemiology study.
Fesinmeyer, MD, North, KE, Lim, U, Bůžková, P, Crawford, DC, Haessler, J, Gross, MD, Fowke, JH, Goodloe, R, Love, SA, et al
BMC medical genetics. 2013;:6
Abstract
BACKGROUND Although smoking behavior is known to affect body mass index (BMI), the potential for smoking to influence genetic associations with BMI is largely unexplored. METHODS As part of the 'Population Architecture using Genomics and Epidemiology (PAGE)' Consortium, we investigated interaction between genetic risk factors associated with BMI and smoking for 10 single nucleotide polymorphisms (SNPs) previously identified in genome-wide association studies. We included 6 studies with a total of 56,466 subjects (16,750 African Americans (AA) and 39,716 European Americans (EA)). We assessed effect modification by testing an interaction term for each SNP and smoking (current vs. former/never) in the linear regression and by stratified analyses. RESULTS We did not observe strong evidence for interactions and only observed two interactions with p-values <0.1: for rs6548238/TMEM18, the risk allele (C) was associated with BMI only among AA females who were former/never smokers (β = 0.018, p = 0.002), vs. current smokers (β = 0.001, p = 0.95, p(interaction) = 0.10). For rs9939609/FTO, the A allele was more strongly associated with BMI among current smoker EA females (β = 0.017, p = 3.5 x 10(-5)), vs. former/never smokers (β = 0.006, p = 0.05, p(interaction) = 0.08). CONCLUSIONS These analyses provide limited evidence that smoking status may modify genetic effects of previously identified genetic risk factors for BMI. Larger studies are needed to follow up our results. CLINICAL TRIAL REGISTRATION NCT00000611.
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A prospective study of telomere length measured by monochrome multiplex quantitative PCR and risk of lung cancer.
Shen, M, Cawthon, R, Rothman, N, Weinstein, SJ, Virtamo, J, Hosgood, HD, Hu, W, Lim, U, Albanes, D, Lan, Q
Lung cancer (Amsterdam, Netherlands). 2011;(2):133-7
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PURPOSE Telomere length plays an important role in chromosomal stability and tumorigenesis, and its measurement in peripheral white blood cell DNA may be a predictor of the development of lung cancer. EXPERIMENTAL DESIGN Using a new method - monochrome multiplex quantitative PCR - which reduces measurement variability, we compared telomere length relative to standard DNA in white blood cell DNA in 229 incident male lung cancer cases and 229 matched controls within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of male smokers. RESULTS Median (10th, 90th percentile) telomere length was 1.13 (0.86, 1.45) in cases and 1.08 (0.85, 1.38) in controls (P=0.038). Telomere length was inversely associated with pack-years of smoking (Spearman's correlation r=-0.16, P=0.02) among controls. Compared to subjects with shorter telomere length (≤median), subjects with greater telomere length (>median) had a 1.6-fold (95% CI, 1.06-2.36) increased risk of lung cancer. There was a significant linear relationship between quartiles of telomere length and risk of lung cancer (odds ratios (95% confidence intervals) by quartile: 1.00, 0.98 (0.55-1.73), 1.62 (0.95-2.77), and 1.50 (0.84-2.68); P(trend)=0.05). In addition, subgroup analysis showed that greater telomere length was associated with an increased risk of lung cancer among longer-term smokers (>38 years) (OR, 1.90; 95% CI, 1.00-3.59) but not among shorter-term smokers (≤38 years) (OR, 1.08; 95% CI, 0.56-2.11) (P(interaction)=0.01). CONCLUSIONS Our results suggest that greater telomere length may be associated with higher risk of lung cancer among male smokers.
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Mendelian randomization: how it can--and cannot--help confirm causal relations between nutrition and cancer.
Schatzkin, A, Abnet, CC, Cross, AJ, Gunter, M, Pfeiffer, R, Gail, M, Lim, U, Davey-Smith, G
Cancer prevention research (Philadelphia, Pa.). 2009;(2):104-13
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Observational epidemiologic studies of nutrition and cancer have faced formidable methodologic obstacles, including dietary measurement error and confounding. We consider whether Mendelian randomization can help surmount these obstacles. The Mendelian randomization strategy, building on both the accuracy of genotyping and the random assortment of alleles at meiosis, involves searching for an association between a nutritional exposure-mimicking gene variant (a type of "instrumental variable") and cancer outcome. Necessary assumptions are that the gene is independent of cancer, given the exposure, and also independent of potential confounders. An allelic variant can serve as a proxy for diet and other nutritional factors through its effects on either metabolic processes or consumption behavior. Such a genetic proxy is measured with little error and usually is not confounded by nongenetic characteristics. Examples of potentially informative genes include LCT (lactase), ALDH2 (aldehyde dehydrogenase), and HFE (hemochromatosis), proxies, respectively, for dairy product intake, alcoholic beverage drinking, and serum iron levels. We show that use of these and other genes in Mendelian randomization studies of nutrition and cancer may be more complicated than previously recognized and discuss factors that can invalidate the instrumental variable assumptions or cloud the interpretation of these studies. Sample size requirements for Mendelian randomization studies of nutrition and cancer are shown to be potentially daunting; strong genetic proxies for exposure are necessary to make such studies feasible. We conclude that Mendelian randomization is not universally applicable, but, under the right conditions, can complement evidence for causal associations from conventional epidemiologic studies.
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A prospective investigation of serum 25-hydroxyvitamin D and risk of lymphoid cancers.
Lim, U, Freedman, DM, Hollis, BW, Horst, RL, Purdue, MP, Chatterjee, N, Weinstein, SJ, Morton, LM, Schatzkin, A, Virtamo, J, et al
International journal of cancer. 2009;(4):979-86
Abstract
Studies indicate that higher sun exposure, especially in the recent past, is associated with reduced risk of non-Hodgkin lymphoma (NHL). Ultraviolet radiation-derived vitamin D may be protective against lymphomagenesis. We examined the relationship between prediagnostic serum 25-hydroxyvitamin D (25(OH)D) and lymphoid cancer risk in a case-control study nested within the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study cohort (1985-2002) of 29,133 Finnish male smokers (ages 50-69). We identified 270 incident lymphoid cancer cases and matched them individually with 538 controls by birth-year and month of fasting blood draw at baseline. In conditional logistic regression models for 10 nmol/L increments or tertile comparisons, serum 25(OH)D was not associated with the risk of overall lymphoid cancers, NHL (n = 208) or multiple myeloma (n = 41). Odds ratios (OR) for NHL for higher tertiles were 0.75 (95% confidence interval (CI), 0.50, 1.14) and 0.82 (95% CI, 0.53, 1.26). The 25(OH)D-NHL association, however, differed by follow-up duration at diagnosis. Cases diagnosed less than 7 years from the baseline showed an inverse association (OR for highest vs. lowest tertile = 0.43; 95% CI: 0.23, 0.83; p for trend = 0.01), but not later diagnoses (OR = 1.52; 95% CI: 0.82, 2.80; p for trend = 0.17). The inverse association found for close exposure to diagnosis was not confounded by other risk factors for lymphoma or correlates of 25(OH)D. Although our findings suggest that circulating 25(OH)D is not likely associated with overall lymphoid cancer, they indicate a potentially protective effect on short-term risk of NHL.
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Prediagnostic total and high-density lipoprotein cholesterol and risk of cancer.
Ahn, J, Lim, U, Weinstein, SJ, Schatzkin, A, Hayes, RB, Virtamo, J, Albanes, D
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2009;(11):2814-21
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BACKGROUND Circulating total cholesterol has been inversely associated with cancer risk; however, the role of reverse causation and the associations for high-density lipoprotein (HDL) cholesterol have not been fully characterized. We examined the relationship between serum total and HDL cholesterol and risk of overall and site-specific cancers among 29,093 men in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort. METHODS Fasting serum total and HDL cholesterol were assayed at baseline, and 7,545 incident cancers were identified during up to 18 years of follow-up. Multivariable proportional hazards models were conducted to estimate relative risks (RR). RESULTS Higher serum total cholesterol concentration was associated with decreased risk of cancer overall (RR for comparing high versus low quintile, 0.85; 95% confidence interval, 0.79-0.91; P trend <0.001; >276.7 versus <203.9 mg/dL), and the inverse association was particularly evident for cancers of the lung and liver. These associations were no longer significant, however, when cases diagnosed during the first 9 years of follow-up were excluded. Greater HDL cholesterol was also associated with decreased risk of cancer (RR for high versus low quintile, 0.89; 95% confidence interval, 0.83-0.97; P trend = 0.01; >55.3 versus <36.2 mg/dL). The inverse association of HDL cholesterol was evident for cancers of lung, prostate, liver, and the hematopoietic system, and the associations of HDL cholesterol with liver and lung cancers remained after excluding cases diagnosed within 12 years of study entry. CONCLUSION Our findings suggest that prior observations regarding serum total cholesterol and cancer are largely explained by reverse causation. Although chance and reverse causation may explain some of the inverse HDL associations, we cannot rule out some etiologic role for this lipid fraction.
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A prospective study of telomere length measured by monochrome multiplex quantitative PCR and risk of non-Hodgkin lymphoma.
Lan, Q, Cawthon, R, Shen, M, Weinstein, SJ, Virtamo, J, Lim, U, Hosgood, HD, Albanes, D, Rothman, N
Clinical cancer research : an official journal of the American Association for Cancer Research. 2009;(23):7429-33
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PURPOSE Telomere length plays an important role in the maintenance of chromosomal stability and in tumorigenesis. We hypothesized that telomere length in peripheral WBC DNA obtained from healthy individuals would be a predictor of future risk of developing non-Hodgkin lymphoma. EXPERIMENTAL DESIGN Using a new assay to measure relative telomere length, monochrome multiplex quantitative PCR, which strongly correlates with telomere length measured by Southern blot (Spearman r = 0.91, P < 0.0001) and has high precision (coefficient of variation = 7%), we compared telomere length in peripheral WBC DNA in 107 incident male non-Hodgkin lymphoma cases and 107 matched controls within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort. RESULTS Median (10th, 90th percentile) telomere length was 1.10 (0.79, 1.43) in cases and 1.02 (0.78, 1.26) in controls (P = 0.0017, Wilcoxon sign test). There was a strong dose-response relationship between quartiles of telomere length and risk of non-Hodgkin lymphoma overall [odds ratios (95% confidence intervals) by quartile: 1.0; 1.1 (0.4-2.7); 1.8 (0.7-4.9); and 3.6 (1.4-8.9); P trend = 0.003], and this association was similar across the most common non-Hodgkin lymphoma subtypes present in this study. CONCLUSION These results suggest that longer telomere length may be a potential predictor for future risk of non-Hodgkin lymphoma.
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One-carbon metabolism biomarkers and risk of colon and rectal cancers.
Weinstein, SJ, Albanes, D, Selhub, J, Graubard, B, Lim, U, Taylor, PR, Virtamo, J, Stolzenberg-Solomon, R
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2008;(11):3233-40
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BACKGROUND Folate intake has been associated with reduced colorectal cancer risk; however, few studies have prospectively examined circulating folate or other related one-carbon biomarkers. METHODS We conducted a nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of 50- to 69-year-old Finnish men to investigate associations between serum folate, vitamin B6, vitamin B12, riboflavin, and homocysteine and risk of colon and rectal cancers. Controls were alive and cancer-free at the time of case diagnosis and matched 1:1 on age and date of baseline fasting serum collection with cases (152 colon and 126 rectal cancers). Multivariate-adjusted odds ratios and 95% confidence intervals were calculated using conditional logistic regression. RESULTS Serum vitamin B6 was inversely associated with colon cancer [odds ratio, 0.30 (95% confidence interval, 0.11-0.82) in the highest versus lowest quintile]. An increased risk of colon cancer was suggested for men in the middle quintile of serum folate, but without indication of a dose-response relationship. None of the other serum biomarkers were associated with colon or rectal cancer, and we observed no interactions with alcohol consumption or methionine or protein intake. A priori combinations of the five one-carbon serum biomarkers provided no clear evidence to support a collective influence on colorectal cancer risk. CONCLUSIONS Our results support the hypothesis that higher vitamin B6 status may play a role in inhibiting colon cancer carcinogenesis; however, folate and other one-carbon related biomarkers were not associated with colon or rectal cancer.