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1.  Adult height and the risk of cause-specific death and vascular morbidity in 1 million people: individual participant meta-analysis 
Wormser, David | Angelantonio, Emanuele Di | Kaptoge, Stephen | Wood, Angela M | Gao, Pei | Sun, Qi | Walldius, Göran | Selmer, Randi | Verschuren, WM Monique | Bueno-de-Mesquita, H Bas | Engström, Gunnar | Ridker, Paul M | Njølstad, Inger | Iso, Hiroyasu | Holme, Ingar | Giampaoli, Simona | Tunstall-Pedoe, Hugh | Gaziano, J Michael | Brunner, Eric | Kee, Frank | Tosetto, Alberto | Meisinger, Christa | Brenner, Hermann | Ducimetiere, Pierre | Whincup, Peter H | Tipping, Robert W | Ford, Ian | Cremer, Peter | Hofman, Albert | Wilhelmsen, Lars | Clarke, Robert | de Boer, Ian H | Jukema, J Wouter | Ibañez, Alejandro Marín | Lawlor, Debbie A | D'Agostino, Ralph B | Rodriguez, Beatriz | Casiglia, Edoardo | Stehouwer, Coen DA | Simons, Leon A | Nietert, Paul J | Barrett-Connor, Elizabeth | Panagiotakos, Demosthenes B | Björkelund, Cecilia | Strandberg, Timo E | Wassertheil-Smoller, Sylvia | Blazer, Dan G | Meade, Tom W | Welin, Lennart | Svärdsudd, Kurt | Woodward, Mark | Nissinen, Aulikki | Kromhout, Daan | Jørgensen, Torben | Tilvis, Reijo S | Guralnik, Jack M | Rosengren, Annika | Taylor, James O | Kiechl, Stefan | Dagenais, Gilles R | Gerry, F | Fowkes, R | Wallace, Robert B | Khaw, Kay-Tee | Shaffer, Jonathan A | Visser, Marjolein | Kauhanen, Jussi | Salonen, Jukka T | Gallacher, John | Ben-Shlomo, Yoav | Kitamura, Akihiko | Sundström, Johan | Wennberg, Patrik | Kiyohara, Yutaka | Daimon, Makoto | de la Cámara, Agustin Gómez | Cooper, Jackie A | Onat, Altan | Devereux, Richard | Mukamal, Kenneth J | Dankner, Rachel | Knuiman, Matthew W | Crespo, Carlos J | Gansevoort, Ron T | Goldbourt, Uri | Nordestgaard, Børge G | Shaw, Jonathan E | Mussolino, Michael | Nakagawa, Hidaeki | Fletcher, Astrid | Kuller, Lewis H | Gillum, Richard F | Gudnason, Vilmundur | Assmann, Gerd | Wald, Nicholas | Jousilahti, Pekka R | Greenland, Philip | Trevisan, Maurizio | Ulmer, Hanno | Butterworth, Adam S | Folsom, Aaron R | Davey-Smith, George | Hu, Frank B | Danesh, John | Tipping, Robert W | Ford, Charles E | Simpson, Lara M | Walldius, Göran | Jungner, Ingmar | Folsom, Aaron R | Demerath, Ellen W | Franceschini, Nora | Lutsey, Pamela L | Panagiotakos, Demosthenes B | Pitsavos, Christos | Chrysohoou, Christina | Stefanadis, Christodoulos | Shaw, Jonathan E | Atkins, Robert | Zimmet, Paul Z | Barr, Elizabeth LM | Knuiman, Matthew W | Whincup, Peter H | Wannamethee, S Goya | Morris, Richard W | Willeit, Johann | Kiechl, Stefan | Weger, Siegfried | Oberhollenzer, Friedrich | Wald, Nicholas | Ebrahim, Shah | Lawlor, Debbie A | Gallacher, John | Ben-Shlomo, Yoav | Yarnell, John WG | Casiglia, Edoardo | Tikhonoff, Valérie | Greenland, Philip | Shay, Christina M | Garside, Daniel B | Nietert, Paul J | Sutherland, Susan E | Bachman, David L | Keil, Julian E | de Boer, Ian H | Kizer, Jorge R | Psaty, Bruce M | Mukamal, Kenneth J | Nordestgaard, Børge G | Tybjærg-Hansen, Anne | Jensen, Gorm B | Schnohr, Peter | Giampaoli, Simona | Palmieri, Luigi | Panico, Salvatore | Pilotto, Lorenza | Vanuzzo, Diego | de la Cámara, Agustin Gómez | Simons, Leon A | Simons, Judith | McCallum, John | Friedlander, Yechiel | Gerry, F | Fowkes, R | Price, Jackie F | Lee, Amanda J | Taylor, James O | Guralnik, Jack M | Phillips, Caroline L | Wallace, Robert B | Kohout, Frank J | Cornoni-Huntley, Joan C | Guralnik, Jack M | Blazer, Dan G | Guralnik, Jack M | Phillips, Caroline L | Phillips, Caroline L | Guralnik, Jack M | Khaw, Kay-Tee | Wareham, Nicholas J | Brenner, Hermann | Schöttker, Ben | Müller, Heiko | Rothenbacher, Dietrich | Wennberg, Patrik | Jansson, Jan-Håkan | Nissinen, Aulikki | Donfrancesco, Chiara | Giampaoli, Simona | Woodward, Mark | Vartiainen, Erkki | Jousilahti, Pekka R | Harald, Kennet | Salomaa, Veikko | D'Agostino, Ralph B | Vasan, Ramachandran S | Fox, Caroline S | Pencina, Michael J | Daimon, Makoto | Oizumi, Toshihide | Kayama, Takamasa | Kato, Takeo | Bladbjerg, Else-Marie | Jørgensen, Torben | Møller, Lars | Jespersen, Jørgen | Dankner, Rachel | Chetrit, Angela | Lubin, Flora | Svärdsudd, Kurt | Eriksson, Henry | Welin, Lennart | Lappas, Georgios | Rosengren, Annika | Lappas, Georgios | Welin, Lennart | Svärdsudd, Kurt | Eriksson, Henry | Lappas, Georgios | Bengtsson, Calle | Lissner, Lauren | Björkelund, Cecilia | Cremer, Peter | Nagel, Dorothea | Strandberg, Timo E | Salomaa, Veikko | Tilvis, Reijo S | Miettinen, Tatu A | Tilvis, Reijo S | Strandberg, Timo E | Kiyohara, Yutaka | Arima, Hisatomi | Doi, Yasufumi | Ninomiya, Toshiharu | Rodriguez, Beatriz | Dekker, Jacqueline M | Nijpels, Giel | Stehouwer, Coen DA | Hu, Frank B | Sun, Qi | Rimm, Eric B | Willett, Walter C | Iso, Hiroyasu | Kitamura, Akihiko | Yamagishi, Kazumasa | Noda, Hiroyuki | Goldbourt, Uri | Vartiainen, Erkki | Jousilahti, Pekka R | Harald, Kennet | Salomaa, Veikko | Kauhanen, Jussi | Salonen, Jukka T | Kurl, Sudhir | Tuomainen, Tomi-Pekka | Poppelaars, Jan L | Deeg, Dorly JH | Visser, Marjolein | Meade, Tom W | De Stavola, Bianca Lucia | Hedblad, Bo | Nilsson, Peter | Engström, Gunnar | Verschuren, WM Monique | Blokstra, Anneke | de Boer, Ian H | Shea, Steven J | Meisinger, Christa | Thorand, Barbara | Koenig, Wolfgang | Döring, Angela | Verschuren, WM Monique | Blokstra, Anneke | Bueno-de-Mesquita, H Bas | Wilhelmsen, Lars | Rosengren, Annika | Lappas, Georgios | Fletcher, Astrid | Nitsch, Dorothea | Kuller, Lewis H | Grandits, Greg | Tverdal, Aage | Selmer, Randi | Nystad, Wenche | Mussolino, Michael | Gillum, Richard F | Hu, Frank B | Sun, Qi | Manson, JoAnn E | Rimm, Eric B | Hankinson, Susan E | Meade, Tom W | De Stavola, Bianca Lucia | Cooper, Jackie A | Bauer, Kenneth A | Davidson, Karina W | Kirkland, Susan | Shaffer, Jonathan A | Shimbo, Daichi | Kitamura, Akihiko | Iso, Hiroyasu | Sato, Shinichi | Holme, Ingar | Selmer, Randi | Tverdal, Aage | Nystad, Wenche | Nakagawa, Hidaeki | Miura, Katsuyuki | Sakurai, Masaru | Ducimetiere, Pierre | Jouven, Xavier | Bakker, Stephan JL | Gansevoort, Ron T | van der Harst, Pim | Hillege, Hans L | Crespo, Carlos J | Garcia-Palmieri, Mario R | Kee, Frank | Amouyel, Philippe | Arveiler, Dominique | Ferrières, Jean | Schulte, Helmut | Assmann, Gerd | Jukema, J Wouter | de Craen, Anton JM | Sattar, Naveed | Stott, David J | Cantin, Bernard | Lamarche, Benoît | Després, Jean-Pierre | Dagenais, Gilles R | Barrett-Connor, Elizabeth | Bergstrom, Jaclyn | Bettencourt, Richele R | Buisson, Catherine | Gudnason, Vilmundur | Aspelund, Thor | Sigurdsson, Gunnar | Thorsson, Bolli | Trevisan, Maurizio | Hofman, Albert | Ikram, M Arfan | Tiemeier, Henning | Witteman, Jacqueline CM | Tunstall-Pedoe, Hugh | Tavendale, Roger | Lowe, Gordon DO | Woodward, Mark | Devereux, Richard | Yeh, Jeun-Liang | Ali, Tauqeer | Calhoun, Darren | Ben-Shlomo, Yoav | Davey-Smith, George | Onat, Altan | Can, Günay | Nakagawa, Hidaeki | Sakurai, Masaru | Nakamura, Koshi | Morikawa, Yuko | Njølstad, Inger | Mathiesen, Ellisiv B | Løchen, Maja-Lisa | Wilsgaard, Tom | Sundström, Johan | Ingelsson, Erik | Michaëlsson, Karl | Cederholm, Tommy | Gaziano, J Michael | Buring, Julie | Ridker, Paul M | Gaziano, J Michael | Ridker, Paul M | Ulmer, Hanno | Diem, Günter | Concin, Hans | Rodeghiero, Francesco | Tosetto, Alberto | Wassertheil-Smoller, Sylvia | Manson, JoAnn E | Marmot, Michael | Clarke, Robert | Fletcher, Astrid | Brunner, Eric | Shipley, Martin | Kivimaki, Mika | Ridker, Paul M | Buring, Julie | Ford, Ian | Robertson, Michele | Ibañez, Alejandro Marín | Feskens, Edith | Geleijnse, Johanna M | Kromhout, Daan | Walker, Matthew | Watson, Sarah | Alexander, Myriam | Butterworth, Adam S | Angelantonio, Emanuele Di | Franco, Oscar H | Gao, Pei | Gobin, Reeta | Haycock, Philip | Kaptoge, Stephen | Seshasai, Sreenivasa R Kondapally | Lewington, Sarah | Pennells, Lisa | Rapsomaniki, Eleni | Sarwar, Nadeem | Thompson, Alexander | Thompson, Simon G | Walker, Matthew | Watson, Sarah | White, Ian R | Wood, Angela M | Wormser, David | Zhao, Xiaohui | Danesh, John
Background The extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain.
Methods We calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual–participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies.
Results For people born between 1900 and 1960, mean adult height increased 0.5–1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96–0.99) for death from any cause, 0.94 (0.93–0.96) for death from vascular causes, 1.04 (1.03–1.06) for death from cancer and 0.92 (0.90–0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12–1.42) for risk of melanoma death to 0.84 (0.80–0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators.
Conclusion Adult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.
doi:10.1093/ije/dys086
PMCID: PMC3465767  PMID: 22825588
Height; cardiovascular disease; cancer; cause-specific mortality; epidemiological study; meta-analysis
2.  Long-Term Coffee Consumption and Risk of Cardiovascular Disease: A Systematic Review and a Dose-Response Meta-Analysis of Prospective Cohort Studies 
Circulation  2013;129(6):643-659.
Background
Considerable controversy exists regarding the association between coffee consumption and cardiovascular disease (CVD) risk. A meta-analysis was performed to assess the dose-response relationship of long-term coffee consumption with CVD risk.
Methods and Results
Pubmed and EMBASE were searched for prospective cohort studies of the relationship between coffee consumption and CVD risk, which included coronary heart disease, stroke, heart failure, and CVD mortality. Thirty-six studies were included with 1,279,804 participants and 36,352 CVD cases. A non-linear relationship of coffee consumption with CVD risk was identified (P for heterogeneity = 0.09, P for trend < 0.001, P for non-linearity < 0.001). Compared with the lowest category of coffee consumption (median: 0 cups/d), the relative risk of CVD was 0.95 (95% CI, 0.87 to 1.03) for the highest (median: 5 cups/d) category, 0.85 (0.80 to 0.90) for the second highest (median: 3.5 cups/d), and 0.89 (0.84 to 0.94) for the third highest category (median: 1.5 cups/d). Looking at separate outcomes, coffee consumption was non-linearly associated with both CHD (P for heterogeneity = 0.001, P for trend < 0.001, P for non-linearity < 0.001) and stroke risks (P for heterogeneity = 0.07, P for trend < 0.001, P for non-linearity< 0.001) (P for trend differences > 0.05).
Conclusions
A non-linear association between coffee consumption with CVD risk was observed in this meta-analysis. Moderate coffee consumption was inversely significantly associated with CVD risk, with the lowest CVD risk at 3 to 5 cups/d, and heavy coffee consumption was not associated with elevated CVD risk.
doi:10.1161/CIRCULATIONAHA.113.005925
PMCID: PMC3945962  PMID: 24201300
coffee; cardiovascular disease; meta-analysis
3.  Television Viewing and Risk of Type 2 Diabetes, Cardiovascular Disease, and All-Cause Mortality A Meta-analysis 
JAMA  2011;305(23):2448-2455.
Context
Prolonged television (TV) viewing is the most prevalent and pervasive sedentary behavior in industrialized countries and has been associated with morbidity and mortality. However, a systematic and quantitative assessment of published studies is not available.
Objective
To perform a meta-analysis of all prospective cohort studies to determine the association between TV viewing and risk of type 2 diabetes, fatal or nonfatal cardiovascular disease, and all-cause mortality.
Data Sources and Study Selection
Relevant studies were identified by searches of the MEDLINE database from 1970 to March 2011 and the EMBASE database from 1974 to March 2011 without restrictions and by reviewing reference lists from retrieved articles. Cohort studies that reported relative risk estimates with 95% confidence intervals (CIs) for the associations of interest were included.
Data Extraction
Data were extracted independently by each author and summary estimates of association were obtained using a random-effects model.
Data Synthesis
Of the 8 studies included, 4 reported results on type 2 diabetes (175 938 individuals; 6428 incident cases during 1.1 million person-years of follow-up), 4 reported on fatal or nonfatal cardiovascular disease (34 253 individuals; 1052 incident cases), and 3 reported on all-cause mortality (26 509 individuals; 1879 deaths during 202 353 person-years of follow-up). The pooled relative risks per 2 hours of TV viewing per day were 1.20 (95% CI, 1.14-1.27) for type 2 diabetes, 1.15 (95% CI, 1.06-1.23) for fatal or nonfatal cardiovascular disease, and 1.13 (95% CI, 1.07-1.18) for all-cause mortality. While the associations between time spent viewing TV and risk of type 2 diabetes and cardiovascular disease were linear, the risk of all-cause mortality appeared to increase with TV viewing duration of greater than 3 hours per day. The estimated absolute risk differences per every 2 hours of TV viewing per day were 176 cases of type 2 diabetes per 100 000 individuals per year, 38 cases of fatal cardiovascular disease per 100 000 individuals per year, and 104 deaths for all-cause mortality per 100 000 individuals per year.
Conclusion
Prolonged TV viewing was associated with increased risk of type 2 diabetes, cardiovascular disease, and all-cause mortality.
doi:10.1001/jama.2011.812
PMCID: PMC4324728  PMID: 21673296
4.  Association between alcohol consumption and plasma fetuin-A and its contribution to incident type 2 diabetes in women 
Diabetologia  2013;57(1):10.1007/s00125-013-3077-8.
Aims/hypothesis
The benefits of moderate alcohol consumption for type 2 diabetes have been postulated to involve a mechanism of improved insulin sensitivity. Fetuin-A, which is known to inhibit insulin signalling, has emerged as a biomarker for diabetes risk. Alcohol consumption may influence circulating fetuin-A concentrations and subsequently diabetes risk by altering the insulin signal. We therefore hypothesised that moderate alcohol consumption would be associated with lower fetuin-A concentration and that fetuin-A would partly explain the association between alcohol consumption and incident type 2 diabetes.
Methods
Among diabetes-free female participants in the Nurses’ Health Study (n=1331), multiple linear regression was conducted to assess the association between alcohol consumption and plasma fetuin-A. Least-squares means (lsmeans) of fetuin-A were estimated in categories of alcohol consumption (0, 0.1-4.9, 5-14.9 and ≥15 g/day). The proportion of alcohol consumption and diabetes association explained by baseline fetuin-A was assessed in 470 matched incident diabetes case–control pairs with follow-up 2000-2006.
Results
Higher alcohol consumption was associated with lower plasma fetuin-A (p for trend=0.009): lsmean±SE 476.5±5.9 μg/ml for abstainers, 468.9±5.2 μg/ml for 0.1-4.9 g/day consumers, 455.9±7.0 μg/ml for 5.0-14.9 g/day consumers, and 450.0±9.4 μg/ml for ≥15.0 g/day consumers. Fetuin-A and fasting insulin explained 18.4% and 54.8%, respectively, of the inverse association between alcohol consumption and diabetes after multiple adjustment (both p for contribution <0.04).
Conclusions/interpretation
Moderate alcohol consumption is associated with lower plasma fetuin-A in diabetes-free women. Fetuin-A and insulin explain a significant proportion of the association between alcohol consumption and incident type 2 diabetes. Further studies are needed to examine potential biological mechanisms underlying this association.
doi:10.1007/s00125-013-3077-8
PMCID: PMC3858443  PMID: 24105100
Alcohol; Fetuin-A; Insulin sensitivity; Type 2 diabetes
5.  Consumption of Plant Seeds and Cardiovascular Health: Epidemiologic and Clinical Trial Evidence 
Circulation  2013;128(5):553-565.
doi:10.1161/CIRCULATIONAHA.112.001119
PMCID: PMC3745769  PMID: 23897849
diet; cardiovascular disease prevention; diabetes mellitus; nutrition; epidemiology; nuts; grains; cocoa; coffee; legumes
6.  Changes in Red Meat Consumption and Subsequent Risk of Type 2 Diabetes: Three Cohorts of US Men and Women 
JAMA internal medicine  2013;173(14):10.1001/jamainternmed.2013.6633.
Context
Red meat consumption has been consistently associated with an increased risk of type 2 diabetes. However, whether changes in red meat intake are related to subsequent type 2 diabetes risk remains unknown.
Objective
We evaluated the association between changes in red meat consumption during a 4-year period and subsequent 4-year risk of type 2 diabetes in US adults.
Design, setting and participants
We followed 26,357 men in the Health Professionals Follow-up Study (HPFS, 1986–2006), 48,709 women in the Nurses’ Health Study (NHS, 1986–2006) and 74,077 women in NHS II (1991–2007). Diet was assessed by validated food frequency questionnaires and updated every 4 years. Time-dependent Cox proportional hazard models were used to calculate hazard ratios (HRs) with adjustment for age, family history, race, marital status, initial red meat consumption, initial and changes in other lifestyle factors (physical activity, smoking status, alcohol intake, energy intake, and dietary quality). Results across cohorts were pooled by inverse-variance-weighted fixed-effect meta-analyses.
Main Outcome Measure
Incident T2D cases validated by supplementary questionnaires.
Results
During 1,965,824 person-years of follow-up, we documented 7,540 incident type 2 diabetes cases. In the multivariate-adjusted models, increasing red meat intake during a 4-year interval was associated with an elevated risk of type 2 diabetes over the subsequent four years in each cohort (all P-trend <0.001): compared with the reference group of no change in red meat intake, increasing red meat intake of >0.5 serving/d was associated with a 48% (pooled HR, 1.48; 95% CI, 1.37–1.59) elevated risk in the subsequent 4-year period, and the association was modestly attenuated after further adjustment for initial body mass index and concurrent weight gain (1.30; 95% CI, 1.21–1.41). A reduction of red meat consumption of >0.5 serving/day from baseline to the first four years of follow-up was associated with a 14% (95% CI, 7%–20%) lower risk during subsequent follow-up through 2006/2007.
Conclusions
Increasing red meat consumption over time is associated with an elevated subsequent risk of type 2 diabetes, and the association is partly mediated by body weight. Our results add further evidence that limiting red meat consumption over time confers benefits for diabetes prevention.
doi:10.1001/jamainternmed.2013.6633
PMCID: PMC3847817  PMID: 23779232
red meat; diabetes; prospective cohort study
7.  Optimal body weight for health and longevity: bridging basic, clinical, and population research 
Aging Cell  2014;13(3):391-400.
Excess body weight and adiposity cause insulin resistance, inflammation, and numerous other alterations in metabolic and hormonal factors that promote atherosclerosis, tumorigenesis, neurodegeneration, and aging. Studies in both animals and humans have demonstrated a beneficial role of dietary restriction and leanness in promoting health and longevity. Epidemiological studies have found strong direct associations between increasing body mass index (BMI) and risks of developing type 2 diabetes, cardiovascular disease, and several types of cancer, beginning from BMI of 20–21 kg m−2. Although a recent meta-analysis suggests that overweight individuals have significantly lower overall mortality than normal-weight individuals, these data are likely to be an artifact produced by serious methodological problems, especially confounding by smoking, reverse causation due to existing chronic disease, and nonspecific loss of lean mass and function in the frail elderly. From a clinical and public health point of view, maintaining a healthy weight through diet and physical activity should remain the cornerstone in the prevention of chronic diseases and the promotion of healthy aging.
doi:10.1111/acel.12207
PMCID: PMC4032609  PMID: 24628815
body mass index; calorie intake; disease prevention; health; obesity
8.  A PROSPECTIVE STUDY OF DIETARY ENERGY DENSITY AND WEIGHT GAIN IN WOMEN 
Background
Little is known about the long-term effects of dietary energy density (ED) on weight gain.
Methods
We conducted a prospective study of 50,026 women (mean age: 36.5; SD: 4.6) in the Nurses' Health Study II followed from 1991 to 1999. Dietary ED and body weight were ascertained in 1991, 1995, and 1999. Total dietary ED was calculated by dividing each subject's daily energy intake (kcal) by the reported weight (g) of all foods consumed.
Results
Dietary ED was positively correlated with saturated fat (r=0.16), trans fat (r=0.15), and the glycemic index (r=0.16), but inversely correlated with vegetable protein (r=−0.30), vegetables (r=−0.27), and fruits (r=−0.17). ED was not significantly correlated with total fat intake (r=0.08). Women who increased their dietary ED during follow-up the most (5th quintile) had a statistical significant greater multivariate-adjusted weight gain as compared with those who decreased their dietary ED most (1st quintile) (in the 8-y time period: 6.42 kg versus 4.57 kg; p for trend < 0.001). However, the amount of weight change over time varied considerably according to the ED of individual foods and beverages.
Conclusion
Increases in total dietary ED were associated with long-term weight gain among younger and middle-aged women. However, public health recommendations cannot be made simply based on ED values of individual foods and beverages only. Reducing consumption of foods high in saturated and trans fats and refined carbohydrates and increasing consumption of fruits and vegetables may help to reduce dietary ED and prevent weight gain.
PMCID: PMC3977032  PMID: 18779295
9.  Changes in water and beverage intake and long-term weight changes: results from three prospective cohort studies 
Objective
To examine the long-term relationship between changes in water and beverage intake and weight change.
Subjects
Prospective cohort studies of 50 013 women aged 40-64 in the Nurses’ Health Study (NHS, 1986-2006), 52 987 women aged 27-44 in the NHS II (1991-2007), and 21 988 men aged 40-64 in the Health Professionals Follow-up Study (1986-2006) without obesity and chronic diseases at baseline.
Measures
We assessed the association of weight change within each 4-year interval with changes in beverage intakes and other lifestyle behaviors during the same period. Multivariate linear regression with robust variance and accounting for within-person repeated measures were used to evaluate the association. Results across the three cohorts were pooled by an inverse-variance-weighted meta-analysis.
Results
Participants gained an average of 1.45 kg (5th to 95th percentile, −1.87 to 5.46) within each 4-year period. After controlling for age, baseline body mass index, and changes in other lifestyle behaviors (diet, smoking habits, exercise, alcohol, sleep duration, TV watching), each 1-cup/d increment of water intake was inversely associated with weight gain within each 4-year period (−0.13 kg; 95% CI: −0.17, −0.08). The associations for other beverages were: SSBs (0.36 kg; 0.24, 0.48), fruit juice (0.22 kg; 0.15, 0.28), coffee (−0.14 kg; −0.19, −0.09), tea (−0.03 kg; −0.05, −0.01), diet beverages (−0.10 kg; −0.14, −0.06), low-fat milk (0.02 kg; −0.04, 0.09), and whole milk (0.02 kg; −0.06, 0.10). We estimated that replacement of 1 serving/d of SSBs by 1 cup/d of water was associated with 0.49 kg (95% CI: 0.32, 0.65) less weight gain over each 4-year period, and the replacement estimate of fruit juices by water was 0.35 kg (95% CI: 0.23, 0.46). Substitution of SSBs or fruit juices by other beverages (coffee, tea, diet beverages, low-fat and whole milk) were all significantly and inversely associated with weight gain.
Conclusion
Our results suggest that increasing water intake in place of SSBs or fruit juices is associated with lower long-term weight gain.
doi:10.1038/ijo.2012.225
PMCID: PMC3628978  PMID: 23318721
water; beverage; body weight; prospective cohort study
10.  Does Being Overweight Really Reduce Mortality? 
Obesity (Silver Spring, Md.)  2013;21(9):10.1002/oby.20602.
There is indisputable evidence from epidemiologic and clinical studies that being overweight and obese elevates the risk of developing debilitating and costly chronic diseases, including hypertension, hypercholesterolemia, type 2 diabetes, cardiovascular diseases (CVD), and cancer (1). Nonetheless, the relationship between body mass index (BMI) and mortality remains the subject of much debate. A recent meta-analysis concluded that compared to those of normal weight (BMI<25.0), overweight individuals (BMI 25.0–29.9) had a significantly lower mortality risk (2). Even Class 1 obesity (BMI 30–34.9) was associated with marginally reduced mortality. In this Perspective, we discuss why this finding is likely to be an artifact of methodological limitations and what the clinical and public health implications may be.
doi:10.1002/oby.20602
PMCID: PMC3806201  PMID: 24078231
Obesity; overweight; mortality; reverse causation; chronic disease; body mass index
12.  The Association between Insomnia Symptoms and Mortality: A Prospective Study of US Men 
Circulation  2013;129(7):737-746.
Background
Insomnia complaints are common in older adults and may be associated with mortality risk. However, evidence regarding this association is mixed. We thus prospectively examined whether men with insomnia symptoms had an increased risk of mortality during 6 years of follow-up.
Methods and Results
A prospective cohort study of 23,447 US men participating in the Health Professionals Follow-up Study and free of cancer, reported on insomnia symptoms in 2004 were followed through 2010. Deaths were identified from state vital statistic records, the National Death Index, family reports, and the postal system. We documented 2025 deaths during 6 years of follow-up (2004-2010). The multivariable-adjusted hazard ratios (HRs) of total mortality were 1.25 (95% confidence interval (CI):1.04-1.50) for difficulty initiating sleep, 1.09 (95%CI:0.97-1.24) for difficulty maintaining sleep, 1.04 (95%CI:0.88-1.22) for early-morning awakenings, and 1.24 (95%CI:1.05-1.46) for non-restorative sleep, comparing men with those symptoms most of the time to men without those symptoms, after adjusting for age, lifestyle factors and presence of common chronic conditions. Men with difficulty initiating sleep and non-restorative sleep most of the time had a 55% (HR:1.55; 95% CI:1.19-2.04; P-trend= 0.01) and 32% (HR:1.32; 95% CI:1.02-1.72; P-trend=0.002) increased risk of CVD mortality, respectively, relative to men without those symptoms.
Conclusion
Some insomnia symptoms, especially difficulty initiating asleep and non-restorative sleep, are associated with a modestly higher risk of mortality.
doi:10.1161/CIRCULATIONAHA.113.004500
PMCID: PMC3987964  PMID: 24226807
Mortality; Sleep Disorders; Cardiovascular Outcomes; Insomnia
13.  A Genome Wide Association Study Identifies Common Variants Associated with Lipid Levels in the Chinese Population 
PLoS ONE  2013;8(12):e82420.
Plasma lipid levels are important risk factors for cardiovascular disease and are influenced by genetic and environmental factors. Recent genome wide association studies (GWAS) have identified several lipid-associated loci, but these loci have been identified primarily in European populations. In order to identify genetic markers for lipid levels in a Chinese population and analyze the heterogeneity between Europeans and Asians, especially Chinese, we performed a meta-analysis of two genome wide association studies on four common lipid traits including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) in a Han Chinese population totaling 3,451 healthy subjects. Replication was performed in an additional 8,830 subjects of Han Chinese ethnicity. We replicated eight loci associated with lipid levels previously reported in a European population. The loci genome wide significantly associated with TC were near DOCK7, HMGCR and ABO; those genome wide significantly associated with TG were near APOA1/C3/A4/A5 and LPL; those genome wide significantly associated with LDL were near HMGCR, ABO and TOMM40; and those genome wide significantly associated with HDL were near LPL, LIPC and CETP. In addition, an additive genotype score of eight SNPs representing the eight loci that were found to be associated with lipid levels was associated with higher TC, TG and LDL levels (P = 5.52×10-16, 1.38×10-6 and 5.59×10-9, respectively). These findings suggest the cumulative effects of multiple genetic loci on plasma lipid levels. Comparisons with previous GWAS of lipids highlight heterogeneity in allele frequency and in effect size for some loci between Chinese and European populations. The results from our GWAS provided comprehensive and convincing evidence of the genetic determinants of plasma lipid levels in a Chinese population.
doi:10.1371/journal.pone.0082420
PMCID: PMC3875415  PMID: 24386095
14.  Total and High-Molecular Weight Adiponectin and Resistin in Relation to the Risk for Type 2 Diabetes in Women: A Prospective Study 
Annals of internal medicine  2008;149(5):307-316.
Background
Adiponectin, particularly high-molecular weight adiponectin, and resistin are recently discovered adipokines that may provide a molecular link between adiposity and type 2 diabetes.
Objective
To evaluate whether total and high-molecular weight adiponectin and resistin are associated with the future risk for type 2 diabetes, independent of obesity and other known diabetes risk factors.
Design
Prospective, nested case-control study.
Settings
United States.
Participants
1,038 initially healthy women of the Nurses’ Health Study who developed type 2 diabetes after blood sampling (1989–1990) through 2002 and 1,136 matched control subjects.
Measurements
Plasma concentrations of adipokines were measured by enzyme-linked immunosorbent assays.
Results
In multivariate models adjusting for diabetes risk factors including body-mass index (BMI), both higher total and high-molecular weight adiponectin levels were associated with a substantially lower risk for type 2 diabetes. The odds ratios comparing the highest with the lowest quintiles were 0.17 (95% CI, 0.12–0.25) for total adiponectin and 0.10 (CI, 0.06–0.15) for high-molecular weight adiponectin. In addition, a higher high-molecular weight-to-total adiponectin ratio was associated with a significantly lower risk even after adjusting for total adiponectin (odds ratio, 0.45 [CI, 0.31–0.65]). In the multivariate model adjusting for diabetes risk factors except BMI, high resistin levels were significantly associated with an increased diabetes risk for (odds ratio, 1.68 [CI, 1.25–2.25]). However, after additional adjustment for BMI, this association was no longer statistically significant (odds ratio, 1.28 [CI, 0.93–1.76]).
Limitations
Residual confounding by imperfectly or unmeasured confounders cannot be excluded.
Conclusions
These results indicate that adiponectin, but not resistin is strongly associated with diabetes risk independent of BMI. The high-molecular weight-to-total adiponectin ratio is related to diabetes risk independent of total adiponectin, suggesting an important role of the relative proportion of high-molecular weight adiponectin in diabetes pathogenesis.
PMCID: PMC3874083  PMID: 18765700
15.  Joint Effects of Common Genetic Variants on the Risk for Type 2 Diabetes in U.S. Men and Women of European Ancestry 
Annals of internal medicine  2009;150(8):541-550.
Background
Genome-wide association studies have identified novel type 2 diabetes loci, each of which has a modest impact on risk.
Objective
To examine the joint effects of several type 2 diabetes risk variants and their combination with conventional risk factors on type 2 diabetes risk in 2 prospective cohorts.
Design
Nested case–control study.
Setting
United States.
Participants
2809 patients with type 2 diabetes and 3501 healthy control participants of European ancestry from the Health Professionals Follow-up Study and Nurses’ Health Study.
Measurements
A genetic risk score (GRS) was calculated on the basis of 10 polymorphisms in 9 loci.
Results
After adjustment for age and body mass index (BMI), the odds ratio for type 2 diabetes with each point of GRS, corresponding to 1 risk allele, was 1.19 (95% CI, 1.14 to 1.24) and 1.16 (CI, 1.12 to 1.20) for men and women, respectively. Persons with a BMI of 30 kg/m2 or greater and a GRS in the highest quintile had an odds ratio of 14.06 (CI, 8.90 to 22.18) compared with persons with a BMI less than 25 kg/m2 and a GRS in the lowest quintile after adjustment for age and sex. Persons with a positive family history of diabetes and a GRS in the highest quintile had an odds ratio of 9.20 (CI, 5.50 to 15.40) compared with persons without a family history of diabetes and with a GRS in the lowest quintile. The addition of the GRS to a model of conventional risk factors improved discrimination by 1% (P < 0.001).
Limitation
The study focused only on persons of European ancestry; whether GRS is associated with type 2 diabetes in other ethnic groups remains unknown.
Conclusion
Although its discriminatory value is currently limited, a GRS that combines information from multiple genetic variants might be useful for identifying subgroups with a particularly high risk for type 2 diabetes.
PMCID: PMC3825275  PMID: 19380854
16.  A Prospective Study of Weight Training and Risk of Type 2 Diabetes in Men 
Archives of internal medicine  2012;172(17):10.1001/archinternmed.2012.3138.
Background
The role of weight training in the primary prevention of type 2 diabetes is largely unknown. We examined the association of weight training with risk of type 2 diabetes among U.S. men and assessed the influence of combining weight training and aerobic exercise.
Methods
We performed a prospective cohort study among 32,002 men from the Health Professionals Follow-up Study that were followed from 1990 until 2008. Weekly time spent on weight training and aerobic exercise (including brisk walking, jogging, running, bicycling, swimming, tennis, squash, calisthenics/rowing) was obtained from questionnaires at baseline and biennially during follow-up.
Results
During 508,332 person years of follow-up (18 years), we documented 2,278 new cases of type 2 diabetes. In multivariable adjusted models, we observed a dose-response relationship between an increasing amount of time spent on weight training or aerobic exercise and lower risk of diabetes (p for trend<0.001). Engaging in weight training or aerobic exercise of at least 150 min/week was independently associated with a lower risk of diabetes of 34% (95% CI 7 – 54%) and 52% (95% CI 45 – 58%), respectively. Men who engaged in both aerobic exercise and weight training of at least 150 min/week had the greatest reduction in type 2 diabetes risk (59%, 95% CI 39 – 73%).
Conclusions
Weight training was associated with a significantly lower risk of type 2 diabetes, independent of aerobic exercise. The combination of weight training and aerobic exercise conferred a greater benefit.
doi:10.1001/archinternmed.2012.3138
PMCID: PMC3822244  PMID: 22868691
17.  Gene-environment interactions and obesity: recent developments and future directions 
BMC Medical Genomics  2015;8(Suppl 1):S2.
Obesity, a major public health concern, is a multifactorial disease caused by both environmental and genetic factors. Although recent genome-wide association studies have identified many loci related to obesity or body mass index, the identified variants explain only a small proportion of the heritability of obesity. Better understanding of the interplay between genetic and environmental factors is the basis for developing effective personalized obesity prevention and management strategies. This article reviews recent advances in identifying gene-environment interactions related to obesity and describes epidemiological designs and newly developed statistical approaches to characterizing and discovering gene-environment interactions on obesity risk.
doi:10.1186/1755-8794-8-S1-S2
PMCID: PMC4315311
18.  Body-Mass Index and All-Cause Mortality in US Adults With and Without Diabetes 
ABSTRACT
BACKGROUND
Previous studies found normal weight compared to overweight/obese adults with type 2 diabetes had a higher mortality risk, and body-mass index (BMI)–mortality studies do not typically account for baseline diabetes status.
OBJECTIVE
To determine if diabetes influences the BMI–mortality relationship.
DESIGN
Using a prospective study design, we analyzed data from a nationally representative sample of US adults participating in the National Health Interview Survey from 1997 to 2002, and followed for mortality through 2006.
PARTICIPANTS
Excluding those with heart disease or cancer, our final analytic sample included 74,710 (34,805 never smoker) adults.
MAIN MEASURES
BMI was calculated from self-reported height and weight. Diabetes status was based on self-reported diagnosis from a health professional. We used direct age standardization to calculate all-cause mortality rates and adjusted Cox models for all-cause mortality hazard ratios by BMI quintile; this was done separately for adults with diabetes and without diabetes.
KEY RESULTS
Among never smokers, mean age was 50.1 years and 43 % were men. Mean BMI was 27.4 kg/m2, 26 % were obese, and 2,035 (5 %) reported diagnosed diabetes. After 9 years, there were 4,355 deaths (754 of 4,740 with diabetes; 3,601 of 69,970 without) among 74,710 participants, and 1,238 (247 of 2,035 with diabetes; 991 of 32,770 without) among 34,805 never smokers. We observed a qualitative interaction with diabetes on the BMI–mortality relationship (p = 0.002). Death rates were substantially higher among participants with diabetes compared to those without diabetes across all BMI quintiles. However, death rates in participants with diabetes fell with increasing BMI quintile, while rates followed a J-shaped curve among those without diabetes. In adjusted Cox models, BMI was positively associated with mortality in adults without diabetes, but inversely associated with mortality among participants with diabetes.
CONCLUSIONS
Mortality increased with increasing BMI in adults without diabetes, but decreased with increasing BMI among their counterparts with diabetes. Future studies need to be better designed to answer the question of whether normal weight adults with diabetes have a higher risk of mortality, by minimizing the possibility of reverse causation. Future studies should also account for prevalent diabetes in all investigations of the BMI–mortality relationship.
Electronic supplementary material
The online version of this article (doi:10.1007/s11606-013-2553-7) contains supplementary material, which is available to authorized users.
doi:10.1007/s11606-013-2553-7
PMCID: PMC3889975  PMID: 23929218
diabetes; body mass index; mortality
19.  Circulating Fetuin-A and Risk of Ischemic Stroke in Women 
Clinical chemistry  2013;60(1):165-173.
Background
Fetuin-A, a protein secreted primarily by the liver, has been associated with non-alcoholic fatty liver disease and insulin resistance. In a recent study, higher circulating fetuin-A was associated with cardiovascular events, particularly ischemic stroke. However, these data have not been replicated.
Methods
A nested case-control design was utilized to examine the relationship between fetuin-A and ischemic stroke among female participants of the Nurses’ Health Study. Fetuin-A was measured in blood samples collected and stored between 1989–1990. A total of 459 incident cases of ischemic stroke were identified and confirmed by medical records according to the National Survey of Stroke criteria between 1990–2006 and matched to 459 controls by age, menopausal status, postmenopausal hormone use, and smoking status. The association between fetuin-A and ischemic stroke was modeled using conditional logistic regression.
Results
Circulating Fetuin-A was higher in women (P<0.01), who reported increased body mass index (BMI≥25 kg/m2), total cholesterol ≥200 mg/dL, high-sensitivity C-reactive protein ≥3 mg/L and current hormone use at baseline. Significant partial Spearman correlations (P<0.001), adjusted for matching factors, were found between measured concentrations of fetuin-A and triglycerides (r=0.20), C-reactive protein (r=0.14), and BMI (r=0.15). Fetuin-A quartiles were not significantly associated with increased risk of incident ischemic stroke when adjusted for matching factors (RR=1.03; 95% CI: 0.69–1.54, extreme quartiles); additional adjustment for lifestyle factors or CVD risk factors and biomarkers did not alter results.
Conclusions
In this sample of women, fetuin-A was not significantly associated with risk of ischemic stroke. Further research is needed to explore this association.
doi:10.1373/clinchem.2013.212597
PMCID: PMC3971644  PMID: 24170613
Ischemic stroke; fetuin-A; α2-Heremans-Schmid glycoprotein
20.  Genetic loci associated with circulating levels of very long-chain saturated fatty acids[S] 
Journal of Lipid Research  2015;56(1):176-184.
Very long-chain saturated fatty acids (VLSFAs) are saturated fatty acids with 20 or more carbons. In contrast to the more abundant saturated fatty acids, such as palmitic acid, there is growing evidence that circulating VLSFAs may have beneficial biological properties. Whether genetic factors influence circulating levels of VLSFAs is not known. We investigated the association of common genetic variation with plasma phospholipid/erythrocyte levels of three VLSFAs by performing genome-wide association studies in seven population-based cohorts comprising 10,129 subjects of European ancestry. We observed associations of circulating VLSFA concentrations with common variants in two genes, serine palmitoyl-transferase long-chain base subunit 3 (SPTLC3), a gene involved in the rate-limiting step of de novo sphingolipid synthesis, and ceramide synthase 4 (CERS4). The SPTLC3 variant at rs680379 was associated with higher arachidic acid (20:0 , P = 5.81 × 10−13). The CERS4 variant at rs2100944 was associated with higher levels of 20:0 (P = 2.65 × 10−40) and in analyses that adjusted for 20:0, with lower levels of behenic acid (P = 4.22 × 10−26) and lignoceric acid (P = 3.20 × 10−21). These novel associations suggest an inter-relationship of circulating VLSFAs and sphingolipid synthesis.
doi:10.1194/jlr.M052456
PMCID: PMC4274065  PMID: 25378659
arachidic acid; behenic acid; lignoceric acid; sphingolipids
21.  Genetics of Type 2 Diabetes in European Populations 
Journal of diabetes  2012;4(3):203-212.
Type 2 diabetes (T2D) has become a leading health problem throughout the world. It is caused by both environmental and genetic factors and interactions between them. However, until very recently, the T2D susceptibility genes have been poorly understood. During the past 5 years, with the advent of genome-wide association studies (GWAS), a total of 58 T2D susceptibility loci have been associated with T2D risk at a genome-wide significance level (P <5×10−8) and evidence shows that most of these genetic variants influence pancreatic β-cell function. Most novel T2D susceptibility loci were identified through GWAS in European populations and later confirmed in other ethnic groups. Although the recent discovery of novel T2D susceptibility loci has contributed substantially to our understanding of the pathophysiology of the disease, clinical utility of these loci in disease prediction and prognosis is limited. More studies using multiethnic meta-analysis, gene-environment interaction analysis, sequencing analysis, epigenetic analysis, and functional experiments are needed to identify new susceptibility T2D loci and causal variants and to establish biological mechanisms.
doi:10.1111/j.1753-0407.2012.00224.x
PMCID: PMC3422419  PMID: 22781158
Europeans; Genetics; Genome-wide association studies; Type 2 diabetes
22.  Post Diagnosis Diet Quality and Colorectal Cancer Survival in Women 
PLoS ONE  2014;9(12):e115377.
Background
Dietary factors are known to influence colorectal cancer (CRC) risk, however, their association with CRC survival is unclear. Therefore, we prospectively examined the association between diet quality scores, dietary patterns and colorectal cancer (CRC) survival.
Methods
1201 women diagnosed with stage I–III CRC between 1986 and 2008, were followed through 2010. Diet was assessed via a food frequency questionnaire administered at least 6 months after diagnosis. We computed the Alternate Healthy Eating Index-2010 (AHEI-2010), alternate Mediterranean Diet score (aMED) and Dietary Approaches to Stop Hypertension score (DASH) and derived two dietary patterns, Western (unhealthy) and prudent (healthy), by principal component analysis for each woman.
Results
During follow-up, we documented 435 deaths, including 162 from CRC. After adjusting for potential confounders, only a higher AHEI-2010 score was significantly associated with lower overall mortality (HR comparing extreme quintiles = 0.71, 95% CI 0.52–0.98, p trend = 0.01) as well as borderline significantly with lower risk of CRC mortality by the trend test (HR Q5 vs Q1 = 0.72, 95% CI = 0.43–1.21, p trend = 0.07). When AHEI-2010 components were examined separately, inverse associations for overall mortality were primarily accounted for by moderate alcohol intake (HR comparing abstainers vs 5–15 g/d = 1.30, 95%CI = 1.05–1.61) and lower intake of sugar sweetened beverages and fruit juices combined (HR for each additional serving = 1.11, 95% CI = 1.01–1.23). No other diet quality score or dietary pattern was associated with overall or CRC-specific mortality.
Conclusion
Higher AHEI-2010 score may be associated with lower overall mortality, moderate alcohol consumption and lower consumption of sugar sweetened beverages and juices combined appeared to account for most of the observed associations.
doi:10.1371/journal.pone.0115377
PMCID: PMC4266679  PMID: 25506700
23.  Red Meat Consumption and Mortality: Results from Two Prospective Cohort Studies 
Archives of internal medicine  2012;172(7):555-563.
Background
Red meat consumption has been associated with an increased risk of chronic diseases. However, its relationship with mortality remains uncertain.
Methods
We prospectively followed 37698 men from the Health Professionals Follow-up Study (1986-2008) and 83644 women from the Nurses' Health Study (1980-2008), who were free of cardiovascular disease (CVD) and cancer at baseline. Diet was assessed by validated food-frequency questionnaires and updated every four years.
Results
We documented 23926 deaths (including 5910 CVD and 9464 cancer deaths) during 2.96 million person-years of follow-up. After multivariate adjustment for major lifestyle and dietary risk factors, the pooled hazard ratio (HR) and 95% confidence interval of total mortality was 1.13 (1.07-1.20) for 1-serving per day increase of unprocessed red meat, 1.20 (1.15-1.24) for processed red meat. The corresponding HRs were 1.18 (1.13-1.23) and 1.21 (1.13-1.31) for CVD mortality, 1.10 (1.06-1.14) and 1.16 (1.09-1.23) for cancer mortality. We estimated that substitutions of 1-serving per day of other foods (including fish, poultry, nuts, legumes, low-fat dairy, and whole grains) for 1-serving per day of red meat were associated with a 7%-19% lower mortality risk. We also estimated that 9.3% of deaths in men and 7.6% in women in our cohorts could be prevented at the end of follow-up if all individuals consumed <0.5 serving/d (≈42 g/d) of red meat.
Conclusions
Red meat consumption is associated with an increased risk of total, CVD and cancer mortality. Substitution of other healthy protein sources for red meat is associated with a lower mortality risk.
doi:10.1001/archinternmed.2011.2287
PMCID: PMC3712342  PMID: 22412075
24.  Exporting Diabetes to Asia: The Impact of Western-Style Fast Food 
Circulation  2012;126(2):163-165.
doi:10.1161/CIRCULATIONAHA.112.115923
PMCID: PMC3401093  PMID: 22753305
cardiovascular disease risk factors; China; diabetes mellitus type 2; diet; Editorials; nutrition
25.  Systems Epidemiology: A New Direction in Nutrition and Metabolic Disease Research 
Current nutrition reports  2013;2(4):10.1007/s13668-013-0052-4.
Systems epidemiology applied to the field of nutrition has potential to provide new insight into underlying mechanisms and ways to study the health effects of specific foods more comprehensively. Human intervention and population-based studies have identified i) common genetic factors associated with several nutrition-related traits and ii) dietary factors altering the expression of genes and levels of proteins and metabolites related to inflammation, lipid metabolism and/or gut microbial metabolism, results of high relevance to metabolic disease. System-level tools applied type 2 diabetes and related conditions have revealed new pathways that are potentially modified by diet and thus offer additional opportunities for nutritional investigations. Moving forward, harnessing the resources of existing large prospective studies within which biological samples have been archived and diet and lifestyle have been measured repeatedly within individual will enable systems-level data to be integrated, the outcome of which will be improved personalized optimal nutrition for prevention and treatment of disease.
doi:10.1007/s13668-013-0052-4
PMCID: PMC3837346  PMID: 24278790
nutrition; systems; genomics; transcriptomics; proteomics; metabolomics; type 2 diabetes; obesity; metabolic disease; epidemiology; populations; diet; network; nutrigenetics; nutrigenomics

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