0
selected
-
1.
Ultraprocessed Food Consumption and Risk of Type 2 Diabetes Among Participants of the NutriNet-Santé Prospective Cohort.
Srour, B, Fezeu, LK, Kesse-Guyot, E, Allès, B, Debras, C, Druesne-Pecollo, N, Chazelas, E, Deschasaux, M, Hercberg, S, Galan, P, et al
JAMA internal medicine. 2020;(2):283-291
-
-
Free full text
-
Abstract
IMPORTANCE Ultraprocessed foods (UPF) are widespread in Western diets. Their consumption has been associated in recent prospective studies with increased risks of all-cause mortality and chronic diseases such as cancer, cardiovascular diseases, hypertension, and dyslipidemia; however, data regarding diabetes are lacking. OBJECTIVE To assess the associations between consumption of UPF and risk of type 2 diabetes (T2D). DESIGN, SETTING, AND PARTICIPANTS In this population-based prospective cohort study, 104 707 participants aged 18 years or older from the French NutriNet-Santé cohort (2009-2019) were included. Dietary intake data were collected using repeated 24-hour dietary records (5.7 per participant on average), designed to register participants' usual consumption for more than 3500 different food items. These were categorized according to their degree of processing by the NOVA classification system. MAIN OUTCOMES AND MEASURES Associations between UPF consumption and risk of T2D were assessed using cause-specific multivariable Cox proportional hazard models adjusted for known risk factors (sociodemographic, anthropometric, lifestyle, medical history, and nutritional factors). RESULTS A total of 104 707 participants (21 800 [20.8%] men and 82 907 [79.2%] women) were included. Mean (SD) baseline age of participants was 42.7 (14.5) years. Absolute T2D rates in the lowest and highest UPF consumers were 113 and 166 per 100 000 person-years, respectively. Consumption of UPF was associated with a higher risk of T2D (multi-adjusted hazard ratio [HR] for an absolute increment of 10 in the percentage of UPF in the diet, 1.15; 95% CI, 1.06-1.25; median follow-up, 6.0 years; 582 252 person-years; 821 incident cases). These results remained statistically significant after adjustment for several markers of the nutritional quality of the diet, for other metabolic comorbidities (HR, 1.13; 95% CI, 1.03-1.23), and for weight change (HR, 1.13; 95% CI, 1.01-1.27). The absolute amount of UPF consumption (grams per day) was consistently associated with T2D risk, even when adjusting for unprocessed or minimally processed food intake (HR for a 100 g/d increase, 1.05; 95% CI, 1.02-1.08). CONCLUSIONS AND RELEVANCE In this large observational prospective study, a higher proportion of UPF in the diet was associated with a higher risk of T2D. Even though these results need to be confirmed in other populations and settings, they provide evidence to support efforts by public health authorities to recommend limiting UPF consumption. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT03335644.
-
2.
Total and added sugar intakes, sugar types, and cancer risk: results from the prospective NutriNet-Santé cohort.
Debras, C, Chazelas, E, Srour, B, Kesse-Guyot, E, Julia, C, Zelek, L, Agaësse, C, Druesne-Pecollo, N, Galan, P, Hercberg, S, et al
The American journal of clinical nutrition. 2020;(5):1267-1279
-
-
Free full text
-
Abstract
BACKGROUND Excessive sugar intake is now recognized as a key risk factor for obesity, type 2 diabetes, and cardiovascular diseases. In contrast, evidence on the sugar-cancer link is less consistent. Experimental data suggest that sugars could play a role in cancer etiology through obesity but also through inflammatory and oxidative mechanisms and insulin resistance, even in the absence of weight gain. OBJECTIVE The objective was to study the associations between total and added sugar intake and cancer risk (overall, breast, and prostate), taking into account sugar types and sources. METHODS In total, 101,279 participants aged >18 y (median age, 40.8 y) from the French NutriNet-Santé prospective cohort study (2009-2019) were included (median follow-up time, 5.9 y). Sugar intake was assessed using repeated and validated 24-h dietary records, designed to register participants' usual consumption for >3500 food and beverage items. Associations between sugar intake and cancer risk were assessed by Cox proportional hazard models adjusted for known risk factors (sociodemographic, anthropometric, lifestyle, medical history, and nutritional factors). RESULTS Total sugar intake was associated with higher overall cancer risk (n = 2503 cases; HR for quartile 4 compared with quartile 1: 1.17; 95% CI: 1.00, 1.37; Ptrend = 0.02). Breast cancer risks were increased (n = 783 cases; HRQ4vs.Q1 = 1.51; 95% CI: 1.14, 2.00; Ptrend = 0.0007). Results remained significant when weight gain during follow-up was adjusted for. In addition, significant associations with cancer risk were also observed for added sugars, free sugars, sucrose, sugars from milk-based desserts, dairy products, and sugary drinks (Ptrend ≤ 0.01). CONCLUSIONS These results suggest that sugars may represent a modifiable risk factor for cancer prevention (breast in particular), contributing to the current debate on the implementation of sugar taxation, marketing regulation, and other sugar-related policies. This trial was registered at clinicaltrials.gov as NCT03335644.
-
3.
Prospective association between a dietary quality index based on a nutrient profiling system and cardiovascular disease risk.
Adriouch, S, Julia, C, Kesse-Guyot, E, Méjean, C, Ducrot, P, Péneau, S, Donnenfeld, M, Deschasaux, M, Menai, M, Hercberg, S, et al
European journal of preventive cardiology. 2016;(15):1669-76
Abstract
BACKGROUND Public health strategies are essential to guide consumers' choices and produce a substantial population impact on cardiovascular disease risk prevention through nutrition. Our aim was to investigate the prospective association between the Food Standards Agency nutrient profiling system dietary index (FSA-NPS DI) and cardiovascular disease risk. The FSA-NPS has been proposed to serve as a basis for a five-colour nutrition label suggested in France to be put on the front of pack of food products. METHODS AND RESULTS A total of 6515 participants to the SU.VI.MAX cohort (1994-2007), who completed at least six 24-hour dietary records during the first two years of the study, were followed for a median of 12.4 years (25th-75th percentiles: 11.0-12.6). Multivariable Cox proportional hazards models were used to characterise the associations between FSA-NPS DI (continuous and sex-specific quartiles) and the incidence of cardiovascular diseases. Interactions with individual characteristics were tested; 181 major cardiovascular events were reported (59 myocardial infarctions, 43 strokes, 79 anginas). A higher FSA-NPS DI, characterising poorer food choices, was associated with an overall increase in cardiovascular disease risk (HRfor a 1-point increment = 1.14 (1.03-1.27); HRQ4vs.Q1 = 1.61 (1.05-2.47), Ptrend Q4-Q1 = 0.03). This association tended to be stronger in smokers (HRfor a 1-point increment = 1.39 (1.11-1.73); Pinteraction = 0.01) and those less physically active (HRfor a 1-point increment = 1.26 (1.08-1.46); Pinteraction = 0.04). CONCLUSIONS Our results suggest that poorer food choices, as reflected by a higher FSA-NPS DI, may be associated with a significant increase in cardiovascular risk, especially in at-risk individuals (smokers and physically inactive persons). This score could be a useful tool for public health prevention strategies. CLINICAL TRIAL REGISTRATION ClinicalTrials.gov identifier: NCT00272428.
-
4.
Prospective Association Between the Dietary Inflammatory Index and Cardiovascular Diseases in the SUpplémentation en VItamines et Minéraux AntioXydants (SU.VI.MAX) Cohort.
Neufcourt, L, Assmann, KE, Fezeu, LK, Touvier, M, Graffouillère, L, Shivappa, N, Hébert, JR, Wirth, MD, Hercberg, S, Galan, P, et al
Journal of the American Heart Association. 2016;(3):e002735
Abstract
BACKGROUND Cardiovascular diseases (CVD) are the leading cause of death in the world, and diet plays a major role in CVD incidence, especially through lipid oxidation mechanisms. This, in turn, leads to tissue inflammation and formation of atheromatous plaques. METHODS AND RESULTS Our objective was to evaluate the association between the inflammatory potential of the diet and the incidence of overall CVD or its subclasses. We included 7743 participants from the Supplémentation en Vitamines et Minéraux AntioXydants (SU.VI.MAX) cohort. All cardiovascular events were recorded using self-reported information or clinical visits, and were validated. The dietary inflammatory index (DII) was computed using repeated 24-hour dietary records (mean=9.5±3.4 records/subject). Hazard ratio and 95% CI for outcomes (CVD and subclasses) were estimated across sex-specific quartiles of the DII using Cox proportional hazard models. A total of 292 cardiovascular events were recorded and validated during an average of 11.4 years of follow-up: 93 myocardial infarctions, 58 strokes, 128 angina pectoris and revascularization interventions, and 13 sudden deaths. When considering CVD subclasses, a diet with pro-inflammatory properties, as expressed by higher DII scores, was significantly associated with a higher risk of myocardial infarction (hazard ratioQuartile 4 versus Quartile 1=2.24, 95% CI: 1.08-4.67). No significant association was observed between the DII score and stroke or both angina pectoris and revascularization intervention. CONCLUSIONS A pro-inflammatory diet, as measured by a higher DII score, was prospectively associated with a higher risk of myocardial infarction. Promotion of a diet exhibiting anti-inflammatory properties may help prevent myocardial infarctions.
-
5.
Prospective association between the Dietary Inflammatory Index and mortality: modulation by antioxidant supplementation in the SU.VI.MAX randomized controlled trial.
Graffouillère, L, Deschasaux, M, Mariotti, F, Neufcourt, L, Shivappa, N, Hébert, JR, Wirth, MD, Latino-Martel, P, Hercberg, S, Galan, P, et al
The American journal of clinical nutrition. 2016;(3):878-85
-
-
Free full text
-
Abstract
BACKGROUND Chronic inflammation is a central mechanism involved in cardiovascular diseases, cancer, diabetes, and chronic respiratory diseases, 4 leading causes of mortality. Diet is a major source of pro- and anti-inflammatory bioactive compounds. The Dietary Inflammatory Index (DII) was designed to estimate the overall inflammatory potential of the diet. OBJECTIVE Our aim was to study the prospective association between the DII and mortality, as well as assess whether antioxidant supplementation could modulate this association. DESIGN The Supplémentation en Vitamines et Minéraux Antioxydants study was a randomized, double-blind, placebo-controlled trial in which participants received low-dose antioxidants or a placebo from 1994 to 2002. In this observational prospective analysis, 8089 participants (mean ± SD age at baseline: 49.0 ± 6.3 y) were followed between 1994 and 2007 (median: 12.4 y). The DII was calculated from repeated 24-h dietary records; higher scores correspond to more proinflammatory diets. A total of 207 deaths occurred during follow-up, including 123 due to cancer and 41 due to cardiovascular events. Multivariate Cox proportional hazards models were computed. RESULTS Sex-specific tertiles of the DII were positively associated with cardiovascular + cancer mortality (HR for tertile 3 compared with tertile 1 = 1.53; 95% CI: 1.01, 2.32; P-trend = 0.05) and specific cancer mortality (HR for tertile 3 compared with tertile 1 = 1.83; 95% CI: 1.12, 2.99; P-trend = 0.02). The corresponding P value was 0.07 for all-cause mortality. The DII was statistically significantly associated with increased all-cause mortality in the placebo group (HR for tertile 3 compared with tertile 1 = 2.10; 95% CI: 1.15, 3.84; P-trend = 0.02) but not in the antioxidant-supplemented group (P-trend = 0.8; P-interaction = 0.098). CONCLUSION These results suggest that a proinflammatory diet is associated with increased all-cause and cancer mortality and antioxidants may counteract some of the proinflammatory effects of the diet. This trial was registered at clinicaltrials.gov as NCT00272428.