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Added sugar intake and its forms and sources in relation to risk of non-alcoholic fatty liver disease: results from the Tianjin Chronic Low-grade Systemic Inflammation and Health cohort study.
Zhang S
,Li H
,Meng G
,Zhang Q
,Liu L
,Wu H
,Gu Y
,Zhang T
,Wang X
,Zhang J
,Dong J
,Zheng X
,Cao Z
,Zhang X
,Dong X
,Sun S
,Wang X
,Zhou M
,Jia Q
,Song K
,China Cohort Consortium
,Borné Y
,Sonestedt E
,Qi L
,Niu K
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Dietary patterns and risk of non-alcoholic fatty liver disease in adults: A prospective cohort study.
Prospective cohort studies linking dietary patterns and non-alcoholic fatty liver disease (NAFLD) are limited, especially in Asian populations. This study aimed to prospectively investigate the association between dietary patterns and risk of NAFLD in a general Chinese adult population.
This study included a total of 17,360 participants free from NAFLD at baseline. Dietary patterns at baseline were identified with factor analysis based on responses to a validated 100-item food frequency questionnaire. NAFLD was diagnosed by abdominal ultrasound after excluding other causes related to chronic liver disease. Cox proportional regression models were used to assess the association between dietary patterns and risk of NAFLD.
During a median follow-up of 4.2 years, 4034 NAFLD cases were documented. Three main dietary patterns were extracted: sugar rich dietary pattern, vegetable rich dietary pattern, and animal food dietary pattern. After adjusting for age, sex, body mass index, smoking, alcohol, education, occupation, income, physical activity, total energy intake, personal and family history of disease, depressive symptoms, dietary supplement use, inflammation markers, and each other dietary pattern score, comparing the highest with the lowest quartiles of dietary pattern scores, the multivariable hazard ratios (95% confidence interval) of NAFLD were 1.11 (1.01, 1.23) for sugar rich dietary pattern, 0.96 (0.86, 1.07) for vegetable rich dietary pattern, and 1.22 (1.10, 1.36) for animal food dietary pattern. Further adjustment for waist circumference instead of body mass index provided similar results.
Dietary patterns rich in animal foods or sugar were associated with a higher risk of NAFLD among Chinese adults, whereas a vegetable rich dietary pattern was not associated.
Zhang S
,Gu Y
,Bian S
,Górska MJ
,Zhang Q
,Liu L
,Meng G
,Yao Z
,Wu H
,Wang Y
,Zhang T
,Wang X
,Sun S
,Wang X
,Zhou M
,Jia Q
,Song K
,Qi L
,Niu K
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Soft drink consumption and risk of nonalcoholic fatty liver disease: results from the Tianjin Chronic Low-Grade Systemic Inflammation and Health (TCLSIH) cohort study.
Epidemiological evidence for the association of soft drink consumption with nonalcoholic fatty liver disease (NAFLD) is inconsistent, and such association has not been prospectively examined in the general adult population.
We aimed to investigate the prospective association between soft drink consumption and the risk of NAFLD in a Chinese adult population.
This prospective cohort study investigated 14,845 participants [mean age: 39.3 y; 6203 (41.8%) men] who were free of liver disease, cardiovascular disease, and cancer at baseline. Soft drink consumption (mainly sugar-containing carbonated beverages) was measured at baseline using a validated FFQ. NAFLD was diagnosed based on abdominal ultrasound without significant alcohol consumption and other causes of liver disease. Hepatic steatosis index (HSI) was calculated based on sex, BMI, and blood transaminase levels. Cox proportional hazards regression models were used to examine the association of soft drink consumption with incident NAFLD.
A total of 2888 first-incident cases of NAFLD occurred during 42,048 person-years of follow-up (median follow-up: 4.2 y). After adjusting for demographic characteristics, lifestyle factors, dietary intake, and inflammatory markers, the multivariable HRs (95% CIs) for incident NAFLD were 1.00 (reference) for <1 serving/wk, 1.18 (1.03, 1.34) for 1 serving/wk, 1.23 (1.08, 1.40) for 2-3 servings/wk, and 1.47 (1.25, 1.73) for ≥4 servings/wk, respectively (P for trend < 0.0001). Further sensitivity analysis showed that the corresponding multivariable HRs (95% CIs) for incident HSI-defined NAFLD were 1.00 (reference), 0.96 (0.70, 1.31), 1.16 (0.83, 1.62), and 1.59 (1.07, 2.37), respectively (P for trend < 0.0001).
The results from our prospective study indicate that soft drink consumption is associated with an increased risk of NAFLD in Chinese adults. This study was registered at UMIN Clinical Trials Registry as UMIN000027174.
Zhang S
,Gu Y
,Bian S
,Lu Z
,Zhang Q
,Liu L
,Meng G
,Yao Z
,Wu H
,Wang Y
,Zhang T
,Wang X
,Sun S
,Wang X
,Zhou M
,Jia Q
,Song K
,Qi L
,Niu K
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Ultra-processed food consumption and the risk of non-alcoholic fatty liver disease in the Tianjin Chronic Low-grade Systemic Inflammation and Health Cohort Study.
Growing evidence supports a link between ultra-processed food consumption and human health outcomes. However, the association between ultra-processed food consumption and non-alcoholic fatty liver disease (NAFLD) is not known. We aimed to explore the association between ultra-processed food consumption and risk of NAFLD.
The prospective study included 16 168 participants aged 18-90 years from the Tianjin Chronic Low-grade Systemic Inflammation and Health (TCLSIH) Cohort Study. Information on ultra-processed food consumption was collected at baseline using a validated food frequency questionnaire. NAFLD was defined as the presence of sonographic fatty liver in the absence of significant alcohol intake (≥210 g/week for men and ≥140 g/week for women, respectively) and other liver diseases. Multivariable Cox proportional hazards models were used to examine the association between ultra-processed food consumption and risk of NAFLD.
During 56 935 person-years of follow-up, we documented 3752 incident NAFLD cases. After adjusting for age, sex, body mass index, smoking, alcohol drinking, education, occupation, income, physical activity, total energy intake, personal and family history of disease and overall diet quality, the multivariable hazard ratios (95% confidence interval) of NAFLD across increasing quartiles of ultra-processed food consumption were 1.00 (reference), 0.99 (0.90, 1.08), 1.13 (1.03, 1.25) and 1.18 (1.07, 1.30), respectively (P for trend <0.0001). The hazard ratio (95% confidence interval) per one standard deviation increase in ultra-processed food consumption, equivalent to a 62.7 g/1000 kcal per day, was 1.06 (1.03, 1.09), P = 0.0001.
Our study indicates that higher ultra-processed food consumption is associated with a higher risk of NAFLD. This finding suggests that ultra-processed food, which is widely consumed worldwide, might be a modifiable dietary target to reduce the risk of NAFLD.
Zhang S
,Gan S
,Zhang Q
,Liu L
,Meng G
,Yao Z
,Wu H
,Gu Y
,Wang Y
,Zhang T
,Wang X
,Sun S
,Wang X
,Zhou M
,Jia Q
,Song K
,Qi L
,Niu K
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Total and added sugar intakes, sugar types, and cancer risk: results from the prospective NutriNet-Santé cohort.
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.
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.
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).
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).
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.
Debras C
,Chazelas E
,Srour B
,Kesse-Guyot E
,Julia C
,Zelek L
,Agaësse C
,Druesne-Pecollo N
,Galan P
,Hercberg S
,Latino-Martel P
,Deschasaux M
,Touvier M
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