Jiantao Ma

Fructose, high-fructose corn syrup, sucrose, and nonalcoholic fatty liver disease or indexes of liver health: a systematic review and meta-analysis

Background: Concerns have been raised about the concurrent temporal trend between simple sugar intakes, especially of fructose or high-fructose corn syrup (HFCS), and rates of nonalcoholic fatty liver disease (NAFLD) in the United States. Objective: We examined the effect of different amounts and forms of dietary fructose on the incidence or prevalence of NAFLD and indexes of liver health in humans. Design: We conducted a systematic review of English-language, human studies of any design in children and adults with low to no alcohol intake and that reported at least one predetermined measure of liver health. The strength of the evidence was evaluated by considering risk of bias, consistency, directness, and precision. Results: Six observational studies and 21 intervention studies met the inclusion criteria. The overall strength of evidence for observational studies was rated insufficient because of high risk of biases and inconsistent study findings. Of 21 intervention studies, 19 studies were in adults without NAFLD (predominantly healthy, young men) and 1 study each in adults or children with NAFLD. We found a low level of evidence that a hypercaloric fructose diet (supplemented by pure fructose) increases liver fat and aspartate aminotransferase (AST) concentrations in healthy men compared with the consumption of a weight-maintenance diet. In addition, there was a low level of evidence that hypercaloric fructose and glucose diets have similar effects on liver fat and liver enzymes in healthy adults. There was insufficient evidence to draw a conclusion for effects of HFCS or sucrose on NAFLD. Conclusions: On the basis of indirect comparisons across study findings, the apparent association between indexes of liver health (ie, liver fat, hepatic de novo lipogenesis, alanine aminotransferase, AST, and γ-glutamyl transpeptase) and fructose or sucrose intake appear to be confounded by excessive energy intake. Overall, the available evidence is not sufficiently robust to draw conclusions regarding effects of fructose, HFCS, or sucrose consumption on NAFLD.

Genetic Risk Score and Risk of Myocardial Infarction in Hispanics

Background— Genome-wide association studies have identified loci associated with coronary heart disease in whites of European ancestry. This study evaluated whether genetic markers previously identified in whites are associated with nonfatal acute myocardial infarction (MI) in Hispanics. Methods and Results— Cases (n=1989) with a first nonfatal acute MI and population-based controls (n=2096) living in Costa Rica were studied. Fourteen single-nucleotide polymorphisms were genotyped. Seven single-nucleotide polymorphisms at 3 independent loci showed significant associations with MI. The odds ratios for the loci with the strongest associations were 1.16 (95% confidence interval [CI], 1.05 to 1.27) for rs4977574 (CDKN2A/2B), 1.15 (95% CI, 1.03 to 1.29) for rs646776 (CELSR2-PSRC1-SORT1), and 1.22 (95% CI, 1.08 to 1.38) for rs501120 (CXCL12); the corresponding PARs were 6.8%, 10.5%, and 15.2%; respectively. We developed a genetic risk score by summing the number of the top 3 associated risk alleles. The OR for MI per genetic risk score unit was 1.18 (95% CI, 1.11 to 1.25; P=4.83×10−8). Discrimination of MI was significantly improved (P=0.02) when the genetic risk score was added to a model including clinical predictors. However, the increase in the area under the receiver-operating characteristic curve after the genetic risk score was added was moderate, from 0.67 (95% CI, 0.65 to 0.69) to 0.68 (95% CI, 0.66 to 0.70). Conclusions— These results indicate both the consistency and disparity of genetic effects on risk of MI between Hispanic and white populations. The improvement in the identified genetic markers on discrimination of MI in Hispanics was modest.

Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts

BACKGROUND & AIMS Non-alcoholic fatty liver disease affects ∼30% of US adults, yet the role of sugar-sweetened beverages and diet soda on these diseases remains unknown. We examined the cross-sectional association between intake of sugar-sweetened beverages or diet soda and fatty liver disease in participants of the Framingham Offspring and Third Generation cohorts. METHODS Fatty liver disease was defined using liver attenuation measurements generated from computed tomography in 2634 participants. Alanine transaminase concentration, a crude marker of fatty liver disease, was measured in 5908 participants. Sugar-sweetened beverage and diet soda intake were estimated using a food frequency questionnaire. Participants were categorized as either non-consumers or consumers (3 categories: 1 serving/month to <1 serving/week, 1 serving/week to <1 serving/day, and ⩾1 serving/day) of sugar-sweetened beverages or diet soda. RESULTS After adjustment for age, sex, smoking status, Framingham cohort, energy intake, alcohol, dietary fiber, fat (% energy), protein (% energy), diet soda intake, and body mass index, the odds ratios of fatty liver disease were 1, 1.16 (0.88, 1.54), 1.32 (0.93, 1.86), and 1.61 (1.04, 2.49) across sugar-sweetened beverage consumption categories (p trend=0.04). Sugar-sweetened beverage consumption was also positively associated with alanine transaminase levels (p trend=0.007). We observed no significant association between diet soda intake and measures of fatty liver disease. CONCLUSION In conclusion, we observed that regular sugar-sweetened beverage consumption was associated with greater risk of fatty liver disease, particularly in overweight and obese individuals, whereas diet soda intake was not associated with measures of fatty liver disease.

Sugar-Sweetened Beverage Consumption is Associated With Change of Visceral Adipose Tissue Over 6 Years of Follow-Up

Background— Sugar-sweetened beverage (SSB) intake has been linked to abnormal abdominal adipose tissue. We examined the prospective association of habitual SSB intake and change in visceral adipose tissue (VAT) and subcutaneous adipose tissue. Methods and Results— The quantity (volume, cm3) and quality (attenuation, Hounsfield Unit) of abdominal adipose tissue were measured using computed tomography in 1003 participants (mean age 45.3 years, 45.0% women) at examination 1 and 2 in the Framingham’s Third Generation cohort. The 2 exams were ≈6 years apart. At baseline, SSB and diet soda intake were assessed using a valid food frequency questionnaire. Participants were categorized into 4 groups: none to <1 serving/mo (nonconsumers), 1 serving/mo to <1 serving/week, 1 serving/week to 1 serving/d, and ≥1 serving/d (daily consumers) of either SSB or diet soda. After adjustment for multiple confounders including change in body weight, higher SSB intake was associated with greater change in VAT volume (P trend<0.001). VAT volume increased by 658 cm3 (95% confidence interval [CI], 602 to 713), 649 cm3 (95% CI, 582 to 716), 707 cm3 (95% CI, 657 to 757), and 852 cm3 (95% CI, 760 to 943) from nonconsumers to daily consumers. Higher SSB intake was also associated with greater decline of VAT attenuation (P trend=0.007); however, the association became nonsignificant after additional adjustment for VAT volume change. In contrast, diet soda consumption was not associated with change in abdominal adipose tissue. Conclusions— Regular SSB intake was associated with adverse change in both VAT quality and quantity, whereas we observed no such association for diet soda.

Sugar-Sweetened Beverage Consumption Is Associated with Abdominal Fat Partitioning in Healthy Adults

Abdominal adiposity, particularly visceral adipose tissue (VAT), is independently linked to the pathogenesis of diabetes and cardiovascular diseases. Emerging evidence suggests that greater intake of sugar-sweetened beverages (SSBs) may be associated with abnormal fat accumulation in VAT. We examined whether habitual SSB consumption and diet soda intakes are differentially associated with deposition of body fat. We conducted a cross-sectional analysis using previously collected data in 2596 middle-aged adults (1306 men and 1290 women) from the Framingham Heart Study Offspring and Third Generation cohorts. VAT and abdominal subcutaneous adipose tissue (SAT) were measured using multidetector computed tomography. Habitual intake of SSBs and diet soda was assessed by a validated food frequency questionnaire. We observed that SSB consumption was positively associated with VAT after adjustment for SAT and other potential confounders (P-trend < 0.001). We observed an inverse association between SSB consumption and SAT (P-trend = 0.04) that persisted after additional adjustment for VAT (P-trend < 0.001). Higher SSB consumption was positively associated with the VAT-to-SAT ratio (P-trend < 0.001). No significant association was found between diet soda consumption and either VAT or the VAT-to-SAT ratio, but diet soda was positively associated with SAT (P-trend < 0.001). Daily consumers of SSBs had a 10% higher absolute VAT volume and a 15% greater VAT-to-SAT ratio compared with nonconsumers, whereas consumption of diet soda was not associated with either volume or distribution of VAT.

Bi-directional analysis between fatty liver and cardiovascular disease risk factors

BACKGROUND & AIMS The relations of non-alcoholic fatty liver disease to cardiovascular disease (CVD) risk factors are not fully understood. The objective of our study is to explore the bi-directional relationships of fatty liver to CVD risk factors. METHODS We prospectively evaluated whether liver fat predicted the development of CVD risk factors and whether CVD risk factors predicted new onset fatty liver during 6years of follow-up in middle- to older-aged Framingham Heart Study participants. We estimated liver fat using multi-detector computed tomography. RESULTS We included 1051 participants (mean age 45±6years, 46% women). The prevalence of fatty liver was 18% at baseline. In participants without fatty liver at baseline, 101 participants developed incident fatty liver over approximately 6years. Baseline liver fat (per standard deviation increase) was associated with increased odds of incident hypertension (OR 1.42; 95% CI 1.15-1.76; p=0.001) and incident type 2 diabetes (OR 1.43; 95% CI 1.09-1.88, p<0.001). In a parallel analysis, individuals with hypertension (OR 3.34; 95% CI 2.04-5.49), hypertriglyceridemia (OR 3.04; 95% CI: 1.84-5.02), impaired fasting glucose (OR 2.92; 95% CI 1.76-4.82), or type 2 diabetes (OR 4.15; 95% CI 1.19-14.46) at baseline had higher odds of incident fatty liver compared to individuals without those conditions (all p<0.03). In both analyses, the observed associations remained similar after additional adjustments for measures of adiposity. CONCLUSIONS The present study demonstrated bi-directional relationships between fatty liver and CVD risk factors among middle- to older-aged Framingham Heart Study participants. LAY SUMMARY It is not fully understood whether non-alcoholic fatty liver (NAFLD) disease precedes or develops after increased cardiovascular disease (CVD) risk factors. The findings of our study suggest a bi-directional relationship between NAFLD and CVD risk factors.

Mid-adulthood cardiometabolic risk factor profiles of sarcopenic obesity.

Midlife and contemporaneous cardiometabolic risk factors associated with sarcopenic obesity were examined.

Associations of Dairy Intake with Incident Prediabetes or Diabetes in Middle-Aged Adults Vary by Both Dairy Type and Glycemic Status

Background: Inconsistent evidence describes the association between dietary intake of dairy and milk-based products and type 2 diabetes (T2D) risk.Objective: Our objective was to assess associations between consumption of milk-based products, incident prediabetes, and progression to T2D in the Framingham Heart Study Offspring Cohort.Methods: Total dairy and milk-based product consumption was assessed by ≤4 food-frequency questionnaires across a mean of 12 y of follow-up in 2809 participants [mean ± SD age: 54.0 ± 9.7 y; body mass index (in kg/m2): 27.1 ± 4.7; 54% female]. Prediabetes was defined as the first occurrence of fasting plasma glucose ≥5.6 to <7.0 mmol/L (≥100 to <126 mg/dL), and T2D was defined as the first occurrence of fasting plasma glucose ≥7.0 mmol/L (≥126 mg/dL) or diabetes treatment. Proportional hazards models were used to estimate the risk of incident outcomes relative to dairy product intake in subsets of the cohort who were at risk of developing the outcomes. Spline regressions were used to examine potential nonlinear relations.Results: Of 1867 participants free of prediabetes at baseline, 902 (48%) developed prediabetes. Total, low-fat, and high-fat dairy consumptions were associated with a 39%, 32%, and 25% lower risk of incident prediabetes, respectively, in the highest compared with the lowest intakes (≥14 compared with <4 servings/wk). Total, low-fat and skim milk, whole-milk, and yogurt intakes were associated nonlinearly with incident prediabetes; moderate intake was associated with the greatest relative risk reduction. Neither cheese nor cream and butter was associated with prediabetes. Of 925 participants with prediabetes at baseline, 196 (21%) developed T2D. Only high-fat dairy and cheese showed evidence of dose-response, inverse associations with incident T2D, with 70% and 63% lower risk, respectively, of incident T2D between the highest and lowest intake categories (≥14 compared with <1 serving/wk for high-fat dairy, ≥4 compared with <1 serving/wk for cheese).Conclusion: Associations of dairy with incident prediabetes or diabetes varied both by dairy product and type and by baseline glycemic status in this middle-aged US population. Baseline glycemic status may partially underlie prior equivocal evidence regarding the role of dairy intake in diabetes.

Barriers to medication adherence and links to cardiovascular disease risk factor control: the Framingham Heart Study: Medication adherence and CVD risk

In the elderly, impaired cognition may weaken medication adherence and compromise treatment for cardiovascular disease (CVD).

A simple clinical model predicts incident hepatic steatosis in a community-based cohort: The Framingham Heart Study

The factors associated with incident hepatic steatosis are not definitively known. We sought to determine factors associated with incident hepatic steatosis, as measured on computed tomography, in the community.