METHODS: This is a cross sectional study conducted in adults living at urban area of Yogyakarta, Indonesia. Data of adiposity, lifestyle, triglyceride, high density lipoprotein (HDL) cholesterol, leptin and UCP2 gene polymorphism were obtained in 380 men and female adults.
RESULTS: UCP2 gene polymorphism was not significantly associated with adiposity, leptin, triglyceride, HDL cholesterol, dietary intake and physical activity (allp> 0.05). Leptin was lower in overweight subjects with AA + GA genotypes than those with GG genotype counterparts (p= 0.029). In subjects with AA + GA genotypes there was a negative correlation between leptin concentration (r= -0.324;p< 0.0001) and total energy intake and this correlation was not seen in GG genotype (r= -0.111;p= 0.188).
CONCLUSIONS: In summary, we showed how genetic variation in -866G/A UCP2 affected individual response to leptin production. AA + GA genotype had a better leptin sensitivity shown by its response in dietary intake and body mass index (BMI) and this explained the protective effect of A allele to obesity.
METHODS: The cross-sectional Family Diet Study (n = 236) was conducted at five primary schools in central of Peninsular Malaysia. Each family consisted of a Malay child, aged 8-12 years, and their main caregiver(s). Information on socio-demographics, dietary intake and anthropometry were collected. Correlations and regression analyses were used to assess dietary relationships within family dyads.
RESULTS: Approximately 29.6% of the children and 75.0% parents were categorised as being overweight or obese. Intakes of nutrients and food groups were below the national recommended targets for majority of children and adults. A large proportion of energy intake mis-reporters were identified: mothers (55.5%), fathers (40.2%) and children (40.2%). Children's body mass index (BMI) was positively associated with parental BMI (fathers, r = 0.37; mothers, r = 0.34; P < 0.01). For dietary intakes, moderate-to-strong (0.35-0.72) and weak-to-moderate (0.16-0.35) correlations were found between mother-father and child-parent dyads, respectively. Multiple regression revealed that maternal percentage energy from fat (β = 0.09, P < 0.01) explained 81% of the variation in children's fat intake.
CONCLUSIONS: Clear parental dietary relationships, especially child-mother dyads, were found. Despite a significant proportion of families with members who were overweight or obese, the majority reported dietary intakes below recommended levels, distorted by energy mis-reporting. The findings of the present study can inform interventions targeting parent-child relationships to improve family dietary patterns in Malaysia.
OBJECTIVES: To investigate the combined effect of FTO rs9930501, rs9930506, and rs9932754 and ADRB2 rs1042713 and rs1042714 using PRS on (1) the odds of obesity and (2) post-intervention differences in dietary, anthropometric, and cardiometabolic parameters in response to high-protein calorie-restricted, high-vitamin E, high-fiber (Hipcref) diet intervention in Malaysian adults.
METHODS: Both a cross-sectional study (n = 178) and a randomized controlled trial (RCT) (n = 128) were conducted to test the aforementioned objectives. PRS was computed as the weighted sum of the risk alleles possessed by each individual participant. Participants were stratified into first (PRS 0-0.64), second (PRS 0.65-3.59), and third (PRS 3.60-8.18) tertiles.
RESULTS: The third tertile of PRS was associated with significantly higher odds of obesity: 2.29 (95% CI = 1.11-4.72, adjusted p = 0.025) compared to the first tertile. Indians (3.9 ± 0.3) had significantly higher PRS compared to Chinese (2.1 ± 0.4) (p = 0.010). In the RCT, a greater reduction in high-sensitivity C-reactive protein (hsCRP) levels was found in second and third tertiles after Hipcref diet intervention compared to the control diet (p interaction = 0.048).
CONCLUSION: Higher PRS was significantly associated with increased odds of obesity. Individuals with higher PRS had a significantly greater reduction in hsCRP levels after Hipcref diet compared to the control diet.
METHODS: This was a cross-sectional study of 22,210 adult men and women who underwent a comprehensive health screening examination between 2011 and 2013 (median age 40 years). Sugar-sweetened carbonated beverage consumption was assessed using a validated food frequency questionnaire, and CAC was measured by cardiac computed tomography. Multivariable-adjusted CAC score ratios and 95% CIs were estimated from robust Tobit regression models for the natural logarithm (CAC score +1).
RESULTS: The prevalence of detectable CAC (CAC score >0) was 11.7% (n = 2,604). After adjustment for age; sex; center; year of screening examination; education level; physical activity; smoking; alcohol intake; family history of cardiovascular disease; history of hypertension; history of hypercholesterolemia; and intake of total energy, fruits, vegetables, and red and processed meats, only the highest category of sugar-sweetened carbonated beverage consumption was associated with an increased CAC score compared with the lowest consumption category. The multivariable-adjusted CAC ratio comparing participants who consumed ≥5 sugar-sweetened carbonated beverages per week with nondrinkers was 1.70 (95% CI, 1.03-2.81). This association did not differ by clinical subgroup, including participants at low cardiovascular risk.
CONCLUSION: Our findings suggest that high levels of sugar-sweetened carbonated beverage consumption are associated with a higher prevalence and degree of CAC in asymptomatic adults without a history of cardiovascular disease, cancer, or diabetes.
METHODS: This is a prospective observational study conducted among critically ill patients aged ≥18 years, intubated and mechanically ventilated within 48 h of ICU admission and stayed in the ICU for at least 72 h. Information on baseline characteristics and nutritional risk status (the modified Nutrition Risk in Critically ill [NUTRIC] score) was collected on day 1. Nutritional intake was recorded daily until death, discharge, or until the twelfth evaluable days. Mortality status was assessed on day 60 based on the patient's hospital record. Patients were divided into 3 groups a) received <2/3 of prescribed energy and protein (both <2/3), b) received ≥2/3 of prescribed energy and protein (both ≥2/3) and c) either energy or protein received were ≥2/3 of prescribed (either ≥2/3). The relationship between the three groups with 60-day mortality was examined by using logistic regression with adjustment for potential confounders. Sensitivity analysis was performed to examine the influence of ICU length of stay (≥7 days) and nutritional risk status.
RESULTS: Data were collected from 154 mechanically ventilated patients (age, 51.3 ± 15.7 years; body mass index, 26.5 ± 6.7 kg/m2; 54% male). The mean modified NUTRIC score was 5.7 ± 1.9, with 56% of the patients at high nutritional risk. The patients received 64.5 ± 21.6% of the amount of energy and 56.4 ± 20.6% of the amount of protein prescribed. Provision of energy and protein at ≥2/3 compared with <2/3 of the prescribed amounts was associated with a trend towards increased 60-day mortality (Adjusted odds ratio [Adj OR] 2.23; 95% confidence interval [CI], 0.92-5.38; p = 0.074). No difference in mortality status was found between energy and protein provision at either ≥2/3 compared with <2/3 of the prescribed amounts (Adj OR 1.61, 95% CI, 0.58-4.45; p = 0.357). Nutritional risk status, not ICU length of stay, influenced the relationship between nutritional adequacy and 60-day mortality.
CONCLUSIONS: Energy and protein adequacy of ≥2/3 of the prescribed amounts were associated with a trend towards increased 60-day mortality among mechanically ventilated critically ill patients. However, neither energy nor protein adequacy alone at ≥ or <2/3 adequacy affect 60-day mortality. Increased mortality was associated with provision of energy and protein at ≥2/3 of the prescribed amounts, which only affected patients with low nutritional risk.