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: This was a cross-sectional study conducted in male and female adults living in the urban area of Yogyakarta, Indonesia. Adiposity was determined based on body weight, body mass index (BMI), percent body fat, and waist and hip circumference. Data on coffee consumption and other dietary components were collected using a semiquantitative food frequency questionnaire along with other caffeine-containing beverages such as tea, chocolate, and other beverages. The -866 G/A UCP2 gene variation was analyzed using polymerase chain reaction-restriction fragment length polymorphism. The correlation between coffee intake and adiposity was tested using linear regression test with adjustment for sex, age, energy intake, table sugar intake, and total caffeine intake.
Results: In all subjects, coffee intake was inversely correlated with body weight (β = -0.122, p=0.028), BMI (β = -0.157, p=0.005), and body fat (β = -0.135, p=0.009). In subjects with AA + GA genotypes, coffee intake was inversely correlated with body weight (β = -0.155, p=0.027), BMI (β = -0.179, p=0.010), and body fat (β = -0.148, p=0.021). By contrast, in subjects with GG genotype, coffee intake was not correlated with body weight (β = -0.017, p=0.822), BMI (β = -0.068, p=0.377), and body fat (β = -0.047, p=0.504).
Conclusion: We showed that coffee intake was negatively correlated with adiposity, and this was independent of total caffeine intake. Additionally, we showed that the -866 G/A UCP2 gene variation influences the relationship between coffee intake and adiposity.
DESIGN: We systematically searched Ovid MEDLINE and Ovid EMBASE for observational studies assessing VDD among healthy children in the SEA region as the primary or secondary outcome from database inception to 6 April 2021. PubMed was used for e-pubs and publications not indexed in Medline. Publications that included abstracts in English were included. We performed a systematic review to describe the prevalence of VDD in SEA children.
RESULTS: Our initial search identified 550 publications with an additional 2 publications from manual screening. Of those, 21 studies from 5 different countries (Thailand, Indonesia, Vietnam, Malaysia and Cambodia) were summarised and included in forest plots. The prevalence of VDD (<50 nmol/L) ranged from 0.9% to 96.4%, with >50% of newborns having VDD, and severe VDD (<30 nmol/L) ranged from 0% to 55.8%. Female sex and urban living were the most common determinants of VDD.
CONCLUSIONS: VDD among healthy children living in the SEA region is common. Efforts to detect VDD and the implementation of preventive measures, including education on safe sun exposure and oral vitamin D supplementation or food fortification, should be considered for key target groups, including adolescent females and pregnant and lactating women to improve the vitamin D status of newborns.
PROTOCOL REGISTRATION NUMBER: This study is registered with PROSPERO (CRD42020181600).
OBJECTIVES: We examined whether the inclusion of folic acid in weekly IFA supplements conferred any benefit on hemoglobin (Hb) concentration, anemia reduction, or iron status [ferritin and soluble transferrin receptor (sTfR)], over iron alone.
METHODS: In this secondary analysis of a randomized controlled trial in Malaysia, n = 311 nonpregnant women (18-45 y old) received 60 mg Fe with either 0, 0.4, or 2.8 mg folic acid once-weekly for 16 wk. Fasting blood was collected at baseline and 16 wk. A generalized linear model (normal distribution with identity link) was used to assess Hb concentration at 16 wk (primary outcome).
RESULTS: At baseline, 84% of women had low folate status (plasma folate 0.05). Baseline plasma folate concentration did not modify the effect of treatment on Hb concentration at 16 wk. Among all women, the risks of anemia [risk ratio (RR): 0.65; 95% CI: 0.45, 0.96; P = 0.03] and iron deficiency based on ferritin (RR: 0.30; 95% CI: 0.20, 0.44; P
METHODS AND ANALYSIS: We will recruit non-pregnant women (n=300; 18-45 years) from Selangor, Malaysia. Women will be randomised to receive either 2.8, 0.4 or 0.0 (placebo) mg folic acid with 60 mg iron weekly for 16 weeks, followed by a 4-week washout period. The primary outcome will be erythrocyte folate concentration at 16 weeks and the mean concentration will be compared between randomised treatment groups (intention-to-treat) using a linear regression model adjusting for the baseline measure.
ETHICS AND DISSEMINATION: Ethical approval was obtained from the University of British Columbia (H18-00768) and Universiti Putra Malaysia (JKEUPM-2018-255). The results of this trial will be presented at scientific conferences and published in peer-reviewed journals.
TRIAL REGISTRATION NUMBERS: ACTRN12619000818134 and NMRR-19-119-45736.
METHODS: We conducted a three-arm double-blind efficacy trial in Malaysia. Non-pregnant women (n=331) were randomised to receive 60 mg iron and either 0, 0.4, or 2.8 mg folic acid once weekly for 16 weeks.
RESULTS: At 16 weeks, women receiving 0.4 mg and 2.8 mg folic acid per week had a higher mean RBC folate than those receiving 0 mg (mean difference (95% CI) 84 (54 to 113) and 355 (316 to 394) nmol/L, respectively). Women receiving 2.8 mg folic acid had a 271 (234 to 309) nmol/L greater mean RBC folate than those receiving 0.4 mg. Moreover, women in the 2.8 mg group were seven times (RR 7.3, 95% CI 3.9 to 13.7; p<0.0001) more likely to achieve an RBC folate >748 nmol/L, a concentration associated with a low risk of NTD, compared with the 0.4 mg group.
CONCLUSION: Weekly IFA supplements containing 2.8 mg folic acid increases RBC folate more than those containing 0.4 mg. Increased availability and access to the 2.8 mg formulation is needed.
TRAIL REGISTRATION NUMBER: This trial is registered with the Australian New Zealand Clinical Trial Registry (ACTRN12619000818134).