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OBJECTIVE: Ultraprocessed food (UPF) intake is associated with BMI, but effects on regional adipose depots or related to minimally processed food (MPF) intake are unknown. METHODS: Data included 12,297 adults in the National Health and Nutrition Examination Survey (NHANES), 2011 to 2016. This study analyzed associations between usual percentage of kilocalories from UPFs and MPFs and three adiposity indicators: supine sagittal abdominal diameter to height ratio (SADHtR, estimates visceral adiposity); waist circumference to height ratio (WHtR, estimates abdominal adiposity); and BMI, using linear and multinomial logistic regression. RESULTS: Standardized β coefficients per 10% increase in UPF intake were 0.0926, 0.0846, and 0.0791 for SADHtR, WHtR, and BMI, respectively (all p < 0.001; p > 0.26 for pairwise differences). For MPF intake, the β coefficients were −0.0901, −0.0806, and −0.0688 (all p < 0.001; p > 0.18 pairwise). Adjusted odds ratios (95% CI) for adiposity tertile 3 versus tertile 1 (comparing UPF intake quartiles 2, 3, and 4 to quartile 1) were 1.33 (1.22-1.45), 1.67 (1.43-1.95), and 2.24 (1.76-2.86), respectively, for SADHtR; 1.31 (1.19-1.44), 1.62 (1.37-1.91), and 2.13 (1.63-2.78), respectively, for WHtR; and 1.27 (1.16-1.39), 1.53 (1.31-1.79), and 1.96 (1.53-2.51), respectively, for BMI. MPF intake showed inverse associations with similar trends in association strength. CONCLUSIONS: Among US adults, abdominal and visceral adiposity indictors were positively associated with UPFs and inversely associated with MPFs.

Objective The purpose of this study was to investigate the association of sodium intake with obesity in US children and adolescents. Methods Cross-sectional data were analyzed for 9,026 children and adolescents in the National Health and Nutrition Examination Survey (NHANES) 2009-2016. Usual sodium intake was estimated from 24-hour dietary recalls using a measurement error model. Logistic regression was used to assess the association of sodium intake with overweight/obesity, obesity, and central obesity (waist to height ratio [WtHR] ≥ 0.5; waist circumferences (WC) ≥ age- and sex-specific 90th percentile). Results Mean (SE) sodium intake was 3,010 (9) and 3,404 (20) mg/d for children and adolescents, respectively. The adjusted odds ratio (AOR) comparing Q4 versus Q1 (87.5th vs. 12.5th percentile of sodium intake) among children was 1.98 (95% CI: 1.19-3.28) for overweight/obesity, 2.20 (1.30-3.73) for obesity, 2.10 (1.12-3.95) for WC ≥ 90th percentile, and 1.68 (0.95-2.97) for WtHR ≥ 0.5, adjusting for demographics, energy, and sugar-sweetened beverage intake. Among adolescents, AOR was 1.81 (0.98-3.37) for overweight/obesity, 1.71 (0.82-3.56) for obesity, 1.62 (0.71-3.66) for WC ≥ 90th percentile, and 1.73 (0.85-3.50) for WtHR ≥ 0.5. Conclusions Sodium intake was positively associated with overweight/obesity, obesity, and central obesity among US children independent of energy and SSB intake, but the association did not reach significance among adolescents.

Objective Associations of overall and regional body fat measured by dual-energy X-ray absorptiometry with total and cause-specific mortality in the National Health and Nutrition Examination Survey (NHANES) 1999-2006 were investigated. Methods This study included 9,471 participants (≥20 years) free of major chronic diseases at baseline. Death information was obtained from the National Death Index (mean follow-up duration: 8.8 years). Results A total of 682 participants died after 12 months since baseline, with 206 and 170 deaths attributed to cardiovascular diseases (CVD) and cancer, respectively. The second quartile of fat mass percentages (FM%) was used as the reference to account for potential nonlinearity. In the multivariate-adjusted model, participants in the highest quartile of total FM% had increased total mortality; hazard ratio (HR; 95% confidence interval, 95% CI) was 1.48 (1.07-2.04; P

Objective Consider all metabolic syndrome (MetS) components [systolic (SBP) and diastolic (DBP) blood pressures, waist circumference, HDL cholesterol, triglycerides (TG), and fasting glucose] and gender/race differential risk when assessing cardiovascular disease (CVD) risk. Methods We estimated a gender- and race-specific continuous MetS score using structural equation modeling and tested its association with CVD mortality using data from National Health and Nutrition Examination Survey III linked with the National Death Index. Cox proportional hazard regression tested the association adjusted for sociodemographic and behavior characteristics. Results For men, continuous MetS components associated with CVD mortality were SBP (hazard ratio = 1.50, 95% confidence interval = 1.14-1.96), DBP (1.48, 1.16-1.90), and TG (1.15, 1.12-1.16). In women, SBP (1.44, 1.27-1.63) and DBP (1.24, 1.02-1.51) were associated with CVD mortality. MetS score was not significantly associated with CVD mortality in men; but significant associations were found for all women (1.34, 1.06-1.68), non-Hispanic white women (1.29, 1.01-1.64), non-Hispanic black women (2.03, 1.12-3.69), and Mexican-American women (3.57, 2.21-5.76). Goodness-of-fit and concordance were overall better for models with the MetS score than MetS (yes/no). Conclusions When assessing CVD mortality risk, MetS score provided additional information than MetS (yes/no).

Background The objective is to study racial differences in infant mortality attributable to birth defects (IMBD) in the United States. Methods We analyzed 1989-1991 and 1995-2002 linked birth/death files for trends and racial differences in IMBD by selected categories of birth defects for infants of non-Hispanic white, non-Hispanic black, and Hispanic mothers. Results In 1989-2002, the IMBD rates declined. However, the decline in postneonatal mortality attributable to birth defects (PMBD) rate was significantly slower than that of overall postneonatal mortality. The adjusted rate ratio for non-Hispanic black and Hispanic versus non-Hispanic white for neonatal mortality attributable to birth defects (NMBD) remained unchanged from 1989-1991 through 2000-2002. For PMBD, it increased from 0.97 (95% confidence interval [CI], 0.90-1.13) in 1989-1991 to 1.12 (95% CI, 1.04-1.21) in 2001-2002 and from 1.08 (95% CI, 1.00-1.16) to 1.18 (95% CI, 1.10-1.27) for non-Hispanic black and Hispanic, respectively. Infant mortality due to cardiovascular and central nervous system defects were the main contributors to the increased racial disparities in PMBD rates. Conclusions The disparity in PMBD between infants of non-Hispanic black and Hispanic mothers and infants of non-Hispanic white mothers increased significantly from 1989-1991 to 2000-2002. Further studies are needed to assess the extent to which delays in care or lack of access to care for infants with birth defects might be contributing to the disparity in IMBD.

The impact of competing risks on tests of association between disease and haplotypes has been largely ignored. We consider situations in which linkage phase is ambiguous and show that tests for disease-haplotype association can lead to rejection of the null hypothesis, even when true, with more than the nominal 5 per cent frequency. This problem tends to occur if a haplotype is associated with overall mortality, even if the haplotype is not associated with disease risk. A small simulation study illustrates the magnitude of bias (high type I error rate) in the context of a cohort study in which a modest number of disease cases (about 350) occur over time. The bias remains even if the score test is based on a logistic model that includes age as a covariate. For cohort studies, we propose a new test based on a modification of the proportional hazards model and for case-control studies, a test based on a conditional likelihood that have the correct size under the null even in the presence of competing risks, and that can be used when haplotype is ambiguous.

Recent reports suggest that women carrying certain polymorphisms of folate genes associated with suboptimal folate status might be at increased risk for having a child with Down syndrome or other autosomal trisomies, and hypothesized that maternal use of multivitamin supplements might reduce such risk. To evaluate this hypothesis, we examined data from a population-based case-control study, and contrasted cases of Down syndrome, trisomy 18, and trisomy 13, with unaffected controls. Periconceptional multivitamin use, compared to no such use, was associated with an odds ratio (OR) of 0.9 (95% confidence interval [CI], 0.6-1.3) for having a pregnancy affected by an autosomal trisomy. The OR was 0.8 (95% CI, 0.5-1.3) for Down syndrome and 1.4 (95% CI, 0.5-3.6) for trisomies 13 and 18, with little variation by maternal race or age. Periconceptional multivitamin use was not associated with a major reduction in the risk for common autosomal trisomies.

BACKGROUND Neural tube defect (NTD) rates can be lowered by increased consumption of folic acid (FA) by women before and during early pregnancy. The crude proportion of reproductive-aged women taking FA supplements has been used to predict a decline of the NTD rate in the general population. In this study we examine the potential error in using the crude proportion to predict NTD risk reduction, and offer an alternative method. METHODS The crude proportion measures the number of women taking FA. It ignores the substantial variability by maternal age in the probability of giving birth. Age-specific fertility rates (ASFRs) reflect the probability that a woman in a specific age group will give birth in a given year. In this study, we show how to calculate a proportion weighted by ASFRs to predict a decline in the NTD rate, and to assess the effectiveness of FA consumption in preventing NTDs. RESULTS Our results show that a crude proportion of 50% of women (15–49 years old) taking FA is associated with a range of 24–77% in weighted proportions. Assuming a 40% risk reduction from taking 400 μg of FA daily, the expected NTD rate decline could vary from 9.6% to 30.6%, depending on the age distribution of women taking FA. CONCLUSIONS The ASFR-weighted proportion estimates the proportion of babies born to women taking FA, as opposed to the crude proportion of women taking FA. We recommend using the ASFR-weighted proportion to predict an NTD rate decline and measure the success of FA education campaigns. We found that when women in high-fertility age groups increased their FA consumption, the decline in the NTD rate was greater than when women in low-fertility age groups did so. Our findings suggest that the more efficient approach to NTD prevention is to focus on women with a higher probability of giving birth. For example, by focusing on

We applied the transmission/disequilibrium test (TDT) for sibs (S-TDT) and for families with one parent (1-TDT), to the Collaborative Study on the Genetics of Alcoholism data set. The combined test is used to screen the whole genome to locate genes responsible for alcohol dependence. This analysis supports the previous finding that the region close to GABRB1 on chromosome 4 might be associated with alcohol dependence. The regions close to D6S474 and D11S1998 are also of particular interest. We found segregation distortion at the GR1K1 locus. The segregation distortion might be due to the binning method used in genotyping at this locus.

We used a case-control design to scan the genome for any associations between genetic markers and disease susceptibility loci using the first two replicates of the Mycenaean population from the GAW11 (Problem 2) data. Using a case-control approach, we constructed a series of 2-by-3 tables for each allele of every marker on all six chromosomes. Odds ratios (ORs) and 95% confidence intervals (95% CI) were estimated for all alleles of every marker. We selected the one allele for which the estimated OR had the minimum p-value to plot in the graph. Among these selected ORs, we calculated 95% CI for those that had a p-value < or = adjusted alpha level. Significantly high ORs were taken to indicate an association between a marker locus and a suspected disease-susceptibility gene. For the Mycenaean population, the case-control design identified allele number 1 of marker 24 on chromosome 1 to be associated with a disease susceptibility gene, OR = 2.10 (95% CI 1.66-2.62). Our approach failed to show any other significant association between case-control status and genetic markers. Stratified analysis on the environmental risk factor (E1) provided no further evidence of significant association other than allele 1 of marker 24 on chromosome 1. These data indicate the absence of linkage disequilibrium for markers flanking loci A, B, and C. Finally, we examined the effect of gene x environment (G x E) interaction for the identified allele. Our results provided no evidence of G x E interaction, but suggested that the environmental exposure alone was a risk factor for the disease.

In the 1960s, thalidomide caused limb deficiencies in thousands of infants world-wide. The limb deficiencies were frequently of the intercalary type. As a result, numerous countries started birth defect surveillance programs. In 1967, the Centers for Disease Control (CDC) started the Metropolitan Atlanta Congenital Defects Program (MACDP), a population-based surveillance system, to provide early warning against new teratogens. Recent studies have shown that thalidomide may be beneficial for a range of conditions, including cancer and AIDS, and it may once again become widely available. Here, we examine the ability of MACDP to detect an increase in the birth prevalence of limb deficiency as an early warning of fetal exposure to thalidomide. We calculated base rates for all limb deficiencies, for bilateral nonsyndromic intercalary or preaxial deficiencies, and for all nonsyndromic intercalary limb deficiencies among Atlanta infants born from 1968 through 1993. We used relative risk estimates from previous studies and a range of pregnancy exposure rates for thalidomide. We tested the statistical power of MACDP to detect subtle changes in the birth prevalence of these defects using Poisson and cumulative sum (CUSUM) techniques. The base rates for all limb deficiencies, for bilateral intercalary or preaxial deficiencies, and for all intercalary limb deficiencies, were 0.53, 0.035, and 0.022/1,000, and the estimated relative risks were 175, 4,570, and 8,180, respectively. We varied the assumed rate of exposure to thalidomide from 1/10,000 to 5/100. With a 1/1,000 exposure rate, both Poisson and CUSUM techniques will detect a rate change in intercalary limb deficiency in about 6 months of monitoring, and a rate change in bilateral intercalary or preaxial deficiencies in about 12 months of monitoring. When monitoring all limb deficiencies, a pregnancy exposure rate of 3.5% or less would go unnoticed by the Poisson method and would take more than 50 years for the CUSUM method to signal an alarm with a 1/1,000 exposure rate. However, for rates of exposure less than 1/1,000, a progressively longer period of time or larger sample are needed to detect a rate change by both methods. Our findings highlight the importance of enlarging the monitored population and correct case classification in birth defects surveillance. Am. J. Med. Genet. 73:251–258, 1997. © 1997 Wiley-Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.

We applied sib-pair and association methods to a GAW data set of nuclear families with quantitative traits. Our approaches included 1) preliminary statistical studies including correlations and linear regressions, 2) sib-pair methods, and 3) association studies. We used a single data set to screen for linkage and association and, subsequently, additional data sets to confirm the preliminary results. Using this sequential approach, sib-pair analysis provided evidence for the genes influencing Q1, Q2, and Q4. We correctly predicted MG1 for Q1, MG2 for Q2, and MG4 for Q4. We did not find any false positives using this approach. Association studies identified chromosomes 8 and 9 to be associated with Q4; however these are assumed to be false positives as no associations were modeled into the data.

Contemporary information on the trends and patterns of mortality associated with birth defects and genetic diseases is lacking in the United States. To study these trends and patterns, we used the Multiple-Cause Mortality Files of the National Center for Health Statistics. From 1979 through 1992, 320,208 deaths in the United States were associated with birth defects and genetic diseases. The age-adjusted mortality rates for people with birth defects declined from about 8.2/100,000 in 1979 to about 6.7/100,000 in 1992, and the mortality rates for people with genetic diseases increased from 2.2/100,000 in 1979 to 2.5/100,000 in 1992. The mortality rate was higher among men than among women and higher among blacks than among whites or other races for both birth defect- and genetic disease-associated deaths. The rate among infants with birth defects was more than 25 times higher than that among other age groups. About half of the children whose deaths were associated with birth defects had cardiovascular system defects, 15% had central nervous system defects, and 12% had chromosomal defects. For deaths associated with genetic diseases, hereditary neurologic or storage disorders were the most common genetic diseases (38%), followed by metabolic disorders (21%), sickle cell and thalassemia (12%). The decline in the rate of mortality from birth defects in the United States probably reflects improvements in medical and surgical care and other factors. Most of the mortality associated with birth defects remains in the pediatric age group (less than 15 years old). The upward trend we detected for the deaths with genetic diseases was most likely related to improved recognition and reporting of some genetic diseases rather than to the increased prevalence.