The association of cancer-preventive lifestyle with colonoscopy screening use in border Hispanic adults along the Texas-Mexico border.

PURPOSE: The relationship between engaging in two domains of cancer-preventive behaviors, lifestyle behaviors and colonoscopy screening, is unknown in Hispanic adults. Accordingly, the study examined the association between lifestyle and colonoscopy screening in Hispanic adults along the Texas-Mexico border, where there is suboptimal colorectal cancer prevention. METHODS: Lifestyle behavior adherence and compliance with colonoscopy screening schedules were assessed using 2013-2023 data from the Cameron County Hispanic Cohorta population-based sample of Hispanic adults living along the Texas-Mexico border. The 2018 World Cancer Research Fund scoring system characterized healthy lifestyle engagement. Multivariable logistic regression quantified the association between lifestyle behaviors and colonoscopy screening. RESULTS: Among 914 Hispanic adults, there was a mean adherence score of 2.5 out of 7 for recommended behaviors. Only 33.0% (95% CI 25.64-41.39%) were up-to-date with colonoscopy. Complete adherence to fruit and vegetable (AOR [adjusted odds ratio] 5.2, 95% CI 1.68-16.30; p = 0.004), fiber (AOR 2.2, 95% CI 1.06-4.37; p = 0.04), and ultra-processed foods (AOR 2.8, 95% CI 1.30-6.21; p = 0.01) consumption recommendations were associated with up-to-date colonoscopy screening. Having insurance versus being uninsured (AOR 10.8, 95% CI 3.83-30.62; p < 0.001) and having local medical care versus in Mexico (AOR 7.0, 95% CI 2.26-21.43; p < 0.001) were associated with up-to-date colonoscopy. CONCLUSIONS: Adherence to dietary lifestyle recommendations was associated with being up-to-date with colonoscopy screenings. Those with poor dietary behavior are at risk for low-colonoscopy use. Improving lifestyle behaviors may complement colonoscopy promotion interventions. Healthcare accessibility influences up-to-date colonoscopy prevalence. Our findings can inform cancer prevention strategies for the Hispanic population.

Genetic correlations between liver fat content, metabolic health, and adiposity distribution in the Fels Longitudinal Study.

BACKGROUND AND AIMS: Hepatic steatosis is known to be heritable, but its genetic basis is mostly uncharacterized. Steatosis is associated with metabolic and adiposity features; recent studies hypothesize that shared genetic effects between these traits could account for some of the unexplained heritability. This study aimed to quantify these genetic associations in a family-based sample of non-Hispanic white adults. METHODS AND RESULTS: 704 participants (18-95 years, 55.8% female) from the Fels Longitudinal Study with an MRI assessment of liver fat were included. Quantitative genetic analyses estimated the age- and sex-adjusted heritability of individual traits and the genetic correlations within trait pairs. Mean liver fat was 5.95% (SE = 0.23) and steatosis (liver fat >5.56%) was present in 29.8% of participants. Heritability (h2± SE) of steatosis was 0.72 ± 0.17 (p = 6.80e-6). All other traits including liver enzymes, fasting glucose, HOMA-IR, visceral and subcutaneous adipose tissue (VAT, SAT), body mass index, body fat percent, waist circumference, lipids and blood pressure were also heritable. Significant genetic correlations were found between liver fat and all traits except aspartate aminotransferase (AST), and among most trait pairs. Highest genetic correlations were between liver fat and HOMA-IR (0.85 ± 0.08, p = 1.73e-8), fasting glucose and ALT (0.89 ± 0.26, p = 6.68e-5), and HOMA-IR with: waist circumference (0.81 ± 0.12, p = 3.76e-6), body fat percent (0.78 ± 0.12 p = 2.42e-5) and VAT (0.73 ± 0.07, p = 6.37e-8). CONCLUSIONS: Common genes may exist between liver fat accumulation, metabolic features and adiposity phenotypes.

A high burden of diabetes and ankle brachial index abnormalities exists in Mexican Americans in South Texas.

Ethnic differences exist in the United States in the interrelated problems of diabetes (DM), peripheral arterial disease (PAD), and leg amputations. The purpose of this study was to determine the prevalence and risk factor associations for subclinical PAD in a population sample of Mexican Americans using the ankle brachial (ABI) index. The ABI-High (higher of the two ankle pressures/highest brachial pressure) and ABI-Low (lower of the two ankle pressures/highest brachial pressure) were calculated to define PAD. Toe brachial index (TBI) was also calculated. 746 participants were included with an age of 53.4 ± 0.9 years, 28.3 % had diabetes mellitus (DM), 12.6 % were smokers, and 51.2 % had hypertension (HTN). Using ABI-High ≤ 0.9, the prevalence of PAD was 2.7 %. This rose to 12.7 % when an ABI-Low ≤ 0.9 was used; 4.0 % of the population had an ABI-High > 1.4. The prevalence of TBI < 0.7 was 3.9 %. DM was a significant risk factor for ABI-High ≤ 0.9 and ABI-High > 1.4, and TBI < 0.7. Increased age, HTN, smoking was associated with ABI-High ≤ 0.9, while being male was associated with ABI-High > 1.4. Increased age, smoking, and lower education were all associated with abnormal TBI. Despite relatively younger mean age than other studied Hispanic cohorts, the present population has a high burden of ABI abnormalities. DM was a consistent risk factor for PAD. These abnormalities indicate an important underlying substrate of vascular and metabolic disease that may predispose this population to the development of symptomatic PAD and incident amputations.

Anti-Müllerian hormone levels are associated with skeletal maturity in adolescent girls in the Fels Longitudinal Study.

The role of anti-Müllerian hormone (AMH), a potential marker of the hypothalamic-pituitary-ovarian axis, is not well established in adolescent females. Most studies use secondary sexual characteristics or chronological age as predictors for AMH. Skeletal maturity, an indicator of bone development, has not been examined to predict AMH. This study sought to examine patterns of change in AMH in relation to skeletal maturity. Demographics, anthropometry, hand-wrist radiographs, and cardiometabolic risk factors from 88 females (212 observations), between the ages of 8 to 18 years from the Fels Longitudinal Study were used in this study. AMH was analyzed using ELISA from stored frozen serum samples. Generalized linear mixed effect modeling was used. In the stepwise regression models, log-transformed AMH (AMHlog) was regressed on relative skeletal age as the skeletal maturity indicator (calculated as chronological age minus skeletal age) and adjusted for chronological age, adiposity, and cardiometabolic risk factors. Skeletal maturity significantly predicted lower AMHlog (ß= -0.073, SE=0.032, p=0.023). Glucose was significantly associated with decreases in AMHlog (ß= -0.008, SE=0.004, p=0.044). Chronological age modeled as a cubic function was not significant. AMH and skeletal maturity may provide correlated information on growth and pubertal status in adolescent females.

The impact of metabolic syndrome on mental health-related quality of life and depressive symptoms.

PURPOSE: Results examining associations between metabolic syndrome (MetS) and depression, as well as on quality of life (QoL), are inconsistent. We aimed to determine whether individuals with MetS had decreased mental health-related QoL (MH-QoL) and higher frequency of depressive symptoms. METHODS: Data from 1,015 participants from the Fels Longitudinal Study were analyzed (mean age ± SD: 49.6 ± 18.7 years, 29.3% MetS, 51% females). MetS was determined using American Heart Association/National Heart, Lung, and Blood Institute criteria. Depressive symptoms (yes vs. no) were assessed with The Patient Health Questionnaire-9 (PHQ-9). MH-QoL (low (≤ 42) vs. high) was assessed with The Medical Outcomes 36-Item Short Form Survey (SF-36). Sex- and age-stratified mixed effects logistic regressions were used to examine the longitudinal relationship between MetS and MH-QoL while adjusting for covariates such as age, smoking status, and drinking status. RESULTS: In cross-sectional analysis, MetS was significantly associated with elevated depressive symptoms in women (OR 2.14, 95% CI 1.22-3.78, p < 0.01), but not in men. In the longitudinal analysis, MetS was observed to have a protective effect among men in the older age group as it approached significance (OR 0.34, 95% CI 0.11-1.05, p = 0.06). CONCLUSION: MetS was adversely associated with depressive symptoms and poor MH-QoL. Our cross-sectional results suggest that depressive symptoms are higher among women with MetS. Interestingly, our longitudinal results suggest that MH-QoL in men with MetS may improve with age.

Mexican American and South Asian population-based cohorts reveal high prevalence of type 2 diabetes and crucial differences in metabolic phenotypes.

OBJECTIVE: Prevalence of type 2 diabetes varies by region and ancestry. However, most guidelines for the prevention of diabetes mellitus (DM) are based on European or non-Hispanic white populations. Two ethnic minority populations-Mexican Americans (MAs) in Texas, USA, and South Indians (SIs) in Tamil Nadu, India-have an increasing prevalence of DM. We aimed to understand the metabolic correlates of DM in these populations to improve risk stratification and DM prevention. RESEARCH DESIGN AND METHODS: The Cameron County Hispanic Cohort (CCHC; n=3023) served as the MA sample, and the Population Study of Urban, Rural, and Semi-Urban Regions for the Detection of Endovascular Disease (PURSE; n=8080) served as the SI sample. Using design-based methods, we calculated the prevalence of DM and metabolic comorbidities in each cohort. We determined the association of DM with metabolic phenotypes to evaluate the relative contributions of obesity and metabolic health to the prevalence of DM. RESULTS: In the CCHC (overall DM prevalence 26.2%), good metabolic health was associated with lower prevalence of DM, across age groups, regardless of obesity. In PURSE (overall prevalence 27.6%), probability of DM was not strongly associated with metabolic phenotypes, although DM prevalence was high in older age groups irrespective of metabolic health. CONCLUSION: Our study provides robust, population-based data to estimate the prevalence of DM and its associations with metabolic health. Our results demonstrate differences in metabolic phenotypes in DM, which should inform DM prevention guidelines in non-European populations.

Multiethnic genome-wide meta-analysis of ectopic fat depots identifies loci associated with adipocyte development and differentiation.

Variation in body fat distribution contributes to the metabolic sequelae of obesity. The genetic determinants of body fat distribution are poorly understood. The goal of this study was to gain new insights into the underlying genetics of body fat distribution by conducting sample-size-weighted fixed-effects genome-wide association meta-analyses in up to 9,594 women and 8,738 men of European, African, Hispanic and Chinese ancestry, with and without sex stratification, for six traits associated with ectopic fat (hereinafter referred to as ectopic-fat traits). In total, we identified seven new loci associated with ectopic-fat traits (ATXN1, UBE2E2, EBF1, RREB1, GSDMB, GRAMD3 and ENSA; P < 5 × 10-8; false discovery rate < 1%). Functional analysis of these genes showed that loss of function of either Atxn1 or Ube2e2 in primary mouse adipose progenitor cells impaired adipocyte differentiation, suggesting physiological roles for ATXN1 and UBE2E2 in adipogenesis. Future studies are necessary to further explore the mechanisms by which these genes affect adipocyte biology and how their perturbations contribute to systemic metabolic disease.

New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk.

To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P<5 × 10(-8)), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk.

Validation of Maturity Offset in the Fels Longitudinal Study.

Sex-specific equations for predicting maturity offset, time before or after peak height velocity (PHV), were evaluated in 63 girls and 74 boys from the Fels Longitudinal Study. Serially measured heights (0.1 cm), sitting heights (0.1 cm), weights (0.1 kg), and estimated leg lengths (0.1 cm) from 8 to 18 years were used. Predicted age at PHV (years) was calculated as the difference between chronological age (CA) and maturity offset. Actual age at PHV for each child was derived with a triple logistic model (Bock-Thissen-du Toit). Mean predicted maturity offset was negative and lowest at 8 years and increased linearly with increasing CA. Predicted ages at PHV increased linearly with CA from 8 to 18 years in girls and from 8 to 13 years in boys; predictions varied within relatively narrow limits from 12 to 15 years and then increased to 18 years in boys. Differences between predicted and actual ages at PHV among youth of contrasting maturity status were significant across the age range in both sexes. Dependence of predicted age at PHV upon CA at prediction and on actual age at PHV limits its utility as an indicator of maturity timing and in sport talent programs.

Gene-by-age effects on BMI from birth to adulthood: the Fels Longitudinal Study.

OBJECTIVES: Genome wide association studies have shown 32 loci to influence BMI in European-American adults but replication in other studies is inconsistent and may be attributed to gene-by-age effects. The aims of this study were to determine if the influence of the summed risk score of these 32 loci (GRS) on BMI differed across age from birth to 40 years, and to determine if additive genetic effects other than those in the GRS differed by age. METHODS: Serial measures of BMI were calculated at 0, 1, 3, 6, 9, 12, 18, and 28 months, and 4, 7, 11, 15, 19, 23, 30, and 40 years for 1,176 (605 females, 571 males) European-American participants in the Fels Longitudinal Study. SOLAR was used for genetic analyses. RESULTS: GRS was significant (P < 0.05) at ages: 6, 9 months, 4-15 years, and 23-40 years. Remaining additive genetic effects independently influenced BMI (P < 5.3 × 10(-5) , 0.40 < h(2) < 0.76). Some genetic correlations between ages were not significant. Differential GRS effects did not retain significance after multiple comparisons adjustments. CONCLUSIONS: While well-known BMI variants do not appear to have significant differential effects, other additive genes differ over the lifespan.

The positive association of obesity variants with adulthood adiposity strengthens over an 80-year period: a gene-by-birth year interaction.

OBJECTIVE: To test the hypothesis that the statistical effect of obesity-related genetic variants on adulthood adiposity traits depends on birth year. METHODS: The study sample included 907 related, non-Hispanic White participants in the Fels Longitudinal Study, born between 1901 and 1986, and aged 25-64.99 years (474 females; 433 males) at the time of measurement. All had both genotype data from which a genetic risk score (GRS) composed of 32 well-replicated obesity-related common single nucleotide polymorphisms was created, and phenotype data [including body mass index (BMI), waist circumference, and the sum of four subcutaneous skinfolds]. Maximum likelihood-based variance components analysis was used to estimate trait heritabilities, main effects of GRS and birth year, GRS-by-birth year interaction, sex, and age. RESULTS: Positive GRS-by-birth year interaction effects were found for BMI (p < 0.001), waist circumference (p = 0.007), and skinfold thickness (p < 0.007). For example, each one-allele increase in GRS was estimated to result in a 0.16 increase in BMI among males born in 1930 compared to a 0.47 increase among those born in 1970. CONCLUSIONS: These novel findings suggest the influence of common obesity susceptibility variants has increased during the obesity epidemic.

Systematic examination of infant size and growth metrics as risk factors for overweight in young adulthood.

OBJECTIVE: To systematically examine infant size and growth, according to the 2006 WHO infant growth standards, as risk factors for overweight status in young adulthood in a historical cohort. Specifically, to assess: Whether accounting for length (weight-for-length) provides a different picture of risk than weight-for-age, intervals of rapid growth in both weight-for-age and weight-for-length metrics, and what particular target ages for infant size and intervals of rapid growth associate most strongly with overweight as a young adult. PATIENTS/METHODS: Data analysis of 422 appropriate for gestational age white singleton infants enrolled in the Fels Longitudinal Study. Odds ratios (OR) for overweight and obesity in young adulthood (age 20-29) were calculated using logistic regression models for the metrics at each target age (0, 1, 3, 6, 9, 12, 18, 24 months) comparing ≥85(th) v. <85(th) percentile, as well as rapid growth (Δ≥0.67 Z-score) through target age intervals. Models accounted for both maternal and paternal BMI. RESULTS: Infants ≥85(th) percentile of weight-for-age at each target age (except 3 months) had a greater odds of being overweight as a young adult. After accounting for length (weight-for-length) this association was limited to 12, and 18 months. Rapid weight-for-age growth was infrequently associated with overweight as a young adult. Rapid weight-for-length growth from 0 to 24 months, 1 to 6, 9, 12, 18, and 24 months and from 3 to 9, 12, 18, and 24 months was strongly associated with overweight status as a young adult. CONCLUSIONS: The WHO weight-for-length metric associates differently with risk of being overweight as a young adult compared to weight-for-age. Intervals of rapid weight-for-length growth ranging from months (0-24), (1-12, 18, and 24) and (3-9, and 12) displayed the largest OR for being overweight as a young adult.

Genome-wide analysis of BMI in adolescents and young adults reveals additional insight into the effects of genetic loci over the life course.

Genetic loci for body mass index (BMI) in adolescence and young adulthood, a period of high risk for weight gain, are understudied, yet may yield important insight into the etiology of obesity and early intervention. To identify novel genetic loci and examine the influence of known loci on BMI during this critical time period in late adolescence and early adulthood, we performed a two-stage meta-analysis using 14 genome-wide association studies in populations of European ancestry with data on BMI between ages 16 and 25 in up to 29 880 individuals. We identified seven independent loci (P < 5.0 × 10⁻8) near FTO (P = 3.72 × 10⁻²³), TMEM18 (P = 3.24 × 10⁻¹7), MC4R (P = 4.41 × 10⁻¹7), TNNI3K (P = 4.32 × 10⁻¹¹), SEC16B (P = 6.24 × 10⁻9), GNPDA2 (P = 1.11 × 10⁻8) and POMC (P = 4.94 × 10⁻8) as well as a potential secondary signal at the POMC locus (rs2118404, P = 2.4 × 10⁻5 after conditioning on the established single-nucleotide polymorphism at this locus) in adolescents and young adults. To evaluate the impact of the established genetic loci on BMI at these young ages, we examined differences between the effect sizes of 32 published BMI loci in European adult populations (aged 18-90) and those observed in our adolescent and young adult meta-analysis. Four loci (near PRKD1, TNNI3K, SEC16B and CADM2) had larger effects and one locus (near SH2B1) had a smaller effect on BMI during adolescence and young adulthood compared with older adults (P < 0.05). These results suggest that genetic loci for BMI can vary in their effects across the life course, underlying the importance of evaluating BMI at different ages.

Characterization of the infant BMI peak: sex differences, birth year cohort effects, association with concurrent adiposity, and heritability.

OBJECTIVES: To characterize an early trait in the BMI-for-age curve, the infant BMI peak. METHODS: BMI-for-age curves were produced for 747 non-Hispanic, white Fels Longitudinal Study participants, from which individual age (AgePeak ) and BMI (BMIPeak ) at maximum infant BMI were estimated. Multivariable general linear regression was used to examine the effects of sex and birth year cohort (1929-1950, 1951-1970, and 1971-2010) on AgePeak and BMIPeak , with associations between BMIPeak and concurrent sum of four skinfold thicknesses assessed in a subsample (N = 155). Heritability (h(2) ) of AgePeak and BMIPeak was estimated using maximum-likelihood variance components analysis. RESULTS: AgePeak occurred at 9 months of age in both sexes, but BMIPeak was 0.4 kg/m(2) higher for boys than for girls (P-value < 0.001). Infants born between 1971 and 2010 experienced a 1.5 month earlier AgePeak and a 0.35 kg/m(2) lower BMIPeak than infants born between 1929 and 1950 (P-values < 0.001). Skinfold thickness explained 37% of the variance in BMIPeak in boys and 20% of the variance in girls (p-values < 0.001). AgePeak and BMIPeak were significantly heritable (h(2) = 0.54 and 0.75, respectively). CONCLUSIONS: Both AgePeak and BMIPeak decreased over successive birth year cohorts in the Fels Longitudinal Study. Despite a positive association of BMIPeak with concurrent adiposity, AgePeak appears to occur later than does the well-documented peak in infant fat mass and BMIPeak does not capture known sex differences in infant adiposity. Strong heritability of these infant BMI traits suggests investigation of genetic control, and validation of their relationship to body composition is greatly needed.

Genetic risk for earlier menarche also influences peripubertal body mass index.

It is unclear whether earlier age at menarche is associated with higher body mass index (BMI) because they share a common genetic underpinning. We investigated the impact of single nucleotide polymorphisms (SNPs) influencing menarche timing on peripubertal BMI. For 556 Fels Longitudinal Study children (277 boys/279 girls) born 1928-1992, a genetic risk score (GRS(42)) was computed as the sum of the number of risk alleles in 42 putative menarche SNPs. Serial BMI Z-scores within ±6.99 years from each individual's age at peak height velocity (Age@PHV) were grouped into seven time points (-6 years, -4 years, -2 years, Age@PHV, +2 years, +4 years, and +6 years). Heritability of BMI ranged from 0.53 to 0.85 across the time points. The effect of GRS(42) on BMI Z-scores at each time point was modeled using variance components-based procedures. GRS(42) had a significant (P < 0.05) effect at every time point; an increase of one risk allele was associated with an increase of 0.03-0.08 BMI Z-scores. A separate score (GRS(29)) was computed that excluded 13 of the menarche SNPs previously documented to also influence adiposity; significant main effects were observed at Age@PHV+4 and +6 years. This finding supports a causal effect of advanced sexual development on post-Age@PHV BMI. Significant positive GRS(42) (or GRS(29))-by-birth year interactions indicate that some genetic influences on BMI have amplified over the 20th century. This gene-by-environment interaction also suggests that children with a genetic predisposition to earlier sexual development might avoid elevated BMI through alteration of their nutritional environment.

Meta-analysis of genome-wide studies identifies WNT16 and ESR1 SNPs associated with bone mineral density in premenopausal women.

Previous genome-wide association studies (GWAS) have identified common variants in genes associated with variation in bone mineral density (BMD), although most have been carried out in combined samples of older women and men. Meta-analyses of these results have identified numerous single-nucleotide polymorphisms (SNPs) of modest effect at genome-wide significance levels in genes involved in both bone formation and resorption, as well as other pathways. We performed a meta-analysis restricted to premenopausal white women from four cohorts (n = 4061 women, aged 20 to 45 years) to identify genes influencing peak bone mass at the lumbar spine and femoral neck. After imputation, age- and weight-adjusted bone-mineral density (BMD) values were tested for association with each SNP. Association of an SNP in the WNT16 gene (rs3801387; p = 1.7 × 10(-9) ) and multiple SNPs in the ESR1/C6orf97 region (rs4870044; p = 1.3 × 10(-8) ) achieved genome-wide significance levels for lumbar spine BMD. These SNPs, along with others demonstrating suggestive evidence of association, were then tested for association in seven replication cohorts that included premenopausal women of European, Hispanic-American, and African-American descent (combined n = 5597 for femoral neck; n = 4744 for lumbar spine). When the data from the discovery and replication cohorts were analyzed jointly, the evidence was more significant (WNT16 joint p = 1.3 × 10(-11) ; ESR1/C6orf97 joint p = 1.4 × 10(-10) ). Multiple independent association signals were observed with spine BMD at the ESR1 region after conditioning on the primary signal. Analyses of femoral neck BMD also supported association with SNPs in WNT16 and ESR1/C6orf97 (p < 1 × 10(-5) ). Our results confirm that several of the genes contributing to BMD variation across a broad age range in both sexes have effects of similar magnitude on BMD of the spine in premenopausal women. These data support the hypothesis that variants in these genes of known skeletal function also affect BMD during the premenopausal period.

Associations between trunk, leg and total body adiposity with arterial stiffness.

BACKGROUND: Obesity and arterial stiffness are associated, but fat distribution patterns may be more strongly related to arterial stiffness than general obesity because of the possible increased inflammation associated with increased abdominal adiposity. The aims of this study were to examine whether fat patterning is associated with arterial stiffness, and determine whether these associations are mediated by low-grade inflammation. METHODS: Adult participants from the Fels Longitudinal Study (228 males and 254 females) were assessed for brachial-ankle pulse wave velocity (BaPWV) to determine arterial stiffness. Dual energy X-ray absorptiometry was used to estimate fat percentage of the trunk and legs (e.g., TRUNKFAT% and LEGFAT%). High-sensitivity C-reactive protein (hs-CRP) levels were assayed as a general marker of inflammation. General linear regression analyses were used. RESULTS: BaPWV was positively associated with TRUNKFAT% (r = 0.44 in men and r = 0.38 in women), whereas it was inversely related to LEGFAT% (r = -0.40 in men and r = -0.39 in women). In multiple regression analyses, each SD increase in TRUNKFAT% was associated with an ~1.03 m/s increase in BaPWV in both men and women. Each SD increase in LEGFAT% was related to a similar magnitude of decrease (1.03 m/s) in BaPWV in both sexes. The relationships of TRUNKFAT% and LEGFAT% with BaPWV were attenuated slightly when including hs-CRP in the models, but remained significant. CONCLUSIONS: We found that trunk and leg fat are related to BaPWV in opposite directions when total body adiposity was accounted for. However, the associations between regional fat patterning and arterial stiffness did not appear to be mediated by low-grade inflammation.

A changing pattern of childhood BMI growth during the 20th century: 70 y of data from the Fels Longitudinal Study.

BACKGROUND: The BMI distribution shifted upward in the United States between the 1960s and the 1990s, but little is known about secular trends in the pattern of BMI growth, particularly earlier in the century and early in childhood. OBJECTIVE: The objective was to examine differences in BMI growth in children born in 1929-1999. DESIGN: BMI curves from ages 2 to 18 y were produced for 855 European-American children in the Fels Longitudinal Study born in 1929-1953, 1954-1972, and 1973-1999. Age (A(min)) and BMI (BMI(min)) at adiposity rebound and age (AV(max)), BMI (BMIV(max)), and velocity (V(max)) at maximum velocity were derived; multivariable regression was used to examine whether maternal BMI, infant weight gain, and other covariates mediated the cohort effects on these traits. RESULTS: BMI curves showed that children born in 1973-1999 had the lowest BMI values until age 5 y but had the largest values from age 8 y onward. In adjusted models, boys and girls born in 1973-1999 had a 0.15-kg/m(2) per year faster V(max) and a 1-kg/m(2) higher BMIV(max) than did children of the same sex born in 1929-1953, and girls had a 0.8-y earlier A(min) (P < 0.01). Maternal BMI and infant weight gain were associated with an obesity-prone pattern of BMI growth but did not account for the observed trends. CONCLUSIONS: Shifts in the BMI growth rate around the time of pubertal initiation were apparent starting after 1973. The BMI growth curve did not increase monotonically over time; rather, children born during the obesity epidemic were characterized by lower BMI values before the adiposity rebound and by rapid subsequent BMI gain.

Eighty-year trends in infant weight and length growth: the Fels Longitudinal Study.

OBJECTIVES: To investigate secular trends in weight and length growth from birth to 3 years of age in infants born from 1930 to 2008, and to assess whether these trends were associated with concurrent trends in pace of infant skeletal maturation and maternal body mass index. STUDY DESIGN: Longitudinal weight and length data from 620 infants (302 girls) were analyzed with mixed effects modeling to produce growth curves and predicted anthropometry for infants born from 1930 to 1949, 1950 to 1969, 1970 to 1989, and 1990 to 2008. RESULTS: The most pronounced differences in growth occurred in the first year of life. Infants born after 1970 were approximately 450 g heavier and 1.4 cm longer at birth, but demonstrated slower growth to 1 year of age than infants born before 1970. Growth trajectories converged after 1 year of age. There was no evidence that relative skeletal age, maternal body mass index, or maternal age together mediated associations between cohort and growth. CONCLUSIONS: Recent birth cohorts may be characterized not only by greater birth size, but also by subsequent catch-down growth. Trends over time in human growth do not increase monotonically, and growth velocity in the first year may have declined compared with preceding generations.

Sugar-sweetened and diet beverages in relation to visceral adipose tissue.

Frequent sugar-sweetened beverage (SSB) intake has been consistently associated with increased adiposity and cardio-metabolic risk, whereas the association with diet beverages is more mixed. We examined how these beverages associate with regional abdominal adiposity measures, specifically visceral adipose tissue (VAT). In a cross-sectional analysis of 791 non-Hispanic white men and women aged 18-70 we examined how beverage consumption habits obtained from a food frequency questionnaire associate with overall and abdominal adiposity measures from MRI. With increasing frequency of SSB intake, we observed increases in waist circumference (WC) and the proportion of visceral to subcutaneous abdominal adipose tissue (VAT%), with no change in total body fat (TBF%) or BMI. Greater frequency of diet beverage intake was associated with greater WC, BMI, and TBF%, but was not associated with variation in visceral adiposity We conclude that increased frequency of SSB consumption is associated with a more adverse abdominal adipose tissue deposition pattern.