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Growth in early infancy is hypothesized to affect chronic disease risk factors later in life. To date, most reports draw on European-ancestry cohorts with few repeated observations in early infancy. We investigated the association between infant growth before 6 months and lipid levels in adolescents in a Hispanic/Latino cohort. We characterized infant growth from birth to 5 months in male (n = 311) and female (n = 285) infants from the Santiago Longitudinal Study (1991-1996) using 3 metrics: weight (kg), length (cm), and weight-for-length (g/cm). Superimposition by translation and rotation (SITAR) and latent growth mixture models (LGMMs) were used to estimate the association between infant growth characteristics and lipid levels at age 17 years. We found a positive relationship between the SITAR length velocity parameter before 6 months of age and high-density lipoprotein cholesterol levels in adolescence (11.5, 95% confidence interval; 3.4, 19.5), indicating higher high-density lipoprotein cholesterol levels occurring with faster length growth. The strongest associations from the LGMMs were between higher low-density lipoprotein cholesterol and slower weight-for-length growth, following a pattern of associations between slower growth and adverse lipid profiles. Further research in this window of time can confirm the association between early infant growth as an exposure and adolescent cardiovascular disease risk factors.

Context Uric acid's role in cardiovascular health in youth with type 1 diabetes is unknown. Objective Investigate whether higher uric acid is associated with increased blood pressure (BP) and arterial stiffness over time in adolescents and young adults with type 1 diabetes and if overweight/obesity modifies this relationship. Methods Longitudinal analysis of data from adolescents and young adults with type 1 diabetes from 2 visits (mean follow up 4.6 years) in the SEARCH for Diabetes in Youth multicenter prospective cohort study from 2007 to 2018. Our exposure was uric acid at the first visit and our outcome measures were the change in BP, pulse wave velocity (PWV), and augmentation index between visits. We used multivariable linear mixed-effects models and assessed for effect modification by overweight/obesity. Results Of 1744 participants, mean age was 17.6 years, 49.4% were female, 75.9% non-Hispanic White, and 45.4% had a follow-up visit. Mean uric acid was 3.7 mg/dL (SD 1.0). Uric acid was not associated with increased BP, PWV-trunk, or augmentation index over time. Uric acid was marginally associated with PWV-upper extremity (β =.02 m/s/year, 95% CI 0.002 to 0.04). The magnitude of this association did not differ by overweight/obesity status. Conclusion Among adolescents and young adults with type 1 diabetes, uric acid was not consistently associated with increased BP or arterial stiffness over time. These results support findings from clinical trials in older adults with diabetes showing that lowering uric acid levels does not improve cardiovascular outcomes. [ABSTRACT FROM AUTHOR]

Growth in early infancy is hypothesized to affect chronic disease risk factors later in life. To date, most reports draw on European-ancestry cohorts with few repeated observations in early infancy. We investigated the association between infant growth before 6 months and lipid levels in adolescents in a Hispanic/Latino cohort. We characterized infant growth from birth to 5 months in male (n  = 311) and female (n  = 285) infants from the Santiago Longitudinal Study (1991–1996) using 3 metrics: weight (kg), length (cm), and weight-for-length (g/cm). Superimposition by translation and rotation (SITAR) and latent growth mixture models (LGMMs) were used to estimate the association between infant growth characteristics and lipid levels at age 17 years. We found a positive relationship between the SITAR length velocity parameter before 6 months of age and high-density lipoprotein cholesterol levels in adolescence (11.5, 95% confidence interval; 3.4, 19.5), indicating higher high-density lipoprotein cholesterol levels occurring with faster length growth. The strongest associations from the LGMMs were between higher low-density lipoprotein cholesterol and slower weight-for-length growth, following a pattern of associations between slower growth and adverse lipid profiles. Further research in this window of time can confirm the association between early infant growth as an exposure and adolescent cardiovascular disease risk factors. [ABSTRACT FROM AUTHOR]

Background: Several innate and environmental factors affect the rate and degree of cognitive decline with each factor representing a potentially valuable intervention point to slow progression of this decline. Serum urate, a product of purine metabolism and potent antioxidant, and weight loss have been associated with cognitive decline. The aim of this study was to determine the relation among urate, body weight, and their interaction with cognitive function. Methods: In the context of a larger study, 133 adults aged 65‐80 at baseline (mean baseline age 72.7 years, 56.5% male) were recruited to participate in a double‐blind, randomized controlled trial. The Montreal Cognitive Assessment (MoCA) was administered to assess cognitive function. Those with MoCA scores >25 were considered cognitively typical, whereas those with MoCA scores below this threshold were deemed to be experiencing mild cognitive decline (MCD). The cognitively typical group was instructed to maintain their regular diet and served as a reference, whereas MCD groups were randomized to receive either 35mg lyophilized wild blueberries or dextrose (serving as control) daily in addition to their regular diet. MoCA, anthropometric measures, and serum were collected at baseline and repeated at 3 and 6 months. The statistical analysis was performed using MiniTab v.19. Results: A regression‐based analysis showed that changes in serum urate were positively associated with changes in MoCA scores (ß = 0.94, SE = 0.47, p < 0.05) at 6 months. Groupwise analyses showed that changes in MoCA scores were not correlated with changes in urate or body weight in individuals with typical cognition or those in the blueberry group. However, in the control group, changes in serum urate (ß = 1.96, SE = 0.92, p<0.05), changes in body weight (ß = ‐0.31, SE = 0.13, p<0.05), and interaction between urate and body weight significantly impacted the change in MoCA scores. (ß = 0.663, SE = 0.20, p<0.05). Individuals with increased urate and decreased body weight showed less cognitive decline as compared to those who had weight gain and decreased urate. Conclusion: Our findings show that changes in urate and body weight interact with each other to significantly impact changes in cognitive function. [ABSTRACT FROM AUTHOR]

Background: Exaggerated cardiovascular reactivity for blood pressure (BP) and heart rate (HR) to laboratory stress tests has been proposed as a predictor of cardiovascular disease.Subjects and Methods: The study was conducted in normal subject; 262 males and 280 females (mean age 30 ± 9 years, BMI 23.5 ± 4 years), from five large and highly consanguineous homogeneous Arab families of OFS. Hemodynamic parameters: Heart rate (HR), systolic, diastolic, mean BP (mmHg), Stroke index (SI, SI (ml/beat/m2), cardiac index (CI,L/min/m2) ), total peripheral resistance index (TPRI, yne∗s∗/cm2)), left ventricular ejection time (LVET, ms) and cardiac contractility (IC, 1000/sec ) were computed from beat-to-beat BP, ECG and impedance cardiography (TFM, CNSystems). Autonomic parameters ( LF; sympathetic , HF; parasympathetic, normalized) and baroreceptor sensitivity (BRS, ms/mmHg) were computed using spectral analysis and the sequence method, respectively. Hemodynamic and autonomic eactivity were averaged after 3 minutes of the word conflict (Δ WCT) and the cold presser (Δ CPT) tests. Results were compared using the Student’s paired ‘t’ test. A P value of < 0.05 was considered as significant.Results: Males had significantly higher or lower reactivity than females for ΔWCT HR( 9.3 ±7 vs. 6.8 ± 6.3), SBP (9.9 ± 11 vs. 7.5 ±6.) , DBP (7.9 ± 8 vs. 6.3± 6), MBP (9.4 ±9.5, (SI -1.9 ± 5.5 vs. - 0.8 ± 4.7) and BRS ( -7.5± 15.9 vs. -4 ±10.5) . In contrast ΔCPT in females evoked significantly higher HR (8.2 ± 8 vs. 5.1 ± 8), CI (0.19 ± 0.4 vs. 0.08 ±0.4) and LF (11.6 ± 16.vs. 5.8 ±15.9) but significantly lower LVET (-8.7 ±16.6 vs. -3.8 ±9) and , BRS ( -6 ± 13 vs.-3.4 ±14 )Conclusion: In this genetically and environmentally homogeneous cohort of OFS we found significant gender differences in hemodynamic and autonomic responses during the WCT and CPT tests. This may indicate that biological mechanism and genetic factors may contribute to such differences and should be receive special emphasis in cardiovascular research. [ABSTRACT FROM AUTHOR]

Inflammatory factors, such as C-reactive protein (CRP), adiponectin, and zinc, are abnormal in obesity, suggesting the presence of a low level of systemic inflammation. This research will explore the relationship between inflammation, weight status and factors of metabolic syndrome in overweight/obesity women in early postpartum. Women with 1-4 months old infants participated in a weight loss program for 8 weeks. Weight, height, blood pressure, blood lipids, CRP, adiponectin and zinc were measured pre-and post-intervention. Metabolic syndrome was defined according to the NCEP-ATP Ill guidelines. Subjects with higher BMI had lower adiponectin and zinc, but increased CRP (P<0.05). Blood concentrations of CRP, adiponectin and zinc were related with risk factors of metabolic syndrome (P<0.05). Serum CRP was reduced with elevations of adiponectin and zinc (r= -0.245 and r= -0.256 respectively, P<0.05). Modest weight loss improved the status of CRP, adiponectin, zinc and decreased incidence of metabolic syndrome (P<0.05). Changes in metabolic syndrome factors were positively related with those of adiponectin (r=0.281, P<0.05). Higher systemic inflammation due to obesity is strongly associated with metabolic syndrome and weight loss appears to be effective in its reduction. [ABSTRACT FROM AUTHOR]

Variation in body weight and composition, as well as adipose tissue function, is regulated by environmental and genetic factors, combined with a variety of interactions, including environment-by-environment, gene-by-gene, and gene-by-environment interactions. Although the recent increase in obesity can in large part be attributed to the increased availability of low-cost but energy-dense foods and an increasingly sedentary lifestyle throughout most of the developed world, the impact of these factors is more pronounced in individuals who are genetically susceptible to these environmental insults. Hence, it is likely to be the response of an individual's genetic background to a given environment that determines susceptibility to obesity. Candidate gene studies, genome-wide linkage studies, and more recently genome-wide association studies (GWASs) have been used to decipher the effect of genetics on obesity. Heritability estimates suggest that 40-70% of the variation in obesity-related phenotypes is attributable to underlying genetic variation. To date, the findings from human cohort studies (both family and case/control studies) summarized in this chapter suggest that there are likely numerous genes impacting the expression of obesity-related phenotypes, with many of these genes seeming to have modest effects. The establishment of many population-based studies that have collected genome-wide data on genetic variation has recently led to the formation of multiple consortia facilitating powerful meta-analyses in order to identify additional genetic variation influencing obesity-related traits through GWAS, as well as to replicate and further characterize previously identified genetic variants and their gene regions. These consortia may have the power to elucidate how genetic and environmental factors act and interact to produce variation in obesity-related phenotypes., (Copyright © 2010 Elsevier Inc. All rights reserved.)