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This study explored (1) the effect of applying an autocalibration algorithm on accelerometer data analyzed using different signal processing techniques and (2) how these techniques changed the signal composition. Using a dataset of preschoolers (n = 137; 4.31 ± 0.87 years; Actigraph accelerometers (100 Hz) on right hip 24 hours/7 days) the vector magnitude (VM) was calculated as a reference; highpass, bandpass and lowpass filters were applied and the "Euclidean Norm Minus One" (ENMO) was calculated. Amplitude probability distribution functions were created to compare the (1) uncalibrated versus calibrated data and, (2) amplitude distribution across the techniques. Results showed that the calibration correction significantly impacted ENMO, VM lowpass and VM data, but the impact on VM highpass and bandpass data was minimal. Comparing across the techniques, results showed the lowest outputs were derived according to ENMO, followed by the VM highpass/VM bandpass and the VM lowpass/VM which yielded very similar results.

Background: The early exposure of nutrients during pubertal mammary gland development may reduce the risk of developing breast cancer later in life. Anticancer n-3 polyunsaturated fatty acids (n-3 PUFA) are shown to modulate pubertal mammary gland development; however, the mechanisms of action remain unclear. Prior work focused on effects at the whole tissue level, and little is known at the cellular level, such as at the level of mammary epithelial cells (MECs), which are implicated in cancer development. Methods: This pilot study examined the effects of lifelong n-3 PUFA exposure on the transcriptome by RNA-Seq in the isolated MECs of pubertal (6–8-week-old) female fat-1 transgenic mice capable of de novo n-3 PUFA synthesis. edgeR and DESeq2 were used separately for the differential expression analysis of RNA sequencing data followed by the Benjamani–Hochberg procedure for multiple testing correction. Results: Nine genes were found concordant and significantly different (p ≤ 0.05) by both the DESeq2 and edgeR methods. These genes were associated with multiple pathways, suggesting that n-3 PUFA stimulates estrogen-related signaling (Mlltl0, Galr3, and Nrip1) and a glycolytic profile (Soga1, Pdpr, and Uso1) while offering protective effects for immune and DNA damage responses (Glpd1, Garre1, and Rpa1) in MECs during puberty. Conclusions: This pilot study highlights the utility of RNA-Seq to better understanding the mechanistic effects of specific nutrients such as n-3 PUFA in a cell-specific manner. Thus, further studies are warranted to investigate the cell-specific mechanisms by which n-3 PUFA influences pubertal mammary gland development and breast cancer risk later in life. [ABSTRACT FROM AUTHOR]

In obesity, circulating saturated fatty acids (SFAs) and inflammatory cytokines interfere with skeletal muscle insulin signaling, leading to whole body insulin resistance. Further, obese skeletal muscle is characterized by macrophage infiltration and polarization to the inflammatory M1 phenotype, which is central to the development of local inflammation and insulin resistance. While skeletal muscle-infiltrated macrophage–myocyte crosstalk is exacerbated by SFA, the effects of other fatty acids, such as n-3 and n-6 polyunsaturated fatty acids (PUFAs), are less studied. Thus, the objective of this study was to determine the effects of long-chain n-3 and n-6 PUFAs on macrophage M1 polarization and subsequent effects on myocyte inflammation and metabolic function compared to SFA. Using an in vitro model recapitulating obese skeletal muscle cells, differentiated L6 myocytes were cultured for 24 h with RAW 264.7 macrophage-conditioned media (MCM), followed by insulin stimulation (100 nM, 20 min). MCM was generated by pre-treating macrophages for 24 h with 100 µM palmitic acid (16:0, PA–control), arachidonic acid (20:4n-6, AA), or docosahexaenoic acid (22:6n-3, DHA). Next, macrophage cultures were stimulated with a physiological dose (10 ng/mL) of lipopolysaccharide for an additional 12 h to mimic in vivo obese endotoxin levels. Compared to PA, both AA and DHA reduced mRNA expression and/or secreted protein levels of markers for M1 (TNFα, IL-6, iNOS; p < 0.05) and increased those for M2 (IL-10, TGF-β; p < 0.05) macrophage polarization. In turn, AA- and DHA-derived MCM reduced L6 myocyte-secreted cytokines (TNFα, IL6; p < 0.05) and chemokines (MCP-1, MIP-1β; p < 0.05). Only AA-derived MCM increased L6-myocyte phosphorylation of Akt (p < 0.05), yet this was inconsistent with improved insulin signaling, as only DHA-derived MCM improved L6 myocyte glucose uptake (p < 0.05). In conclusion, dietary n-3 and n-6 PUFAs may be a useful strategy to modulate macrophage–myocyte inflammatory crosstalk and improve myocyte insulin sensitivity in obesity. [ABSTRACT FROM AUTHOR]

Background: Chronic stress is an important risk factor in the development of obesity. While research suggests chronic stress is linked to excess weight gain in children, the biological or behavioral mechanisms are poorly understood. Objective: The objectives of the Family Stress Study are to examine behavioral and biological pathways through which chronic stress exposure (including stress from COVID-19) may be associated with adiposity in young children, and to determine if factors such as child sex, caregiver-child relationship quality, caregiver education, and caregiver self-regulation moderate the association between chronic stress and child adiposity. Methods: The Family Stress Study is a prospective cohort study of families recruited from 2 Canadian sites: the University of Guelph in Guelph, Ontario, and McMaster University in Hamilton, Ontario. Participants will be observed for 2 years and were eligible to participate if they had at least one child (aged 2-6 years) and no plans to move from the area within the next 3 years. Study questionnaires and measures were completed remotely at baseline and will be assessed using the same methods at 1- and 2-year follow-ups. At each time point, caregivers measure and report their child's height, weight, and waist circumference, collect a hair sample for cortisol analysis, and fit their child with an activity monitor to assess the child's physical activity and sleep. Caregivers also complete a web-based health and behaviors survey with questions about family demographics, family stress, their own weight-related behaviors, and their child's mental health, as well as a 1-day dietary assessment for their child. Results: Enrollment for this study was completed in December 2021. The final second-year follow-up was completed in April 2024. This study's sample includes 359 families (359 children, 359 female caregivers, and 179 male caregivers). The children's mean (SD) age is 3.9 years (1.2 years) and 51% (n=182) are female. Approximately 74% (n=263) of children and 80% (n=431) of caregivers identify as White. Approximately 34% (n=184) of caregivers have a college diploma or less and nearly 93% (n=499) are married or cohabiting with a partner. Nearly half (n=172, 47%) of the families have an annual household income ≥CAD $100,000 (an average exchange rate of 1 CAD=0.737626 USD applies). Data cleaning and analysis are ongoing as of manuscript publication. Conclusions: Despite public health restrictions from COVID-19, the Family Stress Study was successful in recruiting and using remote data collection to successfully engage families in this study. The results from this study will help identify the direction and relative contributions of the biological and behavioral pathways linking chronic stress and adiposity. These findings will aid in the development of effective interventions designed to modify these pathways and reduce obesity risk in children. Trial Registration: ClinicalTrials.gov NCT05534711; https://clinicaltrials.gov/study/NCT05534711 International Registered Report Identifier (IRRID): DERR1-10.2196/48549 [ABSTRACT FROM AUTHOR]

Dietary guidance promotes plant-based foods, yet minimal research has examined intake in children. This study examined plant-based food intake in preschool-aged children using plant-based dietary index (PDI) metrics and related these metrics to nutrient and food group intakes. Dietary data were collected from preschool-aged children (n = 283, 3.45 ± 1.22 years) from the Guelph Family Health Study at baseline using the Automated Self-Administered 24-Hour Dietary Assessment Tool. Food intake servings were assigned to 16 food groups for calculation of overall PDI (oPDI), healthful PDI (hPDI), and less healthful (lhPDI) scores and summarized into tertiles for energy-adjusted comparisons. For oPDI, participants in the highest vs. lowest tertile had higher intakes of nutrients and food groups to encourage (e.g., dietary fiber, fruits) as well as lower intakes of nutrients to encourage (e.g., calcium, vitamin D). For hPDI, participants in the highest vs. lowest tertile had higher intakes of nutrients and food groups to encourage and lower intakes of those to limit (e.g., saturated fat, sweets and desserts). For lhPDI, participants in the highest vs. lowest tertile had higher intakes of nutrients and food groups to limit and lower intakes of those to encourage. These results can inform dietetic practice for dietary guidance that promotes plant-based foods in children. [ABSTRACT FROM AUTHOR]

Excess dietary sugar intake increases the risk of unhealthy weight gain, an important cardiometabolic risk factor in children. To further our understanding of this relationship, we performed a narrative review using two approaches. First, research examining dietary sugar intake, its associations with cardiometabolic health, impact of genetics on sweet taste perception and intake, and how genetics moderates the association of dietary sugar intake and cardiometabolic risk factors in preschool-aged children 1.5-5 years old is reviewed. Second, methodological considerations for collecting and analyzing dietary intake of sugar, genetic information, and markers of cardiometabolic health among young children are provided. Our key recommendations include the following for researchers: (1) Further longitudinal research on sugar intake and cardiometabolic risk factors is warranted to inform policy decisions and guidelines for healthy eating in preschool-aged children. (2) Consistency in sugar definitions is needed across research studies to aid with comparisons of results. (3) Select dietary collection tools specific to each study's aim and sugar definition(s). (4) Limit subjectivity of dietary assessment tools as this impacts interpretation of study results. (5) Choose non-invasive biomarkers of cardiometabolic disease until the strengths and limitations of available biomarkers in preschool-aged children are clarified. (6) Select approaches that account for the polygenic nature of cardiometabolic disease such as genome risk scores and genome wide association studies to assess how genetics moderates the relationship between dietary sugar intake and cardiometabolic risk. This review highlights potential recommendations that will support a research environment to help inform policy decisions and healthy eating policies to reduce cardiometabolic risk in young children. [ABSTRACT FROM AUTHOR]

Past research in rodents suggests that fatty acid (FA) desaturase expression and activity may be modified by vitamin A; however, this has not been investigated in humans. The primary objective of this study was to examine associations between dietary retinoid intakes, plasma retinoid concentrations, and FA desaturase indices in young adults. As a secondary objective, biological sex and estrogen‐containing contraceptive (EC) use were investigated due to prior evidence demonstrating that both can influence plasma retinol concentration and FA desaturase indices. Dietary retinoid intake (food frequency questionnaire), plasma retinoid concentrations (high‐performance liquid chromatography–tandem mass spectrometry), plasma FA (gas chromatography), and FA desaturase indices (product‐to‐precursor ratios) from 945 adults recruited for the cross‐sectional Toronto Nutrigenomics and Health study were analyzed. Participants were stratified into quartiles based on plasma retinol concentration and data analyzed by one‐way analysis of covariance. Dietary retinoid intakes were not associated with the overall n‐3 pathway, overall n‐6 pathway, delta‐5 desaturase, delta‐6 desaturase, or delta‐9 desaturase indices (all r < 0.10, p > 0.05). The overall n‐6 pathway index was significantly higher (p = 0.0004) and the delta‐5 desaturase index was significantly lower (p = 0.0003) in individuals with higher plasma retinol levels; however, these differences were lost when participants were grouped by biological sex and EC use. Although weak relationships were observed between plasma retinol and some FA desaturase indices in the total population, these associations appear to be driven by biological sex and EC usage rather than retinoids. We therefore find little evidence of a relationship between retinoids and FA desaturase indices in young, healthy adults. [ABSTRACT FROM AUTHOR]

Simple Summary: The sociodemographic characteristics of a parent and child may predispose young children to excessive dietary sugar intake; however, there is limited research available on this topic. The aim of this cross-sectional analysis was to examine the impact of sociodemographic characteristics such as child age, child sex, child ethnicity, parent number of years living in Canada, annual household income, parent education and parent marital status on total, free and added sugar intake in young children. Dietary and sociodemographic data including 267 children from 210 families participating in the Guelph Family Health Study were examined. The results indicate that child age, child ethnicity and annual household income can play a crucial role in shaping sugar intake in young children. This research may help inform future research and program interventions early in life along with guiding parents to decrease sugar intake in young children. Background: It is crucial to develop strategies targeted to promote healthy eating patterns in vulnerable populations, especially young children from diverse sociodemographic groups. Thus, the study objective was to investigate the associations between child age, child sex, child ethnicity, parent number of years living in Canada, annual household income, parent education and parent marital status with total, free and added sugar intakes in young children. Methods: This cross-sectional study was a secondary analysis of data gathered in the Guelph Family Health Study. The study included 267 children (129M; 138F) from 210 families aged 1.5 to 5 years. Parents completed questionnaires for children on sociodemographic characteristics and an online 24-hour diet recall. The associations between sociodemographic characteristics and sugar intakes were determined using generalized estimating equations applied to linear regression models. Results: The mean age of the children was 3.5 ± 1.2 years (mean ± std dev.). As children's age increased, there was a greater intake of free and added sugar ( β ^ = 8.6, p = 0.01, 95% CI = 2.4 to 14.7 and β ^ = 6.5, p = 0.03, 95% CI = 0.8 to 12.2, respectively). Those children who identified as white had a higher total sugar intake than children of other ethnicities ( β ^ = 31.0, p = 0.01, 95% CI = 7.2 to 54.7). Additionally, higher annual household income was associated with lower was free sugar intake in children ( β ^ = −2.4, p = 0.02, 95% CI = −4.5 to −0.4). Conclusions: This study underscores the significant influence of multiple sociodemographic characteristics on sugar intake in young children, providing valuable insights for public health policy and nutrition interventions. Moreover, this study highlights the need for early behaviour interventions focusing on reducing sugar intake in young children, while considering sociodemographic factors. [ABSTRACT FROM AUTHOR]