Dietary Flaxseed and Flaxseed Oil Differentially Modulate Aspects of the Microbiota Gut-Brain Axis Following an Acute Lipopolysaccharide Challenge in Male C57Bl/6 Mice.

The microbiota gut-brain axis (mGBA) is an important contributor to mental health and neurological and mood disorders. Lipopolysaccharides (LPS) are endotoxins that are components of Gram-negative bacteria cell walls and have been widely shown to induce both systemic and neuro-inflammation. Flaxseed (Linum usitatissimum) is an oilseed rich in fibre, n3-poly-unsaturated fatty acid (alpha-linolenic acid (ALA)), and lignan, secoisolariciresinol diglucoside, which all can induce beneficial effects across varying aspects of the mGBA. The objective of this study was to determine the potential for dietary supplementation with flaxseed or flaxseed oil to attenuate LPS-induced inflammation through modulation of the mGBA. In this study, 72 5-week-old male C57Bl/6 mice were fed one of three isocaloric diets for 3 weeks: (1) AIN-93G basal diet (BD), (2) BD + 10% flaxseed (FS), or (3) BD + 4% FS oil (FO). Mice were then injected with LPS (1 mg/kg i.p) or saline (n = 12/group) and samples were collected 24 h post-injection. Dietary supplementation with FS, but not FO, partially attenuated LPS-induced systemic (serum TNF-α and IL-10) and neuro-inflammation (hippocampal and/or medial prefrontal cortex IL-10, TNF-α, IL-1ß mRNA expression), but had no effect on sickness and nest-building behaviours. FS-fed mice had enhanced fecal microbial diversity with increased relative abundance of beneficial microbial groups (i.e., Lachnospiraceae, Bifidobacterium, Coriobacteriaceae), reduced Akkermansia muciniphila, and increased production of short-chain fatty acids (SCFAs), which may play a role in its anti-inflammatory response. Overall, this study highlights the potential for flaxseed to attenuate LPS-induced inflammation, in part through modulation of the intestinal microbiota, an effect which may not be solely driven by its ALA-rich oil component.

Active Videogaming Compared to Unstructured, Outdoor Play in Young Children: Percent Time in Moderate- to Vigorous-Intensity Physical Activity and Estimated Energy Expenditure.

OBJECTIVE: The majority of children do not achieve recommended amounts of moderate- to vigorous-intensity physical activity (MVPA). Active videogames (AVGs) may be a source of MVPA for young children. Thus, the purpose of this study was to compare, in children 5-8 years of age, percentage of time engaged in MVPA, assessed via accelerometry and direct observation (DO), and estimated energy expenditure (EE), assessed via accelerometry, while playing AVG and unstructured, outdoor play (OP). MATERIALS AND METHODS: Sixteen normal-weight young children (6.4±0.8 years old, 62.5 percent male, 81.3 percent white, standardized body mass index=-0.18±0.66) completed two 15-minute sessions of AVG and OP. For AVG, participants played "River Rush" (Xbox(®) 360 Kinect(®); Microsoft Corp., Redmond, WA), and OP was conducted in an outdoor playground. Three Actical (Philips Respironics Co. Inc., Bend, OR) accelerometers (hip and left and right wrists) measured percentage MVPA and estimated EE. DO was conducted using the Children's Activity Rating Scale, from which percentage MVPA was coded. RESULTS: Repeated-measures analysis of variance controlling for condition differences in humidity and condition order found greater percentage MVPA in AVG condition with the accelerometer located on the hip (AVG=74.6±31.1 percent versus OP=67.5±31.1 percent; P<0.05, d=0.23) and with DO (AVG=23.8±12.4 percent versus OP=13.2±13.0 percent; P<0.05, d=0.83). CONCLUSIONS: These findings suggest that AVGs may be a source of MVPA for young children.

Elevated breast cancer mortality in women younger than age 40 years compared with older women is attributed to poorer survival in early-stage disease.

BACKGROUND: We investigated differences in breast cancer mortality between younger (younger than 40 years of age) and older (40 years of age and older) women by stage at diagnosis to identify patient and tumor characteristics accounting for disparities. STUDY DESIGN: We conducted a retrospective study of women diagnosed with breast cancer in the 1988 to 2003 Surveillance, Epidemiology, and End Results Program data. Multivariate Cox regression models calculated adjusted hazard ratios (aHR) and 95% confidence intervals to compare overall and stage-specific breast cancer mortality in women younger than 40 years old and women 40 years and older, controlling for potential confounding variables identified in univariate tests. RESULTS: Of 243,012 breast cancer patients, 6.4% were younger than 40 years old, and 93.6% were 40 years of age or older. Compared with older women, younger women were more likely to be African American, single, diagnosed at later stages, and treated by mastectomy. Younger women had tumors that were more likely to be higher grade, larger size, estrogen receptor/progesterone receptor-negative, and lymph-node positive (p < 0.001). Younger women were more likely to die from breast cancer compared with older women (crude HR = 1.39; CI, 1.34 to 1.45). Controlling for confounders, younger women were more likely to die compared with older women if diagnosed with stage I (aHR = 1.44; CI, 1.27 to 1.64) or stage II (aHR = 1.09; CI, 1.03 to 1.15) disease and less likely to die if diagnosed with stage IV disease (aHR = 0.85; CI, 0.76 to 0.95). CONCLUSIONS: Higher breast cancer mortality in younger women was attributed to poorer outcomes with early-stage disease. Additional studies should focus on specific tumor biology contributing to the increased mortality of younger women with early-stage breast cancer.