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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., Competing Interests: The authors declare no conflicts of interest.

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 (20:4 n -6, AA), or docosahexaenoic acid (22:6 n -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, IL-6; 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.

Altered intestinal health is also associated with the incidence and severity of many chronic inflammatory conditions, which could be attenuated via dietary n -3 PUFA interventions. However, little is known about the effect of lifelong exposure to n -3 PUFA from plant and marine sources (beginning in utero via the maternal diet) on early life biomarkers of intestinal health. Harems of C57Bl/6 mice were randomly assigned to one of three isocaloric AIN-93G modified diets differing in their fat sources consisting of the following: (i) 10% safflower oil (SO, enriched in n -6 PUFA), (ii) 3% flaxseed oil + 7% safflower oil (FX, plant-based n -3 PUFA-enriched diet), or (iii) 3% menhaden fish oil + 7% safflower oil (MO, marine-based n -3 PUFA-enriched diet). Mothers remained on these diets throughout pregnancy and offspring (n = 14/diet) continued on the same parental diet until termination at 3 weeks of age. In ileum, villi:crypt length ratios were increased in both the FX and MO dietary groups compared to SO ( p < 0.05). Ileum mRNA expression of critical intestinal health biomarkers was increased by both n -3 PUFA-enriched diets including Relmβ and REG3γ compared to SO ( p < 0.05), whereas only the FX diet increased mRNA expression of TFF3 and Muc2 ( p < 0.05) and only the MO diet increased mRNA expression of ZO-1 ( p < 0.05). In the proximal colon, both the FX and MO diets increased crypt lengths compared to SO ( p < 0.05), whereas only the MO diet increased goblet cell numbers compared to SO ( p < 0.05). Further, the MO diet increased proximal colon mRNA expression of Relmβ and REG3γ ( p < 0.05) and both MO and FX increased mRNA expression of Muc2 compared to SO ( p < 0.05). Collectively, these results demonstrate that lifelong exposure to dietary n -3 PUFA, beginning in utero, from both plant and marine sources, can support intestinal health development in early life. The differential effects between plant and marine sources warrants further investigation for optimizing health.

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.

Over the years, there has been heightened interest in the health benefits of n -3 polyunsaturated fatty acids (PUFA) in reducing chronic diseases such as, cardiovascular disease (CVD), cancer, type 2 diabetes, and acute macular degeneration (AMD). Due to inconsistent findings in the evidence, a review to critically examine the plethora of evidence from randomized controlled trials (RCTs) in n -3 PUFA research was undertaken. The aim of this review is to study the highest level of evidence and to identify gaps in n -3 PUFA research. RCTs were originally designed for pharmaceutical research and later adopted for nutrition and food-related research. RCTs with active diseases assume that n -3 PUFA will have "drug" like effects, and this high expectation may have led to the inconsistent evidence in the literature. The inconsistency in the literature may be related to varying doses of n -3 PUFA, sources of n -3 PUFA (food vs. supplement; plant vs. marine), type of n -3 PUFA (mixture vs. purified), trial duration, population characteristics, sample size, and genetic variation. For future research, there is a need to distinguish between primary and secondary prevention, and to focus RCTs on primary prevention of chronic diseases by n -3 PUFA which is lacking in the literature.

Short-chain fatty acids (SCFA) produced from dietary non-digestible carbohydrate fermentation have metabolic effects in skeletal muscle; however, their effect on inflammatory mediator production is unknown. In this study, L6 myotubes were cultured with individual SCFA (acetate, propionate, and butyrate) at 0.5 mM and 2.5 mM ± 10 ng/mL lipopolysaccharide (LPS) or ± 500 µM palmitic acid (PA) for 24 h. In response to LPS, only butyrate had an effect at the lower concentration (0.5 mM), whereas at the higher concentration (2.5 mM) both propionate and butyrate reduced MCP-1, MIP-1α, and RANTES secretion (p < 0.05), and only butyrate reduced IL-6 secretion and intracellular protein levels of phospho-STAT3 (p < 0.05). In response to PA, 0.5 mM butyrate reduced protein expression of phospho-NFκB p65 and the secretion of IL-6, MIP-1α, and MCP-1, whereas all three SCFA reduced RANTES secretion (p < 0.05). At the 2.5 mM SCFA concentration combined with PA stimulation, all three SCFA reduced intracellular protein expression of phospho-NFκB p65 and phospho-STAT3 and secreted protein levels of MCP-1, IL-6, and RANTES, whereas only butyrate reduced secretion of MIP-1α (p < 0.05). Thus, SCFA exhibit differential effects on inflammatory mediator expression in response to LPS and PA stimulation, which has implications for their individual impacts on inflammation-mediated skeletal muscle dysfunction.

There is limited research on the intake of non-nutritive sweeteners (NNS) among preschool-aged children. Canada’s Food Guide suggests limiting intake of NNS for all population groups and Health Canada recommends that young children (<2 years) avoid consuming beverages containing NNS. The aim of this study was to investigate the frequency and type of non-nutritive sweetener (NNS) intake in preschool-aged children participating in the Guelph Family Health Study pilots. Parents (n = 78 families) completed 3-day food records (n = 112 children; n = 55 females, n = 57 males; 3.6 years ± 1.3). Nineteen children (17%) reported consumption of foods or beverages containing NNS. Food sources with NNS included: freezies, oral nutritional supplements, flavored water, carbonated drinks, sugar free jam and protein powder. The majority of NNS contained in these foods were identified as stevia leaf extract, acesulfame K, sucralose, monk fruit extract and aspartame. Future research should continue to study NNS intake patterns longitudinally in children and examine the association of NNS intake with diet quality and health outcomes.

Concussions and mild traumatic brain injury (m-TBI) have been identified as a consequential public health concern because of their potential to cause considerable impairments in physical, cognitive, behavioral, and social functions. Given their prominent structural and functional roles in the brain, n-3 polyunsaturated fatty acids (PUFA) have been identified as a potentially viable prophylactic agent that may ameliorate the deleterious effects of m-TBI on brain function. The purpose of the present pilot study was to investigate the effect of n-3 PUFA on neurologic function using a weight drop injury (WDI) model. Fat-1 mice, capable of synthesizing n-3 PUFA endogenously from n-6 PUFA, and their wild-type (WT) counterparts, were subjected to a mild low-impact WDI on the closed cranium, and recovery was evaluated using the neurological severity score (NSS) to assess the motor and neurobehavioral outcomes. In comparison to the WT mice, the fat-1 mice had a significantly ( p ≤ 0.05) lower NSS at all time points post-WDI, and significantly greater neurological restoration measured as the time to first movement. Overall, these findings demonstrate the protective effect of n-3 PUFA against mild brain injury.

Background: EPA and DHA n-3 FA play crucial roles in both neurological and cardiovascular health and high dietary intakes along with supplementation suggest potential neuroprotection and concussion recovery support. Rugby athletes have a high risk of repetitive sub-concussive head impacts which may lead to long-term neurological deficits, but there is a lack of research looking into n-3 FA status in rugby players. We examined the dietary n-3 FA intake through a FFQ and n-3 FA status by measuring the percentage of n-3 FA and O3I in elite Canadian Rugby 7s players to show distribution across O3I risk zones; high risk, <4%; intermediate risk, 4 to 8%; and low risk, >8%., Methods: n-3 FA profile and dietary intake as per FFQ were collected at the beginning of the 2017-2018 Rugby 7s season in male ( n = 19; 24.84 ± 2.32 years; 95.23 ± 6.93 kg) and female ( n = 15; 23.45 ± 3.10 years; 71.21 ± 5.79 kg) athletes., Results: O3I averaged 4.54% ± 1.77, with female athlete scores slightly higher, and higher O3I scores in supplemented athletes (4.82% vs. 3.94%, p = 0.183), with a greater proportion of non-supplemented athletes in the high-risk category (45.5% vs. 39.1%). Dietary intake in non-supplemented athletes did not meet daily dietary recommendations for ALA or EPA + DHA compared to supplemented athletes., Conclusions: Overall, despite supplementation, O3I score remained in the high-risk category in a proportion of athletes who met recommended n-3 FA dietary intakes, and non-supplemented athletes had a higher proportion of O3I scores in the high-risk category, suggesting that dietary intake alone may not be enough and athletes may require additional dietary and n-3 FA supplementation to reduce neurological and cardiovascular risk.

Past research using hepatic rat microsomes showed that soy protein suppressed delta-6 desaturase activity (D6D) compared to casein (a dairy protein). The effects of soy and dairy on desaturase pathway activity in humans remain poorly investigated. The objective of this analysis was to investigate the association between soy and dairy consumption with plasma fatty acids and estimate the desaturase pathway activity in a multiethnic Canadian population of young adults. We analyzed data from men ( n = 319) and women ( n = 764) previously collected for the Toronto Nutrigenomics and Health Study. Food frequency questionnaires and plasma fatty acids were assessed. Relationships between soy and dairy beverages and food consumption with estimated desaturase activities were assessed by regression models and by grouping participants according to beverage and food intake data. Weak inverse associations ( p ≤ 0.05) were found between soy consumption and the overall desaturation pathway activity, specifically D6D activity. When participants were grouped based on soy and dairy consumption habits, omega-6 LC-PUFAs, as well as various estimates of the desaturase pathway activity, were significantly lower in individuals consuming soy (with or without dairy) compared to individuals consuming only fluid milk and dairy products. In conclusion, soy consumption, not dairy consumption, appears to suppress desaturase pathway activity.

Chronic stress is known to influence dietary choices, and stressed families often report poorer diet quality; however, little is known about how family-based stress is linked with dietary patterns that promote inflammation. This study investigated associations between family-based stress and the inflammatory potential of the diet among preschool-aged children and their parents. Parents ( n = 212 mothers, n = 146 fathers) and children ( n = 130 girls, n = 123 boys; aged 18 months to 5 years) from 241 families participating in the Guelph Family Health Study were included in the analyses. Parents reported levels of parenting distress, depressive symptoms, household chaos, and family functioning. The inflammatory potential of parents' and children's diets was quantified using the Dietary Inflammatory Index (DII ® ), adjusted for total energy intake (i.e., the E-DII TM ). E-DII scores were regressed onto family stress using generalized estimating equations to account for shared variance among family clusters. Compared to those in homes with low chaos, parents in chaotic homes had significantly more proinflammatory dietary profiles ( β = 0.973; 95% CI: 0.321, 1.624, p = 0.003). Similarly, compared to those in well-functioning families, parents in dysfunctional families had significantly more proinflammatory dietary profiles ( β = 0.967; 95% CI: 0.173, 1.761, p = 0.02). No significant associations were found between parents' E-DII scores and parenting distress or depressive symptoms, nor were any associations found for children's E-DII scores. Results were not found to differ between males and females. Parents in chaotic or dysfunctional family environments may be at increased risk of chronic disease due to proinflammatory dietary profiles. Children's dietary inflammatory profiles were not directly associated with family stress; however, indirect connections through family food-related behaviours may exist. Future research should prioritize elucidating these mechanisms.

Dietary fatty acids (FA) are essential for overall human health, yet individual FA reference ranges have yet to be established. Developing individual FA reference ranges can provide context to reported concentrations and whether an individual displays deficient, or excess amounts of FA. Reference ranges of sixty-seven individual FA (μmol/L) were profiled and analyzed using gas chromatography with a flame ionization detector from serum samples collected from 476 middle-aged Singaporean males (BMI:23.3 ± 2.9) and females (BMI:21.8 ± 3.6). Measures of triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and total cholesterol (TC) (mmol/L) were also collected. The mean FA concentration seen in this cohort (11,458 ± 2478 was similar to that of overweight North American cohorts assessed in past studies. Ten biologically relevant FA were compared between sexes, with females exhibiting significantly higher concentrations in four FA ( p < 0.05). A multiple regression model revealed the ten FA contributed significantly to nearly all lipid biomarkers ( p < 0.05). A majority of participants who had FA concentrations in the ≥95th percentile also exhibited TG, HDL, LDL, and TC levels in the "high" risk classification of developing cardiovascular disease. Future studies profiling individual FA reference ranges in many unique, global cohorts are necessary to develop cut-off values of individual FA concentrations highly related to disease-risk.

Lifestyle habits, such as the consumption of a healthy diet, may prevent up to 30-50% of breast cancer (BC) cases. Dietary fats are of specific interest, as research provides strong evidence regarding the association of dietary fats and BC. However, there is limited research on the role of different types of fats including polyunsaturated (PUFA), monounsaturated (MUFA), and saturated fatty acids (SFA). The objective of this study was to determine the effects of lifelong exposure to various dietary fats on mammary tumour development over a 20-week period. Female heterozygous MMTV-neu (ndl) YD5 mouse models were fed five maternal diets containing (1) 10% safflower oil (n-6 PUFA, control), (2) 3% menhaden oil + 7% safflower oil (marine n-3 PUFA, control), (3) 3% flaxseed + 7% safflower oil (plant-based n-3 PUFA), (4) 10% olive oil (MUFA), or (5) 10% lard (SFA). The primary measures, tumour latency, volume, and multiplicity differed by diet treatment in the following general order, n-6 PUFA > plant n-3 PUFA, SFA, MUFA > marine n-3 PUFA. Overall, these findings show that the quality of the diet plays a significant role influencing mammary tumour outcomes.

The COVID-19 pandemic has disrupted many aspects of daily life. The purpose of this study was to identify how health behaviors, level of stress, financial and food security have been impacted by the pandemic among Canadian families with young children. Parents (mothers, n = 235 and fathers, n = 126) from 254 families participating in an ongoing study completed an online survey that included close and open-ended questions. Descriptive statistics were used to summarize the quantitative data and qualitative responses were analyzed using thematic analysis. More than half of our sample reported that their eating and meal routines have changed since COVID-19; most commonly reported changes were eating more snack foods and spending more time cooking. Screen time increased among 74% of mothers, 61% of fathers, and 87% of children and physical activity decreased among 59% of mothers, 52% of fathers, and 52% of children. Key factors influencing family stress include balancing work with childcare/homeschooling and financial instability. While some unhealthful behaviors appeared to have been exacerbated, other more healthful behaviors also emerged since COVID-19. Research is needed to determine the longer-term impact of the pandemic on behaviors and to identify effective strategies to support families in the post-COVID-19 context.

Parents' stress is independently associated with increased child adiposity, but parents' stress may also interfere with childhood obesity prevention programs. The disruptions to the family dynamic caused by participating in a behaviour change intervention may exacerbate parent stress and undermine overall intervention efficacy. This study explored how family stress levels were impacted by participation in a home-based obesity prevention intervention. Data were collected from 77 families (56 fathers, 77 mothers) participating in the Guelph Family Health Study (GFHS), a pilot randomized control trial of a home-based obesity prevention intervention. Four measures of stress were investigated: general life stress, parenting distress, depressive symptoms, and household chaos. Multiple linear regression was used to compare the level of stress between the intervention and control groups at post-intervention and 1-year follow-up, adjusted for baseline stress. Analyses for mothers and fathers were stratified, except for household chaos which was measured at the family level. Results indicate no significant differences between intervention and control groups for any stress measure at any time point, indicating a neutral effect of the GFHS intervention on family stress. Future work should investigate the components of family-based intervention protocols that make participation minimally burdensome and consider embedding specific stress-reduction messaging to promote family health and wellbeing.

Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been associated with reduced breast cancer risk; however, the exact mechanism remains elusive. Female wildtype (WT) and fat-1 mice were fed a 10% safflower diet until 6 weeks of age. Mammary gland epithelial cells (EC) were isolated and EC populations were determined by CD24 surface expression. Fat-1 mice expressed 65%, 20%, and 15% while WT mice expressed 65%, 26% and 9% for non-, myo- and luminal ECs, respectively. The luminal EC population was significantly greater in fat-1 mice ( p ≤ 0.05), while the total number of mammary ECs were similar between groups ( p = 0.79). Caveolae was isolated from ECs and Her-2/neu, ER-α and cav-1 protein expression was determined by Western blotting. Fat-1 mice had a two-fold greater ER-α ( p ≤ 0.05) and a 1.5-fold greater cav-1 ( p ≤ 0.05) expression than WT with a similar amount of Her-2/neu protein ( p = 0.990) between groups. Overall, this study provides novel mechanistic evidence by which n-3 PUFA modifies early mammary gland development that may potentially reduce breast cancer risk later in life., Competing Interests: The authors declare no conflict of interest.

Background: People living with human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS) (PLWH) are at an increased risk of cardiovascular disease. Diet-related factors may contribute. The aim of this pilot study was to determine, in PLWH, the relationship between atherosclerosis assessed by carotid intima-media thickness (CIMT) and (A) plasma antioxidant micronutrients and oxidative stress or (B) red blood cell polyunsaturated fatty acids (RBC PUFA), particularly long chain omega-3 polyunsaturated fatty acids (n-3 PUFA)., Methods: (A) In a cross-sectional study, subjects had CIMT evaluated by high resolution carotid artery ultrasound. Plasma was collected for vitamin C, measured by spectrophotometry; and alpha- and gamma-tocopherol, retinol, and malondialdehyde-a marker of oxidative stress-using high pressure liquid chromatography and fluorescence spectrophotometry. (B) In a prospective cohort study, other subjects had RBC PUFA measured at baseline, using gas chromatography, and CIMT assessed at baseline and repeated after 2 years. Clinical data was also collected., Results: (A) 91 PLWH participated. Only alpha- and gamma-tocopherol levels were positively correlated with CIMT. In a multivariate analysis, age and systolic blood pressure were significantly associated with CIMT with gamma-tocopherol near significance ( p = 0.053). (B) 69 PLWH participated. At baseline, docosahexaenoic acid (n-3 PUFA) and the ratio of docosahexaenoic acid to arachidonic acid (n-6 PUFA) were significantly and negatively correlated with CIMT. However, a multivariate analysis failed to detect a significant relationship either at baseline or 2 years after., Conclusion: In addition to age and systolic blood pressure, atherosclerosis assessed by CIMT might be associated with higher serum gamma-tocopherol levels. There was a non-significant association between CIMT and RBC n-3 PUFA or the ratio of n-3 to n-6 PUFA.

Taste is a fundamental determinant of food selection, and inter-individual variations in taste perception may be important risk factors for poor eating habits and obesity. Characterizing differences in taste perception and their influences on dietary intake may lead to an improved understanding of obesity risk and a potential to develop personalized nutrition recommendations. This study explored associations between 93 single nucleotide polymorphisms (SNPs) in sweet, fat, bitter, salt, sour, and umami taste receptors and psychophysical measures of taste. Forty-four families from the Guelph Family Health Study participated, including 60 children and 65 adults. Saliva was collected for genetic analysis and parents completed a three-day food record for their children. Parents underwent a test for suprathreshold sensitivity (ST) and taste preference (PR) for sweet, fat, salt, umami, and sour as well as a phenylthiocarbamide (PTC) taste status test. Children underwent PR tests and a PTC taste status test. Analysis of SNPs and psychophysical measures of taste yielded 23 significant associations in parents and 11 in children. After adjusting for multiple hypothesis testing, the rs713598 in the TAS2R38 bitter taste receptor gene and rs236514 in the KCNJ2 sour taste-associated gene remained significantly associated with PTC ST and sour PR in parents, respectively. In children, rs173135 in KCNJ2 and rs4790522 in the TRPV1 salt taste-associated gene remained significantly associated with sour and salt taste PRs, respectively. A multiple trait analysis of PR and nutrient composition of diet in the children revealed that rs9701796 in the TAS1R2 sweet taste receptor gene was associated with both sweet PR and percent energy from added sugar in the diet. These findings provide evidence that for bitter, sour, salt, and sweet taste, certain genetic variants are associated with taste function and may be implicated in eating patterns. (Support was provided by the Ontario Ministry of Agriculture, Food, and Rural Affairs).

Snacking is an integral component of eating habits in young children that is often overlooked in nutrition research. While snacking is a substantial source of calories in preschoolers' diets, there is limited knowledge about the factors that drive snacking patterns. The genetics of taste may help to better understand the snacking patterns of children. The rs1761667 single nucleotide polymorphism (SNP) in the CD36 gene has been linked to fat taste sensitivity, the rs35874116 SNP in the TAS1R2 gene has been related to sweet taste preference, and the rs713598 SNP in the TAS2R38 gene has been associated with aversion to bitter, green leafy vegetables. This study seeks to determine the cross-sectional associations between three taste receptor SNPs and snacking patterns among preschoolers in the Guelph Family Health Study. Preschoolers' snack quality, quantity, and frequency were assessed using three-day food records and saliva was collected for SNP genotyping ( n = 47). Children with the TT genotype in TAS1R2 consumed snacks with significantly more calories from sugar, and these snacks were consumed mostly in the evening. Total energy density of snacks was highest in the CC and CG genotypes compared to the GG genotype in TAS2R38 , and also greater in the AA genotype in CD36 compared to G allele carriers, however this difference was not individually attributable to energy from fat, carbohydrates, sugar, or protein. Genetic variation in taste receptors may influence snacking patterns of preschoolers., Competing Interests: The authors declare no conflict of interest.

Breast cancer (BC) is the most common cancer among women worldwide. Dietary fatty acids, especially n-3 polyunsaturated fatty acids (PUFA), are believed to play a role in reducing BC risk. Evidence has shown that fish consumption or intake of long-chain n-3 PUFA, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are beneficial for inhibiting mammary carcinogenesis. The evidence regarding α-linolenic acid (ALA), however, remains equivocal. It is essential to clarify the relation between ALA and cancer since ALA is the principal source of n-3 PUFA in the Western diet and the conversion of ALA to EPA and DHA is not efficient in humans. In addition, the specific anticancer roles of individual n-3 PUFA, alone, have not yet been identified. Therefore, the present review evaluates ALA, EPA and DHA consumed individually as well as in n-3 PUFA mixtures. Also, their role in the prevention of BC and potential anticancer mechanisms of action are examined. Overall, this review suggests that each n-3 PUFA has promising anticancer effects and warrants further research.

Globally, the prevalence of obesity is increasing which subsequently increases the risk of the development of obesity-related chronic diseases. Low-grade chronic inflammation and dysregulated adipose tissue inflammatory mediator/adipokine secretion are well-established in obesity, and these factors increase the risk of developing inflammation-associated cancer. Breast cancer is of particular interest given that increased inflammation within the subcutaneous mammary adipose tissue depot can alter the local tissue inflammatory microenvironment such that it resembles that of obese visceral adipose tissue. Therefore, in obese women with breast cancer, increased inflammatory mediators both locally and systemically can perpetuate inflammation-associated pro-carcinogenic signaling pathways, thereby increasing disease severity. Herein, we discuss some of these inflammation-associated pro-carcinogenic mechanisms of the combined obese breast cancer phenotype and offer evidence that dietary long chain n-3 polyunsaturated fatty acids (PUFA) may have utility in mitigating the severity of obesity-associated inflammation and breast cancer.

A growing body of research suggests a linkage between pubertal mammary gland development and environmental factors such as diet as modifiers of long term breast cancer risk. Much of this research is dependent upon mouse models, which may vary between studies. However, effects may be strain dependent and further modified by diet, which has not been previously examined. Therefore, the objective of the present study was to determine whether mammary gland development differs between FVB and C57Bl/6 strains on diets containing either n-6 or n-3 polyunsaturated fats. Developmental measures related to onset of puberty and mammary gland development differed between strains. Mice fed the n-3 polyunsaturated fatty acids (PUFA) diet were shown to have lower numbers of terminal end buds, a marker of mammary gland development. This study helps to further clarify differences in development and dietary response between FVB and C57Bl/6 mice in order to more appropriately relate mammary gland research to human populations.