Parental feeding practices to manage snack food intake: Associations with energy intake regulation in young children

© 2017 Elsevier. This manuscript version is made available under the CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0/ This author accepted manuscript is made available following 24 month embargo from date of publication (Dec 2017) in accordance with the publisher’s archiving policyBackground Little attention has been directed to understanding the relationship between restriction and regulation of snack food intake in toddlers. Objective The aim of this study was to examine the effects of parental restriction of toddlers' eating of snacks in the absence of hunger (EAH) and to examine the impact of three contextual factors; snack food access, frequency of snack food consumption, and attraction to snack food. Design 64 parents and toddlers (aged 22–36 months) took part in a protocol to measure EAH (defined as kJ of energy-dense snack foods consumed). Mean EAH was 199 kJ (SD = 299), with 43 children consuming at least some snacks. Restriction was measured with the Child Feeding Questionnaire Restriction subscale. Snack food access was measured with Allow Access from the Toddler Snack Food Feeding Questionnaire (TSFFQ), snack food consumption was measured with a short snack food frequency questionnaire, and attraction to snack foods was measured with Child's Attraction from the TSFFQ. Moderated regression analyses tested interactions between Restriction and contextual factors in predicting EAH. Results EAH was associated with Restriction (r = 0.25, p = .05, 95% CI 0.004 - 0.47). There was an interaction between Restriction and accessibility of snack foods (R2 change = 0.08, p = .025); restriction was associated with EAH only when access to snack foods in the home was, on average, higher. The effect of Restriction on EAH was not moderated by frequency of snack food consumption or Child's Attraction. Conclusions These finding have practical relevance and reinforce the importance of the home food environment for managing young children's snack food intake

Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease

Background: Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this. Objectives: To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids. Search methods: We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors. Selection criteria: We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake. Data collection and analysis: Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression. Main results: We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias. Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet. Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence), cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs), cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence), coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs), stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials) or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs). There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk. All evidence was of moderate GRADE quality, except as noted. Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence). However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT). Effects on stroke are unclear. Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection. LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes. There were no dose or duration effects in subgrouping or meta-regression. There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence). Authors' conclusions: This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia

Polyunsaturated fatty acids for the primary and secondary prevention of cardiovascular disease

Background: Evidence on the health effects of total polyunsaturated fatty acids (PUFA) is equivocal. Fish oils are rich in omega-3 PUFA and plant oils in omega-6 PUFA. Evidence suggests increasing PUFA-rich foods, supplements or supplemented foods can reduce serum cholesterol, but may increase body weight, so overall cardiovascular effects are unclear. Objectives: To assess effects of increasing PUFA intake on cardiovascular disease (CVD) and all-cause mortality in adults. Search method: We searched CENTRAL, MEDLINE and Embase to April 2017 and ClinicalTrials.com and World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews. Selection criteria: We included randomised controlled trials (RCTs) comparing higher with lower PUFA intakes in adults with or without CVD that assessed effects over ≥12 months. We included full-text, abstracts, trials registry entries and unpublished data. Outcomes were all-cause mortality, CVD mortality and events, risk factors (blood lipids, adiposity, blood pressure), and adverse events. We excluded trials where we could not separate effects of PUFA intake from other dietary, lifestyle or medication interventions. Data collection and analysis: Two authors independently screened titles/abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias. We wrote to authors of included studies for further data. Meta-analyses used random-effects analysis, sensitivity analyses included fixed-effects and limiting to low summary risk of bias. We assessed GRADE quality of evidence. Main result: We included 49 RCTs randomising 24,272 participants, with duration of one to eight years. Twelve included trials were at low summary risk of bias, 33 recruited participants without cardiovascular disease. Baseline PUFA intake was unclear in most trials, but 3.9% to 8% of total energy intake where reported. Most trials gave supplemental capsules, but eight gave dietary advice, eight gave supplemental foods such as nuts or margarine, and three used a combination of methods to increase PUFA. Increasing PUFA intake probably has little or no effect on all-cause mortality (risk 3.4% vs 3.3% in primary prevention, 11.7% vs 11.5% in secondary prevention, risk ratio (RR) 0.98, 95% confidence interval (CI) 0.89 to 1.07, 24 trials in 19290 participants), but probably reduces risk of CVD events from 5.8% to 4.9% in primary prevention, 23.3% to 20.8% in secondary prevention (RR 0.89, 95% CI 0.79 to 1.01, 20 trials in 17,073 participants), both moderate quality evidence. Increasing PUFA may reduce risk of CHD events from 13.4% to 7.1% primary prevention, 14.3% to 13.7% secondary prevention (RR 0.87, 95% CI 0.72 to 1.06, 15 trials, 10,076 participants), CHD death (5.2% to 4.4% primary prevention, 6.8% to 6.1% secondary prevention, RR 0.91, 95% CI 0.78 to 1.06, 9 trials, 8810 participants) and may slightly reduce stroke risk (2.1% to 1.5% primary prevention, RR 0.91, 95% CI 0.58 to 1.44, 11 trials, 14,742 participants), but has little or no effect on cardiovascular mortality (RR 1.02, 95% CI 0.82 to 1.26, I2 31%, 16 trials, 15,107 participants) all low quality evidence. Effects of increasing PUFA on major adverse cardiac and cerebrovascular events and atrial fibrillation are unclear as evidence is of very low quality. Event outcomes were all downgraded for indirectness, as most events occurred in men in westernised countries. Increasing PUFA intake reduces total cholesterol (MD -0.12 mmol/L, 95% CI -0.23 to -0.02, I2 79%, 8072 participants, 26 trials) and probably decreases triglycerides (TG, MD -0.12 mmol/L, 95% CI -0.20 to -0.04, I2 50%, 3905 participants, 20 trials), but has little or no effect on HDL (MD -0.01 mmol/L, 95% CI -0.02 to 0.01, I2 0%, 4674 participants, 18 trials) and LDL (MD -0.01 mmol/L, 95% CI -0.09 to 0.06, I2 44%, 3362 participants, 15 trials). Increasing PUFA probably causes slight weight gain (MD 0.76 kg, 95% CI 0.34 to 1.19, I2 59%, 7100 participants, 12 trials). Effects of increasing PUFA on serious adverse events such as pulmonary embolism and bleeding are unclear as the evidence is of very low quality. Authors' conclusions: Increasing PUFA intake probably reduces risk of CVD events, may reduce risk of CHD events and CHD mortality,and may slightly reduce stroke risk, but has little or no effect on all-cause or CVD mortality. The mechanism may be via lipid reduction, but increasing PUFA probably slightly increases weight

Assessing lifetime diet: reproducibility of a self-administered, non-quantitative FFQ

Objective: To demonstrate test–retest reliability (reproducibility) of a new self-administered lifetime diet questionnaire, with a focus on foods relevant to cognitive health in older age. Design: The reproducibility of dietary recall over four or five life periods was assessed by administering the questionnaire at two time points to an older cohort. The period between questionnaire administrations was 7 weeks. Polychoric correlations measured the association between recall at time 1 and time 2 and the weighted κ statistic measured the level of recall agreement for food groups across the two administrations of the questionnaire. Setting: Adelaide, South Australia. Subjects: Fifty-two cognitively healthy, older-age, community-dwelling adults completed the Lifetime Diet Questionnaire; mean age 81•8 (SD 4•4) years, range 70–90 years. Results: The questionnaire showed very good reproducibility in this sample with a mean polychoric correlation coefficient of 0•81 between administration at time 1 and time 2, and an average weighted κ of 0•49 for the level of recall agreement between food groups. Conclusions: The demonstrated reliability of this lifetime diet questionnaire makes it a useful tool to assess potential relationships between long-term dietary intake and later-age cognitive outcomes.Diane Hosking, Vanessa Danthiir, Ted Nettelbeck and Carlene Wilso

The older people, omega-3, and cognitive health (EPOCH) trial design and methodology: A randomised, double-blind, controlled trial investigating the effect of long-chain omega-3 fatty acids on cognitive ageing and wellbeing in cognitively healthy older adults

Extent: 18p.Background: Some studies have suggested an association between omega-3 long-chain polyunsaturated fatty acids (n-3 LC PUFAs) and better cognitive outcomes in older adults. To date, only two randomised, controlled trials have assessed the effect of n-3 LC PUFA supplementation on cognitive function in older cognitively healthy populations. Of these trials only one found a benefit, in the subgroup carrying the ApoE-ε4 allele. The benefits of n-3 LC PUFA supplementation on cognitive function in older normal populations thus still remain unclear. The main objective of the current study was to provide a comprehensive assessment of the potential of n-3 LC PUFAs to slow cognitive decline in normal elderly people, and included ApoE-ε4 allele carriage as a potential moderating factor. The detailed methodology of the trial is reported herein. Methods: The study was a parallel, 18-month, randomised, double-blind, placebo-controlled intervention with assessment at baseline and repeated 6-monthly. Participants (N = 391, 53.7% female) aged 65-90 years, English-speaking and with normal cognitive function, were recruited from metropolitan Adelaide, South Australia. Participants in the intervention arm received capsules containing fish-oil at a daily dosage of 1720 mg of docosahexaenoic acid and 600 mg of eicosapentaenoic acid while the placebo arm received the equivalent amount of olive oil in their capsules. The primary outcome is rate of change in cognitive performance, as measured by latent variables for the cognitive constructs (encompassing Reasoning, Working Memory, Short-term Memory, Retrieval Fluency, Inhibition, Simple and Choice-Reaction Time, Perceptual Speed, Odd-man-out Reaction Time, Speed of Memory Scanning, and Psychomotor Speed) and assessed by latent growth curve modeling. Secondary outcomes are change in the Mini-mental State Examination, functional capacity and well-being (including health status, depression, mood, and self-report cognitive functioning), blood pressure, and biomarkers of n-3 LC PUFA status, glucose, lipid metabolism, inflammation, oxidative stress, and DNA damage.Vanessa Danthiir, Nicholas R Burns, Ted Nettelbeck, Carlene Wilson and Gary Witter

Omega 3 fatty acid for the prevention of cognitive decline and dementia.

BACKGROUND: Evidence from observational studies suggests that diets high in omega-3 long-chain polyunsaturated fatty acids (PUFA) may protect people from cognitive decline and dementia. The strength of this potential protective effect has recently been tested in randomised controlled trials. OBJECTIVES: To assess the effects of omega-3 PUFA supplementation for the prevention of dementia and cognitive decline in cognitively healthy older people. SEARCH METHODS: We searched ALOIS - the Cochrane Dementia and Cognitive Improvement Group's Specialized Register on 6 April 2012 using the terms: "omega 3", PUFA, "fatty acids", "fatty acid", fish, linseed, eicosapentaenoic, docosahexaenoic. SELECTION CRITERIA: Randomised controlled trials of an omega-3 PUFA intervention which was provided for a minimum of six months to participants aged 60 years and over who were free from dementia or cognitive impairment at the beginning of the study. Two review authors independently assessed all trials. DATA COLLECTION AND ANALYSIS: The review authors sought and extracted data on incident dementia, cognitive function, safety and adherence, either from published reports or by contacting the investigators for original data. Data were extracted by two review authors. We calculated mean difference (MD) or standardised mean differences (SMD) and 95% confidence intervals (CI) on an intention-to-treat basis, and summarised narratively information on safety and adherence. MAIN RESULTS: Information on cognitive function at the start of a study was available on 4080 participants randomised in three trials. Cognitive function data were available on 3536 participants at final follow-up.In two studies participants received gel capsules containing either omega-3 PUFA (the intervention) or olive or sunflower oil (placebo) for six or 24 months. In one study, participants received margarine spread for 40 months; the margarine for the intervention group contained omega-3 PUFA. Two studies had cognitive health as their primary outcome; one study of cardiovascular disease included cognitive health as an additional outcome.None of the studies examined the effect of omega-3 PUFA on incident dementia. In two studies involving 3221 participants there was no difference between the omega-3 and placebo group in mini-mental state examination score at final follow-up (following 24 or 40 months of intervention); MD -0.07 (95% CI -0.25 to 0.10). In two studies involving 1043 participants, other tests of cognitive function such as word learning, digit span and verbal fluency showed no beneficial effect of omega-3 PUFA supplementation. Participants in both the intervention and control groups experienced either small or no cognitive declines during the studies.The main reported side-effect of omega-3 PUFA supplementation was mild gastrointestinal problems. Overall, minor adverse events were reported by fewer than 15% of participants, and reports were balanced between intervention groups. Adherence to the intervention was on average over 90% among people who completed the trials. All three studies included in this review are of high methodological quality. AUTHORS' CONCLUSIONS: Direct evidence on the effect of omega-3 PUFA on incident dementia is lacking. The available trials showed no benefit of omega-3 PUFA supplementation on cognitive function in cognitively healthy older people. Omega-3 PUFA supplementation is generally well tolerated with the most commonly reported side-effect being mild gastrointestinal problems.Further studies of longer duration are required. Longer-term studies may identify greater change in cognitive function in study participants which may enhance the ability to detect the possible effects of omega-3 PUFA supplementation in preventing cognitive decline in older people

Decision speed in intelligence tasks: Correctly an ability?

Relatively little is known regarding the broad factor of correct decision speed (CDS), which is represented in the theory of fluid and crystallized intelligence. The current study (N = 186) examined the possibility that distinct CDS factors may exist that are specific to the broad ability assessed by the tasks from which the correct response latencies are derived, in this instance fluid and crystallized intelligence (Gf and Gc) tasks. Additionally, the relationships between the correct response latencies and Gf, Gc, and processing speed (Gs) were investigated. Two distinct yet correlated factors of CDS were identified for Gf and Gc tasks, respectively. Both CDS factors were related to their ability factor counterparts, and CDSGc was lowly related to Gs. However, item difficulty moderated the relationships between CDS and the abilities. When item difficulty was considered relative to groups of participants differing in ability level, differences in the speed of responses were found amongst the ability groups. The pattern of differences in speed amongst the ability groups was similar across all levels of item difficulty. It is argued that this method of analysis is the most appropriate for assessing the relationship between ability level and CDS. The status of CDS as a broad ability construct is considered in light of these findings. (PsycINFO Database Record (c) 2019 APA, all rights reserved