No abstract

Consumption of 100% fruit juice remains controversial for its potential adverse impact on weight and displacement of essential foods in the diets of children. A systematic review of the literature published from 1995-2013 was conducted using the PubMed database to evaluate associations between intake of 100% fruit juice and weight/adiposity and nutrient intake/adequacy among children of 1 to 18 years of age. Weight status outcome measures included body mass index (BMI), BMI z-score, ponderal index, obesity, weight gain, adiposity measures, and body composition. Nutrient outcome measures included intake and adequacy of shortfall nutrients. Data extraction and analysis was conducted according to the Academy of Nutrition and Dietetics Evidence Analysis Process. Twenty-two studies on weight status provided evidence that did not support an association between 100% fruit juice consumption and weight/adiposity in children after controlling for energy intake. Limited evidence from eight studies suggests that children consuming 100% fruit juice have higher intake and adequacy of dietary fiber, vitamin C, magnesium, and potassium. Differences in methodology and study designs preclude causal determination of 100% fruit juice as sole influencer of weight status or nutrient intake/adequacy of shortfall nutrients. In context of a healthy dietary pattern, evidence suggests that consumption of 100% fruit juice may provide beneficial nutrients without contributing to pediatric obesity.

Apoptosis, programmed cell death type I, is a critical part of neurodegeneration in cerebral ischemia, Parkinson’s, and Alzheimer’s disease. Apoptosis begins with activation of pro-death proteins Bax and Bak, release of cytochrome c and activation of caspases, loss of membrane integrity of intracellular organelles, and ultimately cell death. Approaches that block apoptotic pathways may prevent or delay neurodegenerative processes. Carotenoids are a group of pigments found in fruits, vegetables, and seaweeds that possess antioxidant properties. Over the last several decades, an increasing number of studies have demonstrated a protective role of carotenoids in neurodegenerative disease. In this review, we describe functions of commonly consumed carotenoids including lycopene, β-carotene, lutein, astaxanthin, and fucoxanthin and their roles in neurodegenerative disease models. We also discuss the underlying cellular mechanisms of carotenoid-mediated neuroprotection, including their antioxidant properties, role as signaling molecules, and as gene regulators that alleviate apoptosis-associated brain cell death.

Guideline recommendation for a plant bioactive such as flavan-3-ols is a departure from previous recommendations as it is not based on deficiencies but rather improvement in health outcomes. Nevertheless, there is a rapidly growing body of clinical data reflecting benefits of flavan-3-ol intake that outweigh potential harms. Thus, the objective of the Expert Panel was to develop an intake recommendation for flavan-3-ols and cardiometabolic outcomes to inform multiple stakeholders including clinicians, policymakers, public health entities, and consumers. Guideline development followed the process set forth by the Academy of Nutrition and Dietetics which includes use of Evidence to Decision Framework. Studies informing this guideline (157 randomized controlled trials and 15 cohort studies) were previously reviewed in a recently published systematic review and meta-analysis. Quality and strength-of-evidence along with risk-of-bias in reporting was reviewed. In drafting the guideline, data assessments and opinions by authoritative scientific bodies providing guidance on the safety of flavan-3-ols were considered. Moderate evidence supporting cardiometabolic protection resulting from flavan-3-ol intake in the range of 400-600 mg/d was supported in the literature. Further, increasing consumption of dietary flavan-3-ols may help improve blood pressure, cholesterol levels, and blood sugar. Strength of evidence was strongest for some biomarkers (i.e., systolic blood pressure, total cholesterol, HDL-cholesterol, and insulin/glucose dynamics). It should be noted that this is a food-based guideline and not a recommendation for flavan-3-ol supplements. This guideline was based on beneficial effects observed across a range of disease biomarkers and endpoints. While a comprehensive assessment of available data has been reviewed, evidence gaps identified herein can inform scientists whereby guiding future randomized clinical trials.

Cardiometabolic risk factors increase the likelihood of cardiovascular disease development by 2-fold. Lycopene, a potent lipophilic antioxidant, may be able to mediate oxidative stress, a mechanism underpinning metabolic syndrome (MetS) and its risk factors. This is, to our knowledge, the first systematic review of the literature with the purpose of investigating the relation between circulating lycopene or dietary intake of lycopene and MetS as well as its risk factors. The review was conducted using PubMed and EBSCOhost databases with the search terms "lycopene"and "metabolic syndrome." Inclusion criteria included human studies published in English in a scholarly, peer-reviewed journal and evaluation of lycopene in relation to ≥3 of the 5 MetS risk factors as defined by the National Cholesterol Education Program's Adult Treatment Panel III (ATP III) report. The process identified 11 studies, including 8 cross-sectional and 3 intervention studies. Cross-sectional studies were grouped into 3 categories, with several studies falling into >1 category, based on results reporting associations of lycopene with the prevalence and outcomes of MetS (5 studies), presence of ATP III risk factors (4 studies), and variables mediating lycopene's influence on MetS risk (3 studies). All studies in each category reported significant protective associations. Of the 3 intervention studies, all reported significant protective effects from a lycopene-rich beverage, despite varying doses and durations of intake. Although a protective relation between lycopene and MetS was generally supported, different MetS components appeared to be influenced by lycopene rather than demonstrating consistent improvement in a single component. Thus, additional research is needed to elucidate the mechanistic effects of lycopene on MetS, as well as to determine evidence-based recommendations concerning dosedurational effects of lycopene and MetS risk reduction. In conclusion, the evidence of lycopene's benefit exists such that lycopene status or lycopene consumption may be associated with favorable alterations to the components of MetS.