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Background

Little is known about zinc intakes and status during complementary feeding. This is particularly true for baby-led approaches, which encourage infants to feed themselves from the start of complementary feeding, although self-feeding may restrict the intake of zinc-rich foods.

Objective

To determine the zinc intakes, sources, and biochemical zinc status of infants following Baby-Led Introduction to SolidS (BLISS), a modified version of Baby-Led Weaning (BLW), compared with traditional spoon-feeding.

Design

Secondary analysis of the BLISS randomized controlled trial.

Participants/setting

Between 2012 and 2014, 206 community-based participants from Dunedin, New Zealand were randomized to a Control or BLISS group.

Intervention

BLISS participants received eight study visits (antenatal to 9 months) providing education and support regarding BLISS (ie, infant self-feeding from 6 months with modifications to address concerns about iron, choking, and growth).

Main outcome measures

Dietary zinc intakes at 7 and 12 months (weighed 3-day diet records) and zinc status at 12 months (plasma zinc concentration).

Statistical analyses performed

Regression analyses were used to investigate differences in dietary intakes and zinc status by group, adjusted for maternal education and parity and infant age and sex.

Results

There were no significant differences in zinc intakes between BLISS and Control infants at 7 (median: 3.5 vs 3.5 mg/day; P=0.42) or 12 (4.4 vs 4.4 mg/day; P=0.86) months. Complementary food groups contributing the most zinc at 7 months were “vegetables” for Control infants, and “breads and cereals” for BLISS infants, then “dairy” for both groups at 12 months. There was no significant difference in mean±standard deviation plasma zinc concentration between the Control (62.8±9.8 μg/dL [9.6±1.5 μmol/L]) and BLISS (62.8±10.5 μg/dL [9.6±1.6 μmol/L]) groups (P=0.75).

Conclusions

BLISS infants achieved similar zinc intake and status to Control infants. However, the BLISS intervention was modified to increase iron intake, which may have improved zinc intake, so these results should not be generalized to infants following unmodified BLW.  相似文献   
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Prevalence of obesity, an established risk factor for many cancers, has increased dramatically over the past 50 years in the United States and across the globe. Relative to normoweight cancer patients, obese cancer patients often have poorer prognoses, resistance to chemotherapies, and are more likely to develop distant metastases. Recent progress on elucidating the mechanisms underlying the obesity?cancer connection suggests that obesity exerts pleomorphic effects on pathways related to tumor development and progression and, thus, there are multiple opportunities for primary prevention and treatment of obesity-related cancers. Obesity-associated alterations, including systemic metabolism, adipose inflammation, growth factor signaling, and angiogenesis, are emerging as primary drivers of obesity-associated cancer development and progression. These obesity-associated host factors interact with the intrinsic molecular characteristics of cancer cells, facilitating several of the hallmarks of cancer. Each is considered in the context of potential preventive and therapeutic strategies to reduce the burden of obesity-related cancers. In addition, this review focuses on emerging mechanisms behind the obesity?cancer link, as well as relevant dietary interventions, including calorie restriction, intermittent fasting, low-fat diet, and ketogenic diet, that are being implemented in preclinical and clinical trials, with the ultimate goal of reducing incidence and progression of obesity-related cancers.  相似文献   
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