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Both food insecurity and malnutrition are associated with adverse health outcomes in the pediatric population. However, the research on the relationship between these factors has been inconsistent, leading to uncertainty regarding whether or how evaluation of food insecurity should be incorporated into nutrition screening or the nutrition care process. The objective of this systematic review was to determine the association between food insecurity and malnutrition related to undernutrition or overnutrition (defined by anthropometrics) in the pediatric population in the United States. A literature search was conducted using Medline, Embase, and CINAHL databases for studies published from January 2002 through November 2017. A total of 23 studies (19 cross-sectional and 4 prospective cohort studies) met inclusion criteria and were included in qualitative analysis. In 6 studies, there was no overall relationship between food insecurity and underweight. All included studies examined the relationship between food insecurity status and overweight/obesity and results were mixed, with large cross-sectional studies demonstrating a positive relationship between food insecurity and overweight/obesity. There were no clear patterns according to subpopulation. Evidence quality was graded as fair due to heterogeneity in how food insecurity was measured and populations included as well as inconsistency in results. Use of a 2-item food insecurity screening tool may allow for efficient, effective screening of food insecurity in order to identify potential contributors overweight and obesity., (Copyright © 2021 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.)

Background: The relation between malnutrition and pulmonary death in patients with cystic fibrosis (CF) has resulted in intensive nutritional intervention over the last few decades, leading to a significant decline in underweight and the emergence of overweight/obesity as a potential new problem., Methods: We performed a cross-sectional database analysis of 484 adults with CF seen at the University of Minnesota CF Center between January 2015-January 2017, to determine the prevalence and pulmonary/cardiovascular risk factors associated with overweight and obesity in this population., Results: Mean age was 35.2 ± 11.6 years. 5.2% were underweight (BMI<18.5 kg/m 2 ), 62.6% normal weight (BMI ≥ 18.5-24.9 kg/m 2 ), 25.6% overweight (BMI ≥ 25-29.9 kg/m 2 ) and 6.6% obese (BMI ≥ 30 kg/m 2 ). In the subgroup with severe genotypes, 25% had BMI ≥ 25 kg/m 2 . In the entire cohort, overweight/obese were likely to be older (OR = 1.04, p < 0.0001) and to have a mild CFTR genotype (OR = 3.33, p = 0.0003) and modestly elevated triglyceride levels (OR = 1.008, p < 0.0001). The prevalence of hypertension was higher in overweight (25%) and obese (31%) than normal (17%) or underweight (16%), p = 0.01. Total cholesterol levels were higher in overweight/obese versus normal/underweight (144-147 vs 123-131 mg/dL, p = 0.04) as were LDL levels (70-71 vs 53-60 mg/dL, p = 0.02), but all were within the normal range. Percent predicted FEV1 was higher in overweight/obese (78-81%) versus underweight (59%) and normal (70%), p < 0.0001, and overweight/obese experienced significantly fewer acute pulmonary exacerbations., Conclusions: Overweight/obesity is common in adults with CF including those with severe genotypes. Lung function is better in the overweight/obese and lipid levels are within the normal range, albeit higher than in normal/underweight., Competing Interests: Declaration of Competing Interest T. Harindhanavudhi, A. Moheet, A. Moran and Q. Wang have no competing interests. J. Dunitz has received grants from Vertex Pharmaceuticals Inc, Hillrom, Proteostasis Therapeutics, Inc, and Cystic Fibrosis Foundation independent from the submitted work., (Copyright © 2019 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.)

Objectives: To examine body mass index (BMI) trajectories with change in lean mass and physical function in old age., Design: Prospective cohort study., Setting: Health, Aging and Body Composition Study., Participants: Black and white men (n = 482) and women (n = 516) aged 73.1 ± 2.7 and initially free of disability., Measurements: A group-based trajectory model was used to determine BMI trajectories, the path a person's BMI followed over 9 years. Lean mass, gait speed, grip strength, and knee extension strength were assessed at baseline and after 9 years, and relative changes were calculated. Multivariable linear regression was used to determine associations between trajectories and relative change in lean mass and physical function., Results: Four BMI trajectories were identified for men and four for women. Although all demonstrated a decline in BMI, the rate of decline differed according to trajectory for women only. Men in Trajectory 4 (mean BMI at baseline 33.9 ± 2.3 kg/m(2) ) declined more than those in Trajectory 1 (mean BMI at baseline 22.9 ± 1.6 kg/m(2) ) in gait speed (-9.91%, 95% confidence interval (CI) = -15.15% to -4.67%) and leg strength (-8.63%, 95% CI = -15.62% to -1.64%). Women in Trajectory 4 (mean BMI at baseline 34.9 ± 3.0 kg/m(2) ) had greater losses than those in Trajectory 1 (mean BMI at baseline 20.5 ± 1.6 kg/m(2) ) in lean mass in the arms (-3.19%, 95% CI = -6.16% to -0.23%). No other associations were observed., Conclusion: Obese men had the highest risk of decline in physical function despite similar weight loss between trajectories, whereas overweight and obese women who lost the most weight had the greatest risk of lean mass loss. The weight at which a person enters old age is informative for predicting loss in lean mass and physical function, illustrating the importance of monitoring weight., (© 2015, Copyright the Authors Journal compilation © 2015, The American Geriatrics Society.)

Objective: We sought to evaluate body composition in children and young adults with Fontan physiology. Leg lean mass (LM) deficits correlate with diminished exercise capacity in other populations and may contribute to exercise limitations in this cohort., Methods: This cross-sectional study included whole body dual energy X-ray absorptiometry scans in 50 Fontan participants ≥5 years, and measures of peak oxygen consumption (VO2) in 28. Whole body and leg LM (a measure of skeletal muscle) were converted to sex- and race-specific Z-scores, relative to age and stature, based on 992 healthy reference participants., Results: Median age was 11.5 (range 5.1-33.5) years at 9.3 (1.1-26.7) years from Fontan. Height Z-scores were lower in Fontan compared with reference participants (-0.47±1.08 vs 0.25±0.93, p<0.0001). Body mass index Z-scores were similar (0.15±0.98 vs 0.35±1.02, p=0.18). LM Z-scores were lower in Fontan compared with reference participants (whole body LM -0.33±0.77 vs 0.00±0.74, p=0.003; leg LM -0.89±0.91 vs 0.00±0.89, p<0.0001). LM Z-scores were not associated with age or Fontan characteristics. Leg LM Z-scores were lower in vitamin D deficient versus sufficient Fontan participants (-1.47±0.63 vs -0.71±0.92, p=0.01). Median per cent predicted peak VO2 was 81% (range 13%-113%) and was associated with leg LM Z-scores (r=0.54, p=0.003)., Conclusions: Following Fontan, children and young adults are shorter than their peers and have significant LM deficits. Skeletal muscle deficits were associated with vitamin D deficiency and reduced exercise capacity. Future studies should examine the progression of these deficits to further understand the contribution of peripheral musculature to Fontan exercise capacity., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Purpose: To evaluate the DSM-5 diagnosis of Avoidant/Restrictive Food Intake Disorder (ARFID) in children and adolescents with poor eating not associated with body image concerns., Methods: A retrospective case-control study of 8-18-year-olds, using a diagnostic algorithm, compared all cases with ARFID presenting to seven adolescent-medicine eating disorder programs in 2010 to a randomly selected sample with anorexia nervosa (AN) and bulimia nervosa (BN). Demographic and clinical information were recorded., Results: Of 712 individuals studied, 98 (13.8%) met ARFID criteria. Patients with ARFID were younger than those with AN (n = 98) or BN (n = 66), (12.9 vs. 15.6 vs. 16.5 years), had longer durations of illness (33.3 vs. 14.5 vs. 23.5 months), were more likely to be male (29% vs. 15% vs. 6%), and had a percent median body weight intermediate between those with AN or BN (86.5 vs. 81.0 and 107.5). Patients with ARFID included those with selective (picky) eating since early childhood (28.7%); generalized anxiety (21.4%); gastrointestinal symptoms (19.4%); a history of vomiting/choking (13.2%); and food allergies (4.1%). Patients with ARFID were more likely to have a comorbid medical condition (55% vs. 10% vs. 11%) or anxiety disorder (58% vs. 35% vs. 33%) and were less likely to have a mood disorder (19% vs. 31% vs. 58%)., Conclusions: Patients with ARFID were demographically and clinically distinct from those with AN or BN. They were significantly underweight with a longer duration of illness and had a greater likelihood of comorbid medical and/or psychiatric symptoms., (Copyright © 2014 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.)

In an aging population, potentially modifiable factors impacting mortality such as diet quality, body mass index (BMI), and health-related quality of life (HRQOL) are of interest. Surviving members of the Geisinger Rural Aging Study (GRAS) (n = 5,993; aged ?74 years) were contacted in the fall of 2009. Participants in the present study were the 2,995 (1,267 male, 1,728 female; mean age 81.4 ± 4.4 years) who completed dietary and demographic questionnaires and were enrolled in the Geisinger Health Plan over follow-up (mean = 3.1 years). Cox proportional hazards multivariate regression models were used to examine the associations between all-cause mortality and BMI, diet quality, and HRQOL. Compared to GRAS participants with BMIs in the normal range, a BMI < 18.5 was associated with increased mortality (HR 1.85 95%CI 1.09, 3.14, P = 0.02), while a BMI of 25-29.9 was associated with decreased risk of mortality (HR 0.71 95%CI 0.55, 0.91, P =0.007). Poor diet quality increased risk for mortality (HR 1.53 95%CI 1.06, 2.22, P = 0.02). Finally, favorable health-related quality of life was inversely associated with mortality (HR 0.09 95%CI 0.06, 0.13, P < 0.0001). Higher diet quality and HALex scores, and overweight status, were associated with reduced all-cause mortality in a cohort of advanced age. While underweight (BMI < 18.5) increased risk of all-cause mortality, no association was found between obesity and all-cause mortality in this aged cohort.

Cigarette smoking protects against preeclampsia but increases the risk of small-for-gestational-age birth (SGA). Regarding body weight, the converse is true: obesity elevates rates of preeclampsia but reduces rates of SGA. The authors assessed the combined effects of smoking and weight among US women developing preeclampsia or SGA, studying 7,757 healthy, primigravid women with singleton pregnancies in 1959-1965. Smoking (never, light, heavy), stratified by prepregnancy body mass index (BMI (weight (kg)/height (m)(2)); underweight, overweight, obese), was examined in relation to preeclampsia and SGA. Among underweight (BMI <18.5) and normal-weight (BMI 18.5-24.9) women, smoking decreased the risk of preeclampsia (for heavy smoking, light smoking, nonsmoking, test for trend p = 0.002 for underweight and p = 0.009 for normal weight) after adjustment for age, race, and socioeconomic status. However, among overweight/obese women (BMI >or=25), this trend was not apparent (p = 0.4). Among both underweight and overweight women, smoking significantly increased SGA risk (trend p < 0.001 for underweight and p = 0.02 for overweight/obese). Obesity eliminated the inverse association between smoking and preeclampsia but did not substantially alter the positive association between smoking and SGA. A possible unifying biologic explanation is discussed in this paper.