Food Is Medicine: A Presidential Advisory From the American Heart Association.

Unhealthy diets are a major impediment to achieving a healthier population in the United States. Although there is a relatively clear sense of what constitutes a healthy diet, most of the US population does not eat healthy food at rates consistent with the recommended clinical guidelines. An abundance of barriers, including food and nutrition insecurity, how food is marketed and advertised, access to and affordability of healthy foods, and behavioral challenges such as a focus on immediate versus delayed gratification, stand in the way of healthier dietary patterns for many Americans. Food Is Medicine may be defined as the provision of healthy food resources to prevent, manage, or treat specific clinical conditions in coordination with the health care sector. Although the field has promise, relatively few studies have been conducted with designs that provide strong evidence of associations between Food Is Medicine interventions and health outcomes or health costs. Much work needs to be done to create a stronger body of evidence that convincingly demonstrates the effectiveness and cost-effectiveness of different types of Food Is Medicine interventions. An estimated 90% of the $4.3 trillion annual cost of health care in the United States is spent on medical care for chronic disease. For many of these diseases, diet is a major risk factor, so even modest improvements in diet could have a significant impact. This presidential advisory offers an overview of the state of the field of Food Is Medicine and a road map for a new research initiative that strategically approaches the outstanding questions in the field while prioritizing a human-centered design approach to achieve high rates of patient engagement and sustained behavior change. This will ideally happen in the context of broader efforts to use a health equity-centered approach to enhance the ways in which our food system and related policies support improvements in health.

Cardiac and inflammatory biomarkers in perinatally HIV-infected and HIV-exposed uninfected children.

OBJECTIVES: To compare distributions of serum cardiac and inflammatory biomarkers between perinatally HIV-infected (PHIV) and perinatally HIV-exposed uninfected (PHEU) children, to evaluate their associations with echocardiographic measures, and among PHIV youth, with antiretroviral therapy (ART) and HIV disease severity measures. DESIGN: Cross-sectional analysis of temporally paired serum samples for biomarkers and echocardiograms in a prospective multicenter cohort study of PHIV and PHEU youth. METHODS: Serum samples were analyzed among 402 youth in the PHACS Adolescent Master Protocol (AMP) for high-sensitivity cardiac troponin-T (hs-cTnT, a cardiomyocyte injury marker), N-terminal-pro-brain natriuretic peptide (NT-proBNP, a myocardial stress marker), and inflammatory markers [high-sensitivity C-reactive protein, interleukin (IL)-1, IL-6, IL-8, IL-10, IL-18, tumor necrosis factor-α (TNF-α), and soluble TNF receptor II (sTNF-RII)]. Echocardiograms were centrally measured and parameters converted to z cores to account for differences in age and body size. RESULTS: Compared with PHEU (N = 156), PHIV youth (N = 246) more often had detectable hs-cTnT and higher levels of sTNF-RII and IL-18. Higher inflammatory biomarkers were generally associated with higher left ventricular (LV) wall stress and lower LV function and LV mass in the two groups. Among PHIV youth, the biomarkers were more strongly associated with current rather than historical immunologic and virologic status. CONCLUSION: PHEU and PHIV have modest, significant differences in serum levels of specific inflammatory and active myocardial injury biomarkers. Higher biomarker levels were associated with lower LV mass and shifts in LV structure. Further study is warranted on the longitudinal role of cardiac and inflammatory biomarkers for targeting interventions among PHIV and PHEU youth.

Right ventricle to pulmonary artery conduit augmentation compared with replacement in young children.

BACKGROUND: Targeted outcome data for young children undergoing right ventricle to pulmonary artery conduit reoperation are sparse, as are data on the use of conduit augmentation as an alternative to conduit replacement at the time of first conduit reoperation (conduit 2). METHODS: We conducted a retrospective chart review including baseline data, operative data, and cross-sectional follow-up on children younger than 10 years of age undergoing a first conduit reoperation (n = 180), comparing conduit replacement (n = 147, 82%) with conduit augmentation (n = 33, 18%). RESULTS: There were no differences between the two groups with respect to age, size, or hemodynamic variables. Augmentation was less often performed in patients with an aortic homograft and by one surgeon. At conduit 2, cardiopulmonary bypass time was longer in replacement patients (101 +/- 35 versus 71 +/- 34 minutes; p < 0.001); cardiac intensive care unit stay was not different. Early mortality was 0.5%, and overall 10-year survival was 95%. Freedom from reoperation was 80% at 5 years and 39% at 10 years, whereas freedom from reintervention (reoperation or catheter intervention) was 55% at 5 years and 26% at 10 years, with no differences between groups. Aortic homograft as a first conduit was associated with shorter freedom from reoperation. Limiting analysis to conduits that were replaced at conduit 2, undersized conduits were associated with shorter freedom from reoperation and smaller body surface area, and undersized conduits were associated with shorter freedom from reintervention. CONCLUSIONS: Freedom from a second conduit reoperation after a first conduit replacement was shorter in smaller children and undersized conduits. Conduit augmentation offers similar clinical outcomes in selected patients.