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Background: Recent research underscores the crucial role of the gut microbiota in human health, particularly during states of altered homeostasis, including pregnancy. Additionally, it is not well understood how dietary changes during pregnancy affect the development of microbiomes of both mother and child., Methods: Here, we describe the study design and methods for our randomized controlled trial, the fermented and fiber-rich foods on maternal and offspring microbiome study (FeFiFo-MOMS). We enrolled 135 women during early pregnancy, randomizing them to one of four diet arms: increased fiber, increased fermented foods, increase in both, and no dietary intervention as a comparator arm. Samples were collected across pregnancy continuing to 18 months post-birth for clinical, microbiome, and immune marker analysis., Results: Our trial design intended to investigate the effects of dietary interventions-specifically, increased intake of high-fiber and fermented foods-on maternal gut microbiota diversity and its subsequent transmission to infants., Conclusion: The FeFiFo-MOMS trial was designed to provide valuable insights into the modifiable dietary factors that could influence maternal and infant health through microbiota-mediated mechanisms and examine the broader implications of diet on pregnant mothers' and infants' health and disease., Clinicaltrials: govID:NCT05123612., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025. Published by Elsevier Inc.)

Importance: Increasing evidence suggests that, compared with an omnivorous diet, a vegan diet confers potential cardiovascular benefits from improved diet quality (ie, higher consumption of vegetables, legumes, fruits, whole grains, nuts, and seeds)., Objective: To compare the effects of a healthy vegan vs healthy omnivorous diet on cardiometabolic measures during an 8-week intervention., Design, Setting, and Participants: This single-center, population-based randomized clinical trial of 22 pairs of twins (N = 44) randomized participants to a vegan or omnivorous diet (1 twin per diet). Participant enrollment began March 28, 2022, and continued through May 5, 2022. The date of final follow-up data collection was July 20, 2022. This 8-week, open-label, parallel, dietary randomized clinical trial compared the health impact of a vegan diet vs an omnivorous diet in identical twins. Primary analysis included all available data., Intervention: Twin pairs were randomized to follow a healthy vegan diet or a healthy omnivorous diet for 8 weeks. Diet-specific meals were provided via a meal delivery service from baseline through week 4, and from weeks 5 to 8 participants prepared their own diet-appropriate meals and snacks., Main Outcomes and Measures: The primary outcome was difference in low-density lipoprotein cholesterol concentration from baseline to end point (week 8). Secondary outcome measures were changes in cardiometabolic factors (plasma lipids, glucose, and insulin levels and serum trimethylamine N-oxide level), plasma vitamin B12 level, and body weight. Exploratory measures were adherence to study diets, ease or difficulty in following the diets, participant energy levels, and sense of well-being., Results: A total of 22 pairs (N = 44) of twins (34 [77.3%] female; mean [SD] age, 39.6 [12.7] years; mean [SD] body mass index, 25.9 [4.7]) were enrolled in the study. After 8 weeks, compared with twins randomized to an omnivorous diet, the twins randomized to the vegan diet experienced significant mean (SD) decreases in low-density lipoprotein cholesterol concentration (-13.9 [5.8] mg/dL; 95% CI, -25.3 to -2.4 mg/dL), fasting insulin level (-2.9 [1.3] μIU/mL; 95% CI, -5.3 to -0.4 μIU/mL), and body weight (-1.9 [0.7] kg; 95% CI, -3.3 to -0.6 kg)., Conclusions and Relevance: In this randomized clinical trial of the cardiometabolic effects of omnivorous vs vegan diets in identical twins, the healthy vegan diet led to improved cardiometabolic outcomes compared with a healthy omnivorous diet. Clinicians can consider this dietary approach as a healthy alternative for their patients., Trial Registration: ClinicalTrials.gov Identifier: NCT05297825.

Objective: The origins of allergic diseases have traditionally been explained by immunoglobulin E-mediated immune responses to account for asthma, atopic dermatitis, atopic rhinitis, and food allergy. Research insights into disease origins support a broader array of factors that predispose, initiate, or exacerbate altered immunity in allergic diseases, such as (1) inherent epithelial barrier dysfunction; (2) loss of immune tolerance; (3) disturbances in the gut; and (4) organ-specific microbiomes, diet, and age. Here, we discuss these influences that together form a better understanding of allergy as a systems disease., Data Sources: We summarize recent advances in epithelial dysfunction, environmental influences, inflammation, infection, alterations in the specific microbiome, and inherent genetic predisposition., Study Selections: We performed a literature search targeting primary and review articles., Results: We explored microbial-epithelial-immune interactions underlying the early-life origins of allergic disorders and evaluated immune mechanisms suggesting novel disease prevention or intervention strategies. Damage to epithelial surfaces lies at the origin of various manifestations of allergic disease. As a sensor of environmental stimuli, the epithelium of the lungs, gut, and skin is affected by an altered microbiome, air pollution, food allergens in a changed diet, and chemicals in modern detergents. This collectively leads to alterations of lung, skin, or gut epithelial surfaces, driving a type 2 immune response that underlies atopic diseases. Treatment and prevention of allergic diseases include biologics, oral desensitization, targeted gut microbiome alterations, and changes in behavior., Conclusion: Understanding the spectrum of allergy as a systems disease will allow us to better define the mechanisms of allergic disorders and improve their treatment., (Copyright © 2020. Published by Elsevier Inc.)

With the rising prevalence, food allergies have become a significant health burden that affects 6% to 13% of the global population. Although oral immunotherapy (OIT) has been promising for food allergies, this therapy has limitations, including high rates of adverse reactions and long treatment periods. Biologics may address these limitations by increasing the safety and tolerability of OIT and decreasing treatment periods. The use of biologics and vaccines are actively being explored as monotherapy as well as adjunctive therapy in combination with allergen specific OIT. A number of biologics that target key molecules known to be involved in food allergy are under investigation, including anti-immunoglobulin E therapy (omalizumab), anti-interleukin (IL) 4 receptor a (dupilumab), anti-IL-5 (mepolizumab and reslizumab), and anti-IL-5R (benralizumab), anti-IL-33 (etokimab), and peanut DNA plasmid vaccines. In the era of precision medicine, the future of food allergy looks promising, and biologics will provide treatment as well as further insights into the molecular mechanisms associated with food allergy., Competing Interests: The authors have no conflicts of interest to declare pertaining to this article, (Copyright © 2020, The Author(s). Published by OceanSide Publications, Inc., U.S.A.)

Food allergies are the result of immune responses that cause adverse reactions to foods. Immune responses to foods may produce a spectrum of symptoms and disorders, including acute allergic reactions and anaphylaxis, food protein-induced allergic proctocolitis, food protein-induced enterocolitis syndrome, food-dependent, exercise-induced anaphylaxis, and oral allergy syndrome (pollen-food allergy syndrome). Food-allergic responses also contribute to chronic inflammatory disorders such as eosinophilic esophagitis and atopic dermatitis. Although food allergy affects people from infancy through adulthood, there are allergic features that differ according to age (ie, presentation, triggers, and natural course) and have important implications for diagnosis, prognosis, and management. New food allergies can develop at any age, and we propose similarities in the etiology of de novo food allergy whether in infancy or adulthood. The approach to managing food allergy changes dramatically over the life course, and physicians and patients must respond accordingly to optimize care. Food allergy therapies are emerging, and the efficacy and safety of these interventions could differ by age group of those treated. In this review, we highlight interesting observations on the etiology and characteristics of food allergy presenting at different ages and discuss clinical management as it relates to life stage., (Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

The disease burden associated with air pollution continues to grow. The World Health Organization (WHO) estimates ≈7 million people worldwide die yearly from exposure to polluted air, half of which-3.3 million-are attributable to cardiovascular disease (CVD), greater than from major modifiable CVD risks including smoking, hypertension, hyperlipidemia, and diabetes mellitus. This serious and growing health threat is attributed to increasing urbanization of the world's populations with consequent exposure to polluted air. Especially vulnerable are the elderly, patients with pre-existing CVD, and children. The cumulative lifetime burden in children is particularly of concern because their rapidly developing cardiopulmonary systems are more susceptible to damage and they spend more time outdoors and therefore inhale more pollutants. World Health Organization estimates that 93% of the world's children aged <15 years-1.8 billion children-breathe air that puts their health and development at risk. Here, we present growing scientific evidence, including from our own group, that chronic exposure to air pollution early in life is directly linked to development of major CVD risks, including obesity, hypertension, and metabolic disorders. In this review, we surveyed the literature for current knowledge of how pollution exposure early in life adversely impacts cardiovascular phenotypes, and lay the foundation for early intervention and other strategies that can help prevent this damage. We also discuss the need for better guidelines and additional research to validate exposure metrics and interventions that will ultimately help healthcare providers reduce the growing burden of CVD from pollution.