Malnutrition and epilepsy share a complex bidirectional relationship, with malnutrition serving as a potential risk factor for epilepsy development, while epilepsy, in turn, often exerts profound effects on nutritional status. Nutritional interventions have emerged as a critical adjunctive approach in epilepsy management.

To explore the multifaceted associations between malnutrition and epilepsy, structured into three primary sections: (1) Elucidating the impact of malnutrition as a risk factor for epilepsy onset; (2) Examining the reciprocal influence of epilepsy on nutritional status, and (3) Evaluating diverse nutritional interventions in the management of epilepsy.

A systematic search was conducted across PubMed, Scopus, and Web of Science databases utilizing defined keywords related to malnutrition, epilepsy, and nutritional interventions. Inclusion criteria encompassed various study types, including clinical trials, animal models, cohort studies, case reports, meta-analyses, systematic reviews, guidelines, editorials, and review articles. Four hundred sixteen pertinent references were identified, with 198 review articles, 153 research studies, 21 case reports, 24 meta-analyses, 14 systematic reviews, 4 guidelines, and 2 editorials meeting the predefined criteria.

The review revealed the intricate interplay between malnutrition and epilepsy, highlighting malnutrition as a potential risk factor in epilepsy development and elucidating how epilepsy often leads to nutritional deficiencies. Findings underscored the importance of nutritional interventions in managing epilepsy, showing their impact on seizure frequency, neuronal function, and overall brain health.

This systematic review emphasizes the bidirectional relationship between malnutrition and epilepsy while emphasizing the critical role of nutritional management in epilepsy treatment. The multifaceted insights underscore the need for a holistic approach to addressing nutritional aspects alongside conventional epilepsy management strategies.

• Epilepsy
• Nutritional management
• Seizure disorders
• Antiepileptic drugs
• Minerals
• L-carnitine
• Vitamins
• Omega-3
• Gut microbiota

• Allergic rhinoconjunctivitis
• Asthma
• Atopic dermatitis
• Eosinophilic esophagitis
• Food allergies

• Dermatitis, Atopic/epidemiology
• Humans
• Comorbidity
• Cardiovascular Diseases/epidemiology
• Neoplasms/epidemiology
• Mental Disorders/epidemiology
• Autoimmune Diseases/epidemiology
• Endocrine System Diseases/epidemiology

• allergic rhinitis
• asthma
• epilepsy
• leukotriene antagonists
• seizures

• Aged
• Humans
• Asthma/drug therapy
• Asthma/epidemiology
• Cohort Studies
• Diabetes Mellitus/drug therapy
• Epilepsy/drug therapy
• Hospitalization
• Leukotriene Antagonists/therapeutic use
• Rhinitis, Allergic/drug therapy
• Seizures/drug therapy

• Shizuoka Prefecture

• atopic dermatitis
• comorbidities
• epilepsy

• Mendelian randomization
• asthma
• epilepsy
• genome-wide association study
• inverse-variance weighted

• Dog
• Epilepsy
• Medium chain triglycerides
• Microbiota-gut-brain axis
• Nutraceuticals

• Dogs
• Animals
• Dog Diseases
• Epilepsy/veterinary
• Diet/veterinary

• atopic dermatitis
• epidemiology
• family
• quality of life
• school attendance

• Allergic diseases
• Asthma
• Eczema
• Epilepsy

• Allergic rhinitis
• Brain inflammation
• Epilepsy
• Mast cells activation

• immunology
• epilepsy

• Adolescent
• Child
• Child, Preschool
• Diet
• Drug Resistant Epilepsy/complications
• Drug Resistant Epilepsy/diet therapy
• Female
• Food Hypersensitivity/complications
• Humans
• Infant
• Male

• Pediatric Neurology Research Center, Mofid Children Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran

• Children with special needs
• delayed care
• social support
• socioeconomic

• Adult
• Child
• Disabled Children/rehabilitation
• Family Relations/psychology
• Female
• Health Services Accessibility
• Health Services Needs and Demand
• Humans
• Male
• Parents/psychology
• Social Class
• Social Support

• Adult onset
• Asthma
• Atopic dermatitis
• Atopic history
• Eczema
• Hay fever
• Severity

• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Child
• Child, Preschool
• Dermatitis, Atopic/diagnosis
• Female
• Humans
• Male
• Middle Aged
• Phenotype
• Prospective Studies
• Self Report
• Severity of Illness Index
• Surveys and Questionnaires
• Young Adult

• K12 HS023011 AHRQ HHS
• UL1 TR001422 NCATS NIH HHS

Epidemiologic data supporting the epilepsy–asthma association are insufficient. Therefore, we examined this association in this study.

By using claims data from the National Health Insurance Research Database (Taiwan), we executed a retrospective cohort analysis. Analysis 1 entailed comparing 150,827 patients diagnosed as having incident asthma during 1996–2013 with disease-free controls who were selected randomly during the same period, frequency matched in terms of age and sex. Similarly, analysis 2 entailed comparing 25,274 patients newly diagnosed as having epilepsy with sex- and age-matched controls who were selected randomly. At the end of 2013, we evaluated in analysis 1 the epilepsy incidence and risk and evaluated in analysis 2 the asthma incidence and risk. We applied Kaplan–Meier analysis to derive plots of the proportion of asthma-free seizures.

In analysis 1, the asthma group exhibited a higher epilepsy incidence than did the control group (3.05 versus 2.26 per 1,000 person-years; adjusted hazard ratio: 1.39, 95% CI [1.33–1.45]). We also noted a greater risk of subsequent epilepsy in women and girls. In analysis 2, we determined that the asthma incidence between the control and epilepsy groups did not differ significantly; however, some age subgroups including children and individuals in their 30s had an increased risk. A negative association was found in adolescents. The Kaplan–Meier analysis revealed epilepsy to be positively associated with subsequent onset of asthma within seven years of epilepsy diagnosis.

Asthma may be associated with high epilepsy risk, and epilepsy may be associated with high asthma risk among children and individuals in their 30s. Nevertheless, people with epilepsy in other age subgroups should be aware of the possibility of developing asthma within seven years of epilepsy diagnosis.

• Age
• Association
• Asthma
• Epilepsy

• Allergy
• Anxiety
• Asthma
• Autism spectrum disorder
• Depression
• Epilepsy
• Schizophrenia spectrum disorder

• Adolescent
• Asthma/epidemiology
• Bone Diseases/epidemiology
• Child
• Child, Preschool
• Eczema/epidemiology
• Female
• Food Hypersensitivity/epidemiology
• Humans
• Infant
• Infant, Newborn
• Joint Diseases/epidemiology
• Male
• Musculoskeletal Diseases/epidemiology
• Rhinitis, Allergic, Seasonal/epidemiology
• Self Report
• Surveys and Questionnaires

• Adverse reaction
• Allergy
• Drug hypersensitivity
• Epilepsy antiepileptic drug
• Exanthema

• adolescent
• atopic dermatitis
• attention-deficit/hyperactivity disorder
• child
• depression
• epilepsy
• migraine

Allergies and their characteristic T_H2-polarized inflammatory reactions affect a substantial part of the population. Since there is increasing evidence that the immune system modulates plasticity and function of the central nervous system (CNS), we investigated the effects of allergic lung inflammation on the hippocampus—a region of cellular plasticity in the adult brain. The focus of the present study was on microglia, the resident immune cells of the CNS, and on hippocampal neurogenesis, i.e., the generation of new neurons. C57BL/6 mice were sensitized with a clinically relevant allergen derived from timothy grass pollen (Phl p 5). As expected, allergic sensitization induced high serum levels of allergen-specific immunoglobulins (IgG1 and IgE) and of T_H2 cytokines (IL-5 and IL-13). Surprisingly, fewer Iba1⁺ microglia were found in the granular layer (GL) and subgranular zone (SGZ) of the hippocampal dentate gyrus and also the number of Iba1⁺MHCII⁺ cells was lower, indicating a reduced microglial surveillance and activation in the hippocampus of allergic mice. Neurogenesis was analyzed by labeling of proliferating cells with bromodeoxyuridine (BrdU) and determining their fate 4 weeks later, and by quantitative analysis of young immature neurons, i.e., cells expressing doublecortin (DCX). The number of DCX⁺ cells was clearly increased in the allergy animals. Moreover, there were more BrdU⁺ cells present in the hippocampus of allergic mice, and these newly born cells had differentiated into neurons as indicated by a higher number of BrdU⁺NeuN⁺ cells. In summary, allergy led to a reduced microglia presence and activity and to an elevated level of neurogenesis in the hippocampus. This effect was apparently specific to the hippocampus, as we did not observe these alterations in the subventricular zone (SVZ)/olfactory bulb (OB) system, also a region of high cellular plasticity and adult neurogenesis.

• TH2 polarization
• allergy
• hippocampus
• microglia
• neurogenesis
• systemic inflammation

Epilepsy is one of the most common neurologic disorders in dogs and life-long treatment with antiepileptic drugs (AED) is frequently required. Adverse events of AED targeting the skin are only rarely reported in veterinary medicine and the true incidence and spectrum of cutaneous reactions in epileptic dogs remains unknown. In this study, we hypothesized that cutaneous reactions commonly occur in epileptic dogs and are related to AED treatment. A retrospective case review of 185 dogs treated for epilepsy identified 20.0% with simultaneous appearance of dermatologic signs. In a subsequent prospective case investigation (n = 137), we identified newly appearing or distinct worsening of skin lesions following initiation of AED therapy in 10.9% of dogs treated for epilepsy (95% CI 6.8–17.7%). Cutaneous lesions were classified as probably drug-induced in 40.0% of these cases. Patch testing and intradermal testing were further investigated as potential diagnostic methods to confirm AED hypersensitivity. They were of high specificity but sensitivity and positive predictive value appeared inappropriate to recommend their routine use in clinical practice.

• adverse reaction
• antiepileptic drug
• dermatologic
• epilepsy
• patch test
• phenobarbital
• side effects
• skin

• anxiety
• depression
• prenatal
• rhinitis
• wheeze

Eczema often precedes the development of asthma in a disease course called the ‘atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P=2.1 × 10⁻⁸) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P=5.3 × 10⁻⁹). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.

The development of asthma following eczema is known as the atopic march. Here the authors conduct a GWAS on affected children and identify two novel loci associated with the disease phenotype.

• Atopic dermatitis
• Comorbidities
• Epilepsy