Published online Jun 20, 2025. doi: 10.5493/wjem.v15.i2.104328
Revised: February 24, 2025
Accepted: March 18, 2025
Published online: June 20, 2025
Processing time: 119 Days and 21.9 Hours
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 manage
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 un
Core Tip: This systematic review underscores the intricate relationship between nutrition and epilepsy, emphasizing the bidirectional impact of malnutrition on seizure susceptibility and the potential of tailored dietary interventions to improve epilepsy management. Through systematic search and analysis of various studies, the review highlights malnutrition as both a risk factor for epilepsy onset and a consequence of epilepsy, underscoring the importance of nutritional interventions in epilepsy management. While nutritional strategies such as ketogenic diets and medium-chain fatty acids offer promising benefits, their implementation is challenged by factors including patient compliance, resource allocation, and healthcare system support. The review calls for further research to elucidate the mechanisms underlying these interventions and highlights the need for a personalized, multidisciplinary approach to integrate nutrition into epilepsy care effectively.
- Citation: Al-Beltagi M, Saeed NK, Bediwy AS, Elbeltagi R. Unraveling the nutritional challenges in epilepsy: Risks, deficiencies, and management strategies: A systematic review. World J Exp Med 2025; 15(2): 104328
- URL: https://www.wjgnet.com/2220-315x/full/v15/i2/104328.htm
- DOI: https://dx.doi.org/10.5493/wjem.v15.i2.104328
Epilepsy is a neurological disorder characterized by recurrent and unprovoked seizures. Seizures are temporary and paroxysmal disruptions in brain function that result in abnormal brain electrical activity. These seizures can take various forms, from momentary lapses in awareness to convulsions. Epilepsy can affect people of all ages and results from a wide range of causes, including genetic factors, brain injuries, infections, and other underlying conditions[1]. Epilepsy is one of the most common neurological disorders globally, affecting about 0.6%-1% of the world's population with an annual incidence of 0.5/1000 population[2]. The prevalence of epilepsy varies by region and population. Low and middle-income countries have a higher prevalence of epilepsy due to factors such as limited access to healthcare, higher incidence of infectious diseases, and increased risk of head injuries[3]. In the United States, around 3.47 million people have epilepsy, making it one of the most common neurological conditions. About 0.6% of American children up to 17 years of age have active epilepsy. Epilepsy can develop at any age, but it is often diagnosed in childhood or the elderly population. Males are slightly more likely to develop epilepsy than females[4].
Epilepsy can have various causes, including genetic factors, brain injuries, brain tumors, infections (such as meningitis), developmental disorders, and metabolic disorders. In some cases, the cause of epilepsy may not be identified, leading to a diagnosis of "idiopathic" or "cryptogenic" epilepsy. Certain risk factors, such as a family history of epilepsy, can increase the likelihood of developing the condition[5]. Epilepsy is a neurological disorder that is classified into different types based on the characteristics of the seizures and the part of the brain where they originate. There are mainly two categories of epilepsy: Focal (previously known as partial) and generalized seizures. Focal seizures affect one specific part of the brain, leading to localized symptoms, while generalized seizures affect the entire brain, causing loss of consciousness and more widespread symptoms. Along with these two categories, two more categories were introduced: Combined focal and generalized epilepsy and unknown epilepsy. There are several specific epilepsy syndromes, each having distinct features and causes[6,7].
Diagnosing epilepsy involves a thorough medical history, neurological examination, and typically an electroencephalogram (EEG) to measure brain activity during seizures. Antiepileptic drugs (AEDs) are the most common treatment for epilepsy and are tailored to the individual's seizure type and underlying cause[1]. For some individuals with epilepsy who do not respond to medications, surgical interventions, such as brain surgery to remove the seizure focus, may be considered[8].
Recent research increasingly supports a bidirectional relationship between nutritional status and epilepsy. On one side, malnutrition—characterized by deficiencies in critical micronutrients such as vitamins B6, D, and folate, as well as essential minerals like magnesium and zinc—can disrupt neurotransmitter synthesis, impair mitochondrial function, and increase oxidative stress and neuroinflammation. These alterations not only lower the seizure threshold but may also predispose individuals to the onset of epilepsy[9]. Conversely, epilepsy and its management contribute to nutritional challenges. AED and the metabolic stress associated with recurrent seizures can lead to appetite suppression, gas
Recent epidemiological studies underscore that while malnutrition is more prevalent in socioeconomically disadvantaged regions—where food insecurity and nutrient deficiencies are common—the burden of epilepsy is by no means confined to these areas[11]. In developed countries, despite generally better overall nutritional status, specific dietary patterns, lifestyle factors, and subclinical nutrient imbalances have also been associated with an increased risk of epilepsy[9]. For instance, studies have reported that even in high-income nations, variations in dietary quality, such as high consumption of processed foods and low intake of essential micronutrients, may contribute to altered neuronal excitability and an increased seizure threshold. This observation suggests that malnutrition and nutritional imbalances are critical factors influencing epileptogenesis globally[12]. Such findings emphasize the reciprocal relationship between nutritional status and epilepsy—where poor nutrition may predispose individuals to seizure disorders. Conversely, the management of epilepsy can further impact nutritional status through factors such as AED effects and altered metabolism[13]. Therefore, understanding the nuances of this bidirectional link is essential for developing comprehensive, region-specific strategies for epilepsy prevention and management.
In addition to the reciprocal effects of malnutrition and epilepsy, it is important to elucidate how specific dietary patterns and nutritional deficiencies influence epilepsy susceptibility. Diets high in processed foods, refined sugars, and unhealthy fats have been associated with systemic inflammation and metabolic dysregulation, both of which may trigger neuroinflammatory responses and oxidative stress in the brain. These processes can lower the seizure threshold and promote epileptogenesis[14]. Conversely, diets rich in whole foods—encompassing fruits, vegetables, lean proteins, and whole grains—provide essential micronutrients and antioxidants that support neurotransmitter synthesis, maintain mitochondrial function, and modulate immune responses[15]. For example, chronic deficiencies in vitamins such as B6, D, and folate and minerals like magnesium and zinc have been linked to impaired GABAergic and glutamatergic neurotransmission, further increasing neuronal excitability[16,17]. Additionally, dietary patterns influence the com
Various dietary therapies have been studied for their effectiveness in managing epilepsy, particularly in cases of drug-resistant epilepsy. Dietary interventions such as the Ketogenic Diet, Modified Atkins Diet, Low Glycemic Index Diet, Medium-Chain Triglyceride (MCT) Diet, Gluten-Free Diet, probiotics, prebiotics, and other gut manipulation, and Omega-3 Fatty Acids have shown some evidence of benefits in treating patients with epilepsy[19,20]. Furthermore, epilepsy can impact the patient's nutritional status, making dietary considerations even more crucial[21]. This review explores the bidirectional relationship between diet and epilepsy, discussing the benefits and limitations of these dietary approaches, their potential mechanisms of action, and the factors that may influence their effectiveness in different individuals with epilepsy.
This systematic review aimed to comprehensively evaluate the intricate relationship between malnutrition, epilepsy, and the nutritional management strategies pertinent to epilepsy. The review was structured into three primary sections: (1) The impact of malnutrition as a risk factor for epilepsy; (2) The reciprocal influence of epilepsy on nutritional status; and (3) Nutritional interventions targeting epilepsy management. A systematic search was conducted across PubMed, Scopus, and Web of Science databases, utilizing a predefined set of keywords related to malnutrition, epilepsy, and nutritional interventions. The search strategy included a combination of Medical Subject Headings terms and free-text keywords to retrieve relevant studies comprehensively.
We included various study types to ensure a broad perspective on the topic, encompassing human clinical trials, animal models, cohort studies, case reports, meta-analyses, systematic reviews, guidelines, editorials, and review articles. Studies were included if they provided data on the relationship between malnutrition and epilepsy or discussed nutritional interventions in epilepsy management. The selection process involved two independent reviewers who screened titles and abstracts based on predefined eligibility criteria. Discrepancies were resolved through discussion or by consulting a third reviewer. Full-text articles were then assessed for inclusion, selecting 402 relevant references: 189 review articles, 149 research studies, 21 case reports, 24 meta-analyses, 14 systematic reviews, 4 guidelines, and 2 editorials.
Data extraction was conducted systematically using a standardized form to capture critical elements from each study, including study design, participant demographics, nutritional status assessments, epilepsy-related outcomes, mechanistic insights, and key findings. Two reviewers independently verified the extracted data to ensure accuracy and completeness. Any disagreements were resolved through consensus. The quality of included studies was assessed using appropriate tools depending on the study design. For randomized controlled trials (RCTs), the Cochrane Risk of Bias Tool was employed. For observational studies, the Newcastle-Ottawa Scale was used. The quality of review articles was assessed using the AMSTAR 2 checklist. Each study was rated on several criteria, including selection bias, measurement of exposure and outcomes, and control of confounding factors. Studies were classified as high, moderate, or low quality based on these assessments.
The synthesis of extracted data was performed using a thematic analysis approach. Studies were grouped into thematic categories corresponding to the three primary sections of the review. Within each theme, findings were synthesized to highlight the multifaceted relationships between malnutrition and epilepsy onset, the bidirectional effects of epilepsy on nutrition, and the impact of nutritional interventions on seizure frequency, neuronal function, and overall brain health. While our review did not involve original statistical analyses, we critically appraised and summarized the statistical methods employed in the studies reviewed. We focused on the methodologies used to assess the effectiveness of nutritional interventions, such as effect size calculations, confidence intervals, and p-values. In cases where meta-analyses were included, we reported the pooled effect estimates and heterogeneity measures (I² statistics).
This review acknowledges the potential limitations inherent in the literature, including publication bias, variations in study methodologies, language biases, and heterogeneity among study populations and designs. These factors may influence the generalizability of the findings. By structuring the review into these three distinct sections and providing a detailed methodology, this work aims to offer a comprehensive and structured analysis of the interplay between malnutrition and epilepsy, emphasizing the importance of nutritional management in epilepsy treatment and care.
Through a comprehensive analysis, this review underscores the intricate interrelationship between malnutrition and epilepsy. The examination of malnutrition as a risk factor for epilepsy elucidates the impact of nutrient deficiencies on neurological vulnerabilities. The relationship between nutrition and epilepsy is bidirectional, with each exerting influence on the other in intricate ways. Poor nutrition, characterized by deficiencies in essential vitamins and minerals, can elevate the risk of developing epilepsy and act as seizure triggers. Conversely, epilepsy itself, along with medications used for its management, can affect appetite, metabolism, and dietary habits, potentially leading to malnutrition or nutrient imbalances. Exploring how epilepsy affects nutrition unveils the multifaceted alterations in dietary patterns and metabolic disruptions observed in individuals with epilepsy. Moreover, the investigation into nutritional management strategies highlights the potential of dietary modifications and supplements in mitigating seizure susceptibility and supporting overall brain health. Specialized dietary therapies, like the ketogenic diet, have emerged as effective treatments for epilepsy, highlighting the significant role of nutrition in seizure control. Moreover, nutritional inter
Figure 1 illustrates the flow chart of our systematic review process. This diagram details each step—from the initial search across PubMed, Scopus, and Web of Science to the screening, eligibility, and final inclusion of 416 studies. The studies are categorized as follows: 198 review articles, 153 research studies, 21 case reports, 24 meta-analyses, 14 systematic reviews, 4 guidelines, and 2 editorials. The synthesis of these studies highlights the bidirectional relationship between nutrition and epilepsy, including the role of malnutrition as a potential risk factor, the impact of epilepsy on nutritional status, and the efficacy of dietary interventions.
We assessed RCTs using the Cochrane Risk of Bias Tool, which identified a moderate-to-high risk of bias in most trials due to small sample sizes, lack of blinding, and short follow-up durations. Observational studies were assessed using the Newcastle-Ottawa Scale, with the majority rated as moderate quality, though some exhibited limitations related to selection bias and confounding variables. Systematic reviews and meta-analyses were evaluated using AMSTAR 2, revealing that while most adhered to rigorous methodological standards, some exhibited limitations in heterogeneity reporting and risk of bias assessment.
Summary tables (Tables 1-3) present key study characteristics, sample sizes, primary outcomes, and quality assessment scores. Among studies evaluating nutritional interventions for epilepsy management:
| Ref. | Vitamin studied | Sample size | Risk of bias (Cochrane tool) | Main outcome | Statistical findings (P value, 95%CI, etc.) |
| Holló et al[97], 2012 | Vitamin D3 | 13 | Moderate (small sample, no control group) | 40% seizure reduction after vitamin D3 supplementation | P = 0.04 (significant reduction in seizure frequency) |
| Mehvari et al[105], 2016 | Vitamin E | 65 | Low (double-blind, placebo-controlled) | Improved seizure control and EEG findings | P < 0.001 (seizure frequency reduction), P = 0.001 (EEG improvement) |
| Elmazny et al[96], 2020 | Vitamin D | 42 | Moderate (case-control design) | Lower vitamin D levels correlated with higher seizure frequency | P < 0.001 (vitamin D lower in epilepsy patients), P = 0.004 (seizure frequency correlation) |
| Nemati et al[59], 2021 | Folate (Vitamin B9) | 60 | Moderate (cross-sectional, no intervention) | Association between low folate and epilepsy in children | Mean folate: 11.60 ± 6.89 nmol/L; correlation with neurodevelopmental delay |
| Kirik et al[73], 2021 | Vitamin B12 | 26 | High (retrospective, small sample) | Seizures in children resolved with vitamin B12 supplementation | No P values reported, high homocysteine levels noted |
| Portillo et al[75], 2023 | Vitamin B12 | 1 (case report) | Not applicable | Seizures and psychosis improved with B12 supplementation | No statistical data |
| Specht et al[102], 2020 | Vitamin D3 (Neonatal) | 403 (cases), 1163 (controls) | Low (large sample, well-controlled) | High neonatal vitamin D levels correlated with increased epilepsy risk | HR adjust 1.86 (95%CI: 1.21-2.86), P trend = 0.004 |
| Leandro-Merhi et al[85], 2023 | Vitamin D | 93 | Moderate (cross-sectional, statistical correlation only) | Low vitamin D associated with worse seizure control in adults | P = 0.048 (seizure control linked to vitamin D levels) |
| Ref. | Mineral studied | Sample size (n) | Risk of bias (Cochrane tool) | Main outcome | Statistical findings (P value, 95%CI, etc.) |
| Baek et al[122], 2018 | Magnesium | 274 (133 cases, 141 controls) | Moderate (case-control, potential confounders) | Hypomagnesemia more common in febrile seizure patients | OR = 22.12 (95%CI = 9.23-53.02), P < 0.001 |
| Abdelmalik et al[124], 2012 | Magnesium | 22 | High (retrospective, no control group) | Magnesium supplementation reduced seizure frequency | Seizure days reduced (P = 0.021 at 3-6 months, P = 0.004 at 6-12 months) |
| Guo et al[125], 2023 | Magnesium, calcium | 44889 (15212 cases, 29677 controls) | Low (mendelian randomization, large sample) | Higher serum magnesium associated with lower epilepsy risk | OR = 0.28 (95%CI = 0.12-0.62), P = 0.002 |
| Abdullahi et al[126], 2019 | Magnesium, calcium | 90 (40 idiopathic epilepsy, 20 symptomatic epilepsy, 30 controls) | Moderate (case-control, small sample) | Lower serum magnesium and calcium in epilepsy patients | Mg: P = 0.007 (95%CI = -0.189 to -0.031), Ca: P < 0.01 |
| Saghazadeh et al[131], 2015 | Magnesium, zinc, copper, selenium | 60 studies (Meta-analysis) | Low (large sample, multiple studies) | Altered trace element levels in epilepsy and febrile seizures | Magnesium significantly lower in epilepsy (P < 0.001) |
| Kheradmand et al[132], 2014 | Zinc, copper | 70 (35 intractable epilepsy, 35 controlled epilepsy) | Moderate (case-control, small sample) | Zinc deficiency more common in intractable epilepsy | P < 0.05 (71.45% deficiency in intractable vs 25.72% in controlled epilepsy) |
| Saad et al[133], 2014 | Zinc, selenium | 80 (40 epilepsy, 40 controls) | Moderate (case-control, small sample) | Lower Zn, Se in epilepsy patients, higher oxidative stress markers | Zn, Se significantly lower (P < 0.001), Plasma MDA higher (P < 0.001) |
| Chen et al[134], 2019 | Zinc | Animal study (Sprague-Dawley rats) | Moderate (preclinical, no human data) | Zinc deficiency worsened seizure-related brain damage | No direct P value reported, hippocampal ZnT-3 and MBP levels altered |
| Sharif et al[158], 2015 | Iron | 200 (100 febrile seizure, 100 controls) | Moderate (case-control, single-center) | Iron deficiency more common in febrile seizure patients | 45% iron deficiency in seizure group vs 22% in controls (P < 0.05) |
| Bidabadi et al[159], 2009 | Iron | 200 (100 febrile seizure, 100 controls) | Moderate (case-control, single-center) | No protective effect of iron deficiency against febrile seizures | OR = 1.175, temperature peak higher in seizure group (P < 0.0001) |
| Zimmer et al[160], 2021 | Iron | Human and animal study | Low (well-controlled, experimental) | Seizures linked to iron accumulation in temporal lobe epilepsy | P < 0.01, iron metabolism changes observed in TLE |
| Ashrafi et al[168], 2007 | Selenium | 160 (80 intractable epilepsy, 80 controls) | Moderate (case-control, no intervention) | Serum selenium lower in intractable epilepsy patients | P < 0.05 (lower selenium in epilepsy group) |
| Omrani et al[175], 2019 | Omega-3 fatty acids | 50 (randomized clinical trial) | Low (double-blind, placebo-controlled) | Omega-3 reduced seizure frequency and inflammation | P < 0.001 (seizure reduction), lower TNF-α and IL-6 |
| Liang et al[174], 2023 | Omega-3 fatty acids | Mendelian randomization | Low (genetic analysis, large sample) | Higher blood omega-3 levels linked to increased epilepsy risk | OR = 1.16 (95%CI = 1.051-1.279, P = 0.003) |
| Ref. | Supplement studied | Sample size | Risk of bias (Cochrane tool) | Main outcome | Statistical findings (P value, 95%CI, etc.) |
| Schauwecker et al[189], 2012 | Glycemic control | Animal study | Moderate (preclinical, no human data) | Glycemic modulation affects seizure-induced brain injury | Glucose rescue reduced hippocampal pathology (P < 0.001) |
| Hamerle et al[204], 2018 | Alcohol | 310 | Moderate (retrospective, self-reported) | Alcohol-related seizures linked to heavy consumption | OR = 5.79 for genetic epilepsy, OR = 8.95 for chronic alcohol use |
| Samsonsen et al[206], 2018 | Alcohol | 134 | Moderate (observational, cross-over design) | Hazardous drinking and sleep deprivation linked to seizures | AUDIT score ≥ 8 in 28% of patients, seizures peaked on Sundays and Mondays |
| Pelliccia et al[211], 1999 | Food allergy | 3 (case report) | Not applicable | Seizures improved with cow’s milk elimination | EEG normalized after diet change (no statistical data) |
| Silverberg et al[212], 2014 | Allergic disease | 91642 (population-based) | Low (large sample, well-controlled) | Allergies associated with increased epilepsy risk | OR = 1.79 (95%CI: 1.37-2.33) for ≥ 1 allergic disease, OR = 2.69 (95%CI: 1.38-4.01) for food allergies |
| Gorjipour et al[220], 2019 | Hypoallergenic diet | 34 | Moderate (quasi-experimental, no blinding) | Significant reduction in seizure frequency in children with food allergies | 50% seizure-free after 8 weeks, 85% had ≥ 50% reduction (P < 0.001) |
| Sarlo et al[222], 2023 | Low glutamate diet | 33 | Moderate (non-blinded, small sample) | No significant seizure reduction, but 21% were clinical responders | Clinical response likelihood decreased with age (OR = 0.71, 95%CI: 0.50-0.99, P = 0.04) |
| Kaufman et al[224], 2003 | Caffeine | Case report | Not applicable | Excessive caffeine worsened seizure control | Seizures reduced with caffeine elimination (no statistical data) |
| Tényi et al[234], 2021 | Food intake | 100 (596 seizures analyzed) | Low (well-controlled, EEG-monitored) | Food intake significantly precipitated temporal lobe seizures esp. in males | Shorter food-seizure latency linked to less severe seizures (P < 0.05) |
Ketogenic diet: Multiple meta-analyses reported a ≥ 50% reduction in seizure frequency in 42-55% of patients (95%CI: 40%-60%; P < 0.05).
Vitamin D supplementation: A pooled analysis of six RCTs indicated a significant reduction in seizure frequency (mean difference: -1.5 seizures/month; P = 0.02).
Omega-3 fatty acids: Findings were inconclusive, with some studies reporting a modest benefit (effect size: -0.23, P = 0.08) while others showed no statistically significant effect.
L-carnitine and magnesium: Some studies reported improvements in seizure threshold and neuronal stability, though with high variability in effect sizes and lack of large-scale trials.
Table 1 summarizes the methodological quality and key findings of RCTs investigating the role of vitamin supplementation in epilepsy. While Vitamin D and Vitamin E showed potential benefits in seizure reduction, findings on Vitamin B12 and Folate are largely observational. Some studies exhibited a moderate-to-high risk of bias, highlighting the need for larger, well-controlled trials to confirm therapeutic efficacy.
Table 2 provides an overview of studies investigating the role of various minerals (magnesium, calcium, zinc, iron, selenium) and omega-3 fatty acids in epilepsy and seizure disorders. The findings indicate that trace element deficiencies may contribute to seizure susceptibility, though the quality of evidence varies across studies.
Table 3 summarizes RCTs and relevant studies investigating the effects of dietary factors, food allergies, alcohol, caffeine, and glycemic control on epilepsy and seizure disorders. Some dietary modifications reduced seizure frequency, while others showed potential seizure triggers linked to food intake and metabolic changes.
Significant heterogeneity (I² > 50%) was observed across dietary intervention studies, reflecting differences in study designs, intervention dosages, and follow-up periods. While some meta-analyses accounted for this variability through subgroup analyses, the inconsistency in methodologies limits definitive conclusions.
Despite the comprehensive analysis presented in this review, several limitations warrant acknowledgment. We observed significant heterogeneity in study designs. Differences in participant characteristics, diagnostic criteria, intervention measures, and follow-up durations introduce variability affecting the findings' consistency and reliability. In addition, many studies included are observational or based on animal models, lacking RCTs and long-term prospective studies. Furthermore, the interplay between nutrition, neurotransmitter regulation, neuronal plasticity, oxidative stress, and gut microbiota interactions remains incompletely elucidated. We also acknowledge some publication bias. Positive findings may be overrepresented, potentially skewing interpretations. Individual variability is another limitation that should be addressed, as responses to dietary interventions and supplements are influenced by factors such as genetics, comorbidities, medication interactions, and adherence. Future research should prioritize well-designed RCTs, stan
Nutrition can have a significant impact on managing epilepsy, both as a trigger for seizures and as part of treatment. While nutrition cannot cure epilepsy, certain dietary factors can affect seizure risk and management. Nutritional deficiencies, hypoglycemia, skipping meals, dehydration, food allergies and sensitivities, alcohol abuse, caffeine, and stimulants may trigger seizures in an epileptic patient[13]. Recent evidence suggests that nutritional imbalances contribute to epileptogenesis via several interrelated neurobiological pathways. Vitamin deficiencies—for example, inadequate vitamin B6, D, E, and folate levels—can compromise neurotransmitter synthesis and impair antioxidant defenses[22]. These deficiencies increase oxidative stress, as the diminished capacity to neutralize reactive oxygen species (ROS) damages neuronal membranes and mitochondrial structures, thereby reducing energy production[23]. Mineral imbalances, such as low levels of magnesium and zinc, further exacerbate this process by disrupting the balance between excitatory and inhibitory neurotransmission. Specifically, reduced magnesium availability hampers the regulation of N-methyl-D-aspartate (NMDA) receptor activity, while zinc deficiency impairs GABAergic transmission, lowering the seizure threshold[24].
In addition, dysbiosis—an imbalance in gut microbiota—can affect the gut-brain axis by altering the production of neuroactive metabolites such as short-chain fatty acids (SCFAs), which are critical for maintaining anti-inflammatory states in the brain[25]. This imbalance may promote neuroinflammation by increasing pro-inflammatory cytokine levels and compromising the integrity of the blood-brain barrier (BBB). Moreover, certain food additives have been shown to induce mild inflammatory responses or disrupt normal ion channel functioning, thereby further contributing to neuronal hyperexcitability[26].
Collectively, these nutritional factors converge on key pathways, including oxidative stress, mitochondrial dysfunction, and neuroinflammation. This integrated mechanistic framework not only underscores how nutritional deficiencies and imbalances can predispose individuals to seizures but also highlights potential targets for therapeutic intervention. Understanding these pathways is crucial for developing comprehensive nutritional strategies that may serve as adjunctive treatments in epilepsy management. However, the relationship between nutritional deficiencies and epilepsy is complicated and can vary from person to person. Nutritional factors are just one of many factors that can contribute to the development and management of epilepsy. Figure 2 summarizes the different mechanisms of malnutrition that can precipitate aggravating epileptogenesis.
Nutritional deficiencies can play a role in the development of epilepsy by affecting various mechanisms such as neurotransmitter synthesis, mitochondrial function, oxidative stress, myelin synthesis, homocysteine levels, vascular changes, neuroinflammation, epigenetic changes, and AED metabolism[27,28].
Vitamins play essential roles in neurological health and can have implications for epilepsy. Table 4 comprehensively summarizes the effects and roles of various vitamin deficiencies in epileptogenesis. This table details how specific vitamins—such as A, B1 (thiamine), B2 (riboflavin), B6 (pyridoxine), folic acid, B12, C, D, E, and K—contribute to neuronal health, neurotransmitter balance, oxidative stress regulation, and neuroinflammation.
| Vitamin | Role in epileptogenesis | Associated conditions | Causes of deficiency | Treatment/management | Daily recommended dose |
| Vitamin A | Limited evidence of anti-epileptogenic effects by impacting synaptic plasticity, memory impairment, convulsions | Night blindness, xerophthalmia, weakened immune system, skin changes, and impaired growth and development | Dietary Insufficiency, Malabsorption, poor liver function, rapid growth rates in infancy and childhood | Chronic β-carotene/vitamin A intake; Retinoic acid as potential antiepileptic agent | Infants 0-6 months: 400 mcg/day. Infants 7-12 months: 500 mcg/day. Children 1-3 years: 300 mcg/day.Children 4-8 years: 400 mcg/day. Boys 9-13 years: 600 mcg /day. Girls 9-13 years: 600 mcg/day. Male ≥ 14 years: 900 mcg/day. Females ≥ 14 years: 700 mcg/day |
| Thiamine (B1) | Essential for nerve function; deficiency linked to seizures; associated with Wernicke's encephalopathy | Wernicke's encephalopathy; chronic alcohol abuse; poor nutrition | Alcoholism, inadequate dietary intake | Thiamine supplementation and addressing the underlying causes | Infants 0-6 months: 0.2 mg/day. Infants 7-12 months: 0.3 mg/day. Children 1-3 years: 0.5 mg/day. Children 4-8 years: 0.6 mg/day. Boys 9-13 years: 0.9 mg/day. Girls 9-13 years: 0.9 mg/day. Teenagers 14-18 years: 1.2 mg/day. Adult men: 1.2 mg/day. Adult women: 1.1 mg/day. Pregnant women: 1.4 mg/day. Breastfeeding women: 1.4 mg/day |
| Riboflavin (B2) | Important for mitochondrial function; deficiency implicated in riboflavin-responsive epilepsy | Riboflavin-responsive epilepsy; mitochondrial dysfunction | Uncommon in developed countries | Riboflavin supplementation; genetic testing for riboflavin-responsive epilepsy | Infants 0-6 months: 0.3 mg/day. Infants 7-12 months: 0.4 mg/day. Children 1-3 years: 0.5 mg/day. Children 4-8 years: 0.6 mg/day. Children 9-13 years: 0.9 mg/day. Teenagers 14-18 years: Boys: 1.3 mg/day. Girls: 1.0 mg/day. Adult men: 1.3 mg/day. Adult women: 1.1 mg/day. Pregnant women: 1.4 mg/day. Breastfeeding women: 1.6 mg/day |
| Pyridoxine (B6) | Vital for neurotransmitter synthesis; deficiency linked to pyridoxine-dependent epilepsy | Pyridoxine-dependent epilepsy; rare genetic condition | Genetic mutations affecting pyridoxine metabolism | High-dose pyridoxine supplementation; genetic testing for pyridoxine-dependent epilepsy | Infants 0-6 months: 0.1 mg/day. Infants 7-12 months: 0.3 mg/day. Children 1-3 years: 0.5 mg/day. Children 4-8 years: 0.6 mg/day. Children 9-13 years: 1.0 mg/day. Teenagers 14-18 years. Boys: 1.3 mg/day. Girls: 1.2 mg/day. Adult men: 1.3 mg/day. Adult women: 1.3 mg/day. Pregnant women: 1.9 mg/day. Breastfeeding women: 2.0 mg/day |
| Folic acid (B9) | Important for DNA synthesis; deficiency may impact neurological health | Elevated homocysteine levels; disruption of neurotransmitter levels | Antiepileptic drugs, inadequate dietary intake | Folate supplementation: Address dietary and drug-related factors | Infants 0-6 months: 65 mcg/day. Infants 7-12 months: 80 mcg/day. Children 1-3 years: 150 mcg/day. Children 4-8 years: 200 mcg/day. Children 9-13 years: 300 mcg/day. Teenagers 14-18 years: 400 mcg/day. Adult men and women: 400 mcg/day. Pregnant women: 600 mcg/day. Breastfeeding women: 500 mcg/day |
| Vitamin B12 | Crucial for nervous system functioning; deficiency associated with seizures | Demyelination, altered neurotransmitter levels | Malabsorption, dietary deficiencies | Vitamin B12 supplementation and addressing underlying causes | Infants 0-6 months: 0.4 mcg/day. Infants 7-12 months: 0.5 mcg/day. Children 1-3 years: 0.9 mcg/day. Children 4-8 years: 1.2 mcg/day. Children 9-13 years: 1.8 mcg/day Teenagers 14-18 years: 2.4 mcg/day. Adults: 2.4 mcg/day. Pregnant women: 2.6 mcg/day. Breastfeeding women: 2.8 mcg/day |
| Vitamin C | Antioxidant with neuroprotective properties; potential impact on glutamate clearance | Lower levels in patients with epilepsy; neuroprotective effects | Dietary deficiency; oxidative stress | Vitamin C supplementation; antioxidant support | Infants 0-6 months: 40 mg/day. Infants 7-12 mons: 50 mg/day. Children 1-3 years: 15 mg/day. Children 4-8 years: 25 mg per/day. Children 9-13 years: 45 mg/day. Teenagers 14-18 years: Boys: 75 mg/day. Girls: 65 mg/day. Adult men: 90 mg/day. Adult women: 75 mg/day. Pregnant women: 85 mg/day. Breastfeeding women: 120 mg/day |
| Vitamin D | Regulates calcium levels; potential neuroprotective effects | Vitamin D deficiency is associated with increased seizure risk | Limited sun exposure, dietary deficiency | Vitamin D supplementation, sun exposure, and addressing the underlying causes | Infants 0-12 months: 400 IU/day. Children 1-18 years: 600 IU/day. Adults 19-70 years: 600 IU/day. Adults over 70 years: 800 IU/day. Pregnant and breastfeeding women: 600 IU/day |
| Vitamin E | Lipophilic antioxidant with neuroprotective and anti-inflammatory effects | Neuroprotective effects; anticonvulsant properties | Deficiency symptoms include neurological issues | Vitamin E supplementation; antioxidant support | Infants 0-6 months: 4 mg (6 IU)/ day. Infants 7-12 months: 5 mg/day. Children 1-3 years: 6 mg/day. Children 4-8 years: 7 mg/day. Children 9-13 years: 11 mg/day. Teenagers 14-18 years: 15 mg/day. Adults (including pregnant and breastfeeding women): 15 mg/day |
| Vitamin K | Role in gamma-carboxylation of brain proteins; potential anticonvulsant effects | Animal studies show anticonvulsant effects; potential role in brain maturation | Vitamin K antagonist exposure; limited dietary intake | Vitamin K supplementation and addressing underlying causes | Infants 0-6 months: 2.0 mcg/day. Infants 7-12 months: 2.5 mcg/day. Children 1-3 years: 30 mcg/day. Children 4-8 years: 55 mcg/day. Children 9-13 years: 60 mcg/day. Teenagers 14-18 years: Boys: 75 mcg/day. Girls: 75 mcg/day. Adults (including pregnant and breastfeeding women): Men: 120 mcg/day. Women: 90 mcg/day |
Vitamin A: Vitamin A is a fat-soluble vitamin that occurs naturally in many foods. It plays a vital role in maintaining normal vision, strengthening the immune system, fostering reproduction, and promoting growth and development. Moreover, it helps the heart, lungs, and other organs function properly. Vitamin A deficiency can have different adverse effects on the body, impairing neurological functions. Although there is no established relationship between vitamin A deficiency and epilepsy, insufficient levels of specific vitamins, such as vitamin A, could potentially affect neurological health[29].
Vitamin A deficiency can contribute to epileptogenesis through various mechanisms involving structural and functional brain alterations. One key mechanism is related to its role in neurogenesis and neuronal differentiation, as vitamin A is essential for developing and maintaining neural tissue[30]. Inadequate levels of vitamin A may disrupt normal brain development, leading to structural abnormalities and alterations in synaptic connectivity, which can predispose individuals to epileptic seizures. Additionally, vitamin A deficiency can impair neurotransmitter systems, particularly GABAergic and glutamatergic signaling, resulting in an imbalance between excitatory and inhibitory neurotransmission, thereby lowering the seizure threshold[31]. Furthermore, vitamin A deficiency is associated with oxidative stress and neuroinflammation, which can further exacerbate neuronal dysfunction and contribute to epileptogenesis[32]. Overall, vitamin A deficiency can impact various aspects of brain function and structure, ultimately increasing susceptibility to epilepsy.
Vitamin A and retinoids play a crucial role in the synaptic plasticity of the hippocampus[33]. Vitamin A deficiency can lead to memory impairment in adult mice, while steers fed with a Vitamin A-deprived diet can experience convulsions and blindness[34,35]. In a kindling model of epilepsy in mice induced by pentylenetetrazole, it was found that β-carotene and vitamin A exhibit anti-epileptogenic effects when taken on a chronic basis. However, it should be noted that these drugs have no acute anti-seizure effects. It is believed that both non-genomic and genomic mechanisms may contribute to their anti-epileptogenic effects. The bioavailability of β-carotene was increased by brain-targeted nano delivery, correcting the lack of acute anti-seizure effect[36]. Retinoic acid, derived from vitamin A metabolism, exhibits both genomic and nongenomic effects, demonstrating potential as an antiepileptic agent. It interacts with specific receptors—retinoic acid receptors (RARα, β, and γ) and retinoid X receptors (RXRα, β, and γ)—predominantly located in brain regions like the amygdala, pre-frontal cortex, and hippocampus. These receptors undergo significant structural changes upon retinoid binding, prompting the transcription of particular gene networks. Experimental studies suggest that retinoic acid might deter epileptic occurrences by influencing various mechanisms, including gap junctions, neurotransmitters, long-term potentiation, calcium channels, and specific genes. However, there's currently a lack of ongoing or past clinical trials investigating retinoic acid's efficacy in managing seizures[37].
Thiamine: Thiamine, also known as Vitamin B1, is an essential nutrient that is crucial in maintaining proper nerve function and overall neurological health. Thiamine deficiency can lead to epileptogenesis through several interconnected mechanisms primarily related to its crucial role in energy metabolism and neuronal function[38]. Thiamine is a cofactor for key enzymes involved in glucose metabolism, including the pyruvate dehydrogenase complex, which links glycolysis to the citric acid cycle[39]. In thiamine deficiency, impaired glucose metabolism results in decreased energy production, leading to synaptic and neuronal dysfunction and hyperexcitability[40]. Additionally, thiamine deficiency disrupts the function of ion channels and neurotransmitter systems, particularly glutamatergic and GABAergic pathways, further contributing to neuronal hyperexcitability[41]. Moreover, thiamine deficiency-induced oxidative stress and neuroinflammation can exacerbate neuronal damage and epileptogenesis. Overall, thiamine deficiency compromises energy metabolism, neurotransmission, and neuronal integrity, culminating in increased susceptibility to epileptic seizures[42].
A deficiency of thiamine can cause a range of neurological symptoms, including seizures[43]. This deficiency can lead to a neurological disorder called Wernicke's encephalopathy, which is characterized by various neurological symptoms, such as confusion, loss of coordination, and visual disturbances. Seizures may occur in severe cases of Wernicke's encephalopathy[44]. Chronic alcohol abuse is the most common cause of thiamine deficiency, as alcohol can interfere with the absorption of thiamine and increase its excretion. Individuals with alcohol use disorder are at a higher risk of developing thiamine deficiency and, subsequently, Wernicke's encephalopathy, where seizures can be a significant feature[45]. Thiamine deficiency can also occur due to inadequate dietary intake. Individuals with poor nutrition, such as limited access to various foods or certain medical conditions affecting nutrient absorption, can develop thiamine deficiency[38]. In severe cases, this deficiency can cause neurological symptoms, including seizures. It's important to note that thiamine deficiency is relatively rare in the general population. Still, it may be more common in specific at-risk groups, such as chronic alcoholics or individuals with certain medical conditions. If someone with epilepsy is taking AEDs, their healthcare provider needs to monitor their nutritional status and address any potential interactions or deficiencies, including thiamine, as some anti-epileptic medication can decrease thiamine blood levels[13].
Riboflavin: Riboflavin, also known as vitamin B2, is a crucial nutrient that plays a significant role in various metabolic processes in the body. It is essential for mitochondrial function and energy production[32]. Although riboflavin deficiency is uncommon in developed countries because it is present in many foods, it may have implications for people with epilepsy, especially in low-income countries. Riboflavin deficiency can contribute to epileptogenesis through several mechanisms, primarily linked to its roles in energy metabolism, antioxidant defense, and neurotransmitter regulation[46,47].
Riboflavin-responsive epilepsy (RRE) is a specific form of epilepsy that some people with epilepsy may have. In these cases, riboflavin (vitamin B2) supplementation positively affects seizures. RRE is a rare condition, and it is usually diagnosed through genetic testing[48]. Riboflavin is essential for mitochondrial function, which is critical for energy production in cells, including neurons. Mitochondrial dysfunction can increase the excitability of neurons, which may contribute to seizures. In some cases, riboflavin deficiency can worsen mitochondrial dysfunction and affect brain function, which could increase the risk of seizures[49]. It's essential to note that riboflavin deficiency as a direct cause of epilepsy is relatively uncommon. However, for people with a confirmed diagnosis of RRE, riboflavin supplementation can be an effective treatment[50].
Pyridoxine: Pyridoxine, also known as vitamin B6, is an essential nutrient that plays a vital role in various biochemical processes in the body. It is involved in synthesizing neurotransmitters and regulates brain function[51]. Pyridoxine deficiency contributes to epileptogenesis through multiple mechanisms. it disrupts neurotransmitter synthesis, particularly gamma-aminobutyric acid (GABA), leading to increased neuronal excitability[52]. It impairs homocysteine metabolism, causing neurotoxicity and oxidative stress. In addition, it affects heme biosynthesis, leading to the accumulation of neurotoxic intermediates[53]. Pyridoxine deficiency also disrupts sphingolipid metabolism, altering neuronal membrane properties and increasing neuronal excitability. Pyridoxine deficiency compromises various pathways crucial for neuronal function and integrity, ultimately increasing seizure susceptibility[54].
Pyridoxine deficiency can lead to epilepsy, particularly in a rare genetic condition called pyridoxine-dependent epilepsy (PDE). PDE is usually caused by mutations in specific genes, such as ALDH7A1, which impairs pyridoxine metabolism, leading to a deficiency in the pyridoxine-phosphate oxidase enzyme. This enzyme is necessary to convert pyridoxine into its active form, pyridoxal-5'-phosphate, which is essential for the proper function of many enzymes involved in neurotransmitter synthesis and brain function[55]. Seizures are a prominent feature of PDE, and they often do not respond to conventional antiepileptic medications. However, individuals with PDE can control their seizures by taking high doses of pyridoxine supplementation, as it is the only effective treatment for this condition[56]. When individuals with PDE are given pyridoxine, their seizures can be controlled, and they may experience a significant improvement in their neurological symptoms. Genetic testing is usually performed to confirm the diagnosis of PDE[57].
Folic acid: Folic acid (vitamin B9 or folate) is a water-soluble vitamin that plays a vital role in various biochemical processes in the body, including DNA synthesis and repair, cell division, and the formation of red blood cells[58]. While folic acid deficiency can have implications for overall health, it is not commonly considered a direct cause of epilepsy. For several decades, the epilepsy community has been discussing the effects of folic acid. Initially, folic acid was believed to be a cause of seizures, but research has since demonstrated that folic acid in concentrations lower than supraphysiologic does not promote seizures. However, epileptologists are now concerned that individuals with epilepsy taking certain AED may have low levels of folic acid[59,60]. However, there are some indirect ways in which folic acid deficiency can be related to epilepsy. Folate is essential for neurological health; low levels can negatively impact brain function. Folic acid deficiency can lead to elevated levels of homocysteine, increasing the risk of cardiovascular diseases, and may also have implications for neurological health. Elevated homocysteine levels can contribute to vascular changes that affect brain function and potentially increase the risk of seizures in some individuals[60]. A study conducted by Nemati et al[59] revealed that children suffering from refractory epilepsy had lower levels of methyltetrahydrofolate in the cerebrospinal fluid and serum folate. This was particularly noticeable in children with developmental delays[61]. However, it is important to note that this finding does not necessarily imply that folic acid deficiency is the cause of epilepsy. Many anti-epileptic drugs can cause folate deficiency, especially when used in combination or at high doses. In addition, Hirono et al[62] explored the important role of folic acid in polyunsaturated fatty acids desaturation or chain elongation in the developing rats' brains. Therefore, folic acid deficiency is associated with an abnormal myelin lipid profile and damages the myelin sheath, increasing the risk of epilepsy. Deficiency of folic acid can also disrupt neurotransmitter levels, such as serotonin, norepinephrine, and dopamine, increasing seizure risk[63]. Folate deficiency during pregnancy is a well-established risk factor for neural tube defects in the developing fetus. While this is not directly related to epilepsy, pregnant women with epilepsy need to maintain adequate folate intake to prevent birth defects[64].
Vitamin B12: Vitamin B12 is a crucial nutrient that plays a vital role in the functioning of the nervous system. It is necessary to produce myelin, the protective coating surrounding nerve cells[38]. A deficiency of Vitamin B12 can lead to various neurological problems, including epilepsy, hypotonia, and developmental delay. Vitamin B12 deficiency can trigger seizures in people with epilepsy through different mechanisms. It can induce damage to the myelin sheath, making it easier for seizures to occur. Vitamin B12 acts as a coenzyme that helps in myelin synthesis and stabilization by converting methylmalonyl-CoA into succinyl CoA through the enzyme methylmalonyl CoA mutase. Excess of Methylmalonic acid, which is a myelin destabilizer, can cause the synthesis of abnormal fatty acids instead of myelin[65]. These abnormal fatty acids can be incorporated into neuronal lipids, forming a fragile myelin sheath and central nervous system (CNS) dysfunction. Elevated homocysteine and methylmalonic acid levels, with altered methionine synthesis, contribute to demyelination and axonal degeneration[66].
Vitamin B12 deficiency can also disrupt the levels of certain neurotransmitters, increasing the risk of seizures. Altered brain neurotransmitter synthesis with increased excitatory glutamate and altered homocysteic acid pathways can also induce epileptic fits[67]. Homocysteine acts like an excitatory neurotransmitter, competing against GABA. Elevated homocysteine levels mainly cause neural damage[68]. Endothelial dysfunction caused by homocystinuria results in neuronal damage by promoting mitochondrial dysfunction and apoptotic cell death[69]. It has been suggested that cerebral neurons with destroyed myelin sheaths due to vitamin B12 deficiency are more susceptible to the excitatory effects of glutamate[70]. Insufficient synthesis of succinyl-coA cannot fully compensate for sufficient glycine synthesis and can lead to insufficient heme synthesis. Glycine may be deposited in tissues. Glycine is an important excitatory neurotransmitter released from inhibitory interneurons in the spinal cord and brainstem and is an agonist of glycine receptors. Glycine is a co-agonist of glutamate in glutamergic NMDA receptors in the brain and may cause abnormal movements and convulsions[71]. A vitamin B12 supplement is associated with decreased pro-inflammatory cytokines, including interferon-γ, interleukin (IL)-1β, IL-2, IL-6, IL-8, TNF-α, and GM-CSF. Increased levels of these cytokines and anti-inflammatory cytokine IL-10 are involved in the pathogenesis of epilepsy by exacerbating tissue injury. Therefore, Vitamin B12 deficiency may be associated with abnormal pro-inflammatory cytokines that may trigger seizure activity[72]. Kirik and Çatak[73] found that a significant portion of children with afebrile seizures (such as generalized tonic-clonic seizures and infantile spasms) had high Homocysteine as an indication of vitamin B12 deficiency. They suggested that administering vitamin B12 supplementation for an appropriate duration and at an appropriate dosage can prevent unnecessary AED use and eliminate unnecessary tests and examinations[73]. Maternal nutritional deficiency of Vitamin B12 can induce infantile spasms and partial seizures originating from the temporal lobe[74]. Severe vitamin b12 defi
Vitamin C: Vitamin C (Ascorbic acid) is a water-soluble essential vitamin that cannot be formed by the human body and should be dietary supplied. It is found in all bodily organs, with the highest concentration in the brain, as vitamin C can easily be transported through the BBB via the sodium-dependent vitamin C transporter[76]. It is a prototype antioxidant with neuroprotective properties. It is important for neurotransmitter synthesis (e.g., dopamine and norepinephrine), paracrine lipid mediators, and the epigenetic regulation of DNA. It also plays a crucial role in modulating synaptic transmission through glutamate clearance[77]. Despite the role of vitamin C in a wide range of biological functions, its direct role in the management or treatment of epilepsy is not well-established. However, there are several ways in which vitamin C may indirectly influence epilepsy and overall brain health. Vitamin C is a powerful antioxidant that can help protect cells, including brain cells, from oxidative damage caused by free radicals. Vitamin C plays a crucial role in the recycling of vitamin E and lipoic acid[78]. Vitamin C has anticonvulsant effects by activating inhibitory receptors GABA and expressing glutamate transporter genes. It can also reduce the harmful effects of PTZ in rats by decreasing Bax, increasing Bcl-2, and inhibiting caspase-3. These enzymes play important roles in the process of apoptosis[79,80]. This vitamin acts as a neuroprotective factor by strengthening cell membranes, reducing lipid peroxidation, and minimizing oxidative stress reactions in the brain. It also works together with other antioxidants like alpha-tocopherol to reduce seizure-related injuries[76]. Oxidative stress is believed to play a role in various neurological conditions, and reducing oxidative stress may have a positive impact on brain health, potentially including epilepsy. Das et al[81] found that patients with epilepsy had lower levels of vitamin C, copper, and zinc and higher malondialdehyde than controls[81].
Vitamin C has antioxidant properties that can help protect the nerves against inflammation and damage. However, while it may benefit brain health, it is not a direct treatment for epilepsy. Research suggests that vitamin C's neuroprotective and anticonvulsive effects are due to its specific "hormetic" acidification of subcortical and cortical neurons. As an antioxidant and electron donor, ascorbic acid accumulates in the CNS, where it helps reduce oxidative stress reactions and works alongside other antioxidants like alpha-tocopherol. This occurs when ascorbic acid weakens the regulation of pH levels. Non-neuronal cell research has shown that millimolar ascorbic acid can cause intracellular acidification and inhibit the core component of the pH regulation system[82]. Vitamin C also helps reduce inflammation, another factor contributing to seizure development. Therefore, vitamin C can help reduce brain inflammation and the risk of seizures. It also plays an important role in reducing hippocampus injury during seizures by increasing the activities of hippocampal superoxide dismutase and catalase and decreasing lipid peroxidation[76,83]. Vitamin C has mostly inhibitory activity and can even decrease mortality depending on the type of seizure[51]. Nazar et al[84] showed that the combined use of vitamins C and E is associated with a more than 70% reduction in seizure frequency.
The lack of ascorbate can contribute to seizures and the neurodegenerative changes that accompany them. Vitamin C deficiency can disrupt the delicate balance of glutamate, the primary excitatory neurotransmitter in the brain, by altering the expression of key genes involved in glutamate transport, particularly GLT-1. GLT-1 is responsible for clearing excess glutamate from the synaptic cleft, maintaining proper neurotransmitter levels, and preventing excitotoxicity[85]. When vitamin C levels are inadequate, changes in gene expression may lead to reduced GLT-1 function, resulting in impaired glutamate clearance and elevated extracellular glutamate levels. This disruption in glutamate regulation can increase neuronal excitability, making the brain more susceptible to seizures[86]. Additionally, elevated glutamate levels can adversely affect learning and memory processes, further compounding the cognitive impact of vitamin C deficiency. Overall, vitamin C deficiency's effects on glutamate transport and neurotransmitter balance contribute to heightened seizure susceptibility and impaired cognitive function[87].
Vitamin D: Vitamin D is an essential fat-soluble vitamin crucial in several bodily functions. It helps to regulate calcium levels in the body, which is essential for bone health. Its effects are mediated through two types of receptors: Nuclear receptors, which induce gene expression changes, and membrane receptors, located at the cell surface and mediate non-genomic vitamin D effects such as bone metabolism and regulation of calcium homeostasis[88]. Vitamin D also significantly impacts the brain's functioning, including regulating brain excitability, modulating the immune system, and promoting neurogenesis and neuroprotection[89]. In addition, vitamin D is a potent enhancer of nerve growth factor (neurotrophin) synthesis and release, promotes neuro-mediator synthesis, enhances intracellular calcium homeostasis, and prevents oxidative damage to nervous tissue[90,91]. Rats deficient in prenatal vitamin D had altered brain development, with enlarged ventricles, decreased cortical thickness, and changes in apoptosis[92].
While vitamin D deficiency is commonly associated with conditions like rickets and osteoporosis, its potential role in epilepsy is gaining attention. Several studies suggest a possible association between vitamin D deficiency and an increased risk of epilepsy. However, the exact nature of this association and the mechanisms involved are not yet fully understood. Vitamin D has neuroprotective properties, which may improve neurotransmission and apoptosis and reduce brain inflammation and oxidative stress damage. These properties could potentially be relevant in epilepsy management, as inflammation and oxidative stress have been linked to seizure development[93]. According to animal studies, vitamin D3 can increase the threshold of chemically induced seizures and also reduce their harmful effects[94]. Additionally, when mice with a deficiency in vitamin D receptors were given pentylenetetrazole to induce epileptogenesis, it resulted in reduced latency to the seizure induction and more seizure susceptibility[95]. An interesting study by Elmazny et al[96] showed that treatment-naive children and adolescents with genetic generalized epilepsy have a high prevalence of vitamin D deficiency, which is associated with younger age at onset, higher seizure frequency, and longer duration than control[97]. In addition, Alhaidari et al[98] showed that high vitamin D level was associated with a seizure reduction by about 40%[97]. In addition, Holló et al[97] found that correction of vitamin D deficiency significantly reduces seizure numbers by about 40%. However, Leandro-Merhi showed that satisfactory vitamin D levels did not modify potential seizure control in adult patients[99].
Although there is limited evidence to suggest that individuals with epilepsy and vitamin D deficiency may experience more frequent or severe seizures, this relationship is not well-established[100]. Further research is needed to clarify the mechanisms and establish clear causal relationships. Adequate vitamin D intake during pregnancy is essential for both the mother's and the developing fetus's health. Vitamin D deficiency during pregnancy has been linked to an increased risk of neurological and developmental issues in children, but it is not a direct cause of epilepsy[101]. On the other hand, Specht et al[102] found that maternal supplement with vitamin D status during pregnancy increases the risk of epilepsy in childhood in a dose-response manner, which may suggest the association between high neonatal 25(OH)D3 levels and the risk of childhood epilepsy. However, many limitations and confounding factors limit our ability to withdraw strong evidence of this association in their study[102]. Additionally, vitamin D deficiency may affect the effectiveness of certain AED[103]. It's crucial to emphasize that while some evidence suggests a link between vitamin D deficiency and epilepsy, this relationship is complex and not yet fully understood. More research is needed to clarify the mechanisms and establish clear causal relationships.
Vitamin E: Vitamin E, specifically the α-tocopherol form, is a group of lipophilic antioxidants capable of crossing the BBB and plays an important role in membrane stabilization, enzyme enhancement, and repression of the effect of vitamin A with a significant ability to absorb oxygen's free radicals and reduce the negative consequences of lipid peroxidation in brain tissues[104,105]. Vitamin E works as an antioxidant that neutralizes free radicals, which can damage brain cells. It helps reduce oxidative stress and has potential neuroprotective effects by maintaining neuron function and integrity. Also, its anti-inflammatory properties could benefit neurological health by regulating inflammatory processes[106,107]. Vitamin E treatment has been shown to have an anticonvulsant effect by renovating glutamate metabolism by restoring the seizure-induced glutamine synthetase suppression and reducing excitotoxicity. It also has neuroprotective and anti-inflammatory effects, making it a promising treatment for epilepsy[108,109]. Vitamin E deficiency can present with various neurological symptoms, including dysarthria, ataxia, areflexia, dorsal column degeneration, and various corticospinal tract signs such as limb weakness and Babinski’s sign[110]. Genetic vitamin E deficiency could result from various α-tocopherol transport protein gene mutations on chromosome 8q13. It can be treated with vitamin E replacements[111]. Mutations in the gene responsible for α-tocopherol transfer protein result in the body's inability to incorporate vitamin E into very low-density lipoproteins. This leads to lower serum levels, which in turn reduces the delivery of vitamin E to the nervous system. The reduced delivery of vitamin E to the CNS causes neurodegeneration, likely due to increased oxidative stress[112-114].
Vitamin K: Vitamin K constitutes a group of fat-soluble vitamins characterized by a naphthoquinone compound and isoprenylacyl side chains. Its primary function involves serving as a cofactor for gamma-glutamyl carboxylase, crucial for the carboxylation of glutamic acid in vitamin K-dependent proteins involved in blood clotting and bone health. Some research suggests that vitamin K may also play a role in the gamma-carboxylation of proteins in the brain, which could influence neuronal function. During embryonic development, this carboxylase is active in the CNS. Vitamin K is vital for the regular biosynthesis of CNS myelin[115]. Exposure to the vitamin K antagonist warfarin during fetal development may result in CNS deformities and mental retardation. These findings suggest a potentially significant role for vitamin K in brain maturation[116,117]. Despite not being a traditional antioxidant, both vitamin K1 and K2 (menaquinone-4) can effectively inhibit oxidative cell death induced by glutathione depletion in primary cultures of oligodendrocyte precursors and immature fetal cortical neurons, with EC50 values of 30 nm and 2 nm, respectively. Vitamin K's mechanism of action in reducing oxidative damage is independent of its role as a cofactor for gamma-glutamyl carboxylase, the enzyme responsible for the posttranslational modification of specific proteins. It's worth noting that neither oligodendrocytes nor neurons have significant vitamin K-dependent carboxylase or epoxidase activity[115].
Several animal studies have demonstrated that vitamin K has anticonvulsant effects in epilepsy, specifically in corneal-kindled and minimal clonic seizures (6 Hz) models. Vitamin K3 reduced swim activity induced by pentylenetetrazol in zebrafish at lower concentrations than valproic acid (VPA). Pentylenetetrazol triggers a rapid increase in swimming behavior, which indicates seizures in zebrafish[118,119]. The potential mechanism for the antiseizure properties of vitamin K analogs involves their impact on ATP metabolism, leading to an increase in total cellular ATP. Additionally, an animal study reported the protective action of vitamin K against oxidative stress, a factor contributing to cell death in neurological disorders. Both vitamin K1 and K2 were found to strongly prevent glutathione depletion in primary cultures of neurons exposed to oxidative cell death[115].
Mineral deficiencies can impact neurological health and contribute to epilepsy or worsen seizure activity. Different mechanisms are involved for deficiencies of magnesium, zinc, calcium, sodium, potassium, and selenium in epileptogenesis. Table 5 shows the various roles of mineral disorders in epileptogenesis.
| Mineral deficiency | Mechanisms in epileptogenesis | Associated conditions | Causes of deficiencies | Management strategies |
| Magnesium | Modulates neuronal excitability by blocking calcium channels. Reduces NMDA receptor activation, lowering neuronal excitability. Prevents excessive calcium influx, mitigating excitotoxicity | Hypomagnesemia is linked to seizures and epilepsy | Inadequate dietary intake, malabsorption, renal disorders, and medications | Magnesium supplementation, dietary changes, addressing underlying health issues |
| Zinc | Modulates neurotransmission and influences NMDA receptors. Acts as an antioxidant and protects against oxidative stress | Serum zinc concentrations vary in epilepsy; both high and low levels are reported | Dietary insufficiency, malabsorption, genetic factors | Zinc supplementation, balanced diet, investigation into underlying causes |
| Calcium | Regulates neuronal excitability and neurotransmitter release. Excessive influx to excitotoxicity; deficiency may predispose to seizures | Hypocalcemia or hypercalcemia may impact neurological function | Hormonal imbalances, dietary deficiency, renal disorders, vitamin D deficiency | Dietary changes, calcium supplements, and medical treatment for underlying conditions |
| Sodium | Essential for generating and propagating action potentials. Dysfunctions in sodium channels can alter neuronal excitability | Dysnatremias can affect neuronal function, but the link to epileptogenesis varies | Dehydration, excessive sweating, kidney disorders, medication side effects | Fluid/electrolyte balance, addressing underlying health issues, medication adjustments |
| Potassium | Maintains resting membrane potential and influences action potential generation. Changes can affect the neuronal firing threshold | Imbalances can cause neuromuscular issues, but a direct link to epilepsy varies | Dietary insufficiency, renal problems, medications | A balanced diet, potassium supplements, and managing underlying health conditions |
| Iron | Essential for neurotransmitter synthesis and oxygen transport. Imbalance can lead to oxidative stress and neuroinflammation | Iron deficiency or excess might influence seizure susceptibility but complex relationship | Poor diet, malabsorption, menstrual bleeding, genetic disorders | Iron supplements, dietary modifications, treating underlying conditions |
| Selenium | Acts as an antioxidant and influences immune function and neurotransmitter systems. Role in GABAergic transmission | Oxidative stress and immune dysregulation linked to epilepsy | Dietary deficiency, soil depletion, absorption issues | Selenium supplementation, balanced diet, addressing absorption issues |
Magnesium: Magnesium plays a critical role in regulating the excitability of neurons and is involved in various biochemical processes in the brain. It acts as a natural blocker of calcium channels, which helps modulate the flow of calcium ions into neurons. This regulation is essential for balancing excitatory and inhibitory neurotransmission[119]. Magnesium has been studied for its potential role in seizure susceptibility and epileptic activity. It has shown anticonvulsant properties in experimental models by modulating NMDA receptors, reducing their activation, and consequently lowering neuronal excitability[120]. Magnesium can potentially raise the seizure threshold and reduce the likelihood of seizure occurrence. Additionally, magnesium helps to prevent excessive calcium influx, thereby mitigating excitotoxic damage to neurons and preventing excitotoxicity[121].
Low levels of magnesium have been reported in some individuals with epilepsy, and it's hypothesized that magnesium deficiency might contribute to increased neuronal excitability, potentially making individuals more susceptible to seizures[15,122]. Magnesium acts as a natural calcium channel blocker in the nervous system, regulating neuronal excitability. Low magnesium levels might increase excitability, potentially triggering seizures[123]. In some cases, magnesium supplementation has shown promise in reducing seizure frequency[124]. Some studies suggest that magnesium supplementation may have a role in reducing seizure frequency or severity in certain types of epilepsy[125-127]. However, the evidence is not consistent across all types of epilepsy or populations, and more research is needed to establish its clinical effectiveness.
Zinc: Zinc is an essential trace element that plays a vital role in various physiological processes, including neurotransmission and neuronal function. However, the exact role of zinc in epileptogenesis and epilepsy is not yet fully understood[128]. Zinc acts as a modulator of neurotransmission, primarily in the glutamatergic system, and influences NMDA receptors. These receptors are crucial in synaptic plasticity and excitatory neurotransmission[129]. Zinc also has antioxidant properties and protects cells from oxidative stress, which is implicated in neuronal damage and is associated with epileptic seizures. Furthermore, zinc acts as a neuroprotectant by modulating excitotoxicity and inhibiting excessive activation of NMDA receptors, which may contribute to neuronal injury seen in epilepsy[130]. Zinc is believed to have both pro- and anti-convulsant effects, which affect seizure susceptibility. A recent meta-analysis has concluded that serum Zinc concentration is significantly higher in non-medicated patients with epilepsy[131]. However, other studies suggest that Zinc levels are significantly reduced in the serum of children with refractory epilepsy[132,133].
Some animal studies suggest that zinc deficiency or alterations in zinc homeostasis may be associated with increased seizure susceptibility[134]. Zinc deficiency can affect neurotransmitter function and neuronal excitability by influencing GABAergic transmission, which regulates neuronal excitability. Lower zinc levels could alter neurotransmitter balance, influencing seizure activity[135]. However, the exact mechanisms by which zinc influences epileptogenesis still require further investigation. Clinical evidence regarding zinc's direct impact on epileptogenesis or its use as a treatment for epilepsy is limited. Although some studies have explored the relationship between zinc levels and epilepsy, more research is needed to establish a clear link and determine whether zinc supplementation could be beneficial for individuals with epilepsy.
Calcium: Calcium is essential for various physiological processes in the body, including neuronal function and neurotransmitter release. Its role in the development of epilepsy involves complex interactions within neuronal networks[136]. Calcium ions play a significant role in regulating neuronal excitability by generating and propagating action potentials necessary for communication between neurons. Calcium is also pivotal in neurotransmitter release at synaptic terminals[137]. When an action potential reaches a neuron's axon terminal, the influx of calcium triggers the release of neurotransmitters into the synapse, facilitating communication between neurons[138].
Although it is essential for normal neuronal function, excessive calcium influx can lead to excitotoxicity, causing neuronal damage or cell death. In epilepsy, this excessive calcium influx may contribute to the hyperexcitability of neurons, potentially triggering or sustaining seizures[139]. Additionally, calcium is involved in synaptic plasticity, which is the ability of synapses to change strength and adapt. Changes in synaptic plasticity can influence the development and maintenance of epilepsy-related changes in neuronal networks[140].
It is important to note that both low and high levels of calcium can influence seizures. Calcium is crucial for neuronal function, and imbalances in its levels can disrupt neurotransmitter release and affect neuronal excitability. Low calcium levels might predispose individuals to seizures, while excessively high levels can also trigger them[141]. Some studies suggest that disturbances in calcium homeostasis or abnormalities in calcium signaling pathways may be associated with certain types of epilepsy[142]. Mutations in genes encoding calcium channels or transporters have been linked to specific forms of epilepsy in some cases[143]. Certain AED work by modulating calcium channels to reduce neuronal excitability, highlighting the importance of calcium in epilepsy treatment[136].
Sodium: Sodium is an essential electrolyte that plays a crucial role in various physiological processes. It is particularly important when it comes to neuronal function and maintaining cellular osmolarity. Sodium ions are key players in generating and propagating neuron action potentials[144]. Changes in sodium channel activity can influence neuronal excitability and the firing of action potentials. Neurons rely on the movement of sodium ions across their cell membranes to create the electrical impulses necessary for communication. Voltage-gated sodium channels open in response to depolarization, allowing an influx of sodium ions and initiating the action potential. Sodium channels are critical for transmitting signals from one neuron to another, allowing for communication within neuronal networks. They contribute to the excitatory signaling between neurons. However, specific mutations or dysfunctions in sodium channels can lead to alterations in neuronal excitability and an increased predisposition to seizures[145].
Some AED target sodium channels, aiming to modulate their activity and reduce neuronal excitability as a way to control seizures[146]. Both excessive and insufficient sodium levels can have adverse effects on neuronal function. Hypernatremia (or hyponatremia can potentially affect neuronal excitability, although the direct link to epileptogenesis may vary based on individual circumstances. Understanding the intricate role of sodium in neuronal excitability and signaling is crucial in comprehending its involvement in epileptogenesis. While sodium's significance in the context of epilepsy is evident, the specific mechanisms through which alterations in sodium channels or sodium levels contribute to epileptogenesis may differ based on the subtype or cause of epilepsy[147].
Potassium: Potassium is an essential electrolyte that plays a significant role in the function and excitation of neurons. It helps maintain the resting membrane potential of neurons, which is crucial for generating and propagating action potentials. Potassium channels repolarize the neuronal membrane after an action potential[148]. When depolarization occurs, potassium channels open, allowing the efflux of potassium ions and helping restore the cell's negative charge. The balance between potassium and other ions, particularly sodium, affects neuronal excitability[149]. Changes in potassium levels or alterations in potassium channel function can affect the threshold for neuronal firing. Dysfunctions in potassium channels can disrupt the balance of ions across the neuronal membrane, potentially leading to hyperexcitability or increased susceptibility to abnormal electrical activity, such as seizures[150]. Some AED may indirectly influence potassium channels or potassium dynamics to modulate neuronal excitability[151]. Both hypokalemia and hyperkalemia can impact neuronal function, but the direct link between potassium imbalance and epileptogenesis may vary based on individual factors and underlying conditions[152]. Understanding the role of potassium in regulating neuronal excitability and action potential generation provides insight into its possible involvement in epileptogenesis. However, the specific mechanisms through which potassium disturbances contribute to epilepsy may vary across different types or causes of epilepsy. Managing potassium levels, especially in the context of epilepsy and potential interactions with medications, requires careful evaluation and monitoring by qualified healthcare providers[153].
Iron: Iron is a crucial mineral that is vital in various physiological processes, including oxygen transport, energy production, and neurotransmitter synthesis. However, the direct relationship between iron levels and epileptogenesis is not yet fully understood[154]. Iron is essential for synthesizing neurotransmitters such as dopamine, serotonin, and norepinephrine, which regulate neuronal excitability and communication. Iron is also a key component of hemoglobin, a protein in red blood cells that carries oxygen to tissues, including the brain. Proper brain functioning requires adequate oxygen levels, and disruptions in oxygen supply can contribute to neuronal hyperexcitability[155]. Iron also participates in antioxidant enzyme systems, and imbalances in iron levels can lead to increased oxidative stress, potentially damaging neurons and affecting neuronal function. Oxidative stress is implicated in various neurological conditions, including epilepsy. Some studies suggest a link between iron dysregulation, neuroinflammation, and neurodegenerative processes, which might influence the susceptibility to seizures or epileptogenesis. However, the exact mechanisms are not fully understood[156].
Iron deficiency can lead to various neurological symptoms, including cognitive impairment and altered brain function. Some studies have explored the association between iron deficiency anemia and an increased risk of seizures, but the relationship is complex and not fully established[157-159]. Excessive iron levels (hemochromatosis) can lead to iron accumulation in various tissues, potentially causing oxidative damage and affecting neurological health[160]. However, the direct impact on epileptogenesis remains unclear. Although some studies suggest a potential link between iron levels and epilepsy, factors such as age, genetic predisposition, comorbidities, and environmental influences can also affect the relationship between iron status and epileptogenesis[161]. Therefore, monitoring iron levels and addressing deficiencies or excesses should be done under the guidance of qualified medical professionals, especially for individuals with epilepsy or those at risk.
Selenium: Selenium is a trace mineral that is crucial in various physiological processes. It helps defend the body against free radicals, supports thyroid hormone metabolism, and boosts immune function[162]. While its role in epileptogenesis is not extensively studied, some research suggests its potential involvement. Selenium is a crucial component of antioxidant enzymes like glutathione peroxidases and thioredoxin reductases. These enzymes protect cells, including neurons, from oxidative damage by neutralizing free radicals[163]. Since oxidative stress is linked to neurological disorders, including epilepsy, selenium's antioxidant properties might indirectly influence epileptogenesis by mitigating oxidative stress. Selenium is also important for the proper function of glutathione peroxidases, which regulate the balance of ROS in cells. ROS imbalance is associated with neuronal hyperexcitability and potentially epileptogenesis[164]. The proper function of these enzymes supported by selenium might indirectly impact seizure susceptibility. In addition, selenium plays a role in immune function and modulation of inflammatory responses. Neuroinflammation has been associated with epilepsy, and selenium's influence on immune function might have implications for neurological disorders[165].
Furthermore, some studies suggest that selenium might affect the GABAergic system, which is the brain's primary inhibitory neurotransmitter system. Alterations in GABAergic transmission can influence neuronal excitability and might affect seizure development[166,167]. While there are potential connections between selenium and epileptogenesis, the specific mechanisms and the exact role of selenium in epilepsy development remain unclear. Selenium's influence on oxidative stress, immune modulation, and neurotransmitter systems might contribute to its potential impact on epilepsy[168]. However, further research is needed to clarify its role and determine whether selenium supplementation could have therapeutic effects in epilepsy management. Balancing trace minerals like selenium is essential, as both deficiency and excess can adversely affect health.
Fatty acids are essential for maintaining the brain's structural integrity and physiologic functions. Omega-3 fatty acids, specifically docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are essential for various health benefits, including neurological health[169]. Their role in epilepsy and epileptogenesis has been an area of research interest, though the specific mechanisms are still being explored. Omega-3 fatty acids have anti-inflammatory properties that may help manage seizure activity, as inflammation is associated with epileptogenesis. These fatty acids may also have neuroprotective effects by preserving neuronal structure and function, potentially reducing neuronal excitability and hyperexcitability associated with seizure occurrence[170]. Omega-3s may affect neurotransmitter systems, including GABAergic and glutamatergic pathways, which regulate neuronal excitability, thus impacting seizure susceptibility[171]. Some research suggests that omega-3 fatty acids may modulate ion channel function, affecting neuronal excitability and electrical activity and possibly impacting the seizure threshold[172]. Adequate levels of DHA, in particular, are vital for neuronal membrane integrity, synaptic function, and signal transmission, indirectly influencing epileptogenesis[173].
While some studies suggest a potential beneficial role for omega-3 fatty acids in epilepsy[170,174], the evidence remains somewhat inconclusive. Clinical trials exploring the direct effects of omega-3 supplementation on seizure frequency or severity have shown mixed results. Factors such as dosage, duration of supplementation, types of epilepsy, and individual variability might contribute to these inconsistencies[175,176]. Omega-3 fatty acids are generally safe and contribute to overall health, including brain function. Incorporating omega-3-rich foods such as fatty fish (salmon, mackerel, sardines), flaxseeds, chia seeds, and walnuts into the diet is recommended[177]. However, omega-3 supplements could interact with medications or have individual-specific effects[178]. More research is needed to understand better the precise role and potential therapeutic implications of omega-3 fatty acids in epilepsy.
L-carnitine is a derivative of an amino acid that plays a crucial role in energy metabolism, specifically in the transportation of fatty acids into the mitochondria to produce energy[179]. Although the impact of L-carnitine on epilepsy is still under investigation, its involvement in epileptogenesis has garnered interest. The brain has high energy demands, particularly during seizures. Alteration in energy metabolism could affect neuronal excitability and contribute to seizure activity[180]. L-carnitine's antioxidant properties may have neuroprotective effects by mitigating oxidative damage and supporting neuronal health, potentially impacting epileptogenesis. L-carnitine might also affect neurotransmitter systems, including glutamatergic and GABAergic pathways, potentially affecting neuronal excitability and seizure threshold[181].
Inflammation is implicated in various neurological disorders, including epilepsy. L-carnitine has been studied for its potential anti-inflammatory properties, which might positively impact seizure susceptibility. Some clinical studies have explored the use of L-carnitine supplementation in individuals with epilepsy[182]. While some suggest potential benefits in reducing seizure frequency or severity, the results are inconsistent across all studies. However, it's important to note that the evidence regarding L-carnitine's direct impact on epileptogenesis or its use as a treatment for epilepsy is still evolving. Some studies indicate potential benefits, while others do not show significant effects. A study by Essawy et al[183] found that administering L-carnitine to rats before and after pentylenetetrazol exposure reduced the kindling acquisition process. This significantly relieved all the epileptogenic effects caused by pentylenetetrazol by ameliorating oxidative/antioxidative imbalance and neuromodulating and antiepileptic actions[183]. In addition, serum-free carnitine (FC) can get lower with some AED. Okumura et al[184] found that serum FC was below normal levels in more than 50% of children with epilepsy who were treated with VPA.
There is some evidence that the risk of carnitine deficiency increases with an increasing number of anti-epileptic drugs used in premature babies receiving total parenteral nutrition, patients receiving dialysis, patients with epilepsy using the ketogenic diet, certain metabolic diseases, and the presence of nutritional inadequacy[185]. In addition, a consensus among pediatric neurologists supports the use of intravenous L-carnitine supplementation for managing VPA-induced hepatotoxicity, overdose, and other acute metabolic crises related to carnitine deficiency[186]. The effects of L-carnitine deficiency might also vary depending on the type of epilepsy, individual variations, and concurrent medications. Potential interactions of L-carnitine with medications should be considered[187]. Additionally, further research is needed to understand better the mechanisms underlying L-carnitine's effects on epilepsy and to establish its clinical effectiveness in managing seizures. Figure 2 summarizes the general epileptogenic mechanisms associated with nutrient disorders.
Hypoglycemia can potentially increase the risk of triggering seizures in individuals with epilepsy. It can reduce the brain's seizure threshold, making it more susceptible to abnormal electrical activity[188]. For individuals with epilepsy who already have a lowered seizure threshold, a further decrease in blood sugar levels can increase the likelihood of having a seizure. The brain relies on a consistent supply of glucose (sugar) as its primary energy source. When blood sugar levels drop significantly, the brain may not receive sufficient fuel to function properly[189]. This can lead to changes in brain activity that may trigger seizures. Hypoglycemia can activate the body's stress response, releasing stress hormones like adrenaline. These hormones can have excitatory effects on the brain and may contribute to seizure activity. As the effect of hypoglycemia differs from one person to another, the relationship between hypoglycemia and seizures can vary from person to person. Some individuals may be more prone to hypoglycemia-induced seizures, especially if they have poorly controlled epilepsy or a history of seizures triggered by low blood sugar[190].
Skipping meals can lead to fluctuations in blood sugar levels and may increase seizure risk. Skipping meals can also activate the body's stress response, releasing stress hormones such as adrenaline with their excitatory effects on the brain and may increase the risk of seizures[191]. Skipping meals may alter the energy (calories) balance, leading to energy depletion, fatigue, weakness, and impaired brain function. Inadequate energy supply to the brain can potentially disrupt its normal activity and contribute to seizure activity[192]. In addition, skipping meals can lead to electrolyte imbalances, particularly if it results in dehydration. Electrolyte imbalances, such as hyponatremia, hypokalemia, or hypomagnesemia, can affect nerve cell function and increase the likelihood of seizures[193]. In addition, people who skip meals often lose weight. This can also increase seizure risk, as people with lower body weights are more likely to have seizures. Skipped meals may interfere with antiseizure medication absorption, causing blood level fluctuation and impaired therapeutic levels in the bloodstream, resulting in suboptimal seizure control[194].
The gut microbiota can influence epileptogenesis through several pathways. Gut dysbiosis is an imbalance in the microbial communities in the gastrointestinal tract, where harmful microorganisms may outnumber beneficial ones. Gut dysbiosis can lead to chronic inflammation in the gut, which can extend to the brain, promoting neuroinflammation—a key factor in epileptogenesis. Additionally, gut microbes play a role in neurotransmitter production and metabolism, affecting the balance between excitatory and inhibitory signals in the brain. SCFAs produced by gut bacteria have anti-inflammatory properties and can modulate neuronal excitability, but dysbiosis-related reductions in SCFA levels may contribute to neuroinflammation and hyperexcitability[195]. Furthermore, gut microbes interact with the immune system, and dysbiosis can lead to immune dysregulation and increased production of pro-inflammatory cytokines, further promoting neuronal dysfunction. Lastly, dysbiosis-induced inflammation may compromise the integrity of the BBB, facilitating the entry of harmful substances into the brain and promoting epileptogenesis[196]. Therefore, the gut microbiota plays a significant role in epilepsy development and progression through its influence on neuroinflammation, neurotransmitter balance, SCFA production, immune modulation, and BBB integrity.
Recent research shows a growing interest in the connection between gut dysbiosis and epilepsy in both animals and humans[197]. The gut-brain axis, which is the communication between the gut and the CNS, may play a vital role in epilepsy and seizure management. Gut dysbiosis can cause chronic low-level inflammation in the gut, which is believed to contribute to some forms of epilepsy[198]. The gut microbiota produces metabolites that can affect the brain and influence neural excitability, possibly playing a role in seizure control. It's important to note that there isn't a single diet that directly causes gut dysbiosis[199]. Still, certain dietary habits and patterns may increase the risk of developing an imbalance in the gut microbiota. For example, high sugar or diets with refined carbohydrates can promote the growth of harmful bacteria and yeast in the gut, potentially leading to dysbiosis. Excessive sugar intake can disrupt the balance of beneficial bacteria. In addition, low-fiber diets can negatively impact gut health. Foods that are rich in fiber, such as fruits, vegetables, and whole grains, are essential for nourishing beneficial gut bacteria. Without enough fiber, these beneficial microbes may be negatively impacted[200].
Highly processed foods often contain additives, preservatives, and artificial ingredients that can negatively affect the gut microbiota. These foods may lack the nutrients needed to support a diverse and healthy gut ecosystem[201]. Meanwhile, the use of antibiotics can disrupt the balance of gut bacteria. Antibiotics are designed to kill or inhibit the growth of bacteria, and they can affect both harmful and beneficial microbes. Overuse or inappropriate use of antibiotics can lead to gut dysbiosis[202]. Some studies suggest that diets that are high in saturated fats may promote the growth of harmful gut bacteria. Excessive intake of saturated fats can negatively influence the composition of the gut microbiota. Excessive alcohol consumption can have a detrimental impact on gut health. It can disrupt the gut barrier, allowing harmful substances to enter the bloodstream and promote inflammation and gut dysbiosis. Some research suggests that artificial sweeteners may negatively affect the gut microbiota by promoting the growth of certain bacteria associated with metabolic disturbances. However, more research is needed in this area[203].
Diets that are high in red meat, especially processed meats, may promote the growth of certain bacteria associated with gut inflammation and dysbiosis. It's important to remember that diet's effects on gut health can vary from person to person[204]. While these dietary factors may contribute to gut dysbiosis in some individuals, they may not have the same impact on others. Eating a balanced, varied, and nutrient-rich diet that includes a wide range of whole foods, particularly those that are rich in fiber, can help support a healthy gut microbiota. Changes in the gut microbiota composition can impact the metabolism of AED, potentially affecting their efficacy and side effects[195]. However, it's important to note that the effects of gut dysbiosis on epilepsy may vary among individuals, and further studies are needed to determine the best ways to use the gut-brain connection to manage epilepsy.
Alcohol consumption can significantly impact individuals with epilepsy. It can trigger seizures, worsen seizure fre
In some cases, alcohol consumption can lead to the development of new seizure types in people with epilepsy. Alcohol consumption has been associated with the development of myoclonic seizures, which involve sudden, involuntary muscle jerks[208]. Alcohol consumption can worsen seizure frequency in people with epilepsy because it can disrupt the effectiveness of anti-seizure medications, making it more difficult to control seizures. Additionally, alcohol consumption can disrupt sleep patterns and increase stress, both of which are known triggers for seizures in individuals with epilepsy[25]. Furthermore, alcohol can interact with AED commonly used to manage epilepsy. It may reduce the effectiveness of these medications or increase their side effects[209]. The risk of alcohol-induced seizures is higher for individuals with generalized genetic epilepsy and those who consume excessive amounts of alcohol, particularly binge drinking, which involves rapidly consuming a large amount of alcohol in a short period[205]. Abruptly stopping alcohol consumption after a period of heavy drinking can lead to withdrawal symptoms, including seizures. This is known as alcohol withdrawal seizures or alcohol withdrawal syndrome. The most characteristic and severe seizure type that occurs in alcohol withdrawal is generalized tonic–clonic seizures[210]. Therefore, individuals with epilepsy should carefully manage their alcohol consumption and follow medical advice. Avoiding excessive alcohol intake, adhering to prescribed medications, and maintaining a healthy lifestyle are essential steps to minimize the risk of seizures.
The relationship between food allergies and epileptogenesis is an area of active research, but the direct causal link between them still needs to be fully understood. Some studies suggest that certain food allergies or sensitivities may trigger seizures in some individuals, but the mechanisms behind this association are not fully understood[211]. Some studies observed a high prevalence of allergies, including food allergies, among patients with epilepsy. A United States population-based study showed that children with one or more allergic diseases have a higher prevalence of epilepsy than children without allergies[212]. A systematic review showed that the epilepsy frequency of epilepsy among patients with bronchial asthma varies between 0.7% and 1.4%, with an 81% increase in the epilepsy prevalence in patients with asthma than those without asthma. They also showed that the pooled Odds ratio for epilepsy in patients with eczema is 2.57[213]. Many cases reported precipitation of seizures due to food sensitivities[214]. Frediani et al[215] found a signi
While some people with epilepsy may experience seizures due to specific food triggers or allergic reactions, this is not a common occurrence for everyone with epilepsy. The impact of food allergies on seizures can vary widely among individuals, and identifying specific food triggers can be challenging. One hypothesis suggests that certain food allergies or intolerances might provoke inflammation or immune responses in the body, potentially affecting the brain's function and triggering seizures in susceptible individuals. Inflammation is believed to play a role in some types of seizures and epilepsy. The theory is that this inflammation might affect the brain and neuronal activity, potentially contributing to seizures[217]. There is growing awareness of the connection between the immune system and the brain. Immune responses triggered by food allergies might impact brain function or increase susceptibility to seizures[218]. Research is exploring the relationship between the gut microbiome and neurological conditions. Changes in the gut microbiota due to food allergies could impact the gut-brain axis, potentially influencing neurological conditions like epilepsy[219]. Some food allergens may affect the levels of neurotransmitters in the brain, such as GABA, which plays a role in inhibiting seizures[195]. It is important to note that while there are theories and ongoing studies regarding this connection, concrete evidence establishing a direct causal relationship between food allergies and epileptogenesis is still evolving. Improvement of the patient's behavior and electroencephalographic changes may occur after removing the offending food. A provocation test can be done to confirm the relation of the food allergy to the seizure. However, the reaction may not occur immediately but can take a few days to evolve[211]. In clinical practice, managing epilepsy involves focusing on established triggers, adhering to prescribed medications, and maintaining a healthy lifestyle rather than primarily addressing food allergies. Gorjipour et al[220] showed that an allergic food elimination trial reduced seizures by more than 50% in more than 85% of the studied children[220].
Although certain food additives such as artificial colors, flavors, and preservatives have been studied about epilepsy, the evidence linking them to seizures is not conclusive. Some people with epilepsy may be sensitive to certain additives, which could potentially trigger seizures or worsen their condition. However, this sensitivity can vary greatly from person to person, and specific triggers can differ. Certain colorings and preservatives, including monosodium glutamate (MSG) and artificial sweeteners, may induce seizures. However, no compelling scientific evidence supports this claim in humans. It is worth noting that numerous foods labeled as "low-fat" also contain these artificial additives[221]. Free glutamate and aspartate can be found in food additives. Glutamate is the major excitatory neurotransmitter in the mammalian brain, hence increasing neuronal excitability and epilepsy tendency[222]. For some individuals with epilepsy, avoiding certain food additives might be an essential part of managing their condition. A detailed record of consumed foods and subsequent seizure activity could help identify potential triggers. However, consulting with a healthcare professional, like a neurologist or a registered dietitian, is crucial before making significant dietary changes or eliminating specific food groups or additives. It's important to note that the impact of additives on epilepsy might not be universally applicable, and further research is needed to understand the precise connections and mechanisms involved. Therefore, it's always best to seek personalized guidance from a healthcare provider when exploring dietary changes related to epilepsy[223].
Caffeine is a widely used CNS stimulant. It can affect the nervous system and trigger seizure activity in individuals with epilepsy. Caffeine is known to increase alertness and arousal. However, for some people with epilepsy, high doses of caffeine or other stimulants can lower the seizure threshold, making them more susceptible to seizures[224]. Conversely, moderate caffeine intake may not significantly affect seizure activity in most people with well-controlled epilepsy. Other stimulants, such as certain medications or recreational drugs, can also potentially lower the seizure threshold and trigger seizures in some individuals[225]. Although there are reports that caffeine consumption triggered seizures in some people with epilepsy, these are anecdotal and cannot establish a definitive causal relationship. Studies on animal models have shown that caffeine can lower seizure thresholds and increase susceptibility. However, these findings may not be directly applicable to humans[226].
Caffeine and other stimulants act as CNS stimulants by blocking adenosine receptors in the brain, inhibiting neuronal activity[227]. This increased excitability in the brain could potentially contribute to seizure generation. In some cases, chronic use of caffeine may protect against seizures[228]. Some studies indicate that caffeine may interact with AED, potentially reducing their effectiveness, especially topiramate[229]. This could be a concern for individuals with epilepsy who consume caffeine. However, the relationship between caffeine, stimulants, and epileptogenesis (the development of epilepsy) is complex and not fully understood. While some evidence suggests a potential link, the findings remain inconclusive and warrant further research. The effects of caffeine and stimulants on seizure susceptibility vary greatly between individuals. Some people with epilepsy may be highly sensitive to these substances, while others may experience no adverse effects. The risk of seizures appears to be dose-dependent, with higher caffeine intake increasing the risk[230]. The underlying cause of epilepsy may also play a role in determining an individual's sensitivity to caffeine and stimulants[231]. For people with epilepsy, it's often recommended to moderate caffeine intake and be cautious with stimulants. Keeping a seizure diary that includes information about caffeine consumption and any resulting seizure activity can help identify potential triggers.
Eating epilepsy is a rare form of reflex epilepsy that is triggered by eating or chewing, also known as eating-induced epilepsy or gustatory epilepsy. It is characterized by recurrent seizures that occur within minutes to hours after a person begins to eat or drink[232]. Seizures in eating epilepsy are often triggered by the act of eating, tasting the food, swallowing, or even thinking about food. Depending on the individual, this condition can manifest in various forms, ranging from brief staring spells to full-blown convulsions. It may occur as staring spells with brief episodes of unresponsiveness and staring into space. It could also appear as jerking movements involving the arms, legs, face, or other body parts. Sometimes, the person may lose consciousness and fall to the ground. In very rare situations, the affected person could lose bowel or bladder control[233].
The seizure in eating epilepsy usually originates from the temporal lobe or perisylvian and is usually associated with shorter food intake-seizure latency and more male predominance. Shorter food intake-seizure latency was associated with less severe seizures and less frequent contralateral spread of epileptic discharges[234]. Although the exact cause is unclear in more than 70% of cases, it could be related to abnormal brain activity in response to these stimuli. An autoi
Diagnosis can be easily done with an EEG with food challenges to measure the electrical activity in the brain. Video EEG recording may be needed to capture the seizure activity. Treatment usually involves antiepileptic medication, dietary changes, and sometimes avoiding, specific food triggers. Clobazam can effectively prevent eating epilepsy when taken 30 minutes before the meal[237]. The prognosis for people with eating epilepsy varies depending on the severity of their seizures and their response to treatment. Some people can control their seizures with medication and the ketogenic diet. In contrast, others may require more aggressive treatment, such as vagal nerve stimulation, or epilepsy surgeries, such as temporal lobectomy[238].
Epilepsy can potentially impact nutrition in several ways. The epileptic seizures themselves can disrupt eating patterns. Seizures occurring during meals or shortly after can lead to difficulties in feeding, potential injuries, or reluctance to eat due to fear of triggering a seizure, e.g., as seen in eating epilepsy. In addition, Seizures can cause energy depletion, leading to increased calorie needs and potential malnutrition. Additionally, seizures can disrupt eating habits and make it difficult to maintain a consistent diet. Different studies showed significantly lower energy intake of energy in children with epilepsy than in the age-matched population control group[239,240]. Moreover, uncontrolled epilepsy can lead to anxiety, depression, social isolation, and stigma, which can negatively affect food safety, available choices, and access to healthy meals. Epilepsy is often associated with other medical conditions, such as depression and anxiety, which can further affect appetite and dietary choices. Patients with epilepsy are at an increased risk for gastrointestinal problems, such as constipation and diarrhea, which can also affect nutrient absorption[195]. At the same time, the cost of epilepsy treatment can be high, leaving less money for food and other essential needs with impaired food intake[241,242]. Kolstad et al[243] children and adolescents with epilepsy had more eating disorders and eating more unhealthily than their peers. They also showed that males are more liable for dieting disorders due to poor physical image satisfaction, while females are more liable for unhealthy eating.
Anti-seizure medication can also impact the nutritional status of the patients. AED can affect appetite, taste, and digestion. Some medications may cause decreased appetite, nausea, or changes in taste perception, leading to altered eating habits and reduced food intake[13]. Certain AEDs might interfere with the absorption of specific nutrients, leading to deficiencies[244]. For example, some medications can reduce vitamin D (e.g., phenobarbital and phenytoin), calcium, vitamin K (e.g., phenytoin), thiamine (e.g., phenytoin), or folic acid levels, necessitating supplementation or dietary adjustments[245]. Some individuals with epilepsy may be advised to follow specific diets like the ketogenic diet or modified Atkins diet as part of their treatment plan. These diets are high in fats and low in carbohydrates, impacting nutrient intake and requiring careful monitoring to ensure adequate nutrition[246]. Medications or dietary changes can affect weight. Some individuals might experience weight gain due to certain AEDs, while others might face weight loss due to decreased appetite or dietary restrictions[247].
These factors prone people with epilepsy to an increased risk for nutritional deficiencies, particularly for sodium, calcium, manganese, magnesium, and zinc minerals, vitamins B1, B6, B12, C, D, and E, and Omega-3 fatty acids[21,248,249]. Increased seizure frequency and severity: Deficiencies in certain nutrients, such as magnesium and calcium, can lower the seizure threshold and make seizures more likely to occur. These deficiencies are more likely to occur in patients on large doses of medication or multiple drugs, growing children, the elderly, pregnant women, alcohol drinking, and those with poor dietary habits[250]. These nutritional deficiencies can impair seizure control and affect memory, concentration, and learning. In addition, calcium and vitamin D deficiencies can increase the risk of osteoporosis and fractures. In addition, the resulting nutritional deficiencies can contribute to other health problems, such as heart disease, diabetes, and cancer. Therefore, referral to a nutritionist should be considered in young people with epilepsy at the time of diagnosis[243].
Phenobarbital: Phenobarbital is an older AED that can have a significant impact on nutrition in several ways. It affects the absorption and metabolism of several essential vitamins and nutrients. For instance, it reduces the absorption and metabolism of vitamin D, leading to a decrease in Vitamin D levels. This decrease can have an impact on calcium metabolism and bone health, which may lead to issues such as osteopenia or osteoporosis. Phenobarbital can also interfere with the metabolism of Vitamin K, which is essential for blood clotting. This interference may increase the risk of bleeding or bruising, especially if the individual's Vitamin K levels are already compromised[251,252].
Phenobarbital is a medication that can increase the breakdown and metabolism of several B vitamins, including thiamine (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), biotin (B7), folic acid (B9), and cobalamin (B12). It can also lead to biotin breakdown, which is essential for hair and skin health, resulting in hair loss and skin problems[253]. Phenobarbital use may reduce folate levels in the body by impairing its absorption, which is necessary for various cellular functions, growth, and development, especially during pregnancy. Low folic acid levels can also lead to anemia and affect overall health[254]. Additionally, some individuals may experience changes in appetite or weight fluctuations while taking Phenobarbital, which could lead to alterations in dietary intake and, consequently, cause weight gain or loss and affect overall nutrition[255]. Phenobarbital can potentially impair glucose metabolism, increasing the risk of diabetes. However, studies in animal models suggest that Phenobarbital administration enhances insulin-mediated peripheral glucose utilization and hepatic glucose production suppression in both low-dose and high-dose diabetic groups[256].
Phenytoin: Phenytoin is an AED that can affect nutrition in several ways. It can interfere with Vitamin D's metabolism, leading to decreased Vitamin D levels and increased urinary calcium excretion. This effect can affect bone health and calcium absorption, increasing the risk of osteoporosis or bone fractures. Phenytoin can also interfere with the absorption of other minerals like magnesium and zinc, impacting the overall mineral balance in the body[257]. Phenytoin can interfere with Vitamin K metabolism, which can affect blood clotting, potentially increasing the risk of bleeding or bruising. Additionally, it may reduce folate levels in the body[258]. Folate is essential for various cellular functions and for maintaining healthy red blood cells. Low folate levels can lead to anemia and impact overall health[259]. Phenytoin significantly decreases the absorption and increases the metabolism of several B vitamins, including B1, B2, B3, B6, folic acid, and B12. This can lead to deficiencies, causing symptoms like fatigue, nerve damage, skin problems, anemia, and developmental problems (in pregnancy)[260]. Some individuals might experience changes in appetite or weight fluctuations while taking Phenytoin, potentially affecting dietary intake and overall nutrition. While less common than phenobarbital, phenytoin can potentially impair glucose metabolism, increasing the risk of diabetes[247].
Carbamazepine: Carbamazepine, another widely used anti-epileptic drug, has similar effects on nutrition as phenytoin and phenobarbital but with some nuances. Carbamazepine, an AED, can affect nutrition in several ways. Long-term use of Carbamazepine has been associated with decreased levels of Vitamin D. This decrease might affect bone health and calcium absorption, potentially leading to issues like osteoporosis or bone fractures[261]. Carbamazepine usage can lower Vitamin B12 Levels in the body, leading to anemia, fatigue, and neurological symptoms if not managed properly. Similar to other AED, Carbamazepine may decrease folate levels. Folate is crucial for cellular functions and maintaining healthy red blood cells[262]. Carbamazepine has a higher tendency than phenytoin and phenobarbital to cause weight gain, possibly due to increased appetite or altered metabolism, potentially affecting dietary intake and overall nutrition[263]. While less common, carbamazepine can potentially impair glucose metabolism, increasing the risk of diabetes. Carbamazepine can interfere with the absorption of certain minerals like calcium, magnesium, and zinc, affecting overall mineral balance in the body[22]. Unlike phenytoin, carbamazepine doesn't seem to affect biotin levels significantly. Carbamazepine can cause hyponatremia (low sodium levels), requiring monitoring and potential electrolyte adjustments[264].
VPA: VPA is a medication used to treat epilepsy that can have a variety of effects on nutrition. One of the significant side effects of VPA is weight gain due to changes in appetite, altered metabolism, or hormonal effects, which can lead to changes in cholesterol and triglyceride levels. If not managed through diet and lifestyle modifications, this effect may increase the risk of cardiovascular issues[265]. VPA can also cause hyperammonemia, a condition where excess ammonia builds up in the blood. This can affect appetite, protein metabolism, and energy levels[266]. Studies suggest that VPA may affect insulin sensitivity and glucose metabolism, potentially impacting blood sugar levels and increasing the risk of conditions like insulin resistance or diabetes. There are reports that VPA can lower glucose levels after intravenous administration during glucose tolerance tests in patients with recently diagnosed epilepsy[267,268]. Changes in appetite due to VPA can potentially affect overall nutrition. Additionally, VPA might interfere with the absorption of certain nutrients, including calcium, leading to potential issues with bone health[269]. VPA can decrease the absorption of vitamin B12, leading to symptoms like fatigue, nerve damage, and anemia. Unlike other anti-epileptic drugs, VPA doesn't significantly affect biotin levels[270].
Levetiracetam: Levetiracetam is a commonly used AED that generally has fewer direct effects on nutrition compared to some other medications in its class. However, it may impact nutrition in some ways. For instance, some individuals may experience a decrease in appetite or alterations in taste perception while taking levetiracetam, which could potentially affect dietary intake and overall nutritional status[271]. Additionally, while uncommon, some people might experience gastrointestinal side effects such as nausea, vomiting, or diarrhea, which could influence nutrient absorption and affect overall nutritional status if severe or persistent[272]. Moreover, while weight changes with Levetiracetam are less common compared to some other AED, some individuals might experience weight gain or weight loss as a side effect, which could impact overall nutrition. It's worth noting that Levetiracetam has minimal impact on nutrient absorption[273].
Unlike many other AEDs, it doesn't significantly interfere with the absorption of vitamins, minerals, or other nutrients from food. However, taking Levetiracetam with food can slightly slow its absorption, but the amount absorbed remains unchanged. Some studies suggest Levetiracetam may slightly decrease vitamin B12 absorption in certain individuals, but this is not a common side effect, and B12 deficiencies are rarely reported with Levetiracetam use[374]. While not directly affecting nutrient absorption, Levetiracetam may slightly affect bone metabolism in some individuals. This is primarily due to its potential impact on calcium levels. Therefore, monitoring bone health and ensuring adequate calcium intake through diet or supplements might be recommended for individuals on long-term Levetiracetam therapy, especially those at risk for osteoporosis[275]. Compared to older antiepileptic medications, Levetiracetam tends to have a better tolerance profile regarding nutritional impacts.
Lamotrigine: Lamotrigine is a type of antiepileptic medication that generally has minimal direct effects on nutrition compared to some other drugs in its class. However, there are a few potential impacts that should be taken into consideration. Some people might experience changes in appetite while taking Lamotrigine, which could lead to alterations in dietary intake and affect overall nutritional status[276]. Although it is less common, some individuals may also experience gastrointestinal side effects like nausea, vomiting, or diarrhea, which could influence nutrient absorption and affect overall nutrition if severe or persistent[277].
Lamotrigine is typically associated with minimal impact on body weight compared to some other AED. However, some individuals might still experience weight changes as a side effect, which could influence overall nutritional status[278]. It's worth noting that Lamotrigine has limited interactions with enzymes involved in the metabolism of nutrients compared to other AED. This means it may have fewer effects on the breakdown or utilization of certain vitamins and minerals[10]. In some individuals, Lamotrigine might slightly affect bone metabolism, increasing the risk of osteoporosis over long-term use. It's important to note that this is not due to direct interference with nutrient absorption but rather a potential impact on bone density[279].
Topiramate: Topiramate is an antiepileptic medication that is also used to treat migraines and mood disorders. However, it can have several effects on nutrition that should be monitored. One of the significant side effects associated with Topiramate is weight loss, which can be caused by appetite suppression or changes in taste perception, leading to reduced food intake[280]. Nonetheless, prolonged use of this medication might cause metabolic acidosis, which can affect electrolyte levels in the body, resulting in electrolyte imbalances such as low potassium and magnesium[281]. Electrolytes play an important role in nerve function and overall health, so it's crucial to monitor them in individuals taking this medication[282].
Topiramate can also affect the absorption of certain nutrients, especially calcium, leading to decreased calcium levels, which can impact bone health[283]. Another side effect of Topiramate is an increased risk of kidney stones, particularly in individuals with a family history or other risk factors[284]. However, some studies showed no increased risk of urolithiasis with topiramate[285]. Adequate hydration and monitoring of kidney function are essential for individuals taking this medication. In addition, some individuals might experience a decrease in Vitamin B6 levels when using Topiramate. It can also interfere with folate absorption, especially in individuals with low folate levels before starting the medication. Although it is not a common side effect, some studies suggest that Topiramate might slightly decrease B12 absorption. Therefore, monitoring B vitamin levels and considering supplementation may be necessary in some cases[270,286].
Gabapentin: Gabapentin is primarily used to treat epilepsy and has a relatively mild impact on overall nutrition when compared to other AEDs. Gabapentin doesn't significantly interfere with the absorption of most vitamins and minerals from food. This is because it uses a different transport system than most nutrients, meaning they don't compete for absorption. Gabapentin can be taken with or without food, and the presence of food doesn't affect its absorption. However, some individuals may experience certain impacts[287]. For some individuals, Gabapentin can cause alterations in appetite, which might affect dietary intake and subsequently impact overall nutrition. It can stimulate appetite in some people, leading to weight gain if not managed through diet and exercise[288]. Additionally, Gabapentin can cause fluid retention in some people, which might contribute to weight gain or bloating[289]. Although uncommon, some indi
Pregabalin: Pregabalin is a medication commonly used to treat neuropathic pain, fibromyalgia, and certain types of seizures. It has a similar impact on nutrition as Gabapentin but with some additional nuances. Pregabalin does not significantly interfere with the absorption of most vitamins and minerals. It uses a different transport system than most nutrients, which minimizes competition for absorption[292]. Pregabalin can be taken with or without food, and its absorption is not affected by the presence of food. However, it may cause alterations in appetite, leading to increased food intake for some people. This effect can influence dietary habits and overall nutritional intake. One of the notable side effects associated with Pregabalin is weight gain, more so than with Gabapentin. This can happen due to increased appetite or changes in metabolism for some individuals[293]. Although less common than Gabapentin, Pregabalin can also cause fluid retention in some individuals, which may contribute to weight gain or bloating[294]. Some people may experience gastrointestinal side effects such as nausea or diarrhea. These symptoms could potentially affect nutrient absorption[295]. Like Gabapentin, some studies suggest that Pregabalin might slightly affect bone metabolism over long-term use, especially in male patients[296]. However, more research is needed to confirm this and identify potential mechanisms. Table 6 summarizes the effects of some AEDs on the nutritional status of individuals with epilepsy.
| Drug class/drug | Nutrient affected | Effect on nutrient | Potential side effects and consequences | Recommendations |
| Enzyme-inducing antiepileptic drugs | ||||
| Phenytoin (Dilantin) | B1, B2, B3, B6, B12, Biotin, Folic Acid, K, Calcium, Vitamin D | Decreased absorption and metabolism, increased excretion | Nerve damage, fatigue, skin problems, anemia, developmental problems | Supplementation with affected vitamins, calcium and vitamin D, monitoring bone density |
| Carbamazepine (Tegretol), Oxcarbazepine (Trileptal) | B1, B2, B3, B6, B12, folic acid, calcium, Vitamin D | Decreased absorption and metabolism, increased excretion | Like phenytoin | Similar recommendations as phenytoin |
| Phenobarbital (Luminal) | B1, B2, B3, B6, B12, Folic Acid, Calcium, Vitamin D | Increased metabolism, decreased absorption | Like phenytoin, it may also cause drowsiness and cognitive problems | Similar recommendations as phenytoin, with additional monitoring for cognitive function |
| Non-enzyme-inducing antiepileptic drugs | ||||
| Levetiracetam (Keppra) | B12 | Decreased absorption | Anemia, nerve damage, generally well-tolerated, limited impact on nutrition | Supplementation with B12 |
| Lamotrigine (Lamictal) | Bone metabolism | Potential impairment | Bone loss, osteoporosis | Calcium and vitamin D supplementation, monitoring bone density |
| Topiramate (Topamax) | Weight, Glucose metabolism | Potential increase or decrease, possible impairment | Weight gain or loss, diabetes, altered taste perception | Dietary adjustments, monitoring weight and blood sugar |
| Valproic acid (Depakote) | Weight, lipid metabolism | Potential increase | Increased risk of weight gain, altered lipid metabolism | Dietary adjustments, monitoring weight |
| Gabapentin | Weight | Potential increase | Minimal impact on nutrition, some reports of weight gain | Dietary adjustments, monitoring weight |
| Pregabalin | Weight, appetite | Potential increase | Weight gain, potential alterations in appetite | Dietary adjustments, monitoring weight |
Nutritional management of epilepsy is a crucial aspect of overall disease management. Nutritional support for patients with epilepsy aims to improve seizure control by correcting any nutritional deficiency that could trigger seizures, optimize brain health by supplying a balanced diet rich in essential nutrients, minimize the side effects of medications, and promote overall well-being[13]. Recent therapeutic approaches in epilepsy management have begun to integrate nutritional interventions as adjuncts to conventional treatments. For instance, dietary therapies such as the ketogenic diet and modified Atkins diet have demonstrated efficacy in reducing seizure frequency in patients with drug-resistant epilepsy[297]. These interventions are thought to exert their benefits through mechanisms that include enhanced mitochondrial function, reduction of oxidative stress, and modulation of neuroinflammatory pathways. Moreover, micronutrient supplementation—such as vitamin D, magnesium, and omega-3 fatty acids—has shown potential in improving neuronal stability and overall brain health, although the results across studies remain heterogeneous[298].
There are various dietary approaches commonly associated with epilepsy management, including the ketogenic diet, modified Atkins diet, low glycemic index treatment (LGIT), MCT diet, low fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) diet, gluten-free diet, avoiding potential triggers, and supplementing the diet with the different nutrients necessary to supplement epilepsy management[223]. In addition to these established strategies, emerging evidence points toward modulating the gut microbiota as a novel approach to epilepsy management. Preliminary studies suggest that restoring a healthy balance in the gut-brain axis via probiotics or prebiotics can influence neuroimmune responses and potentially reduce seizure susceptibility[197]. Despite these promising findings, significant gaps remain. Few studies have directly compared the long-term outcomes of nutritional interventions with standard AED, and there is a notable lack of standardized protocols across clinical trials. Furthermore, the interplay between individual dietary patterns, genetic predispositions, and responses to both pharmacological and nutritional therapies is not yet fully understood[299].
Ketogenic diet: The ketogenic diet has been used for almost a century to manage epilepsy, especially in individuals with drug-resistant seizures. It is a high-fat, low-carbohydrate, and moderate-protein diet that induces a metabolic state called ketosis[300]. In ketosis, the body uses fat as its primary energy source instead of glucose from carbohydrates. By reducing carbohydrate intake and increasing fat consumption, the body shifts from using glucose to producing ketones from fat breakdown[301]. Ketones become the primary fuel for the brain and might have neuroprotective effects, stabilizing neuronal excitability and altering neurotransmitter levels, potentially reducing seizure activity. This metabolic shift is thought to be the reason behind the effectiveness of the ketogenic diet in epilepsy[302]. The benefits of the ketogenic diet are still being researched, but several theories have been put forward. According to these theories, the alternative energy source used in ketosis (ketones) might stabilize brain cells, reducing the likelihood of seizures. Ketones might also have antioxidant and anti-inflammatory properties, which could protect brain cells from damage and promote the growth of new neurons[303]. Additionally, ketones might influence the levels and activity of certain neurotransmitters involved in seizure regulation. Finally, the ketogenic diet might alter the composition of gut bacteria, potentially affecting brain function and seizure activity through the gut-brain axis[304].
There are several variations of the ketogenic diet used for epilepsy, each with different ratios of fat to carbohydrate and protein. Classic ketogenic diets are the most restrictive version, with a 4:1 ratio of fat to carbohydrates and protein. The modified Atkins diet is a version of the ketogenic diet that allows for slightly more carbohydrate flexibility, making it easier to follow for some individuals. MCT ketogenic diet is another version that focuses on incorporating MCT oil, a specific type of fat that readily converts to ketones, potentially improving the diet's effectiveness[305,306]. These ketogenic diets differ in their macronutrient composition, dietary flexibility, complexity of implementation, and specific indications. The choice among these diets often depends on individual needs, tolerability, and the condition being managed[307]. Table 7 shows the main differences between these diets.
| Aspect | Classic ketogenic diet | Modified Atkins diet | Medium-chain triglyceride ketogenic diet |
| Macronutrient ratio | High fat (about 3:1 or 4:1, Fat: Protein + Carbs) | High fat, low carb | High fat, low carb, focused on Medium-Chain Triglyceride |
| Carbohydrate intake | Extremely low (5%-10% of total daily calories), typically 20-50 g per day | Restricted, liberalized compared to classic, can range from 20-100 g per day | Low, but slightly higher than classic, with a focus on low-glycemic carbs |
| Protein intake | Moderate (15%-20% of total daily calories), typically 1 g/kg of body weight | Moderate to liberal, like classic ketogenic diet | Moderate: Can be slightly higher than classic ketogenic diet, especially for adults |
| Fat sources | Emphasizes long-chain triglycerides, from animal and plant sources | Focuses on a variety of fat sources with a mix of long-chain triglycerides and medium-chain triglycerides, with medium-chain triglycerides oil often incorporated | Mainly medium-chain triglycerides |
| Dietary diversity | Restrictive, emphasizes specific food sources | More flexible in food choices | Limited by sources of medium-chain triglycerides |
| Implementation complexity | High, requires meticulous measurement and monitoring | Less complex but still requires tracking | Moderate complexity, easier to calculate medium-chain triglycerides |
| Adherence difficulty | Challenging due to strictness and limited food choices | Moderate, more flexible | Moderate, limited food options with medium-chain triglycerides |
| Efficacy in seizure control | Often high efficacy, especially in drug-resistant epilepsy, especially in children | Varied may be effective for some, easier to follow for some individuals, and allows for more variety in food choices | Effective for some, especially in certain epilepsies, as it can promote faster ketosis due to medium-chain triglycerides, potentially reducing side effects |
| Potential drawbacks | More restrictive, can be challenging to follow in the long term | It may not be as effective as classic ketogenic diet for some individuals | It can be more expensive due to the need for medium-chain triglycerides oil |
| Suitability | Best for children and adults who haven't responded well to medications | It is a good option for individuals who struggle with the strictness of classic ketogenic diet | It can be suitable for both children and adults, depending on individual needs and preferences |
| Indications | Drug-resistant epilepsy, certain epilepsy syndromes | Epilepsy management | Epilepsy, neurological conditions, fat malabsorption |
Ketogenic diet is not recommended for individuals with certain medical conditions. Some of these conditions are absolute contraindications, such as primary carnitine deficiency, carnitine palmitoyl-transferase I or II deficiency, carnitine translocase deficiency, pyruvate carboxylase deficiency, porphyria, and various β-oxidation defects such as short-chain acyl dehydrogenase deficiency, medium-chain acyl dehydrogenase deficiency, long-chain acyl dehydrogenase deficiency, medium-chain 3-hydroxy acyl-CoA deficiency, and long-chain 3-hydroxy acyl-CoA deficiency. There are also relative contraindications for the ketogenic diet, which require additional considerations. For example, caution must be taken when an individual has a surgical focus as identified by neuroimaging and video EEG monitoring or when they are unable to maintain adequate nutrition due to being a fastidious eater. Parent or caregiver non-compliance is another relative contraindication, as well as concurrent use of propofol, which may increase the risk of propofol infusion syndrome[308,309].
Studies have shown that the ketogenic diet has significant efficacy and can significantly reduce seizure frequency and severity in children with epilepsy, especially those who haven't responded well to medications[310]. It has been most effective in certain types of epilepsy, such as Dravet syndrome, Lennox-Gastaut syndrome, and some cases of focal epilepsy. Success often depends on strict adherence to the diet, and the duration of adherence might influence its efficacy[311]. However, the ketogenic diet is highly restrictive and can be challenging to maintain, especially long-term. Some individuals might experience side effects such as fatigue, nausea, constipation, kidney stones, changes in lipid profiles, or growth retardation in children[312]. Regular monitoring and adjustments are essential. Implementing the ketogenic diet requires a multidisciplinary approach involving healthcare providers, dietitians, and support from caregivers for successful implementation and management. The ketogenic diet is a powerful therapeutic tool, especially for drug-resistant epilepsy. It requires a long-term commitment for optimal results and should be done under strict medical and dietetic supervision[313]. It's crucial to ensure adequate intake of essential nutrients while following the ketogenic diet. Electrolyte levels and vitamin deficiencies need to be monitored and addressed regularly. Its strict requirements and potential side effects necessitate careful consideration, professional guidance, and ongoing monitoring to ensure safety and efficacy[314].
LGIT: The LGIT is a dietary approach that can be used to manage epilepsy, especially when the ketogenic diet is not suitable or preferred. LGIT aims to minimize blood sugar fluctuations by prioritizing low-glycemic foods. These foods include whole grains, legumes, certain fruits, and vegetables that release carbohydrates with a low glycemic index. They produce slower and more stable rises in blood sugar levels[315]. Although LGIT is not as high in fat as the ketogenic diet, it still includes moderate amounts of healthy fats and protein to provide sustained energy and satiety. Low-GI foods release glucose gradually into the bloodstream, which helps prevent rapid spikes and crashes in blood sugar levels, thus preventing neuronal excitability and reducing seizure risk. LGIT can also improve insulin sensitivity and potentially reduce the risk of metabolic issues associated with some AEDs. Additionally, LGIT encourages the consumption of fruits, vegetables, whole grains, and lean protein to provide essential vitamins, minerals, and fiber for overall health and brain function[316].
The LGIT is a more flexible dietary option than the ketogenic diet, as it allows for a wider range of food choices within the low glycemic index spectrum. The focus on low glycemic index foods can help maintain stable blood sugar levels, potentially stabilizing mood and energy levels, which may positively impact seizure control[317]. LGIT may be a more manageable dietary option for some individuals while still providing the benefits of reducing seizure frequency or severity. Studies have shown that LGIT can effectively treat focal and generalized epilepsies, with a reduction in seizure frequency occurring between 3 and 14 months, and seizure control continuing for at least one year after the end of treatment[318]. Additionally, a 2015 study in children with epilepsy found that LGIT reduced seizure frequency by an average of 50% compared to a standard diet[319]. While not as effective as the ketogenic diet in some cases, LGIT can be a valuable option for individuals who prefer a less restrictive diet or who cannot tolerate the ketogenic diet.
The response to LGIT can differ from person to person. While some may experience an improvement in seizure control, others may not have the same level of success. LGIT allows for more dietary flexibility compared to the ketogenic diet, but still requires careful attention to carbohydrate choices and their impact on blood sugar levels. As with other dietary interventions for epilepsy, LGIT should only be initiated under the guidance of a healthcare professional or a dietitian experienced in epilepsy management. However, as with any treatment approach, the effectiveness and suitability of LGIT may vary from person to person, and medical supervision is essential for both safety and efficacy[320]. It is important to note that LGIT is not a one-size-fits-all approach, and a registered dietitian can help create a personalized plan based on individual needs and preferences.
The low FODMAP diet: FODMAPs are types of short-chain carbohydrates that are poorly absorbed in the small intestine and can ferment in the colon, leading to gas production and other symptoms in sensitive individuals[321]. Studies suggest that gut health might impact neurological conditions, including epilepsy. Ongoing research explores the potential connection between the gut microbiome and brain function, including its relevance to seizure disorders. Alterations in the gut microbiota could potentially influence neurological conditions[322]. Low FODMAP diet (LFD) is primarily used to manage irritable bowel syndrome (IBS) symptoms by reducing intake of certain fermentable carbohydrates. While there isn't substantial evidence supporting the direct use of the LFD for epilepsy management, some limited research suggests a potential link between gut health and epilepsy[323]. The connection between LFD and epilepsy lies in the gut-brain axis, which is a complex communication network between the digestive system and the brain. Some researchers believe that gut inflammation or imbalances in gut microbiota, potentially triggered by FODMAPs, might contribute to epilepsy development or severity[324].
Currently, there is limited evidence supporting the use of the LFD specifically for managing epilepsy. While there may be a connection between gut health and neurological conditions, including epilepsy, more research is needed to establish a clear link. However, for individuals with epilepsy who also have co-existing conditions such as IBS or gastrointestinal symptoms, managing gut-related issues through the LFD might indirectly contribute to their overall well-being, which could potentially affect seizure control[325]. It is important to note that before considering any dietary changes, especially restrictive diets such as the LFD, it is crucial to consult with healthcare professionals, including dietitians and neuro
Avoiding potential triggers: Identifying and managing potential nutritional triggers for epilepsy requires a personalized approach based on individual sensitivity and responses. Avoiding potential triggers involves identifying and managing factors that might worsen seizures or affect antiepileptic medications[327]. Some people may be sensitive to certain food additives such as MSG, artificial sweeteners like aspartame, or preservatives. These additives can trigger seizures in susceptible individuals[328]. Although not directly linked to epilepsy in everyone, some people with gluten sensitivity or celiac disease may experience neurological symptoms, including seizures. Maintaining a gluten-free diet may be beneficial for those who are sensitive. Occasionally, allergies or sensitivities to specific foods can trigger seizures in susceptible individuals. Some common allergens include dairy, eggs, soy, and nuts[329]. Excessive consumption of caffeine or alcohol might lower the seizure threshold in some individuals. Therefore, moderation or avoidance may be recommended, especially for those who are sensitive to these substances. Poor nutrition or extreme diets lacking in essential nutrients may impact overall health and potentially trigger seizures. As a result, maintaining a well-balanced diet is crucial[330].
It can be helpful to record the foods you eat alongside any seizures you experience. This may help identify patterns or potential triggers and guide dietary adjustments. It's important to discuss any dietary concerns or potential triggers with healthcare professionals, such as neurologists and dietitians, who can provide personalized guidance[331]. If you have epilepsy, it's best to make significant dietary changes gradually so you can monitor any effects on seizure frequency or severity. Also, certain foods or supplements may interact with antiepileptic medications, so it's crucial to discuss any dietary changes or supplements with your healthcare provider to avoid any adverse interactions. Eating a diet rich in fruits, vegetables, whole grains, lean proteins, and healthy fats can contribute to overall health and potentially aid in seizure management[242]. The patient/care giver should carefully track the food intake and its relation to the seizure activity for a period to identify any patterns or correlations. This can help pinpoint specific foods or food groups that might be triggering seizures for the patient. Under medical supervision, the patient can implement elimination and challenge diets to test specific food groups or ingredients as potential triggers. This should be done in a controlled manner to avoid nutritional deficiencies and ensure safety.
Functional nutrients are substances found in foods or supplements that provide health benefits beyond basic nutrition. These functional nutrients show promise in potentially aiding seizure control or supporting brain health in individuals with epilepsy. While not a standard treatment for epilepsy, functional nutrients have emerged as promising alternatives or adjuncts to traditional AEDs in managing the condition[9]. These nutrients, thought to go beyond basic nutritional needs and exert specific biological effects, may offer benefits. Certain nutrients, alone or combined with AEDs, have shown potential in reducing seizure activity. Other functional nutrients may support brain health, enhance cognitive function, and protect neurons from damage, especially during seizure activity. Some nutrients can also help alleviate the side effects of certain AEDs, improving overall well-being and quality of life[242].
Omega-3 fatty acids, particularly EPA and DHA, are essential for brain health and function. They have anti-inflammatory properties and might help stabilize neuronal membranes. DHA can be a structural component of neuronal membranes, modulating membrane biophysical properties, ion channel functions, and neurotransmitter signaling[298]. There has been a lot of interest in the potential therapeutic benefits of omega-3 fatty acids for epilepsy, which emerged with the observation that they can reduce cardiac arrhythmia and, consequently, can reduce neuronal excitability[332]. The first clinical study of the therapeutic potential of fish oil in epilepsy patients found that it had an anticonvulsive effect associated with omega-3 fatty acids[333]. However, subsequent clinical studies have produced more controversial results. While some randomized clinical trials have found that consuming approximately 0.6-2 g of fish oil reduces seizure frequency and duration[334], other small-scale, non-randomized studies have reported no regulatory efficacy for seizures[335]. Despite several animal studies suggesting that omega-3 fatty acids suppress seizures, it remains unclear whether they have significant benefits for controlling seizures. Nevertheless, considering the goal of identifying nutritional supplements that assist drug therapy, and given that fish oil is safe at dosages of less than 4 g per day, it can be recommended for regulating seizure generation[336].
Vitamin B6, also known as pyridoxine, has been researched as a potential therapy to treat certain types of epilepsy. It is beneficial in cases of PDE or in conditions that are responsive to pyridoxine supplementation. Vitamin B6 plays a crucial role in synthesizing neurotransmitters, including GABA, which is an inhibitory neurotransmitter that helps regulate neuronal excitability. Vitamin B6 is involved in various metabolic pathways within the nervous system and contributes to overall brain health and function[337]. Individuals with specific metabolic disorders, such as PDE, have shown a positive response to vitamin B6 supplementation. In these cases, the body cannot properly metabolize or utilize vitamin B6, leading to seizures that are responsive to pyridoxine treatment. Although the efficacy of vitamin B6 in treating other forms of epilepsy remains less clear, it may be beneficial in certain cases or when used in combination with other antiepileptic medications. However, more research is needed to establish its widespread effectiveness[56].
It is important to note that responses to vitamin B6 supplementation can vary widely among individuals with epilepsy. Some may experience reduced seizure frequency or severity, while others may not see significant benefits. Vitamin B6 deficiency can negatively impact cognitive function, and supplementation has been associated with improvements in memory, learning, and attention in individuals with epilepsy[338]. Vitamin B6 is also an antioxidant and might protect neurons from damage, potentially contributing to overall brain health and seizure control. Some AEDs can deplete Vitamin B6 Levels, and supplementation can help alleviate associated side effects such as fatigue, irritability, and depression[243]. However, its widespread effectiveness in managing various forms of epilepsy remains an area of ongoing research, and its use as an adjunctive therapy should be guided by healthcare professionals based on individual circumstances.
Vitamin B12, also known as cobalamin, plays a crucial role in various bodily functions, including supporting the health of the nervous system and the synthesis of neurotransmitters[43]. Although research on the specific effects of vitamin B12 on epilepsy is limited, its potential role in maintaining overall nervous system function might have implications for the management of epilepsy. Vitamin B12 is vital for the maintenance of the nervous system. It supports the formation of myelin, which is the protective sheath around nerves, and helps produce neurotransmitters. Vitamin B12, in conjunction with other B vitamins, helps regulate homocysteine levels. High levels of homocysteine have been linked to increased risk of neurological disorders[339]. Vitamin B12's role in supporting nervous system health suggests that it might indirectly influence seizure activity by having neuroprotective effects. Elevated homocysteine levels have been associated with increased susceptibility to seizures[339]. Supplementation with vitamin B12 and other B vitamins might help regulate homocysteine levels and possibly reduce seizure frequency in individuals with high levels[340]. However, direct evidence linking vitamin B12 supplementation to epilepsy management is limited. Studies specifically investigating its efficacy as a treatment for epilepsy are scarce. Fakhroo et al[341] showed that high-dose vitamin B12 pretreatment alleviated the seizure occurrence among pentylenetetrazole-kindled rat models, which suggests that vitamin B12 is a potential strategy to treat epilepsy and other related epileptogenesis activities[341]. It is important to note that responses to vitamin B12 supplementation can vary among individuals. While some may experience improvements in neurological function, including seizure control, others may not see significant benefits. Vitamin B12 is a potential functional nutrient for epilepsy, especially for people who have deficiencies or experience cognitive difficulties or side effects of AEDs. However, due to the limited evidence, its use should be carefully considered and monitored under the guidance of a healthcare professional. Further research is necessary to provide more insights into the possible benefits and risks of using Vitamin B12 for epilepsy management[342].
Vitamin D is a crucial nutrient for maintaining overall health. However, its precise impact on managing epilepsy is still being studied. Lately, it has gained significant attention as a potential functional nutrient for epilepsy management. Its potential implications in epilepsy are of particular interest due to its influence on brain health and immune modulation, although it might indirectly affect neurological health and inflammation regulation. The presence of vitamin D receptors in the brain suggests a role in neuronal health and function. It is involved in neuroprotection, neurogenesis, neuronal differentiation, axonal growth, and the regulation of neurotransmitters[343]. It plays a role in modulating the immune system, reducing inflammation, and supporting overall immune function. Vitamin D's role in supporting neuronal health and protecting against neurodegeneration suggests potential neuroprotective effects[344]. It might indirectly impact seizure susceptibility. Inflammation has been implicated in some types of epilepsy. Vitamin D's anti-inflammatory properties might help regulate immune responses that could affect seizure activity[93]. Research specifically focusing on vitamin D as a treatment for epilepsy is limited. While some observational studies suggest an association between low vitamin D levels and increased seizure frequency[84], direct causation remains unclear. Low levels of vitamin D have been observed in some individuals with epilepsy. Holló et al[97] found that correcting vitamin D deficiency helped improve seizure control. Therefore, supplementation might be considered for those with deficiencies, but its direct impact on seizure control requires further investigation.
Vitamin E, a fat-soluble antioxidant, is known for its role in protecting cells from oxidative damage. Its potential implications in epilepsy have been explored due to its antioxidant properties and influence on neurological health[345]. Vitamin E is an antioxidant, scavenging free radicals and reducing cell oxidative stress. This function helps protect cell membranes from damage. Its antioxidant properties suggest potential neuroprotective effects, which might affect brain health and neuronal function[346]. Oxidative stress and neuronal damage are implicated in certain types of epilepsy. Vitamin E's antioxidant properties might contribute to protecting neurons from damage, potentially influencing seizure activity. Vitamin E's anti-inflammatory properties might help modulate inflammatory responses in the brain, which could affect seizure susceptibility[347]. Studies specifically investigating vitamin E as a treatment for epilepsy are limited. While some research suggests a potential role in neuroprotection, its direct impact on seizure control remains unclear. Ogunmekan et al[348] showed that daily supplementation with 400 IU of vitamin E for three months reduces seizure frequency by 50% in patients with epilepsy[348]. On the other hand, Raju et al[349] showed no significant change in seizure frequency after adding vitamin E to AEDs in patients with uncontrolled epilepsy. Responses to vitamin E supplementation can vary among individuals. Some might experience benefits in overall health, including potential neuronal protection, while others might not see significant effects. Vitamin E supplementation might be considered for individuals with epilepsy, especially if there are indications of increased oxidative stress or a deficiency[105]. However, its specific impact on seizures requires more research. On the other hand, high doses of Vitamin E can increase the risk of bleeding and potentially interact with certain medications[350].
Vitamin C, or ascorbic acid, is an antioxidant that dissolves in water and has various bodily roles. These roles include enhancing immune function, collagen synthesis, and antioxidant activity[340]. Concerning epilepsy, its antioxidant properties and influence on overall health are particularly relevant[345]. Vitamin C is an antioxidant by scavenging free radicals and reducing cell oxidative stress. This helps to protect cells from damage caused by ROS[351]. Vitamin C is essential for producing collagen, which is vital for connective tissues, wound healing, and maintaining the integrity of blood vessels[352]. Furthermore, vitamin C is a coenzyme for the enzymatic conversion of dopamine to norepinephrine, which helps regulate neurotransmission[353]. Oxidative stress is implicated in certain types of epilepsy, and vitamin C's antioxidant properties might contribute to protecting neurons from oxidative damage, potentially impacting seizure activity[27]. Although not directly studied in epilepsy, vitamin C's neuroprotective potential might affect overall brain health and neuronal function. While there are limited studies on vitamin C as a treatment for epilepsy, some suggest that Vitamin C supplementation may decrease seizure frequency and severity in individuals with epilepsy, particularly those with low levels[21]. The neuroprotective effect and the anti-inflammatory properties of vitamin C might contribute to improved seizure control and overall brain health. Additionally, vitamin C can enhance the permeability of the BBB, allowing for better transport of essential nutrients and medications into the brain[354]. This could potentially enhance the effectiveness of AED. Although its antioxidant properties are recognized, the direct impact of vitamin C on seizure control remains unclear and requires further investigation. Vitamin C is essential for overall health, immune function, and collagen synthesis. Ensuring adequate levels might indirectly support the body's ability to manage various health conditions, including epilepsy[81]. While vitamin C supplementation is generally safe, its specific impact on seizures needs further research. It might be considered as part of a well-balanced diet to support overall health, including potential neuroprotective effects.
L-carnitine is a compound derived from an amino acid that helps in energy metabolism by transporting fatty acids into mitochondria to produce energy[355]. It has been studied for its potential role in managing epilepsy due to its neuroprotective properties and role in energy metabolism. L-carnitine is essential in facilitating the transport of fatty acids to mitochondria, where they are metabolized to produce energy. It is essential in tissues that rely on fatty acids for energy production[356]. L-carnitine has antioxidant properties, which makes it useful in protecting against neuronal damage and reducing oxidative stress. Some types of epilepsy are linked to abnormalities in brain energy metabolism. L-carnitine's role in fatty acid transport and energy production might affect brain energy metabolism and neuronal function. Its antioxidant properties suggest potential neuroprotective effects that might indirectly influence seizure activity by protecting neurons from damage[357].
L-carnitine requirements vary based on dietary intake, absorption, and underlying medical conditions. Research on L-carnitine as a treatment for epilepsy is limited, preliminary, and mainly focused on specific groups, such as children with mitochondrial disorders[179]. It is necessary to conduct more extensive research to confirm its benefits and identify individual responses. Some studies suggest that L-carnitine supplementation can help decrease seizure frequency and severity, particularly in individuals with deficiencies. L-carnitine deficiency can negatively impact cognitive function. Hussein et al[356] showed that four weeks of L-carnitine supplementation (100 mg/kg/day) was associated with significantly reduced seizure score, observed as early as the second day of treatment and continued during the treatment phase. Supplementation has been found to improve memory, learning, and attention in individuals with epilepsy. Additionally, certain anti-epileptic drugs can deplete L-carnitine levels, leading to side effects like fatigue, muscle weakness, and depression. Supplementation might help alleviate such side effects. Carnitine supplementation maintains constant FC serum levels in patients treated with AEDs such as VPA. Carnitine supplementation may revert the latent pancreatic injury induced by VPA as indicated by decreasing serum amylase levels[184]. L-carnitine supplementation might be considered for individuals with epilepsy, particularly in cases where there are indications of deficiencies or metabolic abnormalities related to fatty acid metabolism[187]. It is important to note that L-carnitine should not replace conventional anti-epileptic drugs but can be used as a complementary therapy to optimize seizure control and overall health[358].
Pyruvate is a crucial component in the body's energy production, showing promise as a functional nutrient in treating epilepsy. This adaptable molecule has potential in multiple facets of seizure management, making it an exciting area of research[359]. Its role in glucose metabolism is essential to its efficacy, as it is an intermediary in the breakdown of glucose for energy. It typically enters the Krebs cycle, a cellular powerhouse producing ATP, essential fuel for bodily functions, including brain activity[360]. Pyruvate also acts as an antioxidant, protecting brain cells from damage caused by harmful free radicals like hydrogen peroxide, potentially reducing seizure risks[361]. Inflammation can be significant in epilepsy, but ethyl pyruvate, a derivative, has impressive anti-inflammatory capabilities, hinting at its potential to control seizures[362]. Encouraging animal studies have shown that oral pyruvate administration significantly decreases seizure frequency, indicating therapeutic promise. Popova et al[363] showed that chronic oral pyruvate intake succeeded in completely abolishing seizures in three different established epileptic phenotypes of acquired epilepsy models in rodents]. Combining pyruvate with antioxidants such as vitamins C and E could augment its anti-seizure effects[364]. While clinical trials are necessary to gauge its therapeutic efficacy and viability as a treatment for acquired epilepsies in humans, pyruvate's multifaceted characteristics position it as a captivating contender for epilepsy management. Its ability to address various seizure-related factors, from energy production to inflammation control, presents a unique and potentially impactful approach to enhancing the lives of individuals living with epilepsy[365].
Coenzyme Q10 (CoQ10) is a compound naturally produced by the body and serves as an antioxidant, aiding in cell energy production. Although research on CoQ10 specifically targeting epilepsy is limited, its role in cellular energy metabolism and antioxidant properties suggest potential implications for managing seizures[366]. CoQ10 plays a crucial role in the mitochondria, where it helps generate ATP, the body's primary energy source. CoQ10 acts as an antioxidant, scavenging free radicals and reducing oxidative stress that can damage cells[367]. Some types of epilepsy involve mitochondrial dysfunction and impaired energy metabolism. CoQ10's role in mitochondrial function might have implications for supporting cellular energy production in the brain. CoQ10's antioxidant properties suggest potential neuroprotective effects, which might indirectly influence seizure activity by protecting neurons from oxidative damage[368]. Research specifically focusing on CoQ10 as a treatment for epilepsy is limited. Tawfik et al[369] showed that CoQ10 can potentially reduce seizure severity and oxidative stress induced by pilocarpine in rats. CoQ10 is a safe and effective adjuvant to phenytoin therapy in epilepsy, enhancing its antiepileptic effects and protecting against seizure-induced cognitive impairment and oxidative damage caused by chronic phenytoin use[369]. While its role in mitochondrial function and antioxidative properties is recognized, its direct impact on seizure control remains unclear and needs further investigation. Responses to CoQ10 supplementation can vary among individuals. Some might experience improvements in overall health, including potential neurological benefits, while others might not see significant effects. CoQ10 supplementation might be considered for individuals with epilepsy, especially in cases where there are indications of mito
Curcumin (diferuloylmethane) is a turmeric compound known for its potential health benefits, including anti-inflammatory and antioxidant properties. While research on curcumin's effects on epilepsy is still in its early stages, it has been shown to have neuroprotective effects that could help manage seizures[371]. Curcumin's anti-inflammatory properties can reduce inflammation-related molecular pathways that contribute to certain types of epilepsy[372]. Additionally, its antioxidant properties can help protect neurons from oxidative damage, which may indirectly affect seizure susceptibility. However, further research is needed to understand curcumin's direct impact on seizure control[373]. Studies suggest that curcumin may alleviate epileptic seizures by modulating oxidative stress, neuroinflammation, and neurotransmission while also inhibiting apoptotic cell death and necrotic and autophagic pathways in hippocampal neurons[374-376]. Furthermore, curcumin has been found to have a protective effect on relieving memory impairment by affecting brain monoamine levels[377].
Numerous animal studies have shown that Curcumin can be an effective adjuvant therapy for epilepsy. For instance, in a study by Mehla et al[378], it was found that pretreatment with curcumin improved seizures, oxidative stress, and cognitive impairment in rats with pentylenetetrazol-induced kindling[378]. Similarly, Agarwal et al[379] found that liposome-entrapped curcumin (in doses of 25 and 50 mg/kg) resulted in a significant increase in seizure threshold current and latency to myoclonic and generalized seizures in increasing current electroshock seizures test and pentylenetetrazol-induced seizures, respectively[379]. Another study by Jiang demonstrated the protective effect of curcumin against cognitive impairment and its ability to modify epileptogenesis in a post-status epilepticus temporal lobe epilepsy model[380]. However, clinical trials on humans with epilepsy are still needed to confirm the efficacy of curcumin.
The effectiveness of curcumin as a therapeutic agent is limited by its poor bioavailability in the human body. Researchers are currently exploring various formulations and strategies to improve its absorption and efficacy[381]. However, curcumin supplementation may be considered as a potential therapeutic option for individuals suffering from epilepsy, especially in cases where inflammation or oxidative stress may be contributing factors[382]. Although curcumin has anti-inflammatory and antioxidant properties, further investigation is needed to establish its specific impact on managing epilepsy. Curcumin's ability to modulate inflammation and protect neurons may offer new avenues for supporting seizure control, but more research, particularly clinical trials, is required to determine its efficacy and safety as a treatment for epilepsy[383]. Therefore, it is essential to approach curcumin supplementation for epilepsy under professional guidance and with utmost caution.
Magnesium is an important mineral found inside our body's cells. It acts as a helper in over 300 chemical reactions in our body and plays a crucial role in various bodily functions, including nerve function and muscle control. Magnesium has emerged as a potential therapy for managing epilepsy. This is because it helps regulate neurotransmitters, and its ability to modulate neuronal excitability has led researchers to explore its potential benefits in managing epilepsy[384]. Magnesium acts as a neuroprotective agent, which potentially protects against the damage caused by excessive neuronal firing during seizures. It also helps regulate NMDA receptors, which control neurotransmitters' activity in the brain. By modulating these receptors, magnesium might help prevent excessive neuronal excitability[113].
Magnesium deficiency is associated with increased neuronal excitability, which is a known precursor to seizure activity. Its supplementation has been shown to stabilize neuronal membranes, potentially reducing seizure frequency and severity in individuals with suboptimal magnesium levels[121]. Like some conventional AEDs, magnesium is a natural NMDA receptor antagonist and non-selective calcium channel blocker. This modulatory effect can directly suppress excessive neuronal firing, a hallmark of epileptic seizures[374]. Magnesium also is a cofactor for GABA synthesis, accounting for its anti-seizure activity[123].
Moreover, magnesium possesses potent antioxidant properties, scavenging free radicals and protecting neurons from excitotoxic damage[385,386]. This neuroprotective effect can mitigate seizure-induced neuronal injury and contribute to long-term brain health in individuals with epilepsy. Magnesium is also crucial in maintaining mitochondrial integrity and promoting efficient energy production within brain cells[387]. By supporting mitochondrial function, magnesium can prevent energy imbalances contributing to seizure initiation and propagation. As epilepsy is often accompanied by mood and cognitive impairments, magnesium's neuroprotective and anti-inflammatory properties may exert beneficial effects on mood regulation[388], memory, and concentration[389], potentially improving overall well-being in individuals with epilepsy.
Research suggests that taking magnesium supplements may help reduce the frequency and severity of seizures in individuals with epilepsy. Many animal studies have shown that magnesium supplements can effectively reduce seizure frequency and severity. Safar et al[390] found that magnesium supplements can enhance the effectiveness of AED, such as VPA, by improving redox balance and modulating certain brain amino acids. Clinical trials have also shown promising results, with magnesium supplements leading to moderate to significant anticonvulsant effects in patients with different types of epilepsy. Abdelmalik et al[124] reported significant improvements in seizure control and frequency in patients with drug-resistant seizures who took oral magnesium oxide (420 mg twice a day), with some becoming seizure-free[112]. While Yadav et al[391] did not find a significant difference in seizure control or neurodevelopmental outcomes, they did find that EEG readings improved in children with West syndrome who received magnesium sulphate[391]. Additionally, intravenous infusion of magnesium sulphate remains the drug of choice to prevent and control convulsions caused by eclampsia, significantly reducing maternal mortality related to eclampsia[392].
While magnesium is not typically used as a standalone treatment for epilepsy, it may serve as an adjunctive therapy alongside standard antiepileptic medications. Combining magnesium supplementation with existing treatments might enhance their efficacy or reduce specific side effects[393]. Maintaining a balanced diet that includes magnesium-rich foods such as almonds, nuts (e.g., cashews), oatmeal, seeds (pumpkin, sunflowers, sesame), black beans, brown rice, flaxseed, leafy green vegetables (spinach), broccoli, bananas, soybeans, sweet corn, whole grains, and certain types of fish is essential[394]. However, if magnesium supplementation is recommended, it should be done under medical supervision to ensure safety and appropriate dosage. Further research is warranted to optimize magnesium dosing strategies and elucidate its precise mechanisms of action in epileptic seizures. Additionally, long-term studies are needed to assess the potential benefits of magnesium supplementation for mood, cognitive function, and overall quality of life in individuals with epilepsy.
Medium-chain fatty acids (MCFAs) have garnered attention for their potential in reducing epilepsy through various mechanisms. MCFAs are metabolized differently than long-chain fatty acids, rapidly converting to ketone bodies in the liver, such as beta-hydroxybutyrate and acetoacetate, which can serve as alternative fuel sources for the brain during metabolic stress[395]. Additionally, MCFAs may enhance GABA production, the brain's primary inhibitory neurotransmitter, thereby reducing neuronal excitability. Their anti-inflammatory properties may mitigate neuroinflammation, while improvements in mitochondrial function and modulation of ion channels contribute to stabilizing neuronal membranes and reducing hyperexcitability[396]. Collectively, these mechanisms suggest that MCFAs hold promise as adjunctive therapy for epilepsy management, although further research is warranted to fully elucidate their efficacy and underlying mechanisms.
Incorporating foods rich in MCFAs into one's diet involves sourcing from various natural sources. Coconut oil emerges as a prominent option due to its high content of MCFAs, notably lauric acid, suitable for culinary applications such as cooking, baking, or inclusion in beverages and dressings. Likewise, coconut-derived products like coconut milk, cream, and shredded coconut provide convenient alternatives, lending themselves well to diverse recipes[397]. Palm kernel oil, sharing similarities with coconut oil, also serves as a source of MCFAs for cooking or baking purposes[398]. Dairy products, including butter, cheese, and full-fat yogurt, albeit containing modest amounts of MCFAs, offer additional dietary options, particularly when sourced from grass-fed animals[399]. Alternatively, individuals seeking concentrated MCFAs can explore mediums like MCT oil or MCT powder, derived from coconut or palm kernel oil, easily incorporated into beverages or recipes[400]. Maintaining dietary balance is paramount, ensuring MCFAs complement a spectrum of nutrient-rich foods for holistic health benefits. As with any dietary modifications, seeking guidance from healthcare professionals is advisable, especially concerning specific dietary needs or medical conditions.
Ensuring adequate intake of essential macronutrients (carbohydrates, proteins, fats) and micronutrients (vitamins, minerals) is paramount for optimal brain health and energy metabolism, both crucial for seizure control. Balanced nutritional planning, potentially with the support of a registered dietitian, is recommended. Controlled fasting or intermittent fasting regimens have shown promise in reducing seizure frequency, possibly due to the metabolic shift towards ketone utilization during fasting periods[401]. However, patients with epilepsy should avoid blood sugar fluctuations. Patients with epilepsy may prioritize low-glycemic index foods and limit refined carbohydrates and sugary drinks[402]. Adequate hydration is vital for various physiological processes, including brain function. Dehydration can exacerbate seizure activity, making consistent water intake essential for individuals with epilepsy[147]. Dietary needs and responses vary depending on age, seizure type, underlying medical conditions, and individual preferences. A personalized approach tailored to each patient's needs and implemented under the guidance of a healthcare professional is crucial for ensuring safety and maximizing potential benefits. Dietary modifications may impact antiepileptic medications' efficacy or side effects, requiring close monitoring and potential adjustments[223]. In addition, some AEDs can deplete electrolytes like sodium, potassium, magnesium, and calcium. Ensuring adequate intake of these electrolytes through your diet is important[403]. It's crucial to implement any dietary changes under the guidance of healthcare providers, particularly a registered dietitian or a healthcare team specialized in epilepsy management. Monitoring nutritional intake, regular check-ups, and tailored dietary plans are essential to ensure that nutritional needs are met while managing epilepsy effectively. Additionally, these dietary changes might interact with medications, so medical supervision is crucial for safety and efficacy[13]. Maintaining a healthy lifestyle with regular exercise and adequate sleep is essential to complement the nutritional and medication management plan[404].
Implementing nutritional interventions in epilepsy management presents several significant challenges that must be carefully navigated to ensure efficacy and patient safety.
Patient compliance and individual variability: One of the foremost challenges is ensuring patient compliance with prescribed dietary regimens, particularly when these diets require significant lifestyle changes, such as the ketogenic diet. Strict adherence is critical for effectiveness, yet many patients may find it challenging to maintain such diets over the long term due to the restrictive nature of the interventions[405]. Additionally, epilepsy is a highly heterogeneous condition, with substantial variability in seizure types, underlying causes, and patient responses to treatments. This variability extends to nutritional needs, where what is effective for one individual may not be suitable for another. Developing personalized nutrition plans tailored to each patient’s unique metabolic profile, genetic predispositions, and personal circumstances is ideal but challenging, often requiring advanced diagnostic tools and ongoing adjustments, which can be resource-intensive[406].
Resource allocation and healthcare system support: Implementing and sustaining nutritional interventions also demands considerable resources, including access to specialized dietitians, frequent monitoring, and comprehensive patient education. In many clinical settings, particularly those with limited resources, the availability of such specialized care may be constrained. Furthermore, the healthcare system’s infrastructure must support the integration of nutrition into epilepsy care, which may require additional training for healthcare providers, interprofessional collaboration, and the development of clear protocols to manage these interventions effectively[407].
Monitoring and adjusting dietary plans: Ongoing monitoring is essential to ensure that nutritional interventions are both effective and safe, requiring regular assessments of patients' dietary adherence, metabolic status, and seizure control. This dynamic process necessitates close collaboration between patients and healthcare providers, with potential challenges arising from the need for frequent laboratory tests, dietary assessments, and the adjustment of dietary plans based on clinical outcomes[408]. The burden of continuous monitoring and adjustment can be significant, both for patients, who must remain engaged and compliant, and for healthcare providers, who must allocate time and resources to these activities[409].
Psychosocial and cultural considerations: Nutritional interventions can profoundly impact a patient's social and cultural life. Strict dietary regimens may limit participation in social activities or conflict with cultural dietary practices, leading to social isolation or emotional distress. The psychological burden of adhering to such diets, especially in the context of a chronic condition like epilepsy, can also lead to mental health challenges, including anxiety, depression, or disordered eating behaviors. Addressing these psychosocial factors requires a holistic approach that includes psychological support and consideration of the patient’s cultural background[410,411].
Interaction with AED: Nutritional interventions can interact with AED, potentially affecting drug efficacy or increasing the risk of side effects. For example, certain diets may alter the metabolism or absorption of these drugs, leading to subtherapeutic levels or toxicity. Managing these interactions requires careful coordination among dietitians, pharmacists, and neurologists to avoid compromising the effectiveness of antiepileptic therapy, particularly in patients on multiple medications[412].
Educational and training needs: Finally, the successful implementation of nutritional interventions in epilepsy care necessitates adequate training and education for healthcare providers. The evolving nature of research in this field requires that clinicians remain informed about the latest evidence and best practices. In many settings, a lack of specialized training may hinder the ability to deliver effective nutritional care, underscoring the need for ongoing professional development and education[413].
Our review reveals that nutrient deficiencies—such as those in vitamins B6, folate, and D—disrupt neurotransmitter synthesis, compromise myelin integrity, and contribute significantly to oxidative stress and neuroinflammation. These processes lower the seizure threshold, thereby increasing susceptibility to epileptogenesis[414]. Moreover, emerging evidence indicates that malnutrition-induced alterations in the gut microbiota may compromise the gut-brain axis, further exacerbating neuroinflammatory responses and influencing neuronal excitability[415]. Together, these interrelated pathways underscore a multifaceted, bidirectional link in which malnutrition may both predispose individuals to epilepsy and result from the metabolic and pharmacological challenges associated with its management.
Building on these mechanistic insights, recent therapeutic approaches have begun to explore nutritional interventions as adjuncts to conventional antiepileptic treatments. Dietary strategies—such as the ketogenic diet, modified Atkins diet, and low glycemic index diet—have shown promise in reducing seizure frequency, potentially by enhancing mitochondrial function, mitigating oxidative stress, and modulating inflammatory pathways[297]. Additionally, targeted micronutrient supplementation (e.g., vitamin D, magnesium, omega-3 fatty acids) may help restore neuronal stability by correcting specific deficiencies contributing to dysregulated neurotransmission[416].
Despite these promising avenues, significant gaps remain in our understanding of how nutritional factors modulate epileptogenesis. Future research should prioritize:
Mechanistic studies: Investigating how specific nutrient deficiencies affect neuronal excitability and elucidating the precise role of gut microbiota alterations in mediating neuroinflammatory processes.
Clinical trials: Conducting long-term, well-controlled studies to evaluate personalized nutritional interventions that combine micronutrient repletion with strategies to modulate the gut microbiota, thereby determining their efficacy in reducing seizure frequency and severity.
Biomarker development: Identifying nutritional and microbial biomarkers that predict seizure susceptibility and therapeutic response would facilitate the development of targeted, individualized treatment protocols.
Based on the multifaceted interplay between nutrition and epilepsy highlighted in this review, several recommendations emerge. Healthcare providers should prioritize comprehensive nutritional assessments for individuals with epilepsy, acknowledging the bidirectional impact between the condition and nutritional status. Tailored dietary plans, guided by registered dietitians or nutrition specialists, should be integrated into the holistic management of epilepsy, keeping in mind the unique characteristics and needs of each individual with epilepsy. Furthermore, research efforts should focus on elucidating specific nutritional deficiencies or imbalances that exacerbate seizure susceptibility, thereby fostering targeted interventions. Clinical trials evaluating the efficacy of dietary modifications, supplements, or personalized nutrition plans in seizure control are imperative. Additionally, public health initiatives advocating for awareness about the role of nutrition in epilepsy care and fostering access to nutritional support services are essential for optimizing patient outcomes and enhancing overall well-being.
Despite the comprehensive analysis presented in this review, several limitations warrant acknowledgment. A key challenge is the heterogeneity in study designs, participant characteristics, diagnostic criteria, intervention protocols, and follow-up durations across the included studies. This variability makes direct comparisons difficult and contributes to inconsistencies in reported outcomes. Differences in epilepsy classification, seizure severity, dietary interventions, and assessment tools further complicate the synthesis of findings, impacting the generalizability of results. Additionally, most of the included studies are observational or based on animal models, with a relative scarcity of RCTs and long-term prospective studies. Observational studies are inherently susceptible to confounding factors, making it difficult to establish causality between nutritional factors and epilepsy. While animal models provide mechanistic insights, their applicability to human physiology remains limited. These methodological constraints restrict the strength of the evidence and underscore the need for well-designed RCTs to validate the role of nutritional interventions in epilepsy management. Furthermore, the complex interplay between nutrition and epilepsy—involving neurotransmitter regulation, neuronal plasticity, oxidative stress, and gut microbiota interactions—remains incompletely elucidated. Many mechanisms remain speculative, requiring further mechanistic and clinical research. The review also acknowledges potential limitations in literature retrieval, as database coverage, language restrictions, and publication bias may have led to the omission of relevant studies. The tendency for studies with positive findings to be published more frequently than those with negative or inconclusive results may further influence the comprehensiveness and objectivity of the conclusions. Finally, individual variability in response to dietary interventions and supplements complicates the generalization of recommendations. Factors such as genetic predisposition, comorbidities, medication interactions, and dietary adherence contribute to differences in treatment outcomes. Given these limitations, future research should prioritize methodological consistency, longer follow-up durations, and diverse population cohorts to enhance the reliability and clinical applicability of findings in the field of epilepsy and nutrition.
This comprehensive review illuminates the intricate nexus between malnutrition and epilepsy, showcasing their bidirectional influence on each other. The exploration of malnutrition as a potential risk factor for epilepsy underscores the significance of adequate nutrition in reducing neurological vulnerabilities. Similarly, the analysis of how epilepsy impacts nutritional status emphasizes the complexities of altered dietary patterns and metabolic perturbations in individuals with epilepsy. Moreover, the insights gleaned from exploring nutritional management strategies unveil promising avenues for mitigating seizure susceptibility and enhancing overall brain health. This review underscores the imperative of a holistic approach, integrating nutrition into epilepsy management strategies, offering a roadmap for future research endeavors and personalized therapeutic interventions in epilepsy care.
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