Emad Alem

Mr. Emad Alem


Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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5 October 2024 in The Journal of Nutrition
Verified
Journal Article
Closed access
HAHamid Abbasi
Hamid Abbasi
SKSara Khoshdooz
Sara Khoshdooz
EAEmad Alem
Emad Alem
FBFarnush Bakhshimoghaddam
Farnush Bakhshimoghaddam
SDSaeid Doaei
Saeid Doaei
MGMark O. Goodarzi
Mark O. Goodarzi

23 August 2024 in Clinical Nutrition ESPEN
Verified
Journal Article
Closed access
HAHamid Abbasi
Hamid Abbasi
EAEmad Alem
Emad Alem
FBFarnush Bakhshimoghaddam
Farnush Bakhshimoghaddam
SKSara Khoshdooz
Sara Khoshdooz
SDSaeid Doaei
Saeid Doaei

1 June 2026 in Precision Nutrition
Verified
Journal Article
Open access
HAHamid Abbasi
Hamid Abbasi
EAEmad Alem
Emad Alem
MAMohammadMehdi Abbasi
MohammadMehdi Abbasi
GEGhazaleh Eslamian
Ghazaleh Eslamian
Background: Epilepsy is one of the most prevalent neurological disorders and is increasingly recognized to coexist with metabolic disturbances, including insulin resistance and impaired insulin sensitivity. This study aimed to examine the association between dietary selenium intake and multiple metabolic indices among adults with epilepsy. Methods: A total of 484 adults with epilepsy were identified from the National Health and Nutrition Examination Survey (NHANES). Dietary selenium intake was assessed using 24-hour dietary recalls and categorized into quartiles. Associations between selenium intake and multiple metabolic indices, including Triglyceride-glucose (TyG), Triglyceride-glucose-body mass index (TyG-BMI), Triglyceride-glucose-waist circumference (TyG-WC), homeostatic model assessment-insulin resistance (HOMA-IR), glucose-to-insulin (GI) ratio, McAuley index, and Quantitative Insulin Sensitivity Check Index (QUICKI), were evaluated using multiple linear regression models. Results: In fully adjusted models (model 4), dietary selenium intake showed a statistically significant positive association with TyG-WC in both continuous ( β = 1.69, [95% confidence interval {CI} = 1.08, 2.31]; P < 0.001) and quartile analyses ( β Q2 vs. Q1 = 290, [95% CI = 260–320], β Q3 vs. Q1 = 194, [95% CI = 159, 230], β Q4 vs. Q1 = 56.5, [95% CI = 20.0, 93.1]; P trend = 0.014). Selenium intake was also positively associated with TyG-BMI ( β = 0.433, [95% CI = 0.190, 0.675]; P < 0.001) and HOMA-IR ( β = 0.030, [95% CI = 0.02, 00.039]; P < 0.001) in continuous analyses. In contrast, insulin sensitivity indices, including QUICKI ( β Q4 vs. Q1 = −0.010 , [95% CI = −0.016, −0.005]; P < 0.001), GI ratio ( β Q4 vs. Q1 = −12.8 , [95% CI = −17.4, −8.22]; P < 0.001), and the McAuley index ( β Q4 vs. Q1 = −1.47, [95% CI = −2.02, −0.921]; P < 0.001), showed inverse associations with higher selenium intake. The association with the TyG index was non-linear after full adjustment. Conclusions: Higher dietary selenium intake was most consistently associated with increased TyG-WC, suggesting a closer link with central adiposity-related insulin resistance in adults with epilepsy. Concurrent inverse associations with insulin sensitivity indices highlight a less favorable metabolic profile at higher selenium intake levels. These findings underscore the importance of considering metabolic heterogeneity when evaluating dietary selenium exposure in individuals with epilepsy.