To determine if weekend catch-up sleep (CUS) impacts body mass index (BMI) in the general population. A stratified random sample (2156 subjects; age 19–82 years old, 43.0 ± 14.5; 1183 male) from the general population was evaluated, in 2010, using face-to-face interviews about sociodemographic characteristics, height, weight, habitual sleep duration, and time-in-bed at night on weekdays and weekend, sleep-related profiles, mood and anxiety scales, and comorbid-medical conditions. Weekend CUS was identified when nocturnal sleep extension occurred over the weekend, and this was quantified. Average sleep duration, BMI, and chronotype were determined. The association of BMI with the presence and the amount of weekend CUS was analyzed, independent of average sleep duration, chronotype, and sociodemographic factors. BMI and average sleep duration was 23.0 ± 3.0 kg/m² and 7.3 ± 1.2 hours, respectively. The weekend CUS group consisted of 932 subjects (43.1%) who slept longer on weekend than weekdays by 1.8 ± 1.1 hours. Weekend CUS subjects had a significantly lower BMI (22.8 ± 0.19 kg/m²) than the non-CUS (23.1 ± 0.19 kg/m²) group, after adjustment for age, sex, average sleep duration, chronotype, other sociodemographic factors, and anxiety/mood status (p = .01) The relationship between weekend CUS and BMI was dose-dependent (p = 0.02): Every additional hour of weekend CUS was associated with a decrease of 0.12 kg/m² in BMI (95% confidence interval, −0.23 to −0.02). Weekend sleep extension may have biological protective effects in preventing sleep-restriction induced or related obesity. The results suggest a simple population-level strategy to minimize effects of sleep loss.

Summary:  Purpose: Men with epilepsy often have sexual or reproductive abnormalities that are attributed to alterations in androgen levels, including subnormal free testosterone. Levels of the major metabolites of testosterone—androsterone (5α‐androstan‐3α‐ol‐17‐one; 5α,3α‐A), a neurosteroid that acts as a positive allosteric modulator of GABA_A receptors, and its 5β‐epimer etiocholanolone (5β‐androstan‐3α‐ol‐17‐one; 5β,3α‐A)—also may be reduced in epilepsy. 5α,3α‐A has been found in adult brain, and both metabolites, which also can be derived from androstenedione, are present in substantial quantities in serum along with their glucuronide and sulfate conjugates. This study sought to determine whether these endogenous steroid metabolites can protect against seizures. Methods: The anticonvulsant activity of 5α,3α‐A and 5β,3α‐A was investigated in electrical and chemoconvulsant seizure models in mice. The steroids also were examined for activity against extracellularly recorded epileptiform discharges in the CA3 region of the rat hippocampal slice induced by perfusion with 55 μM 4‐aminopyridine (4‐AP). Results: Intraperitoneal injection of 5α,3α‐A–protected mice in a dose‐dependent fashion from seizures in the following models (ED₅₀, dose in mg/kg protecting 50% of animals): 6‐Hz electrical stimulation (29.1), pentylenetetrazol (43.5), pilocarpine (105), 4‐AP (215), and maximal electroshock (224). 5β,3α‐A also was active in the 6‐Hz and pentylenetetrazol models, but was less potent (ED₅₀ values, 76.9 and 139 mg/kg, respectively), whereas epiandrosterone (5α,3β‐A) was inactive (ED₅₀, ≤300 mg/kg). 5α,3α‐A (10–100 μM) also inhibited epileptiform discharges in a concentration‐dependent fashion in the in vitro slice model, whereas 5β,3α‐A was active but of lower potency, and 5α,3β‐A was inactive. Conclusions: 5α,3α‐A and 5β,3α‐A have anticonvulsant properties. Although of low potency, the steroids are present in high abundance and could represent endogenous modulators of seizure susceptibility.

Multidrug resistance protein 2 (MRP2, ABCC2) is involved in the transport of antiepileptic drugs and is upregulated in the brain tissues of patients with epilepsy. Therefore, genetic variations in the MRP2 gene may affect individual drug responses to the antiepileptic agent carbamazepine. Associations between MRP2 polymorphisms and the adverse drug reactions (ADRs) of carbamazepine were analyzed using an integrated population genetics and molecular functional approach. In the initial case-control study, five tag single nucleotide polymorphisms in the MRP2 gene were analyzed in 146 patients with epilepsy. Patients were divided into two groups: those who experienced ADRs of the central nervous system and those who did not. An independent replication study was performed using DNA samples from 279 patients. A nonsynonymous polymorphism, c.1249G>A (p.V417I, rs2273697), showed a strong association with the neurological ADR caused by carbamazepine (P=0.005). Logistic regression analysis with multiple clinical variables indicated that the presence of A allele at the MRP2 c.1249G>A locus was an independent determinant of central nervous system ADR caused by carbamazepine. Moreover, the positive association of c.1249A was reproduced in the replication study (P=0.042, joint P value of the replication=0.001). The functional study using ATPase assay and FACScan flow cytometer indicated that carbamazepine was a substrate of MRP2 and that the 417I variation selectively reduced carbamazepine transport across the cell membrane. These results strongly suggest that the A-allele of the MRP2 single nucleotide polymorphism c.1247G>A is associated with adverse neurological drug reactions to carbamazepine.

Although tension-type headache (TTH) is a frequent type of headache disorder and imposes a significant burden, there is scant information about the prevalence and impact of comorbid anxiety and depression among individuals with TTH. We investigated the prevalence and clinical impact of anxiety and depression among patients with TTH in the general population. We recruited Korean participants aged 19–69 years using a two-stage clustered random sampling method. To identify the presence of headache type, anxiety, and depression, we used a semi-structured interview using certain questionnaires. To assess the level of anxiety and depression, we used the Goldberg Anxiety Scale and Patient Health Questionnaire-9, respectively. Among 2,695 participants, 570 people (21.2%) had TTH during previous 1 year. In participants with TTH, the prevalence of anxiety (9.5% vs. 5.3%, p = 0.001) and depression (4.2% vs. 1.8%, p = 0.001) was significantly higher than that of non-headache participants. The prevalence of anxiety among TTH participants with >15 attacks per month [21.4%, odds ratio (OR): 4.0] and 1–14 attacks per month (13.1%, OR: 2.2) was higher than that in those with <1 attack per month (6.4%), however this tendency was not observed in participants with depression. Visual Analogue Scale (VAS) score [median 5.0 vs. 4.0, p = 0.010] and Headache Impact Test-6 (HIT-6) score [median 45.5 vs. 42.0, p < 0.001] were significantly higher among those with anxiety. Furthermore, VAS scores [median 5.0 vs. 4.0, p = 0.010] and HIT-6 scores [median 45.5 vs. 42.0, p = 0.027] were also significantly higher among TTH patients with depression than among those without depression. In conclusion, anxiety and depression were more prevalent in participants with TTH than in non-headache participants. These two conditions were associated with an exacerbation of headache symptoms in individuals with TTH.

Sleep disorder and sleep complaints are common in subjects with migraine. Although the association between sleep disorders and migraine has been reported, the association between perceived insufficient sleep and migraine has rarely reported. The aim of this study is to evaluate the association between insufficient sleep and migraine using the data of the Korean Headache-Sleep Study (KHSS). The KHSS is a nation-wide cross-sectional population-based survey regarding headache and sleep for Korean adults aged 19 to 69 years. A difference of one hour or more between sleep need and average sleep time indicated insufficient sleep. Of 2,695 participants, 727 (27.0%) individuals were classified as having insufficient sleep. The prevalence of insufficient sleep among individuals with migraine (45.5%) was significantly higher compared to that among individuals with non-migraine headache (32.9%, p = 0.004) or among non-headache (20.4%, p < 0.001). Average sleep time did not differ among migraine, non-migraine headache, and non-headache groups (7.3 ± 1.2 vs. 7.2 ± 1.2 vs. 7.3 ± 1.4, p = 0.207). Multivariable logistic regression analyses demonstrated that migraine had an increased odds ratio (OR) for insufficient sleep after adjusting for sociodemographic variables, short sleep time, insomnia, poor sleep quality, anxiety, and depression (OR = 1.8, 95% confidence interval [CI] = 1. 2 – 2.7, p = 0.002). The prevalence of insufficient sleep was significantly higher among migraineurs compared to that in non-migraine headache or non-headache group.