ObjectivesChronic degenerative diseases are closely related to daily eating habits, nutritional status, and, in particular, energy intake. In clarifying these relationships it is very important for dietary surveys to report accurate information about energy intake. This study attempted to identify the prevalence of the under-reporting of energy intake and its related characteristics based on the Korean National Health and Nutrition Examination Survey conducted in the years 2007–2009.MethodsThe present study analyzed dietary intake data from 15,133 adults aged ≥19 years using 24-hour dietary recalls. Basal metabolic rates were calculated from the age- and gender-specific equations of Schofield and under-reporting was defined as an energy intake <0.9, represented by the ratio of energy intake to estimated basal metabolic rate.ResultsUnder-reporters (URs) accounted for 14.4% of men and 23.0% of women and the under-reporting rate was higher in the age group 30–49 years for both men and women. The results from an analysis of the age-specific socioeconomic characteristics of participants classified as URs showed that under-reporting was high in women living alone and in women with only elementary school education or no education. The results from an analysis of the health-specific characteristics of URs showed that a large proportion of URs had poor self-rated health or were obese, or both, compared with non-URs. The proportion of participants who consumed less than the estimated average requirements for nutrients was significantly higher in URs compared with non-URs.ConclusionThe under-reporting of energy intake was associated with age, gender, education level, income level, household status (single-person or multi-person), self-rated health, physical activity, and obesity.

Although inflammation is a host defense mechanism, chronic inflammation mediates several diseases, including cancer, allergy, asthma, and autoimmune diseases, and reportedly, it is associated with a 60% mortality rate. There are several reports on the anti-inflammatory effects of Curcuma longa and Allium hookeri. However, although they can be used as culinary materials and have biological effects, they are not effective anti-inflammatory agents. In this study, we evaluated the synergic effect of C. longa and A. hookeri in order to confirm the possibility of a new anti-inflammatory agent. Based on cell viability and cytokine analyses, the appropriate ratio of C. longa and A. hookeri was confirmed using an air pouch animal model. Then, the anti-inflammatory effect of C. longa and A. hookeri co-treatment was evaluated by measuring the immune cell count and cytokines in the exudate and by comparing the morphological changes and cytokines in inflamed skin samples. Additionally, we evaluated the NF-κB/ COX-2 pathway and iNOS levels. The active constituents detected in C. longa were demethoxycurcumin and bisdemethoxycurcumin, and that detected in A. hookeri was methylsulfonylmethane. An in vitro assessment determined the appropriate drug ratio as 3:7. In a carrageenan-induced inflammatory model, co-treatment effectively suppressed inflammatory cytokines, including IFN-γ, IL-1β, IL-6, IL-13, and IL-17, and recovered inflammation-related morphological changes in the skin. The antiinflammatory effect of the co-treatment was mediated through the NF-κB/COX-2 pathway and iNOS inhibition. We concluded that co-treatment with C. longa and A. hookeri synergistically inhibited inflammation via the NF-κB/COX-2/iNOS pathway. Inflammation is a biological, homeostatic defense mechanism against foreign bodies. However, chronic inflammation can cause additional damage in cases of cancer, allergy, asthma, autoimmune diseases, glomerulonephritis, hepatitis, inflammatory bowel disease, rheumatoid arthritis, and other disorders 1. Moreover, chronic inflammation can result in death. Reportedly, chronic inflammatory diseases 2 are associated with a 60% worldwide mortality. Steroidal hormones are the most potent anti-inflammatory drugs owing to their ability to block all inflammatory pathways; however, tolerance against such drugs is easily developed. Hence, non-steroidal anti-inflammatory drugs (NSAIDs) are broadly used. However, NSAIDs have severe adverse effects as they damage the upper gastrointestinal tract by inhibiting prostaglandin synthesis 3. Several cytokines influence the occurrence or inhibition of inflammation. Pro-inflammatory cytokines that promote inflammation include interleukin-1β (IL-1β), IL-6, IL-13, and tumor necrosis factor-alpha (TNF-α) 4. Conversely, anti-inflammatory cytokines that can inhibit inflammation include IL-1Rα, IL-4, IL-10, IL-11, and TGF-β1 5. Furthermore, the nuclear factor kappa B (NF-κB)/cyclooxygenase 2 (COX-2)/inducible nitric oxide synthase (iNOS) pathway is important in the pathogenesis of inflammat...

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Recent studies showing the improvement of ADHD symptoms obtained with the highly selective noradrenergic reuptake inhibitor, atomoxetine, demonstrate that the noradrenergic system plays the role of pathophysiology in this disorder. It is revealed that the norepinephrine transporter gene (SLC6A2) is a possible candidate gene directly related to ADHD. To determine possible roles of the SLC6A2 as a susceptibility gene for ADHD, we performed the genetic association study for a functional À3081(A/T) polymorphism, located in the promoter region of SLC6A2. For the present study of association between ADHD and the SLC6A2, 103 male patients with ADHD and 103 normal male controls were randomly gathered. Significant differences were found in the allele frequencies (c 2 ¼ 5.60, P ¼ 0.02) and the odds ratio for the allele T between the ADHD and normal subjects was 1.59 (95% CI: 1.08-2.34) suggesting that T allele is critical to make the group difference. Significant group difference was also found in AA, AT, TT genotypes (c 2 ¼ 7.1, P ¼ 0.02). The odds ratio for TT and AT genotypes was 4.57 (95% CI: 2.56-8.15) and 1.96 (95% CI: 0.96-3.78), respectively. Findings in the present study provided further evidence of association between ADHD and À3081(A/T) polymorphism of SLC6A2.