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  • 标题:Low-Energy Diet in Atopic Dermatitis Patients: Clinical Findings and DNA Damage
  • 本地全文:下载
  • 作者:Katsuyasu Kouda ; Toshio Tanaka ; Mitsuo Kouda
  • 期刊名称:Journal of PHYSIOLOGICAL ANTHROPOLOGY and Applied Human Science
  • 印刷版ISSN:1345-3475
  • 出版年度:2000
  • 卷号:19
  • 期号:5
  • 页码:225-228
  • DOI:10.2114/jpa.19.225
  • 出版社:Japan Society of Physiological Anthropology
  • 摘要:

    Undernutrition without malnutrition (low-energy diet) increases maximum longevity, reduces the incidence of several cancers and delays their onset, in animal studies. It has also been demonstrated by experimental study that caloric restriction provides a beneficial effect on various inflammatory diseases. In this study, we offered a low-energy diet to patients with atopic dermatitis (AD). Nineteen adult patients (5 males and 14 females aged 15 to 36 years) were enrolled in the study which lasted 8 weeks. The energy intake was 550f nutritional requirements; protein was 75%, calcium 180%, iron 130%, vitamin A 105%, vitamin C 250% and vitamin E 1100f the daily requirement. No patient experienced adverse reaction, and none dropped out of the trial. Body weight, body mass index (BMI), and systolic blood pressure had decreased significantly by the end of study. The SCORAD (scoring atopic dermatitis) index, which combines objective (extent and intensity of lesions) and subjective (daytime pruritus and sleep loss) criteria, was reduced significantly. In 11 patients with severe AD, there was a significant reduction in oxidative DNA damage. The change in the inflammatory intensity score and the change in BMI caused by energy restriction showed a significant positive correlation. The change in oxidative DNA damage levels and the change in BMI showed a positive correlation. These results clarify the relationship between weight loss and the improvement of AD. It may be hypothesized that this low-energy diet which included several additional nutrients has a possibility to reduce inflammatory symptoms of patients with AD.

  • 关键词:low-energy diet; oxidative DNA damage; atopic dermatitis
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