著者
Rei Otsuka Koji Tamakoshi Hiroshi Yatsuya Chiyoe Murata Atsushi Sekiya Keiko Wada Hui Ming Zhang Kunihiro Matsushita Kaichiro Sugiura Seiko Takefuji Pei OuYang Nobue Nagasawa Takaaki Kondo Satoshi Sasaki Hideaki Toyoshima
出版者
Japan Epidemiological Association
雑誌
Journal of Epidemiology (ISSN:09175040)
巻号頁・発行日
vol.16, no.3, pp.117-124, 2006 (Released:2006-05-19)
参考文献数
29
被引用文献数
106 191

BACKGROUND: Few epidemiologic studies have examined the association between the rate of eating and obesity. In this study, we cross-sectionally examined the association of the self-reported rate of eating with current Body Mass Index (BMI), and BMI-change from 20 years of age to the current age.METHODS: Subjects were 3737 male (mean age ± standard deviation and mean BMI ± standard deviation: 48.2 ± 7.1 years and 23.3 ± 2.7 kg/m2) and 1005 female (46.3 ± 7.0 years and 21.8 ± 2.8 kg/m2) Japanese civil servants. We measured self-reported categorical rate of eating, current BMI, BMI at age 20, and BMI-change from age 20. Energy intake was assessed over a 1-month period with a brief-type diet history questionnaire.RESULTS: The multiple regression analysis in which the current BMI was regressed by categorical rate of eating, energy intake, age, and lifestyle factors showed that current BMI steadily increased by -0.99, -0.67, 0.81, and 1.47 kg/m2 along with the progress of categorical rate of eating from the 'medium' group to 'very slow', 'relatively slow', 'relatively fast', and 'very fast' groups, respectively, in men. In women, the corresponding values were -1.06, -0.35, 0.50, and 1.34 kg/m2. When the BMI increment from age 20 to current age was regressed in the same manner, the increment was -0.63, -0.34, 0.57, and 1.05 kg/m2 in men and -0.71, -0.32, 0.34, and 1.14 kg/m2 in women, respectively. Additionally, both BMI at age 20 and current height were positively associated with rate of eating.CONCLUSIONS: Our results among middle-aged men and women suggest that eating fast would lead to obesity.J Epidemiol 2006; 16: 117-124.
著者
Ryosuke Fujii Asahi Hishida Takeshi Nishiyama Masahiro Nakatochi Keitaro Matsuo Hidemi Ito Yuichiro Nishida Chisato Shimanoe Yasuyuki Nakamura Tanvir Chowdhury Turin Sadao Suzuki Miki Watanabe Rie Ibusuki Toshiro Takezaki Haruo Mikami Yohko Nakamura Hiroaki Ikezaki Masayuki Murata Kiyonori Kuriki Nagato Kuriyama Daisuke Matsui Kokichi Arisawa Sakurako Katsuura-Kamano Mineko Tsukamoto Takashi Tamura Yoko Kubo Takaaki Kondo Yukihide Momozawa Michiaki Kubo Kenji Takeuchi Kenji Wakai
出版者
Japan Epidemiological Association
雑誌
Journal of Epidemiology (ISSN:09175040)
巻号頁・発行日
vol.32, no.11, pp.483-488, 2022-11-05 (Released:2022-11-05)
参考文献数
38

Background: Inflammation is thought to be a risk factor for kidney disease. However, whether inflammatory status is either a cause or an outcome of chronic kidney disease remains controversial. We aimed to investigate the causal relationship between high-sensitivity C-reactive protein (hs-CRP) and estimated glomerular filtration rate (eGFR) using Mendelian randomization (MR) approaches.Methods: A total of 10,521 participants of the Japan Multi-institutional Collaborative Cohort Study was analyzed in this study. We used two-sample MR approaches (the inverse-variance weighted (IVW), the weighted median (WM), and the MR-Egger method) to estimate the effect of genetically determined hs-CRP on kidney function. We selected four and three hs-CRP associated single nucleotide polymorphisms (SNPs) as two instrumental variables (IV): IVCRP and IVAsian, based on SNPs previously identified in European and Asian populations. IVCRP and IVAsian explained 3.4% and 3.9% of the variation in hs-CRP, respectively.Results: Using the IVCRP, genetically determined hs-CRP was not significantly associated with eGFR in the IVW and the WM methods (estimate per 1 unit increase in ln(hs-CRP), 0.000; 95% confidence interval [CI], −0.019 to 0.020 and −0.003; 95% CI, −0.019 to 0.014, respectively). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 0.005; 95% CI, −0.020 to 0.010 and −0.004; 95% CI, −0.020 to 0.012, respectively). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: −0.008; 95% CI, −0.058 to 0.042; IVAsian: 0.001; 95% CI, −0.036 to 0.036).Conclusion: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.
著者
Ryosuke Fujii Asahi Hishida Takeshi Nishiyama Masahiro Nakatochi Keitaro Matsuo Hidemi Ito Yuichiro Nishida Chisato Shimanoe Yasuyuki Nakamura Tanvir Chowdhury Turin Sadao Suzuki Miki Watanabe Rie Ibusuki Toshiro Takezaki Haruo Mikami Yohko Nakamura Hiroaki Ikezaki Masayuki Murata Kiyonori Kuriki Nagato Kuriyama Daisuke Matsui Kokichi Arisawa Sakurako Katsuura-Kamano Mineko Tsukamoto Takashi Tamura Yoko Kubo Takaaki Kondo Yukihide Momozawa Michiaki Kubo Kenji Takeuchi Kenji Wakai
出版者
Japan Epidemiological Association
雑誌
Journal of Epidemiology (ISSN:09175040)
巻号頁・発行日
pp.JE20200540, (Released:2021-02-20)
参考文献数
38

Background: Inflammation is thought to be a risk factor for kidney disease. However, discussion is controversial whether inflammatory status is either a cause or an outcome of chronic kidney disease. We aimed to investigate the causal relationship between high-sensitivity C-reactive protein (hs-CRP) and estimated glomerular filtration rate (eGFR) using mendelian randomization (MR) approaches.Methods: A total of 10,521 participants of the Japan Multi-institutional Collaborative Cohort Study was analyzed in this study. We used two-sample MR approaches (the inverse-variance weighted (IVW), the weighted median (WM), and the MR-Egger method) to estimate the effect of genetically determined hs-CRP on kidney function. We selected four and three hs-CRP associated single nucleotide polymorphisms (SNPs) as two instrumental variables (IV): IVCRP and IVAsian, based on SNPs previously identified in European and Asian populations. IVCRP and IVAsian explained 3.4% and 3.9% of the variation in hs-CRP, respectively.Results: Using the IVCRP, genetically determined hs-CRP was not significantly associated with eGFR in the IVW and the WM methods (estimate per 1 unit increase in ln(hs-CRP), 95%CI: 0.000, –0.019 to 0.020 and –0.003, –0.019 to 0.014). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 95% CI: –0.005, –0.020 to 0.010 and –0.004, –0.020 to 0.012). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: –0.008, –0.058 to 0.042; IVAsian: 0.001, –0.036 to 0.036).Conclusions: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.