1 / 37

Journal Club

Journal Club. de Ruyter JC, Olthof MR, Seidell JC, Katan MB. A Trial of Sugar-free or Sugar-Sweetened Beverages and Body Weight in Children . N Engl J Med. 2012 Sep 21. Ebbeling CB, Feldman HA, Chomitz VR, Antonelli TA, Gortmaker SL, Osganian SK, Ludwig DS .

denise
Télécharger la présentation

Journal Club

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Journal Club de Ruyter JC, Olthof MR, Seidell JC, Katan MB. A Trial of Sugar-free or Sugar-Sweetened Beverages and Body Weight in Children. N Engl J Med. 2012 Sep 21. Ebbeling CB, Feldman HA, Chomitz VR, Antonelli TA, Gortmaker SL, Osganian SK, Ludwig DS. A Randomized Trial of Sugar-Sweetened Beverages and Adolescent Body Weight. N Engl J Med. 2012 Sep 21. Qi Q, Chu AY, Kang JH, Jensen MK, Curhan GC, Pasquale LR, Ridker PM, Hunter DJ, Willett WC, Rimm EB, Chasman DI, Hu FB, Qi L. Sugar-Sweetened Beverages and Genetic Risk of Obesity. N Engl J Med. 2012 Sep 21. 埼玉医科大学 総合医療センター 内分泌・糖尿病内科 Department of Endocrinology and Diabetes, Saitama Medical Center, Saitama Medical University 松田 昌文 Matsuda, Masafumi 2012年9月27日8:30-8:55 8階 医局

  2. Man Drinking Fat. NYC Health Anti-Soda Ad. Are You Pouring on the Pounds? http://www.youtube.com/watch?v=-F4t8zL6F0c&feature=player_embedded

  3. New York City consists of five boroughs, each of which is a state county. The five boroughs—The Bronx, Brooklyn, Manhattan, Queens, and Staten Island—were consolidated into a single city in 1898. With a Census-estimated 2011 population of 8,244,910 distributed over a land area of just 305 square miles (790 km2). Super Size Me is a 2004 American documentary film directed by and starring Morgan Spurlock, an American independent filmmaker. Spurlock's film follows a 30-day period from February 1 to March 2, 2003 during which he ate only McDonald's food.

  4. May 30, 2012 米ニューヨーク市のマイケル ブルームバーグ市長は、肥満対策に取り組むために、レストラン、映画館、食料品店での高カロリーの清涼飲料の販売を規制するプランを発表した。 September 13, 2012 The New York City Board of Health approved a measure that says sugary beverages with more than 25 calories per eight ounces can only be sold in portions of 16 ounces or less. The ban on larger quantities applies to the following food service establishments: restaurants, mobile food carts, delis and concessions at movie theaters, stadiums and arenas. The new regulation, which goes into effect on March 12, 2013, will give establishments six months to comply.

  5. the Department of Health Sciences, EMGO Institute for Health and Care Research, VU University Amsterdam, Amsterdam, the Netherlands. N Engl J Med 2012.DOI: 10.1056/NEJMoa1203034

  6. Figure 1. Screening, Randomization, and Follow-up of the Study Participants. A total of 164 children stopped consuming the study beverages. Measurements in 136 of these children (79 children in the sugar-free group and 57 in the sugar group) were available at 18 months. Thus, measurements in 28 children who did not complete the study (15 children in the sugar-free group and 13 in the sugar group) were not available at 18 months. We randomly assigned 641 children, not 642, as previously reported, since after unblinding, one child whom we believed to have undergone randomization had not undergone randomization.

  7. Figure 2. Urinary Sucralose Concentrations. The sucralose concentration was determined in spot urine samples by means of liquid chromatography with mass spectrometry.21 Samples were obtained from randomly selected children who completed the study. We assigned a value of 0.01 to samples below the detection limit of 0.02 mg per liter. The upper and lower ends of the boxes indicate the 25th and 75th quartiles, the black dots means, the horizontal lines within the boxes medians, the upper whisker the maximum value, and the lower whisker the minimum value. Values for the sugar-free group are based on samples obtained from 116 children at 6 months and from 117 children at 12 and 18 months. Mean (±SD) urinary sucralose concentrations were 6.3±3.7 mg per liter at 6 months, 6.6±4.5 mg per liter at 12 months, and 7.0±5.6 mg per liter at 18 months; sucralose was undetectable in 3% of samples at 6 months, 8% of samples at 12 months, and 10% of samples at 18 months. Values for the sugar group are based on samples obtained from 54 children at 6 months and 36 children at 12 and 18 months. Mean values were 0.04±0.13 mg per liter at 6 months, 0.03±0.14 mg per liter at 12 months, and 0.31±0.56 mg per liter at 18 months; sucralose was undetectable in 93% of samples at 6 months, 97% of samples at 12 months, and 67% of samples at 18 months. We also pooled 543 samples from participants at baseline to produce 20 pools. The mean sucralose concentration in these samples was 0.06±0.07 mg per liter. Sucralose is an artificial sweetener.

  8. Figure 3. Body-Mass Index (BMI) z Score in the 477 Children Who Drank the Study Beverages for the Full 18 Months. The z score for BMI is the BMI expressed as the number of standard deviations by which a child differed from the mean in the Netherlands for his or her age and sex. Panel A shows mean z scores for the two study groups over the 18-month study period. Panel B shows the between-group difference in the mean change from baseline (the mean change in the BMI z score in the sugar-free group minus the mean change in the sugar group), as a function of time. T bars in both panels indicate standard errors.

  9. the New Balance Foundation Obesity Prevention Center (C.B.E., D.S.L.) and the Clinical Research Center (H.A.F., T.A.A., S.K.O.), Boston Children’s Hospital, Boston; the Institute for Community Health, Cambridge (V.R.C.); and the Department of Society, Human Development, and Health, Harvard School of Public Health, Boston (S.L.G.) — all in Massachusetts. N Engl J Med 2012.DOI: 10.1056/NEJMoa1203388

  10. Figure 1. Screening, Randomization, and Follow-up of the Study Participants. Among the 538 adolescents who were excluded, 15 of the 49 who did not meet the sugar-sweetened–beverage (SSB) criterion also had other reasons and are included in the counts for those reasons. The weight and height of all available participants were measured at each time point in order to calculate BMI.

  11. * Plus–minus values are means ±SD. Means were compared with the use of the Student’s t-test and proportions compared with the use of Fisher’s exact test. Percentages may not sum to 100 owing to rounding. GED denotes General Educational Development, and MET metabolic equivalent. †Race and ethnic group were reported by the parents of the participants. “Multiple” included white–black (8 participants), white–Asian (3), white–black–Asian (1), and white–Arabic (1). “Other” included Latino or Latina (8 participants), Hispanic (7), Brazilian (2), Cape Verdean (2), Puerto Rican (4), Latino or Latina–Brazilian (1), Spanish (1), and American (1). Comparisons of baseline characteristics according to ethnic group are provided in Table S1 in the Supplementary Appendix. ‡Participants at or above the 85th percentile for BMI but below the 95th percentile were classified as overweight, and participants at or above the 95th percentile were classified as obese. The BMI range was 23.2 to 28.8 for overweight participants and 26.7 to 50.7 for obese participants. §The educational level listed is for the father or mother, depending on which parent had the higher level of education.

  12. *Plus–minus values for unadjusted data are means ±SD, and plus–minus values for changes from baseline are means ±SE. Changes were calculated at 1 year and 2 years from the general linear model, without adjustment for covariates. †The P values for changes from baseline in each study group are based on tests of the hypothesis that the mean change was zero. ‡The P values for the between-group differences in changes from baseline are based on tests of the hypothesis that the mean change was the same in the two groups. There were no significant ethnic group–study group interactions for any of the dietary variables.

  13. *Plus–minus values for unadjusted data are means ±SD, and plus–minus values for changes from baseline are means ±SE. Changes were calculated at 1 year and 2 years from the general linear model, and were adjusted for sex, race, ethnic group, household income, parental education, baseline BMI, baseline beverage consumption (energy from sugar-sweetened beverages and fruit juices and servings of artificially sweetened beverages and unsweetened beverages), baseline total energy intake, baseline sugar intake, and baseline obesity-related behavioral measures (physical activity and hours of television viewing). Results specific to ethnic group are from a model that included an interaction term for study group and ethnic group. For the change during the 2 years, before imputation, BMI data were available for 166 non-Hispanic participants (78 in the experimental group and 88 in the control group) and 43 Hispanic participants (27 in the experimental group and 16 in the control group). †The P values for changes from baseline in each study group are based on tests of the hypothesis that the mean change was zero. ‡The P values for the between-group differences in changes from baseline are based on tests of the hypothesis that the mean change was the same in the two groups.

  14. the Departments of Nutrition (Q.Q., M.K.J., D.J.H., W.C.W., E.B.R., F.B.H., L.Q.) and Epidemiology (G.C.C., D.J.H., W.C.W., E.B.R., F.B.H.), Harvard School of Public Health; and the Divisions of Preventive Medicine (A.Y.C., P.M.R., D.I.C.), Cardiovascular Disease (P.M.R.), and Genetics (D.I.C.), and the Channing Division of Network Medicine ( J.H.K., G.C.C., L.R.P., D.J.H., W.C.W., E.B.R., F.B.H., L.Q.), Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School; and the Department of Ophthalmology (L.R.P.), Massachusetts Eye and Ear Infirmary, Harvard Medical School — all in Boston. N Engl J Med 2012. DOI: 10.1056/NEJMoa1203039

  15. GENOTYPING We selected 32 single-nucleotide polymorphisms (SNPs) that represent all 32 loci that are known to be associated with BMI. SNP genotyping and imputation have been described in detail elsewhere. Most of the SNPs were genotyped or had a high imputation quality score (r2≥0.8), as assessed with the use of MACH software, version 1.0.16 (Center for Statistical Genetics, University of Michigan) (Table S1 in the Supplementary Appendix). GENETIC-PREDISPOSITION SCORE The genetic-predisposition score was calculated on the basis of the 32 SNPs with the use of a previously reported weighting method; scores range from 0 to 64, with higher scores indicating a higher genetic predisposition to obesity. Each SNP was weighted according to its relative effect size (β coefficient). To obtain a more accurate and precise effect size of each SNP on BMI, we used β coefficients derived from a meta-analysis of studies involving a total of approximately 126,000 persons. We rescaled the weighted score to reflect the number of risk alleles: each point of the genetic-predisposition score corresponded to one risk allele.

  16. Chr: chromosome; EAF: effect allele frequency. *Allele coding based on the forward strand. †Effect sizes in kg/m2 of BMI obtained from GWAS. ‡r2 refers to the measurement of SNPs imputation quality.

  17. Figure S1 Genetic predisposition score and body mass index in three cohorts The histograms represent the percentage of participants; and the means (±SE) of BMI are plotted, with the trend lines across the genetic predisposition score.

  18. * Plus–minus values are means ±SD. Baseline data were from 6934 women in the Nurses’ Health Study (NHS, 1980), 4423 men in the HealthProfessionals Follow-up Study (HPFS, 1986), and 21,740 women in the Women’s Genome Health Study (WGHS, 1992). Physical activity was assessed in 1986 for the NHS cohort. Television watching was assessed in 1992 for the NHS cohort and in 1988 for the HPFS cohort. † P values are for the trend across the four categories of intake of sugar-sweetened beverages. ‡ The body-mass index (BMI) is the weight in kilograms divided by the square of the height in meters. § MET denotes metabolic equivalents. . Scores on the Alternative Healthy Eating Index range from 2.5 to 87.5, with higher scores indicating a healthier diet. ‖ The genetic-predisposition score ranges from 0 to 64, with higher scores indicating a higher genetic predisposition to obesity.

  19. In the NHS, there were 1107 incident cases of obesity among 6402 initially nonobese women during 18 years of follow-up (1980 to 1998), and in the HPFS, there were 297 incident cases of obesity among 3889 initially nonobese men during 12 years of follow-up (1986 to 1998). The results were similar in the WGHS cohort (Fig. 1), in which 2280 women (of 18,127 women who were nonobese at baseline) became obese during 6 years of follow-up (1992 to 1998).

  20. * Plus–minus values are β coefficients ±SE. Data were derived from repeated-measures analysis for women in the NHS (five measures during the period from 1980 to 1998) and for men in the HPFS (three measures during the period from 1986 to 1998). Data on beverage intake were assessed 4 years before the assessment of BMI. † Data were adjusted for age and source of genotyping data. ‡ Data were further adjusted for level of physical activity, time spent watching television, status with respect to current smoking, alcohol intake, Alternative Healthy Eating Index score, and total energy intake. §Results for the two cohorts were pooled by means of inverse-variance–weighted, fixed-effects meta-analyses.

  21. Figure 1. Relative Risk of the Development of Obesity per Increment of 10 Risk Alleles, According to Intake of Sugar-Sweetened Beverages. For the discovery phase, with data from the Nurses’ Health Study (NHS) and Health Professionals Follow-up Study (HPFS) cohorts, the analyses were based on 18 years of follow-up for 6402 initially nonobese women (1980 to 1998, 1107 incident cases of obesity) and 12 years of follow-up for 3889 initially nonobese men (1986 to 1998, 297 incident cases of obesity). Shown are the pooled relative risks of incident obesity, with adjustment for age, source of genotyping data, level of physical activity, status with respect to current smoking, alcohol intake, time spent watching television, Alternative Healthy Eating Index score, and total energy intake. For the replication phase, with data from the Women’s Genome Health Study (WGHS) cohort, the analyses were based on a median of 6 years of follow-up for 18,127 initially nonobese women (1992 to 1998, 2280 incident cases of obesity). Shown are the relative risks of incident obesity, with adjustment for age, geographic region, eigenvectors, level of physical activity, status with respect to current smoking, alcohol intake, and total energy intake. Horizontal bars indicate 95% confidence intervals.

  22. Figure 2. Difference in BMI Associated with One Serving of a Sugar-Sweetened Beverage per Day, According to the Quartile of the Genetic-Predisposition Score. Data are effect sizes (β coefficients [±SE]) of sugar-sweetened beverage intake (one serving per day) on body-mass index (BMI; the weight in kilograms divided by the square of the height in meters), stratified according to the quartile of the genetic-predisposition score. In the NHS cohort, the median scores across the quartiles were 24.5 (range, 13.1 to 26.3), 27.8 (range, 26.4 to 29.0), 30.3 (range, 29.1 to 31.7), and 33.6 (range, 31.8 to 43.4); in the HPFS cohort, 24.9 (range, 16.0 to 26.5), 27.9 (range, 26.6 to 29.1), 30.4 (range, 29.2 to 31.7), and 33.6 (range, 31.8 to 41.9); and in the WGHS cohort, 24.7 (range, 15.3 to 26.5), 27.8 (range, 26.6 to 29.1), 30.3 (range, 29.2 to 31.6), and 33.4 (range, 31.7 to 43.4). In the NHS and HPFS cohorts, the analyses were based on data from the first 4 years in women (1980 to 1984) and men (1986 to 1990), respectively, with adjustment for age, source of genotyping data, level of physical activity, time spent watching television, status with respect to current smoking, alcohol intake, and Alternative Healthy Eating Index score. In the WGHS cohort, the analyses were based on data from the first 3 years, with adjustment for age, geographic region, eigenvectors, level of physical activity, status with respect to current smoking, and alcohol intake. P values are for interaction. I bars indicate standard errors.

  23. Message 3つの論文でSugar-Sweetened Beverages(糖で甘くした飲み物)に関するものがNew York市で制限する法律が通るとほぼ同時にNew England Journal of Medicine誌に掲載された! オランダのDRINK研究。平均8歳の正常体重児641人を対象に、糖で甘くした飲み物の代わりのノンカロリー飲料摂取による体重増加抑制効果を無作為化試験で検討。18カ月の試験で、体重増加は人口甘味料使用の無糖飲料群で6.35kg、糖で甘くした飲み物群で7.37kgだった。皮下脂肪厚、腹囲身長比、体脂肪量の増加も無糖群で有意に少なかった。(差は小さい気もしますが。...) ボストンで平均15歳での体重が多めの224人を1年ほど糖で甘くした飲み物の制限とそうでない群で検討。2年目は介入しないで両群を比較した。1年の介入で食事や体重に差が出た(BMI (−0.57, P = 0.045) で体重(−1.9 kg, P = 0.04) )。特にHispanicでは2年めについても差が継続していた。 ボストン周辺の疫学研究で遺伝子を解析できる3つの研究(the Nurses’ Health Study (NHS), Health Professionals Follow-up Study (HPFS), the Women’s Genome Health Study (WGHS) )について、肥満傾向の遺伝素因と糖で甘くした飲み物の量の関連を検討。BMI増加と肥満の発生について肥満遺伝子あたりのリスクは糖で甘くした飲み物が増えるほど影響が大きことが示された。

More Related