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Dive into the research topics where David S. Ludwig is active.

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Featured researches published by David S. Ludwig.


The Lancet | 2002

Childhood obesity: public-health crisis, common sense cure

Cara B. Ebbeling; Dorota B. Pawlak; David S. Ludwig

During the past two decades, the prevalence of obesity in children has risen greatly worldwide. Obesity in childhood causes a wide range of serious complications, and increases the risk of premature illness and death later in life, raising public-health concerns. Results of research have provided new insights into the physiological basis of bodyweight regulation. However, treatment for childhood obesity remains largely ineffective. In view of its rapid development in genetically stable populations, the childhood obesity epidemic can be primarily attributed to adverse environmental factors for which straightforward, if politically difficult, solutions exist.


The Lancet | 2001

Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis

David S. Ludwig; Karen E. Peterson; Steven L. Gortmaker

BACKGROUND The rising prevalence of obesity in children has been linked in part to the consumption of sugar-sweetened drinks. Our aim was to examine this relation. METHODS We enrolled 548 ethnically diverse schoolchildren (age 11.7 years, SD 0.8) from public schools in four Massachusetts communities, and studied them prospectively for 19 months from October, 1995, to May, 1997. We examined the association between baseline and change in consumption of sugar-sweetened drinks (the independent variables), and difference in measures of obesity, with linear and logistic regression analyses adjusted for potentially confounding variables and clustering of results within schools. FINDINGS For each additional serving of sugar-sweetened drink consumed, both body mass index (BMI) (mean 0.24 kg/m2; 95% CI 0.10-0.39; p=0.03) and frequency of obesity (odds ratio 1.60; 95% CI 1.14-2.24; p=0.02) increased after adjustment for anthropometric, demographic, dietary, and lifestyle variables. Baseline consumption of sugar-sweetened drinks was also independently associated with change in BMI (mean 0.18 kg/m2 for each daily serving; 95% CI 0.09-0.27; p=0.02). INTERPRETATION Consumption of sugar-sweetened drinks is associated with obesity in children.


The Lancet | 2005

Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis

Mark A. Pereira; Alex I. Kartashov; Cara B. Ebbeling; Linda Van Horn; Martha L. Slattery; David R. Jacobs; David S. Ludwig

BACKGROUND Fast-food consumption has increased greatly in the USA during the past three decades. However, the effect of fast food on risk of obesity and type 2 diabetes has received little attention. We aimed to investigate the association between reported fast-food habits and changes in bodyweight and insulin resistance over a 15-year period in the USA. METHODS Participants for the CARDIA study included 3031 young (age 18-30 years in 1985-86) black and white adults who were followed up with repeated dietary assessment. We used multiple linear regression models to investigate the association of frequency of fast-food restaurant visits (fast-food frequency) at baseline and follow-up with 15-year changes in bodyweight and the homoeostasis model (HOMA) for insulin resistance. FINDINGS Fast-food frequency was lowest for white women (about 1.3 times per week) compared with the other ethnic-sex groups (about twice a week). After adjustment for lifestyle factors, baseline fast-food frequency was directly associated with changes in bodyweight in both black (p=0.0050) and white people (p=0.0013). Change in fast-food frequency over 15 years was directly associated with changes in bodyweight in white individuals (p<0.0001), with a weaker association recorded in black people (p=0.1004). Changes were also directly associated with insulin resistance in both ethnic groups (p=0.0015 in black people, p<0.0001 in white people). By comparison with the average 15-year weight gain in participants with infrequent (less than once a week) fast-food restaurant use at baseline and follow-up (n=203), those with frequent (more than twice a week) visits to fast-food restaurants at baseline and follow-up (n=87) gained an extra 4.5 kg of bodyweight (p=0.0054) and had a two-fold greater increase in insulin resistance (p=0.0083). INTERPRETATION Fast-food consumption has strong positive associations with weight gain and insulin resistance, suggesting that fast food increases the risk of obesity and type 2 diabetes.


Circulation | 2004

Prevalence of the Metabolic Syndrome in American Adolescents Findings From the Third National Health and Nutrition Examination Survey

Sarah D. de Ferranti; Kimberlee Gauvreau; David S. Ludwig; Ellis J. Neufeld; Jane W. Newburger; Nader Rifai

Background—Metabolic syndrome (MetS) is defined by the Third Report of the Adult Treatment Panel (ATP III) using criteria easily applied by clinicians and researchers. There is no standard pediatric definition. Methods and Results—We defined pediatric MetS using criteria analogous to ATP III as ≥3 of the following: (1) fasting triglycerides ≥1.1 mmol/L (100 mg/dL); (2) HDL <1.3 mmol/L (50 mg/dL), except in boys aged 15 to 19 years, in whom the cutpoint was <1.2 mmol/L (45 mg/dL); (3) fasting glucose ≥6.1 mmol/L (110 mg/dL); (4) waist circumference >75th percentile for age and gender; and (5) systolic blood pressure >90th percentile for gender, age, and height. MetS prevalence in US adolescents was estimated with the Third National Health and Nutritional Survey 1988 to 1994. Among 1960 children aged ≥12 years who fasted ≥8 hours, two thirds had at least 1 metabolic abnormality, and nearly 1 in 10 had MetS. The racial/ethnic distribution was similar to adults: Mexican-Americans, followed by non-Hispanic whites, had a greater prevalence of MetS compared with non-Hispanic blacks (12.9%, [95% CI 10.4% to 15.4%]; 10.9%, [95% CI 8.4% to 13.4%]; and 2.5%, [95% CI 1.3% to 3.7%], respectively). Nearly one third (31.2% [95% CI 28.3% to 34.1%]) of overweight/obese adolescents had MetS. Conclusions—Our definition of pediatric MetS, designed to be closely analogous to ATP III, found MetS is common in adolescents and has a similar racial/ethnic distribution to adults in this representative national sample. Because childhood MetS likely tracks into adulthood, early identification may help target interventions to improve future cardiovascular health.


Pediatrics | 2007

Recommendations for Treatment of Child and Adolescent Overweight and Obesity

Bonnie A. Spear; Sarah E. Barlow; Chris Ervin; David S. Ludwig; Brian E. Saelens; Karen E. Schetzina; Elsie M. Taveras

In this article, we review evidence about the treatment of obesity that may have applications in primary care, community, and tertiary care settings. We examine current information about eating behaviors, physical activity behaviors, and sedentary behaviors that may affect weight in children and adolescents. We also review studies of multidisciplinary behavior-based obesity treatment programs and information about more aggressive forms of treatment. The writing group has drawn from the available evidence to propose a comprehensive 4-step or staged-care approach for weight management that includes the following stages: (1) Prevention Plus; (2) structured weight management; (3) comprehensive multidisciplinary intervention; and (4) tertiary care intervention. We suggest that providers encourage healthy behaviors while using techniques to motivate patients and families, and interventions should be tailored to the individual child and family. Although more intense treatment stages will generally occur outside the typical office setting, offices can implement less intense intervention strategies. We not ony address specific patient behavior goals but also encourage practices to modify office systems to streamline office-based care and to prepare to coordinate with professionals and programs outside the office for more intensive interventions.


Journal of Clinical Investigation | 2001

Melanin-concentrating hormone overexpression in transgenic mice leads to obesity and insulin resistance

David S. Ludwig; Nicholas A. Tritos; Jason W. Mastaitis; Rohit N. Kulkarni; Efi Kokkotou; Joel K. Elmquist; Bradford B. Lowell; Jeffrey S. Flier; Eleftheria Maratos-Flier

Several lines of investigation suggest that the hypothalamic neuropeptide melanin-concentrating hormone (MCH) regulates body weight in mammals. Obese mice lacking functional leptin overexpress the MCH message in the fed or fasted state. Acute intracerebroventricular injection of MCH increases energy intake in rats. Mice lacking the MCH gene are lean. To test the hypothesis that chronic overexpression of MCH in mice causes obesity, we produced transgenic mice that overexpress MCH (MCH-OE) in the lateral hypothalamus at approximately twofold higher levels than normal mice. On the FVB genetic background, homozygous transgenic animals fed a high-fat diet ate 10% more and were 12% heavier at 13 weeks of age than wild-type animals, and they had higher systemic leptin levels. Blood glucose levels were higher both preprandially and after an intraperitoneal glucose injection. MCH-OE animals were insulin-resistant, as demonstrated by markedly higher plasma insulin levels and a blunted response to insulin; MCH-OE animals had only a 5% decrease in blood glucose after insulin administration, compared with a 31% decrease in wild-type animals. MCH-OE animals also exhibited a twofold increase in islet size. To evaluate the contribution of genetic background to the predisposition to obesity seen in MCH-OE mice, the transgene was bred onto the C57BL/6J background. Heterozygote C57BL/6J mice expressing the transgene showed increased body weight on a standard diet, confirming that MCH overexpression can lead to obesity.


The New England Journal of Medicine | 2009

The Public Health and Economic Benefits of Taxing Sugar-Sweetened Beverages

Kelly D. Brownell; Thomas Farley; Walter C. Willett; Barry M. Popkin; Frank J. Chaloupka; Joseph W. Thompson; David S. Ludwig

Consumption of sugar-sweetened beverages has increased in recent decades; evidence suggests that consumption of these beverages contributes to obesity and adverse health outcomes. The authors discuss the potential public health and economic benefits of taxing sugar-sweetened beverages.


Pediatrics | 2006

Effects of Decreasing Sugar-Sweetened Beverage Consumption on Body Weight in Adolescents: A Randomized, Controlled Pilot Study

Cara B. Ebbeling; Henry A. Feldman; Stavroula K. Osganian; Virginia R. Chomitz; Sheila J. Ellenbogen; David S. Ludwig

OBJECTIVE. The role of sugar-sweetened beverages (SSBs) in promoting obesity is controversial. Observational data link SSB consumption with excessive weight gain; however, randomized, controlled trials are lacking and necessary to resolve the debate. We conducted a pilot study to examine the effect of decreasing SSB consumption on body weight. METHODS. We randomly assigned 103 adolescents aged 13 to 18 years who regularly consumed SSBs to intervention and control groups. The intervention, 25 weeks in duration, relied largely on home deliveries of noncaloric beverages to displace SSBs and thereby decrease consumption. Change in SSB consumption was the main process measure, and change in body mass index (BMI) was the primary end point. RESULTS. All of the randomly assigned subjects completed the study. Consumption of SSBs decreased by 82% in the intervention group and did not change in the control group. Change in BMI, adjusted for gender and age, was 0.07 ± 0.14 kg/m2 (mean ± SE) for the intervention group and 0.21 ± 0.15 kg/m2 for the control group. The net difference, −0.14 ± 0.21 kg/m2, was not significant overall. However, baseline BMI was a significant effect modifier. Among the subjects in the upper baseline-BMI tertile, BMI change differed significantly between the intervention (−0.63 ± 0.23 kg/m2) and control (+0.12 ± 0.26 kg/m2) groups, a net effect of −0.75 ± 0.34 kg/m2. The interaction between weight change and baseline BMI was not attributable to baseline consumption of SSBs. CONCLUSIONS. A simple environmental intervention almost completely eliminated SSB consumption in a diverse group of adolescents. The beneficial effect on body weight of reducing SSB consumption increased with increasing baseline body weight, offering additional support for American Academy of Pediatrics guidelines to limit SSB consumption.


JAMA | 2008

Mindfulness in medicine.

David S. Ludwig; Jon Kabat-Zinn

the profession’s code of ethics and is personally damaging to that individual. In a controversial psychobiography of President George W. Bush, Frank, a psychiatrist, characterized the president as a “paranoid megalomaniac” and “untreated alcoholic.” Although these are clearly clinical and diagnostic labels that appear to violate the Goldwater Rule, Frank’s view is that his book is a scholarly psychobiography, not “expert opinion” and, as such, is outside the purview of APA ethics guideline. Still, the line between a careful psychiatric profile and a casual off-the-cuff diagnosis of a public figure is not so clear. Even if the intent of the mental health professional in both situations is very different—understanding the psychology of the person (psychobiography) or assailing the character of a disliked political candidate (the Goldwater case)— both share a similar ethical problem: unauthorized psychiatric assessment of a person who is not examined by the professional.


The New England Journal of Medicine | 2012

A Randomized Trial of Sugar-Sweetened Beverages and Adolescent Body Weight

Cara B. Ebbeling; Henry A. Feldman; Virginia R. Chomitz; Tracy A. Antonelli; Steven L. Gortmaker; Stavroula K. Osganian; David S. Ludwig

BACKGROUND Consumption of sugar-sweetened beverages may cause excessive weight gain. We aimed to assess the effect on weight gain of an intervention that included the provision of noncaloric beverages at home for overweight and obese adolescents. METHODS We randomly assigned 224 overweight and obese adolescents who regularly consumed sugar-sweetened beverages to experimental and control groups. The experimental group received a 1-year intervention designed to decrease consumption of sugar-sweetened beverages, with follow-up for an additional year without intervention. We hypothesized that the experimental group would gain weight at a slower rate than the control group. RESULTS Retention rates were 97% at 1 year and 93% at 2 years. Reported consumption of sugar-sweetened beverages was similar at baseline in the experimental and control groups (1.7 servings per day), declined to nearly 0 in the experimental group at 1 year, and remained lower in the experimental group than in the control group at 2 years. The primary outcome, the change in mean body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) at 2 years, did not differ significantly between the two groups (change in experimental group minus change in control group, -0.3; P=0.46). At 1 year, however, there were significant between-group differences for changes in BMI (-0.57, P=0.045) and weight (-1.9 kg, P=0.04). We found evidence of effect modification according to ethnic group at 1 year (P=0.04) and 2 years (P=0.01). In a prespecified analysis according to ethnic group, among Hispanic participants (27 in the experimental group and 19 in the control group), there was a significant between-group difference in the change in BMI at 1 year (-1.79, P=0.007) and 2 years (-2.35, P=0.01), but not among non-Hispanic participants (P>0.35 at years 1 and 2). The change in body fat as a percentage of total weight did not differ significantly between groups at 2 years (-0.5%, P=0.40). There were no adverse events related to study participation. CONCLUSIONS Among overweight and obese adolescents, the increase in BMI was smaller in the experimental group than in the control group after a 1-year intervention designed to reduce consumption of sugar-sweetened beverages, but not at the 2-year follow-up (the prespecified primary outcome). (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others; ClinicalTrials.gov number, NCT00381160.).

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Cara B. Ebbeling

Boston Children's Hospital

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Henry A. Feldman

Boston Children's Hospital

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Dorota B. Pawlak

Boston Children's Hospital

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