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 December 2003 NCSAC Meeting Summary: Obesity and Physical Development

Appendix V: National Children’s Study Advisory Committee 8th Meeting

Thematic Group Breakout Meeting Summary: Obesity and Physical Development

December 15, 2003
Sheraton Atlanta Hotel
Atlanta, GA

Chair: Robert T. Michael, Ph.D., NCSAC Member, University of Chicago

Working Groups represented at this thematic breakout session included Nutrition, Growth, and Pubertal Development; Community Outreach and Communications; Early Origins of Adult Health; Health Disparities and Environmental Justice; and Health Services. The group reviewed the hypotheses in the ICC subcommittee draft document and attempted to accomplish two things:

  • Identify areas that were not there but that should be. He mentioned obesity, physical development, and pubertal development.
  • Identify measures and timing of capturing the data. He added that what you get, when you get it, and how often you get it are important.

Revisions were made to each and four additional hypotheses were discussed but not added to the existing hypotheses. A list of questions from the ICC was noted. Dr. Michael said that Working Groups should provide answers and then return the document to Jan L. Leahey, NCSAC Executive Secretary, for distribution to the ICC.

Dr. Michael said that this is primarily an observational study, not an interventional study. The important question about obesity is how to solve it, rather than what causes it. The Study wants to know the causes so treatments can be developed. Propose a workshop that measures hormone levels between birth and 18 months. Puberty will be measured early. Potential measures must be reliable and repeatable.

Redundant/Overlapping Hypotheses

Dr. Michael noted that it is important to determine what would be most important for the hypotheses. He asked which measurements are most critical.

The attendees discussed the following hypotheses:

  • Hypothesis 1: Impaired maternal glucose metabolism during pregnancy is directly related to risk of obesity and insulin resistance in offspring.

  • Hypothesis 2: Intrauterine growth restriction, as determined by serial ultrasound examination, is associated with subsequent risk of central obesity and insulin resistance in offspring, independent of subsequent body mass index.

  • Hypothesis 3: Breast milk feeding, compared with infant formula feeding, and breastfeeding duration are associated with lower rates of obesity and lower risk of insulin resistance.

Participants determined that domains that require augmentation in the draft document are:

  • Gene–environment interaction
  • Access to food
  • Location of grocery stores
  • Level of physical activity
  • Amount of television watching
  • Linkage between puberty and obesity.

The group felt that the above domains were not adequately covered by the hypotheses, so they wrote three additional hypotheses. They view these as placeholders for information and measurements that need to be included in the hypotheses.

Soy is a phytoestrogen that is used to measure early exposure.

The Study needs to know what is in breast milk that could cause obesity. Evaluations should include the type of food eaten by mothers and measurement of any natural chemicals found in breast milk. A comparison between breast milk and formula is also needed. The amount of milk a child consumes varies over time. Therefore, duration of breastfeeding and reasons women stop breastfeeding should be studied as well.

Dr. Michael noted that the Study needs to measure what and when, the specifics of the domain of data capture, and at what ages and stages we want to capture.

Paula W. Yoon, Sc.D., M.P.H., National Center for Environmental Health, CDC, DHHS, Co-Chair of the Environment Working Group, added that gene-environment interaction should be included in this research. She also said that her Working Group had done a lot of work on gene-environment interaction and had submitted some hypotheses, although they were not discussed during this meeting.

  • Hypothesis 4: Dietary predictors of obesity and insulin resistance include reduced intake of fiber and whole grains, and high glycemic index.

    Reduced child intake; Type 1 Diabetes.

    The Study needs to specify fibers in dietary intake and food frequencies. What are the dietary predictors of obesity? Track schools they attend.

  • Hypothesis 5: Environmental factors such as distance to parks, availability of walking routes in the neighborhood, and neighborhood safety are associated with risk of obesity and insulin resistance.

    Dr. Chapin proposed that the Fertility and Early Pregnancy Working Group develop a priority list indicating whether the above agents are important. They should also answer whether our list is the same as theirs or are they inverted?

  • Hypothesis 6: Social, behavioral, and family factors that affect development of dietary preferences and physical activity patterns early in childhood determine risk of childhood obesity and insulin resistance.

  • Hypothesis 7: In utero and subsequent exposure to environmental agents that affect the endocrine system (bisphenol A, atrazine, and lead) results in altered age at puberty.
Attendees then discussed additional hypotheses. Hypothesis 8 was written by John H. Himes, Ph.D., M.P.H., School of Public Health, University of Minnesota.

  • Hypothesis 8: Environmental factors, that is, availability and access to foods, community, household, and food insecurity, are associated with dietary patterns and food choices of children. These choices and patterns are associated with increased risk of obesity.

  • Hypothesis 9: Consistent high levels of physical activity throughout childhood are associated with lower rates of obesity, lower risk of insulin resistance, and lower rates of type 1 diabetes.

    Sherry G. Selevan, Ph.D., Office of Research and Development, EPA, added that early childhood obesity or increased growth rate reduces in age at puberty in both onset and duration.

  • Hypothesis 10: Impaired maternal glucose metabolism during pregnancy interacts with the child’s genetic variation and is directly related to risk of obesity, insulin resistance, and Type 1 Diabetes in offspring.

Dr. Yoon noted that glucose challenge women experience during pregnancy is important to include in the study.

Outcome Measures

Discussion of measurements for the Study included:

  • What samples should be collected?
  • Where would the samples be stored?
  • How should the Study measure insulin resistance in very small children who grow rapidly and are prone to insulin resistance?
  • How to measure environmental contaminants in breast milk?
  • What types of chemicals are found in breast milk?
  • Why do women stop breastfeeding?
  • Compare types of formula used by mothers.
  • What is the availability of walking routes, food, and access to food?
  • Study the social, behavioral, and family factors that affect development of dietary preferences and physical activity patterns in early childhood, and how these factors determine risk of childhood obesity and resistance to diabetes.
  • What type of environment is the child living in?
  • What are the child’s attitudes about physical activities and diet?
  • What self-efficacy measures will be studied relative to knowledge and attitudes?
  • How and when will exposures be measured? Develop and list periods of concern. If certain exposures occur around conception, they can alter either pregnancy outcome or development of the reproductive system.
  • How to measure amounts of fibers, carbohydrates, and sugars?
  • Family medical history is very important.

Environmental Agents

Robert E. Chapin, Ph.D., Pfizer, Inc., provided the following partial list of environmental agents:

  • Organophosphates
  • Metals: lead, arsenic, mercury
  • Organochlorines
  • Phthalates (two)
  • Monophenols
  • Bisphenols
  • Triazenes
  • Air pollutants
  • Phytoestrogens
  • Closun [?]

In Attendance

Thematic Group Members

Chair: Robert T.Michael, Ph.D., Harris Graduate School of Public Policy Studies, University of Chicago
Robert E. Chapin, Ph.D., Investigative Development Toxicology Lab, Pfizer, Inc.
John H. Himes, Ph.D., M.P.H., School of Public Health, University of Minnesota
Pauline Mendola, Ph.D., Office of Research and Development, EPA
Nancy Potischman, Ph.D., National Cancer Institute, NIH, DHHS
Sherry G. Selevan, Ph.D., Office of Research and Development, EPA
Kristine O. Suozzi, Ph.D., Bernalillo County (NM) Environmental Health Department
Richard Y. Wang, D.O., National Center for Environmental Health, CDC, DHHS
Paula W. Yoon, Sc.D., M.P.H., National Center for Environmental Health, CDC, DHHS

Observers and Other Participants

Nancy M. Betts, Ph.D., R.D., Agricultural Research Division Education and Human Services, University of Nebraska
Michelle Chiezah, M.P.H., Hennepin County Community Health Department, Minneapolis, MN
Raffael Jovine, Ph.D., Booz Allen Hamilton, Inc.
Jan L. Leahey, NCSAC Executive Secretary, NICHD, NIH, DHHS

  6/26/2008
  6/26/2008