ARTICLE: “Diabetes study looks at impaired prenatal diet: Research in baboons says restricting maternal diet could predispose child to diabetes.” Milwaukee Journal Sentinel [Milwaukee] 28 June 2011, E1-2.
TAKE HOME MESSAGE:
1) Do your homework and ask the right questions.
2) Learn to let go of a story angle that doesn't materialize....you're "on deadline" now.
3) Enjoy every minute of the access you'll get to a fabulous scientist!
QUESTIONS FOR STUDY AUTHOR:
1) Does this study help refute the myth that "the baby takes what it needs"?
2) You describe your findings as changes in "developmental programming" that may predispose a fetus to health effects later in life. Would you say this study helps support the Barker Hypothesis?
3) You developed your studies to better understand how sheep and rodent data can be extrapolated to primates. How closely does data described in promates reflect what has been observed clinically in humans?
4) In the baboon studies, you controlled for lifestyle factors. In human populations, can we ever really tease out prenatal factors predisposing to disease from predisposing lifestyle factors?
5) It appears as though none of the food-restricted females had preterm births, but we know that this can occur in humans. Is it a reasonable hypothesis organ impairments, such as you observed in baboons, could contribute to preterm birth?
6) Prediabetic markers are potentiated with age in type 2 diabetics. Is there a way to reverse the prediabetic state in baboons who experience changes in their developmental programming in utero...or is their fate sealed?
7) A woman who reads this article who suffers from hyperemesis in pregnancy, for example, might be alarmed to learn of these findings. Certainly, there are babies born to undernourished woman who have no apparent health effects. To what extent do you imagine there are compensatory mechanisms for the changes that may occur in a nutrient-stressed fetus?
8) Does the normal diet fed to primates resemble what would be considered normal intake by human females during pregnancy?
9) The group of animals receiving a normal diet had an n=12 and those on a restricted diet had an n=6. Why not equally distribute the number of animals between the two groups?
10) Age of pregancy of baboons was 11.5 years on average. How does this translate in human years?
11) The juveniles were described as 3.5 years og age. At what age would you expect to see the onset of pre-diabetic markers in humans?
12) Diagnosis of pregnancy occurred approximately 30 days into gestation. which is when you began the food restriction protocol. Do you anticipate that food restriction during the first 30 days of pregnancy might also have untoward effects on fetal or adult health?
13) You assayed beta cell function, but alpha cells have also emerged as cells that have some involvement in the pathophysiology of diabetes. Have you looked at any endpoints in alpha cells?
14) Can you describe some of the more mechanistic questions you might ask using an in vitro system?
15) Can you imagines the development of a test to screen for poor maternal or fetal nutrition? What markers might be good candidates for such a test?
QUESTIONS FOR OUTSIDE SOURCES:
1) How do you think this work adds to our understanding of the etiology of type 2 diabetes in children?
2) Do you see any drawbacks of this study? Are there any conclusions in this paper that you believe are too strong?
3) Can you comment on the prevalence of type 2 diabetes in pediatric or adolescent populations with whom you work?
4) Can you comment on the prevalence of “food deserts” or food insecurity in Milwaukee and to what extent a lack of maternal nutrition could be contributing to prediabetic markers in children?
1) I’m curious to know what you think the impact of this work is on our understanding of developmental programming.
2) I’m also interested in knowing how you think this work advances what we already know.
3) On the flip side, do you see any drawbacks of this study? Are there any conclusions you believe are too strong?