Author Interviews, Nutrition, Pediatrics, Sugar, Weight Research / 26.09.2019
Excess Sugar in Childhood Linked to Adult Obesity Epidemic
MedicalResearch.com Interview with:
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Dr. Bentley[/caption]
Professor Alex Bentley
Head of Anthropology
University of Tennessee
Knoxville TN
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: In recent years, considerable evidence has accumulated suggesting that excess sugar consumption, e.g. in sugar-sweetened beverages, has been a major driver of the U.S. obesity crisis. Critics of this idea, however, have asked: why did the rise in sugar consumption precede the U.S. obesity crises by a decade or more, and why did obesity continue to rise even after sugar consumption began declining the early 2000s?
We modeled the delayed onset of obesity by assuming that diet is a cumulative process that begins in childhood. On average, each age cohort (birth year) has its own specific cumulative exposure to excess sugar in their diets. The inherent delay in our model links childhood consumption of excess sugar with propensity for adult obesity as an adult. Our model explains a simple process by which excess sugar in diets of children of the 1970s and 1980s could explain the sharp increase of adult obesity that began in the 1990s.
Dr. Bentley[/caption]
Professor Alex Bentley
Head of Anthropology
University of Tennessee
Knoxville TN
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: In recent years, considerable evidence has accumulated suggesting that excess sugar consumption, e.g. in sugar-sweetened beverages, has been a major driver of the U.S. obesity crisis. Critics of this idea, however, have asked: why did the rise in sugar consumption precede the U.S. obesity crises by a decade or more, and why did obesity continue to rise even after sugar consumption began declining the early 2000s?
We modeled the delayed onset of obesity by assuming that diet is a cumulative process that begins in childhood. On average, each age cohort (birth year) has its own specific cumulative exposure to excess sugar in their diets. The inherent delay in our model links childhood consumption of excess sugar with propensity for adult obesity as an adult. Our model explains a simple process by which excess sugar in diets of children of the 1970s and 1980s could explain the sharp increase of adult obesity that began in the 1990s.










Dr. Hui Wang[/caption]
Prof Hui Wang PhD
Wuhan University
China
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: We started our work in the adverse outcome of maternal caffeine intake during pregnancy about 15 years ago. Then, we found that prenatal caffeine intake could result in nonalcoholic fatty liver disease in the offspring. However, the underlying mechanism was unclear.
So, we start the current work, and found that hat maternal caffeine intake disrupts liver development before and after birth, which might be the trigger of the adult non-alcoholic fatty liver disease in the offspring rats. Moreover, we further found that the fetal programming of liver glucocorticoid – insulin like growth factor 1 axis, a new endocrine axis first reported by our team, might participate in such process.

