In the May/June issue of the journal Childhood Obesity is an editorial titled “Behavioral Research Agenda in a Multietiological Approach to Child Obesity Prevention,” whose authors are Tom Baranowski, Ph.D.; Kathleen J. Motil, M.D.; and Jennette P. Moreno, Ph.D.
It has become pretty clear that the energy balance model of obesity causation does not always hold up. Less clear are the reasons why the energy in/energy out formula seems inadequate to explain all the observed variation in obesity.
According to the authors, adherence to energy balance orthodoxy has resulted in interventions which…
[…] have either not worked, or had small effects, not nearly enough to halt the epidemic. In the process, a serious disconnect has developed between advances in biological and in behavioral sciences in regard to obesity prevention. Experts have criticized [the energy balance model] for not reflecting the likely multifactorial nature of obesity. A substantial number of other possible, even likely, causes of obesity have been identified…
But possibility and likelihood are not proof. Many “obesity villains” have been named as suspects and, regarding most of them, the jury is still out. This paper describes three.
The term “infectobesity” refers to virus-related infection, specifically the province of adenovirus 36. The theory points to two major areas that need solid research: how many infected kids become obese and, conversely, how many obese children are infected.
Scientists face a daunting number of questions, including, “How is adenovirus 36 spread?” That’s right, we don’t even know how it gets around. The hope is the research could lead to a vaccine against it.
This word signifies an imbalance amongst the various kinds of bacteria present in the microbiome. Current thinking is that the particular types of bugs inhabiting our digestive systems are less important than the relative size of their populations. This theory goes beyond the bacterial phyla that are present, and drags viral, fungal, and eukaryotic phyla into the net of obesogenic suspicion.
The intestinal bacteria give evidence of not liking processed foods, antibiotics, morphine and various other medications, sundry household cleaning products, and quite a few other things. When these substances and conditions throw their world into disorder, some of their responses appear to change the host body by making it fatter. Again, an enormous amount of research stands between these clues and any definitive answers.
The microbiome is suspected of influencing obesity for a number of secondary reasons. The bugs have been shown to affect appetite, cravings, addiction, diabetes, mood swings, autism, depression, stress, the immune system, and ghrelin, leptin, and other hormones. All those things are sometimes connected with obesity.
Children’s weight appears to be influenced by the timing of sleep, activity, and meals. American parents have become accustomed to hearing that poor sleep habits can lead to obesity. The screen-time factor enters into this, as many vociferous battles have been fought over how soon before bedtime the electronic screens must be turned off.
But wait. The authors say,
Sleep duration or disturbances have not been related consistently to obesity in children.
The experts conclude that these three factors and many, many others need to be studied in depth. To complicate matters even further, “subsets of children develop obesity at different ages,” and sleep deprivation harmful to a toddler might not affect an older child or teen. When many factors are involved, the possibilities multiply exponentially.
(To be continued…)
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