Join the Discussion On: Obesity and energy balance: is the tail wagging the dog?

Ripe for the weekend ... Has Gary Taubes been right all along? Is the whole tautology of the First Law of Thermodynamics whacked? Do we have this direction wrong?  Well, apparently quite a few have seen the paper I'll be sharing with you through Google Docs, and thought just that!  First, I'd like to thank Matt Metzgar for the PDF.  

OK, so what's this all about?  

Obesity and energy balance: is the tail wagging the dog?
JCK Wells and M Siervo .   European Journal of Clinical Nutrition (2011), 1–17.

But marilynb aka mhb here has decided to share my link over at the LLVLC discussion board attributing the sharing to Matt.  Yes, he provided me with the PDF, and it's not "my" (or his) PDF, but I was sharing it through my Google Docs account via a link for my readers for the purpose of discussion.  I do not appreciate that being linked about without even properly acknowledging the source.  If you want to share and discuss, do it on your own account folks.   Some people are rather ... pathetic.

Anyway, anyone wanting the full text can email me and I'll be glad to provide it.  I'm going to have to rethink how to share full texts apparently.


The scientific study of obesity has been dominated throughout the twentieth century by the concept of energy balance. This conceptual approach, based on fundamental thermodynamic principles, states that energy cannot be destroyed, and can only be gained, lost or stored by an organism. Its application in obesity research has emphasised excessive appetite (gluttony), or insufficient physical activity (sloth), as the primary determinants of excess weight gain, reflected in current guidelines for obesity prevention and treatment. This model cannot explain why weight accumulates persistently rather than reaching a plateau, and underplays the effect of variability in dietary constituents on energy and intermediary metabolism. An alternative model emphasises the capacity of fructose and fructose-derived sweeteners (sucrose, high-fructose corn syrup) to perturb cellular metabolism via modification of the adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio, activation of AMP kinase and compensatory mechanisms, which favour adipose tissue accretion and increased appetite while depressing physical activity. This conceptual model implicates chronic hyperinsulinaemia in the presence of a paradoxical state of ‘cellular starvation’ as a key driver of the metabolic modifications inducing chronic weight gain. We combine evidence from in vitro and in vivo experiments to formulate a perspective on obesity aetiology that emphasises metabolic flexibility and dietary composition rather than energy balance. Using this model, we question the direction of causation of reported associations between obesity and sleep duration or childhood growth. Our perspective generates new hypotheses, which can be tested to improve our understanding of the current obesity epidemic, and to identify novel strategies for prevention or treatment.

I haven't had a chance to read this in full yet, but I will definitely be adding my two cents or more over the weekend.  However I already have some thoughts just from reading the abstract and keeping in mind that the lead author comes from the realm of Childhood Nutrition research.  Still, I'll let you folks have at it first.

Join in below!

Obesity and energy balance: is the tail wagging the dog?