European Journal of Endocrinology (2005) 152 179–184L-Tri-iodothyronine is a major determinant of resting energy expenditure in underweight patients with anorexia nervosa and during weight gainSimone Onur1, Verena Haas1, Anja Bosy-Westphal1, Maren Hauer1, Thomas Paul2, Detlev Nutzinger2, Harald Klein3 and Manfred J Müller1
There's a lot of confusion about the effects of dietary restriction on metabolic rates and whether there is such a thing as "starvation mode." This article clarified a lot of the issues for me--and is pretty fascinating from a physiological perspective. It's a little technical (and may be difficult to understand without the figures, which I couldn't figure out how to post), so here's a summary of the salient points.
The study examined the relationship between resting energy expenditure(REE), lean body mass, and "T3"--the active form of the thyroid hormone that is implicated in metabolic rates. (As you may know, under and over production of thyroid hormones result in metabolic slowdown or increases, respectively). The researchers found that compared with healthy controls, patients with anorexia have significantly lower resting energy expenditure (by about 20%) that correlates both with lower T3 levels and reductions in lean body mass. Notably, both of these factors are independently predictive of REE--implying that a person's metabolism slows not just b/c of muscle wasting, but also b/c of hormonal changes.
Interestingly, when the AN subjects began refeeding regimes, both their T3 levels and REE rates significantly rebounded, suggesting the T3 response may have a stabilizing effect in terms of weight gains or losses. T3 levels correlated strongly with changes in metabolic rates during refeeding. The authors also found that the relative contribution of increased lean mass to REE increases during refeeding is small because most of the weight regained, at least initially, is in the form of body fat.
Given that AN have normal levels of TSH (that stimulates the production of thyroid hormone) and T4 (the inactive/precursor form of the T3), the authors hypothesize that factors released by the fat tissue itself triggers the increase T3 production (i.e. the conversion of T4 to T3). The suggest increases in leptin release, a factor secreted by adipose tissue that is low in patients with AN, may result facillitate the coversion of thyroid hormone into its active form.
A couple of things to think about:
*The increase in REE with increased fat mass can paradoxically make it difficult for patients with AN to gain weight during refeeding, hence the atypically high calorie regimes used in treatment.
*This T3 response is evident in normal or overweight adults when they gain weight, but not to the same degree as in patients with AN.( Collapse )