6 discovered in bone [24], thereby providing a possible mecha- nism for interaction between nutritional and metabolic bone axes and resumption of menses. Our data are consistent with other studies examining the bone and hormonal changes that occur with refeeding in AN [2, 9]. In this present study, however, we searched for and found signiﬁcant correlations between REE and changes in BMD during nutritional rehabilitation. The main limitation was the size of the study population, for a larger sample would allow for control of various variables while examining correlations and would facilitate detection of diﬀerences between those who remained amenorrheic versus those who regained menses. Of note, it would have been interesting to follow the bone markers of the amenorrheics at 90% IBW to see if continuation of adequate nutritional intake would reverse bone loss and amenorrhea, two of the many important complications of AN [25]. In conclusion, we explore here an alternate hypothesis of the increase in REE during refeeding of AN patients to relate the increased energy expenditure to bone formation such that only after substantial BMD recovery are suﬃcient energy stores available for gonadal recovery. Bone recovery from osteopenic and osteoporotic states may take priority because of its survival advantage, a notion consistent with the reproductive then bone loss that occurs in AN. Further research is necessary to identify why one group of AN patients recovers bone mass and menses while undergoing the same nutritional rehabilitation as another group yet to recover either. Nonetheless, our hypothesis that bone recovery utilizes a vast amount of energy oﬀers the exciting possibility that prolonged nutritional rehabilitation may lead to recovery from osteopenia and osteoporosis and resump- tion of menses in the women who remain amenorrheic with low BMD. Disclosure M. Sum and L. Mayer have nothing to disclose. M. P. 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