A Challenging Perspective on Bone Loss in AN

Reprinted from Eating Disorders Review
September/October 2009 Volume 20, Number 5
©2009 Gürze Books

An Australian researcher contends that in-vivo bone densitometry measurements do not prove that anorexia nervosa (AN) induces actual loss of bone mineral. Instead, the researcher states that the changes are actually due to soft-tissue effects from the disease.

Dr. H.H. Bolotin of the Royal Melbourne Institute of Technology, Victoria, Australia, writes that since the advent of noninvasive in-vivo bone densitometry studies, investigators have reported that loss of regional bone mineral material occurs at the onset of AN and continues throughout the course of the illness. However, Dr. Bolotin also notes that over the intervening 20 years of studies of patients with AN, no specific underlying direct bone-biological causal link between AN and trabecular bone loss has yet been uncovered (Bone 2009; 44:1034).

According to Dr. Bolotin, in-vivo single-energy photon absorptiometry (SPA), dual-energy absorptiometry (DXA), and single-energy quantitative computer-assisted tomographic (SEQCT) measurements of bone mineral loss do not constitute evidence of actual loss of bone, and thus that attributing osteopenia and osteoporosis to AN-afflicted adolescent girls is unfounded. Instead, he says, the bone “losses” can be accounted for by the already well-documented AN-induced changes in extra-osseous soft tissues (particularly in extraskeletal fat) and intraosseous bone marrow yellowing (marrow hypoplasia and marrow cell necrosis). Dr. Bolotin points out that these changes in soft tissue composition and the anthropomorphics of this young population are in themselves enough to cause most bone imaging tests to systematically misestimate true bone density and erroneously register changes in bone mineral content.

Thus, Dr. Bolotin believes that DEXA and SEQCT bone density measurements of predominantly trabecular bone sites cannot be relied upon as a gauge of increased risk of early (or late) development of osteoporosis in patients with AN. 
It should be noted that Dr. Bolotin’s hypothesis contradicts most studies that have been published about osteoporosis and osteopenia in relation to AN. Additional research will be needed to resolve this important clinical controversy.

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