COMMENTARY: THYROID HORMONE IN NEANDERTAL EVOLUTION: A NATURAL OR A PATHOLOGICAL ROLE?*

Jerome Dobson recently proposed a controversial explanation for the morphological characteristics found among "classic" Pleistocene Neandertals from central Europe (1998). Chronic iodine deficiency in these hominids, he suggests, either due to low dietary iodine consumption (a pathological causality) or as a consequence of genetically impaired iodine utilization (a biological causality), may have interfered with thyroid hormone metabolism to such an extent that normal human skeletal development was compromised. He states that "the number and quality of morphological similarities between cretins and Neandertals argues for iodine as a key factor in controlling Neandertal morphology.... Iodine deficiency, whether biological or pathological, could explain the apparent ease with which new Cro-Magnon arrivals swept aside their Neandertal predecessors. In either case, biological or pathological, recovery from cretinism may explain the total disappearance of certain Neandertal traits in subsequent populations" (p. 14 ). Although I believe Dobson's explanation is untenable, the apparent similarities he describes between modern endemic cretins and classic Neandertals are intriguing. Both Neandertal and cretin bones, Dobson points out, are particularly robust and thickened: The skull is large relative to body size, and the body trunk is disproportionately long compared with the short limbs. He illustrates the disproportionately short distal limb bones (radius/ulna, tibia/fibula) characteristic of Neandertals (Aiello and Dean 1990), a trait apparently shared with cretins. Similar skeletal traits, however, are seen in modern Inuit and Lapp (Sami) populations and in several Pleistocene carnivores, including the dire wolf and the saber-toothed cat (Stock and Lance 1948; Stock 1956; Kurten and Anderson 1980; Trinkaus and Shipman 1993; Wolpoff 1999). These last two species, now as inexplicably extinct as other members of the Pleistocene megafauna, are described as differing from their Holocene counterparts in skull size, limb proportions, and general robustness. A massive skull, heavy bone structure, and disproportionately shortened distal limb bones compared with those of closely related taxa are not, therefore, traits unique to Neandertals or even to the hominid lineage. I suggest that these skeletal characteristics indeed reflect thyroid hormone synthesis, but in a totally natural rather than pathological manner, because of the role that thyroid hormone plays in growth and development. The pathological changes associated with massive endemic cretinism that Dobson correlates with Neandertal morphology are reflected in the skeleton because they are a consequence of interference in normal fetal growth. This disruption in fetal growth is caused by a chronic deficiency of the iodine required for thyroid hormone synthesis in the mother, because fetuses require thyroid hormone from maternal sources for normal development (Hadley 1984; Geelhoed 1999; Crockford 2002). Iodine deficiency that continues after birth has further developmental repercussions, because the rapid brain and skeletal growth that occurs during the early postnatal period are also dependent on relatively high levels of available thyroid hormone (Hadley 1984; Geelhoed 1999). Consequently, not only do severely afflicted endemic cretins have modified skeletons, but most individuals also suffer such pronounced mental retardation that they are forever dependent on healthy individuals for basic care (Geelhoed 1999). This dependency on thyroid hormone for normal growth and development is characteristic of all vertebrates, not just humans (Waterman 1958; Hadley 1984). Surprisingly, although the essential nature of thyroid hormone in both fetal development and postnatal growth of vertebrates is well recognized, until now the evolutionary significance of this fact was not explored to any appreciable degree. …