Premature Hair Graying and Bone Mineral Density

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Abstract
In a recent case-control study, premature hair graying was found to be associated with osteopenia, suggesting that this might be a clinically useful risk factor for osteoporosis. We report a reexamina- tion of this possibility in 293 healthy postmenopausal women. Sub- jects experiencing onset of hair graying in their 20s tended to have lower bone mineral density throughout the skeleton (adjusted for age and weight) than those with onset of graying later in life. The same was true for those in whom the majority of their hair was gray by the age of 40 yr (n 5 16), in whom bone density was reduced by 7% in the femoral neck, 8% in the femoral trochanter, and 4% in the total body (P , 0.05) when compared with those not prematurely gray. Bone density at the lumbar spine and Ward's triangle showed similar trends that were not significant. However, premature hair graying explained only 0.6 -1.3% of the variance in bone mineral density within the population. We conclude that premature hair graying is associated with low bone density, but that its infrequency in the normal postmenopausal population leads to its accounting for only a tiny fraction of the variance of bone density. (J Clin Endocrinol Metab 82: 3580 -3583, 1997) T HE existence of clinical markers of osteoporosis is an attractive concept to help identify those people at par- ticular risk and may also give some insight into the patho- genesis of the condition. Recently, premature hair graying was reported to be associated with osteopenia (1). In this case-control study, premature hair graying was associated with a greater than 4-fold increased risk of osteopenia (de- fined as a lumbar spine bone mineral density (BMD) T-score ,2 1). This observation was made in subjects in whom there were no other identifiable risk factors for osteopenia nor conditions that might result in hair depig- mentation. This important observation was subject to a number of methodological limitations however. First, the subjects were drawn from three different sources, specifically patients re- ferred by their doctors, self-referrals, and volunteer subjects in clinical trials. It is not clear, therefore, that the cases and controls came from the same reference population, nor whether the proportion of cases and controls from each source were different. Second, although information on a large number of subjects was available for analysis, rigorous exclusion of potentially confounding conditions resulted in only 15% of those subjects with osteoporosis being included in the analysis. However 64% of those with premature hair graying were included, suggesting that the exclusion criteria affected cases and controls differently. Third, the decision to define premature hair graying as the majority of hair gray before age 40 yr was not justified and therefore might rep- resent a post hoc analysis of the data. Supporting this pos- sibility, Rosen et al. (1) were unable to show a significant correlation between age of hair graying and raw or age- adjusted BMD. Furthermore, defining osteopenia as a di- chotomous variable is arbitrary and does not reflect the con- tinuous relationship between BMD and fracture risk. In addition, BMD at sites other than the lumbar spine were not reported. Finally, inclusion of both male and female subjects in the same analysis may have introduced bias if there was gender disproportion in the contingency tables. The appli- cability of this interesting association to an otherwise healthy population at risk of osteoporosis (e.g. normal postmeno- pausal women) is, therefore, uncertain. We readdressed this question by examining the association between premature hair graying and BMD throughout the skeleton in 293 healthy postmenopausal women.

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