unhealthy lifestyle (Otten et al., 1990), which were shown to be associated with shortened LTL (Cherkas et al., 2006; Bekaert et al., 2007). Despite the racial differences in LTL and the rate of its shortening during adulthood, we found LTL to be heritable in both races. Might the longer LTL in African Americans than whites provide clues with regard to racial differences in life expectancy in the USA? Until recently, a controversy existed about the relation between LTL and mortality/survival in elderly persons (Cawthon et al., 2003; Martin-Ruiz et al., 2005; Bischoff et al., 2006; Harris et al., 2006; Honig et al., 2006). Of these, two studies (Cawthon et al., 2003; Honig et al., 2006) showed an association between mortality and LTL. The other three did not. We recently addressed this question in the Longitudinal Study of Aging Danish Twins, which comprises same-sex, elderly twins, whose mortality/survival was monitored for 10 years after leukocyte collection. The same-sex twin model is the most optimal to study the connection between mortality and LTL because it controls for genes, rearing environment, sex and age, all of which might impact LTL. Using Southern blot analysis approach, it was found that the co-twin with the shorter telomere parameters was likely to die first by the 4th year of the 10 years follow-up (Kimura et al., in press). Another study reported similar findings in same-sex Swedish twins (Bakaysa et al., 2007). The mechanisms that define the upper boundary of lifespan – namely, the survival of elderly individuals who withstood or did not suffer aging-related diseases during midlife – might not be the same as those that determine aging in the general population (Kimura et al., 2007). However, assuming that LTL is associated with lifespan in the elderly, there are curious observations regarding differences in mortality/survival between African Americans and whites. African Americans exhibit increased clustering of risk factors not only for CV disease but also other potentially lethal maladies; in the USA they display higher mortality rates and shorter life expectancy than whites (Otten et al., 1990). However, above the age of 70–80 years African Americans have been reported to exhibit lower mortality than whites (Markides & Machalek, 1984; Wing et al., 1985; Ford et al., 1990; Elo & Preston, 1994). This crossover phenomenon was challenged due to concerns that vital statistics data reflect systematic misreporting of age among elderly African Americans (Coale & Kisker, 1986; Preston et al., 1996). However, more recent work further supports the mortality crossover, at least with respect to coronary heart disease mortality (Corti et al., 1999). The etiology of this finding is unknown. The faster LTL short- ening in African Americans would narrow the racial difference in LTL, but the vestigial effect of the LTL ‘advantage’ in African Americans throughout most of adult life might narrow the racial gap in mortality in the elderly. A number of limitations of this study are noteworthy. First, this cross-sectional study is not as powerful as the longitudinal approach to examine leukocyte telomere dynamics. Second, our conclusions that LTL attrition rate is slower in African Americans than in whites between birth and early adulthood is based on Race and leukocyte telomere length, S. C. Hunt et al. 455 indirect evidence. Third, our study focuses on the racial difference in LTL without factoring a host of race-associated circumstances that might account for the narrowing of the racial gap in LTL. How- ever, the racial difference in LTL is of such a magnitude that it would probably eclipse the effect of any single environmental factor. We propose that race and ethnicity should be assessed in future studies that explore the associations between diseases of aging, CV disease, in particular, and leukocyte telomere parameters. Experimental procedures The cohorts The NHLBI FHS is a multicenter investigation of the genetic and epidemiologic basis of CV disease (Higgins et al., 1996). Between January 2002 and January 2004, 3359 family members were studied (2737 whites, 622 African Americans). The LTL data are derived from 1968 individuals from this cohort (1163 women, 805 men, 1395 whites and 573 African Americans) with an age range of 30–93 years. The BHS is a long-term community-based epidemiologic study of early natural history of CV disease beginning in childhood from the semirural, biracial community of Bogalusa, LA (Bogalusa Heart Study, 1995). Between September 1995 and December 1996, 1420 individuals (1011 whites, 409 African Americans) were examined for CV risk factors. The LTL data were derived from 485 individuals of this cohort who had stored blood available (301 women, 184 men, 247 whites and 138 African Americans) with an age range of 19 –37 years. The study protocol was approved by Institutional Review Boards of centers that oversee each of the participating cohorts and each participant gave written informed consent. Telomere length measurements The mean length of the TRFs, determined by Southern blot ana- lysis, was used to measure LTL on DNA extracted from peripheral leukocytes. We obtained the mean TRF length in two ways: our standard method (Okuda et al., 2002) and an ‘overlay’ method (Vasan et al., in press), both utilizing HinfI/RsaI restriction enzymes. (Description of the ‘overlay’ method, used for DNA samples derived from the FHS, is provided in the Supplementary Appendix S1.) For the standard method, the coefficient of variation for duplicate samples, which were resolved on different gels, was 1.43% while for the overlay method it was 2.40%. The correlation between the two methods was r = 0.99, p < 0.0001 (n = 24). In a subset of participants, TRF length was also measured in DNA digested with restriction enzymes HphI/MnII. The TRF length derived from these restriction enzymes highly correlated with that derived from HinfI/RsaI (r = 0.814, p = 0.0001; Supplementary Fig. S1). In the same subset we also measured telomere repeats by qPCR, using minor modification (Gardner et al., 2007) of the method originally described by Cawthon (2002). The coefficient of variation for duplicate samples undergoing qPCR on different days was 6.10%. The laboratory that conducted the TRF length and qPCR assays was blinded to the identity of the subjects. © 2008 The Authors Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2008