ples. We are also indebted to Si-Kang Gou and Si-Fang Wu for technical assistance. The work was supported by NSFC and Nat- ural Science Foundation of Yunnan Province.

Although we did not include centenarians, as did the study by Tanaka et al. (1998), the Old samples considered here can probably well-represent the long-lived popula- tion in China, considering the current longevity situation. The association of the 5178A with aging, as suggested by Tanaka et al. (1998, 2000), should be reflected in the three age samples under study. However, our results failed to detect an expected increase in frequency and thus gave no support to the suggestion of Tanaka et al. (1998, 2000). The disagreement between our results and those of Tanaka and his colleagues (1998, 2000) may reflect the possible error in distinguishing mtDNA haplogroup-specific muta- tion(s) from pathogenic or disease-associated mutation(s), especially when we deduced the possible function of mu- tation(s) in mitochondrial pathological disorders. For ex- ample, the mtDNA 3394 mutation in the NADH dehydro- genase subunit 1 gene (ND1) was reported to be associ- ated with non-insulin-dependent diabetes mellitus (Hirai et al. 1996). However, later studies showed that this muta- tion was a haplogroup-specific mutation for haplogroup M9a (Kivisild et al. 2002, formerly M9 in Yao et al. 2002) and occurred in 0–4.0% of normal Han Chinese from dif- ferent regional samples. Therefore, the statistical correla- tion between the clinical characteristics/habits and certain mtDNA mutation(s), if not tested further by pedigree analyses and mitochondrial function analysis, could be better explained as indications of the complex interactions among mitochondrial genes, nuclear genes, and the envi- ronment (Herrnstadt et al. 2002).

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Acknowledgements We thank Li Tong (The First Affiliated Hos- pital, Kunming Medical University ) for the help to collect sam-