Habitual dietary intake of ß-carotene, vitamin C, folate, or vitamin E may interact with single nucleotide polymorphisms on brachial-ankle pulse wave velocity in healthy adults.

PURPOSE: The interaction between genetics and diet may explain the present disagreement in the protective role of vitamin intake on cardiovascular disease. We cross-sectionally assessed the interaction of habitual dietary intake of ß-carotene, vitamin C, folate, and vitamin E with single nucleotide polymorphisms (SNPs) on brachial-ankle pulse wave velocity (baPWV), a measure of arterial stiffness. METHODS: Dietary intakes of ß-carotene, vitamin C, folate, and vitamin E were quantified by a food frequency questionnaire in 3198 healthy men and women (≥ 40 years) from the Korea Multi-Rural communities Cohort study. baPWV was measured, and 19 SNPs were genotyped. The associations and interactions between dietary vitamin intake, SNP genotype, and baPWV were assessed using general linear models. RESULTS: In both men and women, dietary intake of ß-carotene, vitamin C, folate, or vitamin E and baPWV were not directly associated. Vitamin C, folate, and vitamin E intake had an interaction with rs4961 (ADD1) genotype on baPWV in men. rs4961 also interacted with folate intake on baPWV in women. In women, rs10817542 (ZNF618) and rs719856 (CD2AP) had an interaction with ß-carotene and folate intake and rs5443 (GNB3) had an interaction with vitamin E intake on baPWV. In general, minor allele homozygotes with low vitamin intake had higher baPWV than other subgroups. Results were similar when supplement users were excluded. CONCLUSIONS: Higher intake of dietary vitamin C, folate, and vitamin E may be related to high baPWV in healthy Korean men who are minor allele homozygotes of rs4961. In healthy Korean women, dietary folate, ß-carotene, and vitamin E intake may affect baPWV differently according to rs4961, rs10817542, rs719856, or rs5443 genotype. Greater dietary intake of these nutrients may protect those that are genetically vulnerable to stiffening of the arteries.

Association of a RUNX2 promoter polymorphism with bone mineral density in postmenopausal Korean women.

Osteoporosis is characterized by impaired osteoblastogenesis. Bone mineral density (BMD) is a major determinant of bone strength. RUNX2 is an osteoblast-specific transcription factor involved in osteoblast differentiation and ossification. To determine whether RUNX2 is associated with BMD in an ethnically distinct population, we investigated SNPs within the two RUNX2 promoters (P1 and P2) using the Illuminar GoldenGate system in 729 postmenopausal Korean women. Subjects bearing the minor homozygote genotype (CC) at the RUNX2 -1025 T > C SNP (rs7771980) located in P2 showed a significant association with reduced lumbar spine BMD (p = 0.02) and BMDs at proximal femur sites (trochanter, p = 0.05; total femur, p = 0.04) compared with subjects carrying the major homozygote genotype (TT) or the heterozygote genotype (TC), respectively. These results present an interesting genotype association complementary to the previously reported association of BMD with the RUNX2 -1025 T > C P2 SNP in Spanish and Australian cohorts. Therefore, we suggest that the RUNX2 P2 polymorphism (-1025 T > C) may be a useful genetic marker for bone metabolism and may play an important role in BMD in postmenopausal Korean women.