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Cardiovascular Fitness Is Negatively Associated With Homocysteine Levels in Female Adolescents
Jonatan R. Ruiz, BSc;
Ricardo Sola, MD;
Marcela Gonzalez-Gross, PhD;
Francisco B. Ortega, BSc;
German Vicente-Rodriguez, PhD;
Miguel Garcia-Fuentes, MD, PhD;
Angel Gutierrez, MD, PhD;
Michael Sjöström, MD, PhD;
Klaus Pietrzik, PhD;
Manuel J. Castillo, MD, PhD
Arch Pediatr Adolesc Med. 2007;161(2):166-171.
Objective To examine the association between cardiovascular fitness and homocysteine levels in adolescents.
Design Cross-sectional study.
Setting Madrid, Murcia, Granada, Santander, and Zaragoza, Spain.
Participants One hundred fifty-six Spanish adolescents (76 boys and 80 girls) aged (mean ± SD) 14.8 ± 1.4 years.
Main Exposures Cardiovascular fitness was measured by the 20-m shuttle run test. Pubertal stage, birth weight, smoking status, and socioeconomic status were determined, and the sum of 6 skinfold thickness measurements, and serum folic acid and vitamin B12 levels were measured. Methylenetetrahydrofolate reductase (MTHFR; 677C>T genotype) polymorphism was done by DNA sequencing.
Main Outcome Measure Fasting homocysteine levels.
Results Mean values of homocysteine were significantly higher in the MTHFR 677CT and TT genotype subgroups compared with the CC genotype subgroup in adolescent boys, whereas in adolescent girls, mean values of homocysteine were significantly higher in the MTHFR 677CT and TT genotype subgroup compared with the CC and CT genotype subgroups. Multiple regression analyses showed that cardiovascular fitness was significantly associated with homocysteine levels in female adolescents after controlling for potential confounders including the MTHFR 677C>T genotype (β = –0.40; semipartial correlation = –0.35; P = .007). No associations were found between cardiovascular fitness and homocysteine levels in male adolescents (β = 0.12; semipartial correlation = 0.08; P = .51).
Conclusion The results suggest that cardiovascular fitness is negatively associated with homocysteine levels in female adolescents after controlling for potential cofounders including MTHFR 677C>T genotype.
Author Affiliations: Department of Medical Physiology, School of Medicine, University of Granada (Messrs Ruiz and Ortega and Drs Sola, Gonzalez-Gross, Gutierrez, and Castillo), Unit of Hematology, University Hospital San Cecilio, Granada (Dr Sola), E. U. Ciencias de la Salud, University of Zaragoza (Dr Vicente-Rodriguez), School of Sport Sciences, Universidad Politécnica de Madrid (Dr González-Gross), and Department of Pediatrics, University of Cantabria, Santander (Dr Garcia-Fuentes), Spain; Unit for Preventive Nutrition, Department of Biosciences and Nutrition at NOVUM, Karolinska Institutet, Huddinge, Sweden (Dr Sjöström and Messrs Ruiz and Ortega); and Institut fuer Ernaehrungswissenschaft, Pathophysiologie der Ernährung, Rheinische Friedrich-Wilhelms Universität, Bonn, Germany (Dr Pietrzik).
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ABSTRACT
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