18
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Changes in Body Composition Predict Homocysteine Changes and Hyperhomocysteinemia in Korea

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Cardiovascular disease (CVD) is the primary cause of death in Korea. Hyperhomocysteinemia confers an independent risk for CVD comparable to the risk of smoking and hyperlipidemia. The purpose of this study was to assess the effect of cardiovascular risk factors and body composition change on homocysteine (Hcy) levels in Korean men and women. The association between body composition and Hcy levels was investigated in a 2-yr prospective cohort study of 2,590 Koreans (mean age 45.5±9.6 yr). There were 293 cases of hyperhomocysteinemia (>14 µM/L) at follow-up. Increases in total body fat proportion and decreases in lean body mass (LBM) were significantly associated with increases in Hcy concentration after controlling for confounding factors. Further adjustments for behavioral factors showed that decreases in LBM were associated with Hcy increase. Decrease in LBM also predicted hyperhomocysteinemia at follow-up, after controlling for confounding factors. There was no significant association between change in body mass index (BMI) and Hcy concentrations over time. Hcy changes over time were related to change in LBM and body fat content, whereas BMI or weight change did not predict change in Hcy levels. Changes in ratio of LBM to total fat mass may contribute to hyperhomocysteinemia.

          Related collections

          Most cited references26

          • Record: found
          • Abstract: found
          • Article: not found

          Plasma homocysteine as a risk factor for vascular disease. The European Concerted Action Project.

          Elevated plasma homocysteine is a known risk factor for atherosclerotic vascular disease, but the strength of the relationship and the interaction of plasma homocysteine with other risk factors are unclear. To establish the magnitude of the vascular disease risk associated with an increased plasma homocysteine level and to examine interaction effects between elevated plasma homocysteine level and conventional risk factors. Case-control study. Nineteen centers in 9 European countries. A total of 750 cases of atherosclerotic vascular disease (cardiac, cerebral, and peripheral) and 800 controls of both sexes younger than 60 years. Plasma total homocysteine was measured while subjects were fasting and after a standardized methionine-loading test, which involves the administration of 100 mg of methionine per kilogram and stresses the metabolic pathway responsible for the irreversible degradation of homocysteine. Plasma cobalamin, pyridoxal 5'-phosphate, red blood cell folate, serum cholesterol, smoking, and blood pressure were also measured. The relative risk for vascular disease in the top fifth compared with the bottom four fifths of the control fasting total homocysteine distribution was 2.2 (95% confidence interval, 1.6-2.9). Methionine loading identified an additional 27% of at-risk cases. A dose-response effect was noted between total homocysteine level and risk. The risk was similar to and independent of that of other risk factors, but interaction effects were noted between homocysteine and these risk factors; for both sexes combined, an increased fasting homocysteine level showed a more than multiplicative effect on risk in smokers and in hypertensive subjects. Red blood cell folate, cobalamin, and pyridoxal phosphate, all of which modulate homocysteine metabolism, were inversely related to total homocysteine levels. Compared with nonusers of vitamin supplements, the small number of subjects taking such vitamins appeared to have a substantially lower risk of vascular disease, a proportion of which was attributable to lower plasma homocysteine levels. An increased plasma total homocysteine level confers an independent risk of vascular disease similar to that of smoking or hyperlipidemia. It powerfully increases the risk associated with smoking and hypertension. It is time to undertake randomized controlled trials of the effect of vitamins that reduce plasma homocysteine levels on vascular disease risk.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Aging muscle.

            Age causes structural and functional changes in skeletal muscle in a wide range of species, including humans. Muscle changes in humans start in the fourth decade of life and cause frailty and disabilities. Associated changes in body composition form the basis of many metabolic disorders, such as insulin resistance, type 2 diabetes, hypertension, and hyperlipidemia, which result in an increased incidence of cardiovascular death. Decreases in the synthesis rates of many muscle proteins, specifically of myosin heavy chain and mitochondrial proteins, occur with age. The underlying causes of the reduction in mitochondrial biogenesis and ATP production seem to be decreases in mitochondrial DNA and messenger RNA. Reduced ATP production could be the basis of reduced muscle protein turnover, which requires energy. Both aerobic exercise and resistance exercise enhance muscle protein synthesis and mitochondrial biogenesis. Insulin and amino acids have also been shown to enhance muscle mitochondrial biogenesis and mitochondrial protein synthesis. However, the insulin-induced increase in muscle mitochondrial ATP production is defective in type 2 diabetic patients with insulin resistance. Moreover, a dissociation between increases in muscle mitochondrial biogenesis and insulin sensitivity after exercise has been noted in older persons. It remains to be determined whether muscle mitochondrial dysfunction causes or results from insulin resistance. Exercise seems to enhance the efficiency of muscle mitochondrial DNA in rodents. Reduced physical activity as a contributor of age-related mitochondrial dysfunction remains to be determined. It is proposed that a reduction in tissue mitochondrial ATP production signals the hypothalamic centers to reduce spontaneous physical activities. Voluntary physical activity is regulated by cognitive centers and could attenuate the progressive decline in mitochondrial functions that occurs with age.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Effect of physical activity on thiamine, riboflavin, and vitamin B-6 requirements.

              Because exercise stresses metabolic pathways that depend on thiamine, riboflavin, and vitamin B-6, the requirements for these vitamins may be increased in athletes and active individuals. Theoretically, exercise could increase the need for these micronutrients in several ways: through decreased absorption of the nutrients; by increased turnover, metabolism, or loss of the nutrients; through biochemical adaptation as a result of training that increases nutrient needs; by an increase in mitochondrial enzymes that require the nutrients; or through an increased need for the nutrients for tissue maintenance and repair. Biochemical evidence of deficiencies in some of these vitamins in active individuals has been reported, but studies examining these issues are limited and equivocal. On the basis of metabolic studies, the riboflavin status of young and older women who exercise moderately (2.5-5 h/wk) appears to be poorer in periods of exercise, dieting, and dieting plus exercise than during control periods. Exercise also increases the loss of vitamin B-6 as 4-pyridoxic acid. These losses are small and concomitant decreases in blood vitamin B-6 measures have not been documented. There are no metabolic studies that have compared thiamine status in active and sedentary persons. Exercise appears to decrease nutrient status even further in active individuals with preexisting marginal vitamin intakes or marginal body stores. Thus, active individuals who restrict their energy intake or make poor dietary choices are at greatest risk for poor thiamine, riboflavin, and vitamin B-6 status.
                Bookmark

                Author and article information

                Journal
                J Korean Med Sci
                J. Korean Med. Sci
                JKMS
                Journal of Korean Medical Science
                The Korean Academy of Medical Sciences
                1011-8934
                1598-6357
                July 2013
                03 July 2013
                : 28
                : 7
                : 1015-1020
                Affiliations
                [1 ]Department of Family Practice and Community Health, Ajou University School of Medicine, Suwon, Korea.
                [2 ]Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA.
                Author notes
                Address for Correspondence: Anastasia Georgiades, PhD. Duke University Medical Center, Durham, Box 3842 NC 27710, USA. Tel: +1-919-684-9905, Fax: +1-919-681-7347, anastasia.georgiades@ 123456duke.edu
                Article
                10.3346/jkms.2013.28.7.1015
                3708071
                23853483
                2490c407-92c3-4076-956f-8c9ad04e3c04
                © 2013 The Korean Academy of Medical Sciences.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 February 2012
                : 30 April 2013
                Categories
                Original Article
                Cardiovascular Disorders

                Medicine
                body composition,lean body mass,hyperhomocysteinemia
                Medicine
                body composition, lean body mass, hyperhomocysteinemia

                Comments

                Comment on this article