Distribution of and Factors Associated With Serum Homocysteine Levels in Children

Abstract

HE OPPORTUNITY FOR PRIMARY prevention of cardiovascular disease (CVD) begins during childhood. 1 Specifically,earlylesions of atherosclerosis are present in the arteries of children and adolescents 2 ; some children display moderate to high levels of physiologic risk factors 3 ; and childhood levels of physiologic risk factors may predict adult levels. 3-5 Recent studies suggest that plasma homocysteine concentration may be an independent and modifiable risk factor for CVD in adults. 6 A meta-analysis found for every 5-µmol/L increase in homocysteine, the odds ratio for risk of coronary artery disease was 1.6 (95% confidence interval [CI], 1.4-1.7) for men and 1.8 (95% CI, 1.4-2.3) for women. 7 Although conclusive evidence for a causal association with CVD in adults is lacking, 7-17 the potential for prevention provides a strong rationale for understanding the determinants of homocysteine in children.

Plasma homocysteine concentration and blood pressure in healthy Iranian adults: the Tehran Homocysteine Survey (2003–2004)

“…39,40 Several studies also showed a significant association between Hcy and BP, [4][5][6][41][42][43][44][45] or HTN; 1,46 however, no association was found in other studies 47,48 (Table 6). Recently, a randomized, placebo-controlled, Hcy-lowering trial reported a decrease in BP in response to treatment.…”

Factors associated with risk of low folate intake among adolescents

“…A associação entre níveis plasmáticos elevados de homocisteína e ingestão deficiente de folato foi demonstrada por vários estudos 1,14,15 , em função da necessidade desse nutriente para a conversão de homocisteína em metionina. A partir dos dados da NHANES III (estudo longitudinal de base populacional desenvolvido pelo Departamento de Saúde dos EUA), foi possível constatar que as concentrações de homocisteína plasmática entre os adolescentes e adultos norte-americanos tende a aumentar com a idade em ambos os sexos, sendo que esse aumento é mais acelerado no sexo masculino do que no feminino 16 .…”

Nutritional aspects and possible pathological mechanisms of hyperhomocysteinaemia: an independent risk factor for vascular disease

“…Studies in children and adolescents have found no difference between homocysteine levels of boys and girls (Tonstad et al 1996a(Tonstad et al , 1997Reddy, 1997;De Laet et al 1999;Greenlund et al 1999) until after puberty (Tonstad et al 1997;Vilaseca et al 1997;De Laet et al 1999), when homocysteine levels tend to increase markedly and a male-female difference becomes apparent, probably as a result of increased muscle mass and sex hormone concentration at this stage of development. In terms of ethnic differences, Greenlund et al (1999) found no differences between black and white children, but Ubbink et al (1996) and Osganian et al (1999) found higher homocysteine levels in blacks v. whites. It would be useful to have some longitudinal studies which would assess the potential impact of homocysteine levels in childhood on coronary artery disease risk in later life.…”

“…It is still unknown if vitamin B 6 exerts its effect on vascular disease directly through its various effects on platelets (Subbarao et al 1979;Konecki & Feinberg 1980;Lam et al 1980), connective tissue (Murray et al 1978;Myers et al 1985) and thromobogenesis (Editorial, 1981;Hladovec, 1979), or indirectly by causing the accumulation of homocysteine (Mudd et al 1995). Many studies have found a significant (P < 0·05) inverse relationship between homocysteine levels and vitamin B 6 status (Brattstrom et al 1992b, Stampfer et al 1992Selhub et al 1993;Robinson et al 1995Robinson et al , 1998Verhoef et al 1996Verhoef et al , 1997aGraham et al 1997;Osganian et al 1999) and an accumulation of homocysteine in vitamin B 6 depletion-repletion studies (Smolin et al 1983;Shultz & Hansen, 1998), which would support an indirect relationship between vitamin B 6 and vascular disease mediated via homocysteine. However, some studies have failed to find any relationship between vitamin B 6 and homocysteine (Brattstrom et al 1990;Dalery et al 1995;Riggs et al 1996;Ubbink et al 1996;Dierkes et al 1998;Healy et al 1998;Bates et al 1999), and the findings of vitamin B 6 depletion-repletion studies are contradictory (Smolin et al 1983;Miller et al 1992;Stabler et al 1997;Shultz & Hansen, 1998).…”