Importance of both folic acid and vitamin B12 in reduction of risk of vascular disease

Quinlivan, Eoin P.; McPartlin, Joseph; McNulty, Helene; Ward, Mary; Strain, JJ; Dg, Weir; Scott, J. M.

doi:10.1016/s0140-6736(02)07439-1

Cited by 192 publications

(118 citation statements)

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“…This part of the study examined the possibility that homocysteine-lowering in response to riboflavin may be obscured by a much greater effect of folate status. The hypothesis addressed in part 2 was therefore that once folate status had been optimized, a dependence of tHcy on riboflavin might emerge, similar to the dependence of tHcy on vitamin B 12 that emerges following folic acid supplementation, as recently reported by our group (Quinlivan et al, 2002). The results show that, in response to folic acid supplementation, tHcy concentrations decreased significantly (by 19.6%), demonstrating that baseline tHcy concentrations were indeed lowerable by nutritional intervention in these subjects.…”

Section: Discussionsupporting

confidence: 62%

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status

et al. 2002

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Objective: To investigate the effect of riboflavin supplementation on plasma homocysteine (tHcy) concentrations in healthy elderly people with sub-optimal riboflavin status. Design: A double-blind, randomized, placebo-controlled riboflavin supplementation trial. Setting: Community based study in Northern Ireland. Subjects: From a screening sample of 101 healthy elderly people, 52 had sub-optimal riboflavin status (erythrocyte glutathione reductase activation coefficient, EGRAC ! 1.20) and were invited to participate in the study. Intervention: The intervention had two parts. Part 1 was a 12 week randomized double blind, placebo-controlled intervention with riboflavin (1.6 mg=day). Following completion of part 1, the placebo group went on to part 2 of the study which involved supplementation with folic acid (400 mg=day) for 6 weeks followed by folic acid and riboflavin (1.6 mg=day) for a further 12 weeks, with a 16 week washout period post-supplementation. The purpose of part 2 was: (a) to address the possibility that homocysteine-lowering in response to riboflavin may be obscured by a much greater effect of folate, and that, once folate status was optimized, a dependence of homocysteine on riboflavin might emerge; and (b) to demonstrate that these subjects had homocysteine concentrations which could be lowered by nutritional intervention. Results: Although riboflavin supplementation significantly improved riboflavin status in both parts 1 and 2 of the study (P < 0.001 for each), tHcy concentrations were unaffected (P ¼ 0.719). In contrast, folic acid supplementation (study part 2) resulted in a homocysteine lowering of 19.6% (P ¼ 0.001). Conclusion: Despite the metabolic dependency of tHcy on riboflavin, it did not prove to be an effective homocysteine-lowering agent, even in the face of sub-optimal riboflavin status.

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Section: Discussionsupporting

confidence: 62%

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status

et al. 2002

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“…Hyperhomocysteinaemia has been associated with cardiovascular diseases (Eikelboom et al, 1999;Graham, 1999;Brattström and Wilcken, 2000;Wald et al, 2002) and folate supplements may reduce plasma levels and vascular risk (Chait et al, 1999;Selhub et al, 2000;Quinlivan et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Nutritional determinants of plasma total homocysteine distribution in the Canary Islands

et al. 2006

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Objective: We sought to define plasma homocysteine reference values in healthy individuals in the Canary Islands and to determine its relations to folate and vitamin B12 intakes and concentrations. Design: Cross-sectional study. Setting: Population-based representative sample of 557 participants, aged 18-65 years, from the Canary Islands Nutrition Survey (ENCA). Subjects: All participants completed two 24-h dietary recalls and a general questionnaire collecting socio-demographic and health-related lifestyle information. Interventions: Plasma homocysteine and serum vitamin B12 levels were measured by immunoassay, whereas folate levels through an automated ionic capturing method. Results: Median plasma homocysteine was 11.9 mmol/l, higher in men (13.1 mmol/l) than in women (10.9 mmol/l) (Po0.001) and positively associated with age in both sexes (Po0.001). The prevalence of hyperhomocysteinaemia (X15 mmol/l), 21.4%, was also greater in men (32.2%) than in women (13.4%). There were significant negative correlations between plasma homocysteine and serum (r ¼ À0.32, Po0.001) and erythrocyte (r ¼ À0.26, Po0.001) folate, as well as serum vitamin B12 (r ¼ À0.28, Po0.001) concentrations. When divided in quartiles of vitamin intakes or concentrations, men with the lowest vitamin B12 and folate serum values had significantly higher plasma homocysteine concentrations than those in the other three quartiles. In women, hyperhomocysteinaemia was higher in the lowest quartiles of folate intake and serum and erythrocyte folate concentrations. Conclusions: These data provide further evidence that hyperhomocysteinaemia is a sensitive marker of inadequate folate and vitamin B12 status, allowing for the identification of those with greatest need for nutritional interventions.

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“…In questo caso, il miglioramento della funzione endoteliale e la normalizzazione dei livelli plasmatici di omocisteina sono stati ottenuti senza terapia con acido folico, ma soltanto con un programma riabilitativo. Tale dato conferma i risultati di uno studio in precedenza effettuato su pazienti con cardiopatia ischemica sottoposti a un programma riabilitativo simile a quello effettuato nell'esempio soprariportato [69]. Il meccanismo con cui il training riduce i livelli plasmatici di omocisteina può essere duplice.…”

Section: Aspetti Fisiopatologiciunclassified

“…E stato così evidenziato non solo il suo coinvolgimento nelle reazioni di sintesi degli acidi nucleici (DNA e RNA) e la sua stretta correlazione con la vitamina B12, ma anche nelle malattie vascolari tromboemboliche, nelle malattie cardiovascolari, associato secondo alcuni alla vitamina B12 [69,70], nella depressione [30], molto verosimilmente nella demenza senile e nell'Alzheimer [31,[72][73][74], in alcune forme neoplastiche dell'intestino [75]. Il suo deficit nell'insorgenza delle anomalie del tubo neurale, oramai noto da tempo, ha suggerito la fortificazione delle farine di più comune impiego per aumentare, in tutta la popolazione comprese le donne con possibile gravidanza non programmata (50%), i bassi livelli nell'organismo di tale vitamina secondari soprattutto allo scarso consumo di legumi, vegetali e frutta.…”

Section: Conclusioniunclassified

Hyperhomocysteinemia in developing age and nutritional aspects of folates: an early cardiovascular risk factor

Caramia¹,

Belardinelli²

2016

Monaldi Arch Chest Dis

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RASSEGNA IntroduzioneAlcune malattie dell'età evolutiva sono causate da mutazioni di geni che codificano proteine specifiche con conseguente alterazione della struttura e/o della quantità di proteina sintetizzata. Ne derivano degli errori congeniti del metabolismo in quanto, la capacità funzionale della proteina, sia essa un elemento strutturale o un enzima, o un recettore, o un veicolo di trasporto, o una pompa di membrana, può essere più o meno compromessa.Molte mutazioni genetiche sono prive di conseguenze e determinano solo quel polimorfismo che differenzia gli individui. Altre volte gli errori congeniti del metabolismo che ne derivano danno luogo ad una sintomatologia o ad uno stato di malattia variabile, da molto lieve a letale, nella prima infanzia o nell'età evolutiva o più tardi ancora nel giovane adulto e nell'anziano.Una tale situazione si può verificare anche nel ciclo metabolico dell'aminoacido essenziale metionina. Questa, introdotta con alcuni alimenti quali carne, latte, uova, ma anche fagioli e legumi, per la perdita di un gruppo metilico dà luogo alla formazione di circa 26 mmoli di omocisteina attraverso l'attivazione della metionina ad adenosilmetionina (SAMe), donatore universale del gruppo metilico, che ceduto il metile produce adenosilomocisteina la quale per idrolisi libera omocisteina e adenosina.L'omocisteina può essere a sua volta trasformata di nuovo in metionina attraverso un processo di rimetilazione. Questa reazione risparmiatrice di metionina è catalizzata dall'enzima metionina sintetasi (MS) che richiede il 5 metil-tetraidrofolato (MTHF) come substrato e la metilcobalamina come cofattore per trasferire il gruppo metilico del MTHF all'omocisteina: si formano così metionina e tetraidrofolato (THF). Il ciclo tende a conservare metionina che, nella forma attivata (SAMe), è il maggior donatore di metili per DNA, RNA, etc. [1,2].A livello epatico, dove il metabolismo della metionina è particolarmente attivo, oltre all'enzima folato-dipendente è presente un altro enzima che produce per metilazione metionina da omocisteina: è una metiltransferasi che utilizza come donatore di metili la betaina o trimetilglicina.Se la metionina è introdotta in eccesso viene inibita la metionina sintetasi, per ridurre la sintesi di metionina, e si attiva, con una serie di reazioni di transulfurazione irreversibile ad opera di due enzimi vitamina B6 dipendenti, la Cistationina-β-sintasi e la β-Cistationasi, per formare cistationina e cisteina During the last decade, scientific evidence is mounting that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Despite this evidence, however, there are still concerns about the mechanisms(s) by which homocysteine exerts its pro-atherogenic effect, and it is unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherog...

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Importance of both folic acid and vitamin B12 in reduction of risk of vascular disease

Cited by 192 publications

References 3 publications

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status

Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status

Nutritional determinants of plasma total homocysteine distribution in the Canary Islands

Hyperhomocysteinemia in developing age and nutritional aspects of folates: an early cardiovascular risk factor

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