Local and systemic effects of cigarette smoking on folate and vitamin B−12

Piyathilake, Chandrika J.; Macaluso, Maurizio; Hine, R. Jean; Richards, Evelleen; Krumdieck, Carlos L.

doi:10.1093/ajcn/60.4.559

Cited by 228 publications

(182 citation statements)

References 19 publications

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“…The absence of a relationship between B 12 concentration and smoking is in keeping with most previous findings [24][25][26]29], although not all [30].…”

Section: Homocysteine Folate and Smokingsupporting

confidence: 90%

Homocysteine and coronary heart disease risk in the PRIME study

Troughton

Woodside

Arveiler³

et al. 2007

Atherosclerosis

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Introduction: Despite recent meta-analyses suggesting that homocysteine is an independent predictor of coronary heart disease (CHD), there is debate regarding whether elevated homocysteine may be deleterious only in the presence of other risk factors, with which it acts synergistically to exert a multiplicative effect on CHD risk, emerging only as a CHD predictor in patients with pre-existing risk factors.The Prospective Epidemiological Study of Myocardial Infarction (PRIME) Study is a multicentre prospective study of 10 593 men from France and Northern Ireland, investigating cardiovascular risk factors. We investigated: (1) whether higher homocysteine is associated with increased CHD risk in the PRIME case-control cohort; (2) whether homocysteine interacts synergistically with pre-existing CHD risk factors. Methods: Homocysteine was measured in 323 participants who had developed CHD at 5-year follow-up and in 638 matched controls. Results: There was no significant difference in homocysteine between cases and controls (p = 0.18). Homocysteine was significantly higher in current smokers (geometric mean mol/l (interquartile range mol/l) 9.45 (7.43, 11.75)) compared with non-smokers (8.90 (7.32, 10.70); p = 0.007). There was a significant interaction between homocysteine, smoking and CHD risk (χ 2 = 10.29, d.f. = 2, p = 0.006). Conclusions: These findings suggest that elevated homocysteine is significantly associated with CHD risk in current smokers.

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“…The absence of a relationship between B 12 concentration and smoking is in keeping with most previous findings [24][25][26]29], although not all [30].…”

Section: Homocysteine Folate and Smokingsupporting

confidence: 90%

Homocysteine and coronary heart disease risk in the PRIME study

Troughton

Woodside

Arveiler³

et al. 2007

Atherosclerosis

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“…The finding of an interaction effect between smoking and MTHFR(C677T) genotype has not been reported previously. A suboptimal plasma folate status among smokers (Piyathilake et al, 1994;Cafolla et al, 2000;O'Callaghan et al, 2002) might explain the observed interaction, as plasma folate has been shown to interact with MTHFR(C677T) genotype (Jacques et al, 1996b;Brattstrom et al, 1998;Girelli et al, 1998;McQuillan et al, 1999;Dekou et al, 2001;Saw et al, 2001). The involvement of folate is further supported by another study in which smoking was reported to interact with the dietary intake of folate (De Bree et al, 2001b).…”

Section: Discussionmentioning

confidence: 99%

Effect of lifestyle factors on plasma total homocysteine concentrations in relation to MTHFR(C677T) genotype. Inter99 (7)

et al. 2004

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Objective: To examine the associations between various lifestyle factors-smoking habits, physical activity, dietary habits, coffee, tea, and alcohol consumption-and homocysteine (tHcy) in relation to MTHFR(C677T) genotype. Design: Cross-sectional population-based study. Setting: Residents of Copenhagen County, Denmark. Subjects: A random sample of 6457 men and women aged 30-60 years drawn from the Civil Registration System and invited to a health examination in 1999-2001. A total of 2788 participants were included in the statistical analysis. Main outcome measures: tHcy was measured using a Fluorescent Polarization Immuno Assay. MTHFR-genotype was determined by PCR and RFLP analysis. Information about lifestyle factors was obtained from a self-administered questionnaire. Results: Daily smoking, less healthy dietary habits, and coffee drinking were associated with elevated tHcy concentrations independent of other determinants. Wine consumption was related to tHcy in a J-shaped manner, whereas beer consumption was negatively associated with tHcy after multiple adjustments. Interaction was observed between smoking status and MTHFRgenotype, smoking status and sex, and beer consumption and age. The effect of smoking was more pronounced in persons with the TT genotype and in women. The effect of beer consumption was more pronounced at younger than at older ages. Conclusions: Smoking status, dietary habits, coffee intake, wine, and beer consumption were major lifestyle determinants of tHcy. Changes in these lifestyle factors may reduce tHcy concentrations, thereby lowering cardiovascular risk in the general population.

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“…Low folate intake, tobacco smoking, and alcohol excess lead to hyperhomocysteinemia, probably by altering folate metabolism and by depleting vitamin B 6 stores (Cravo et al, 1996;Nygård et al, 1995Nygård et al, , 1998Piyathilake et al, 1994). Additionally, heavy coffee consumption increases homocysteine levels whereas tea, vitamin supplements, vegetable and fruit intakes, and physical activity are inversely related to circulating homocysteine (Appel et al, 2000;Broekmans et al, 2000;Brouwer et al, 1999;Nygård et al, 1997bNygård et al, , 1998Rasmussen et al, 2000).…”

Section: Aging Gender Lifestyle Factors and Other Causesmentioning

confidence: 99%

Impaired Homocysteine Metabolism and Atherothrombotic Disease

Durand

Prost²,

Loreau

et al. 2001

Laboratory Investigation

232

147

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SUMMARY:Based on recent retrospective, prospective, and experimental studies, mild to moderate elevation of fasting or postmethionine-load plasma homocysteine is accepted as an independent risk factor for cardiovascular disease and thrombosis in both men and women. Hyperhomocysteinemia results from an inhibition of the remethylation pathway or from an inhibition or a saturation of the transsulfuration pathway of homocysteine metabolism. The involvement of a high dietary intake of methionine-rich animal proteins has not yet been investigated and cannot be ruled out. However, folate deficiency, either associated or not associated with the thermolabile mutation of the N 5,10 -methylenetetrahydrofolate reductase, and vitamin B 6 deficiency, perhaps associated with cystathionine ␤-synthase defects or with methionine excess, are believed to be major determinants of the increased risk of cardiovascular disease related to hyperhomocysteinemia. Recent experimental studies have suggested that moderately elevated homocysteine levels are a causal risk factor for atherothrombotic disease because they affect both the vascular wall structure and the blood coagulation system. The oxidant stress that results from impaired homocysteine metabolism, which modifies the intracellular redox status, might play a central role in the molecular mechanisms underlying moderate hyperhomocysteinemia-mediated vascular disorders. Because folate supplementation can efficiently reduce plasma homocysteine levels, both in the fasting state and after methionine loading, results from further prospective cohort studies and from on-going interventional trials will determine whether homocysteine-lowering therapies can contribute to the prevention and reduction of cardiovascular risk. Additionally, these studies will provide unequivocal arguments for the independent and causal relationship between hyperhomocysteinemia and atherothrombotic disease. (Lab Invest 2001, 81:645-672).C ardiovascular diseases remain the leading cause of mortality in Western populations. Hyperlipoproteinemia, hypertension, diabetes, obesity, and tobacco smoking are the main risk factors for atherosclerosis and its thrombotic complications. However, these factors alone cannot account for all of the deaths caused by vascular pathologies.As early as 1969, clinical studies conducted in homocystinuric children revealed the importance of severe hyperhomocysteinemia in premature development of atherosclerosis and thromboembolism (McCully, 1983). According to numerous retrospective case-controlled studies, moderate increases in plasma homocysteine, which can be precisely quantitated by high performance liquid chromatography (HPLC), raise the risk for cardiovascular disease 2-fold, after adjusting for classic risk factors. Moreover, up to 20% to 40% of patients with vascular pathologies present moderate to intermediate hyperhomocysteinemia. However, results from prospective studies are inconsistent. Additionally, molecular mechanisms underlying hyperhomocysteinemia-induced vascular diseas...

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Local and systemic effects of cigarette smoking on folate and vitamin B−12

Cited by 228 publications

References 19 publications

Homocysteine and coronary heart disease risk in the PRIME study

Homocysteine and coronary heart disease risk in the PRIME study

Effect of lifestyle factors on plasma total homocysteine concentrations in relation to MTHFR(C677T) genotype. Inter99 (7)

Impaired Homocysteine Metabolism and Atherothrombotic Disease

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