Förändringar i homocystein- och 8-iso-PGF(2a)-nivåer efter fotbolls- & hockeymatcher

[King Grub]

The aim of the present study was to evaluate the levels of homocysteine and 8-iso PGF(2a) in football and hockey players before and soon after a match, on the predisposition for development of atherosclerosis. We measured 8-iso-PGF(2a) and homocysteine in 21 football athletes aged 21.8 ± 3.7 years old and 18 hockey athletes 22.2 ± 3.3 years old, respectively. All the athletes presented significant increases in serum homocysteine levels following the match (p = 0.001 for football and p = 0.001 for hockey players) Also a statistically significant increase of 8-iso-PGF(2a) levels was found in hockey and football athletes following the match (p < 0.001 and p = 0.071). Our findings suggest that strenuous exercise such as a football or a hockey match causes a marked increase in serum homocysteine and 8-iso-PGF(2a). Due to the fact that homocysteine and 8-iso-PGF(2a) are contributing to atheromatosis, it may be useful to follow a restoration exercise program that involves mild exercise and to pay special attention to folate, vitamin B6, and vitamin B12 balance during the first 24 h after the match.

Res Sports Med. 2011 Apr;19(2):118-128. Changes in Homocysteine and 8-iso-PGF(2a) Levels in Football and Hockey Players After a Match.

[mn8eii]

Mycket intressant!

Samtidigt har man ju inte funnit något vidare stöd för att homocysteinsänkande medel skulle ge någon sänkt risk för kardiovaskulära incidenter.

Background: Cardiovascular disease such as coronary artery disease, stroke and congestive heart failure, is a leading cause of death worldwide. A postulated risk factor is elevated circulating total homocysteine (tHcy) levels which is influenced mainly by blood levels of cyanocobalamin (vitamin B12), folic acid (vitamin B9) and pyridoxine (vitamin B6). There is uncertainty regarding the strength of association between tHcy and the risk of cardiovascular disease.
Objectives: To assess the clinical effectiveness of homocysteine-lowering interventions (HLI) in people with or without pre-existing cardiovascular disease.
Search Strategy: We searched The Cochrane Central Register of Controlled Trials (CENTRAL) on The Cochrane Library (issue 3 2008), MEDLINE (1950 to August 2008), EMBASE (1988 to August 2008), and LILACS (1982 to September 2, 2008). We also searched in Allied and Complementary Medicine (AMED; 1985 to August 2008), ISI Web of Science (1993 to August 2008), and the Cochrane Stroke Group Specialised Register (April 2007). We hand searched pertinent journals and the reference lists of included papers. We also contacted researchers in the field. There was no language restriction in the search.
Selection Criteria: We included randomised clinical trials (RCTs) assessing the effects of HLI for preventing cardiovascular events with a follow-up period of 1 year or longer. We considered myocardial infarction and stroke as the primary outcomes. We excluded studies in patients with end-stage renal disease.
Data Collection and Analysis: We independently performed study selection, risk of bias assessment and data extraction. We estimated relative risks (RR) for dichotomous outcomes. We measured statistical heterogeneity using I(2). We used a random-effects model to synthesise the findings.
Main Results: We included eight RCTs involving 24,210 participants with a low risk of bias in general terms. HLI did not reduce the risk of non-fatal or fatal myocardial infarction, stroke, or death by any cause (pooled RR 1.03, 95% CI 0.94 to 1.13, I(2) = 0%; pooled RR 0.89, 95% CI 0.73 to 1.08, I(2) = 15%); and pooled RR 1.00 (95% CI 0.92 to 1.09, I(2): 0%), respectively.
Authors' Conclusions: Results from available published trials suggest that there is no evidence to support the use of HLI to prevent cardiovascular events.
Martí-Carvajal AJ, Solà I, Lathyris D, Salanti G. Homocysteine lowering interventions for preventing cardiovascular events. Cochrane Database of Systematic Reviews 2009, Issue 4. Art. No.: CD006612. DOI: 10.1002/14651858.CD006612.pub2

[mn8eii]

Inte för att jag på något sätt ifrågasätter att det finns en korrelation mellan förhöjda homocysteinvärden och ateroskleros.

AIMS: Homocysteine upregulates expression of adhesion molecules on endothelial cells which recruits leukocytes and initiates atherosclerosis. Endothelial cells in hyperhomocysteinemic patients are continuously exposed to high levels of homocysteine. This study exposed adult endothelial cells and endothelial cells from immune naïve foetal tissue to homocysteine chronically and studied effects on cellular adhesion molecule expression under static and flow conditions.

METHODS: Human umbilical vein endothelial cells (HUVEC) and human saphenous vein endothelial cells (HSVEC) were cultured in medium containing 1 mM dl-homocysteine or l-cysteine for 5-9 days. Proliferation was assessed. Cells were subjected to flowing neutrophils and numbers of tethered, rolled fixed and transmigrated neutrophils on endothelial cells were counted and compared to controls. Immunofluorescence staining with antibodies against Intercellular adhesion molecule-1 (ICAM-1), E-selectin and P-selectin were used to quantify expression.

RESULTS: Chronic treatment with 1 mM homocysteine inhibited proliferation of HUVEC and HSVEC. Homocysteine treated cells showed significantly increased expression of ICAM-1, E-selectin and to a lesser extent P-selectin. In both cell types, homocysteine significantly increased interactions between neutrophils and endothelial cells under flow conditions (p < 0.05) while cysteine had no effect.

CONCLUSION: Endothelial cells from adult and immune naïve foetal tissue showed similar responses to chronic treatment with homocysteine.
Eur J Vasc Endovasc Surg. 2011 Mar;41(3):429-35. Epub 2010 Dec 14.

En review där de försöker reda ut "homocysteinkontroversen". Finns att läsa gratis dessutom för er som är mer intresserade: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3026670/ .

Mild to moderate hyperhomocysteinemia has been identified as a strong predictor of cardiovascular disease, independent from classical atherothrombotic risk factors. In the last decade, a number of large intervention trials using B vitamins have been performed and have shown no benefit of homocysteine-lowering therapy in high-risk patients. In addition, Mendelian randomization studies failed to convincingly demonstrate that a genetic polymorphism commonly associated with higher homocysteine levels (methylenetetrahydrofolate reductase 677 C>T) is a risk factor for cardiovascular disease. Together, these findings have cast doubt on the role of homocysteine in cardiovascular disease pathogenesis, and the homocysteine hypothesis has turned into a homocysteine controversy. In this review, we attempt to find solutions to this controversy. First, we explain that the Mendelian randomization analyses have limitations that preclude final conclusions. Second, several characteristics of intervention trials limit interpretation and generalizability of their results. Finally, the possibility that homocysteine lowering is in itself beneficial but is offset by adverse side effects of B vitamins on atherosclerosis deserves serious attention. As we explain, such side effects may relate to direct adverse effects of the B-vitamin regimen (in particular, the use of high-dose folic acid) or to proinflammatory and proproliferative effects of B vitamins on advanced atherosclerotic lesions.
J Inherit Metab Dis. 2011 Feb;34(1):93-9. Epub 2010 Jun 22

Och slutligen en sista meta-analys där de utforskar folsyrans eventuella roll i ateroskleros.

Experimental models and observational studies suggest that homocysteine-lowering therapy with folic acid (FA) may prevent cardiovascular disease (CVD). However, FA also stimulates cell proliferation and might promote progression of atherosclerosis. Our objectives were to perform a meta-analysis of FA supplementation trials on CVD events and to explore a potential interaction between FA supplementation and baseline homocysteine levels on CVD events. We searched MEDLINE for randomized controlled trials of FA supplementation to prevent CVD events (January 1966 to July 2009) and performed meta-analyses using random effects models. For trials that reported responses to FA supplementation stratified by baseline levels of homocysteine, we pooled within-trial estimates of differences in log-relative risks by baseline homocysteine levels using a random effects model. Overall, FA supplementation did not affect primary cardiovascular clinical end points (relative risk 1.02, 95% confidence interval [CI] 0.93 to 1.13, p = 0.66) or stroke (relative risk 0.95, 95% CI 0.84 to 1.08, p = 0.43). However, in trials that reported analyses stratified by baseline homocysteine, effect of FA supplementation differed by strata of baseline homocysteine (p for interaction = 0.030). Specifically, risks of primary clinical CVD events comparing FA supplementation to control were 1.06 (95% CI 1.00 to 1.13) in strata with mean baseline homocysteine levels >12 mumol/L and 0.94 (95% CI 0.86 to 1.03) in strata with baseline homocysteine levels <12 micromol/L. In conclusion, FA had no effect on CVD or stroke. However, analysis of within-trial results stratified by baseline homocysteine suggests potential harm in those with high homocysteine at baseline. This interaction may have important implications for recommendations of FA supplement use. In the meantime, FA supplementation should not be recommended as a means to prevent or treat CVD or stroke.
Am J Cardiol. 2010 Aug 15;106(4):517-27.