Lity of detecting an association with homocysteine, if any. The mechanism underlying the association among n3 PUFAs and homocysteine is just not but fully understood.Kume et al. Nutrition Metabolism 2013, 10:41 http://www.nutritionandmetabolism.com/content/10/1/Page 7 ofHomocysteine concentrations are partly determined by genetic things, which includes genes encoding enzymes involved in homocysteine metabolism such as MAT, cystathioninelyase (CSE) and 5methyltetrahydrofolate reductase (MTHFR) [12]. In an experimental study using human HepG2 cell, administration of n3 PUFA upregulated CSE and MTHFR mRNA expressions and downregulated MAT mRNA expression [12]. Compared with EPA and ALA, DHA showed much more pronounced effects in downregulating MAT mRNA expression [12]. Such regulatory effect of n3 PUFA on expression of those genes might cause decreased homocysteine concentration. Main strengths of this study contain a higher participation price (91 ) within a welldefined working population, the use of a biomarker of dietary fatty acid intake and adjustment for potentially crucial confounders like smoking, physical activity, vitamin B6, vitamin B12 and folate. In the present population, serum folate levels have been significantly related with both serum n3 and n6 PUFA and homocysteine levels, and some statistically significant associations within a folateunadjusted model disappeared right after adding serum folate towards the model, suggesting the value of adjustment for blood folate as a confounder. On the other hand, this study has some limitations. 1st, because of its crosssectional design, we can’t infer causality from our acquiring.751470-47-0 site Second, we measured serum fatty acid composition and homocysteine only at one point in time, which may not reflect longterm status.Fmoc-Gln(Trt)-OH In stock Third, because of close intercorrelations among PUFAs, the observed association for a certain fatty acid may well reflect its joint impact with other fatty acids on homocysteine. Fourth, we stored serum samples at 20 till fatty acid measurement. In this condition, there could be selective loss of PUFA as a result of oxidation more than time (30). Fifth, intraassay variation for DHA measurement was relatively big compared with other fatty acids. This measurement error is probably nondifferential and may have attenuated the DHA homocysteine association. Sixth, while we found a statistically considerable association between serum homocysteine levels and DHA, the distinction in mean homocysteine level among the highest and lowest tertiles of DHA was compact (0.PMID:23551549 63 nmol/mL). It remains elusive whether or not such a difference is of clinical significance. Seventh, while we’ve adjusted for recognized and recommended things associated with homocysteine levels, we can not exclude a possibility of bias because of other confounders or residual confounding. For instance, we adjusted for dietary vitamin B6 and B12 intakes, but not for their serum levels because of a lack of those data. The adjustment for blood levels of these vitamins might present distinct final results. Lastly, the study subjects didn’t represent a random sample with the Japanese population and therefore caution is expected in generalizing the present findings.Conclusions Reduced serum homocysteine concentrations had been observed amongst these with higher DHA in serum phospholipids in an apparently wholesome Japanese population. This acquiring adds to evidence to get a part of DHA in lowering homocysteine concentrations at fairly higher DHA levels. The protective effect of n3 PUFA might not be limited to.