Depression is a major health problem, especially for elderly people. According to the “homocysteine hypothesis of depression”, high homocysteine levels may cause depression of mood via cerebrovascular diseases. Whil...Depression is a major health problem, especially for elderly people. According to the “homocysteine hypothesis of depression”, high homocysteine levels may cause depression of mood via cerebrovascular diseases. Whilst biologically plausible, such hypothesis needs yet confirmation. We aimed at: 1) studying the relationships between homocysteinemia (HCY) and depression in a community-dwelling cohort of people aged 70 to 75 years at baseline;2) investigating plasma levels of HCY and 3) comparing these levels between males and females, in the same population. We exploited the data from four waves (2010, 2012, 2014 and 2018) of the longitudinal study “InveCeAb”, with specific regard towards mood assessment, by Geriatric Depression Scale (GDS) scoring, and diagnosis of clinically relevant or subthreshold depression. HCY plasma levels were measured in the waves 2012, 2014 and 2018. Sample attrition was due mainly to death or overall worsening. No statistically significant differences were found in plasma homocysteine levels in each wave, according to depressive symptoms. No correlations were found between plasma HCY levels in each wave with their corresponding GDS scores, even after adjustment for folate and cobalamin blood concentrations. Dichotomized levels of HCY (≤15 vs >15 μM/l) were not associated with dichotomized GDS scores (≤4 vs higher), clinically relevant and subthreshold depression diagnosis and any antidepressive use, in any wave. First (2012) HCY levels increased with participants’ increasing age, cross-sectionally. Listwise HCY concentrations decreased along the 3 waves. HCY levels were always higher in males than in females. Our results may challenge the “homocysteine hypothesis” of depression, whilst supporting the role of high homocysteinemia as a marker of overall bad health.展开更多
AIM： To assess the hypercoagulability in PBC and its relationship with homocysteine （HCY） and various components of the haemostatic system. METHODS： We investigated 51 PBC patients （43F/8M; mean age： 63±13....AIM： To assess the hypercoagulability in PBC and its relationship with homocysteine （HCY） and various components of the haemostatic system. METHODS： We investigated 51 PBC patients （43F/8M; mean age： 63±13.9 yr） and 102 healthy subjects （86 women/16 men, 63±13 yr）, and evaluated the haemostatic process in whole blood by the Sonoclot analysis and the platelet function by PFA-100 device. We then measured HCY （fasting and after methionine loading）, tissue factor （TF）, thrombin-antithrombin complexes （TAT）, D-dimer （D-D）, thrombomodulin （TH）, folic acid, vitamin B6 and B12 plasma levels. C677T 5,10-methylenetetrahydrofolate reductase （HTHFR） polymorphism was analyzed. RESULTS： Sonoclot RATE values of patients were significantly （P〈 0.001） higher than those of controls. Sonoclot time to peak values and PFA-100 closure times were comparable in patients and controls. TAT, TF and HCY levels, both in the fasting and post-methionine loading, were significantly （P〈0.001） higher in patients than in controls. Vitamin deficiencies were detected in 45/51 patients （88.2%）. The prevalence of the homozygous TT677 MTHFR genotype was significantly higher in patients （31.4%） than in controls （17.5%） （P〈 0.05）. Sonodot RATE values correlated significantly with HCY levels and TF.CONCLUSION： In PBC, hyper-HCY is related to hypovitaminosis and genetic predisposing factors. Increased TF and HCY levels and signs of endothelial activation areassociated with hypercoagulability and may have an important role in blood clotting activation.展开更多
Objective To review the association of methylene tetrahydrofolate reductase (MTHFR) C677T mutant with coronary artery disease, as well as to highlight the results of some of these studies and to emphasize the need to ...Objective To review the association of methylene tetrahydrofolate reductase (MTHFR) C677T mutant with coronary artery disease, as well as to highlight the results of some of these studies and to emphasize the need to focus on the genetic architecture of CAD. Data SourcesData used in this article is mainly from relevant articles obtained through Pubmed, OVID and Google Scholar published from 1980 to 2008. Major studies and trials in this period were taken into account to draw accurate conclusion on the relation of those mutations in MTHFR with homocysteinemia and CAD. ResultOur analysis shows that hyperhomocysteinemia, a risk factor for occlusive arterial diseases, can be caused by disruptions of homocysteine metabolism catalyzed by MFTHR. A common alanine to valine mutation in MTHFR may contribute to mild heperhomocysteinemia in CAD. Individuals with the homozygous mutant genotype had higher plasma homocysteine, particularly when plasma folate was below the median value. ConclusionThis MTHFR mutant in the setting of insufficient folate may be a risk factor of CAD and can be regarded as a model of genetic-environmental interaction in the development of CAD.展开更多
文摘Depression is a major health problem, especially for elderly people. According to the “homocysteine hypothesis of depression”, high homocysteine levels may cause depression of mood via cerebrovascular diseases. Whilst biologically plausible, such hypothesis needs yet confirmation. We aimed at: 1) studying the relationships between homocysteinemia (HCY) and depression in a community-dwelling cohort of people aged 70 to 75 years at baseline;2) investigating plasma levels of HCY and 3) comparing these levels between males and females, in the same population. We exploited the data from four waves (2010, 2012, 2014 and 2018) of the longitudinal study “InveCeAb”, with specific regard towards mood assessment, by Geriatric Depression Scale (GDS) scoring, and diagnosis of clinically relevant or subthreshold depression. HCY plasma levels were measured in the waves 2012, 2014 and 2018. Sample attrition was due mainly to death or overall worsening. No statistically significant differences were found in plasma homocysteine levels in each wave, according to depressive symptoms. No correlations were found between plasma HCY levels in each wave with their corresponding GDS scores, even after adjustment for folate and cobalamin blood concentrations. Dichotomized levels of HCY (≤15 vs >15 μM/l) were not associated with dichotomized GDS scores (≤4 vs higher), clinically relevant and subthreshold depression diagnosis and any antidepressive use, in any wave. First (2012) HCY levels increased with participants’ increasing age, cross-sectionally. Listwise HCY concentrations decreased along the 3 waves. HCY levels were always higher in males than in females. Our results may challenge the “homocysteine hypothesis” of depression, whilst supporting the role of high homocysteinemia as a marker of overall bad health.
文摘AIM： To assess the hypercoagulability in PBC and its relationship with homocysteine （HCY） and various components of the haemostatic system. METHODS： We investigated 51 PBC patients （43F/8M; mean age： 63±13.9 yr） and 102 healthy subjects （86 women/16 men, 63±13 yr）, and evaluated the haemostatic process in whole blood by the Sonoclot analysis and the platelet function by PFA-100 device. We then measured HCY （fasting and after methionine loading）, tissue factor （TF）, thrombin-antithrombin complexes （TAT）, D-dimer （D-D）, thrombomodulin （TH）, folic acid, vitamin B6 and B12 plasma levels. C677T 5,10-methylenetetrahydrofolate reductase （HTHFR） polymorphism was analyzed. RESULTS： Sonoclot RATE values of patients were significantly （P〈 0.001） higher than those of controls. Sonoclot time to peak values and PFA-100 closure times were comparable in patients and controls. TAT, TF and HCY levels, both in the fasting and post-methionine loading, were significantly （P〈0.001） higher in patients than in controls. Vitamin deficiencies were detected in 45/51 patients （88.2%）. The prevalence of the homozygous TT677 MTHFR genotype was significantly higher in patients （31.4%） than in controls （17.5%） （P〈 0.05）. Sonodot RATE values correlated significantly with HCY levels and TF.CONCLUSION： In PBC, hyper-HCY is related to hypovitaminosis and genetic predisposing factors. Increased TF and HCY levels and signs of endothelial activation areassociated with hypercoagulability and may have an important role in blood clotting activation.
文摘Objective To review the association of methylene tetrahydrofolate reductase (MTHFR) C677T mutant with coronary artery disease, as well as to highlight the results of some of these studies and to emphasize the need to focus on the genetic architecture of CAD. Data SourcesData used in this article is mainly from relevant articles obtained through Pubmed, OVID and Google Scholar published from 1980 to 2008. Major studies and trials in this period were taken into account to draw accurate conclusion on the relation of those mutations in MTHFR with homocysteinemia and CAD. ResultOur analysis shows that hyperhomocysteinemia, a risk factor for occlusive arterial diseases, can be caused by disruptions of homocysteine metabolism catalyzed by MFTHR. A common alanine to valine mutation in MTHFR may contribute to mild heperhomocysteinemia in CAD. Individuals with the homozygous mutant genotype had higher plasma homocysteine, particularly when plasma folate was below the median value. ConclusionThis MTHFR mutant in the setting of insufficient folate may be a risk factor of CAD and can be regarded as a model of genetic-environmental interaction in the development of CAD.
