Hyperhomocysteinemia as risk factor for depression: A review

Chronic nutritional deficiencies or lack of supplement such as folate, vitamin B-6, omega-3, minerals and vitamin B-12 may disturb normal one-carbon metabolism or methionine cycle, lead to hyperhomocysteinemia and associated with genetic abnormality and epigenetic alterations. It is also associated with DNA hypomethylation that can cause the cell damage and neuronal injury in the brain through the oxidative stress. Hyperhomocysteinemia is also associated with alterations of gene expression and structural change in the chromatin, involved in the pathogenesis of diseases related to homocysteine. MTHFR C677T polymorphism in these pathways can act synergistically with nutritional deficiencies increased the level of homocysteine and convert S-adenosylhomocysteine which is bulky in cell and potent product inhibition of DNA methyltransferases. However, several studies were observed hyperhomocysteinemia along with lower folate, vitamin B12 and vitamin B6 levels in the depression when compared to controls and interventions to treat vitamin B12, vitamin B6 and folate deficiencies in the depressed individuals studied here could help improve cognitive performance and decrease the level of total homocysteine. Further, studies on the biochemical status of other micronutrients in same population will help establish whether a more comprehensive intervention plan is defensible.