Low B vitamin status has long been linked to depressive behaviour, especially individuals with lethargic, apathetic symptomotology (showing no interest, feeling or concern). S-adenosyl methionine (SAMe) has been repeatedly shown 'as effective' as many currently prescribed antidepressants. However, the mechanism by which SAMe elicits its response is unclear at this time. Moreover, bio-available forms of folate and B12, such as methylfolate and methylcobalamin have been touted as depression therapies.
In my previous post I spoke to the gene, MTHFR, and its impact on Autism. Here I will show how MTHFR is linked to depression.
Two meta-analyses of 20 and 26 research studies, respectively, has shown a significant effect from the MTHFR C677T polymorphism on the incidence of depression. A recent study of 3478 European women found a strong association between the MTHFR C677T genotype (your single or grouped traits based on genetic makeup) and three indicators of depression (family history of depression, previous anti-depressant use, elevated depression scores pertaining to the EuroQoL mood questionnaire). A further study involving 402 depressed subjects and 600 controls also found a positive association between high Hamilton Rating Score for Depression and C677T MTHFR. Recently 90 subjects diagnosed with depression secondary to traumatic brain injury found that those individuals with MTHFR C677T predicted greater treatment response to 50 mg of citalopram (anti-depressant).
Interestingly also, is a study of 83 polish women with post-partum depression (89 controls). This study investigated the association of MTHFR polymorphism according to depression severity. After stratification of symptoms, MTR genotype was shown to increase the risk of depression 5 fold. Individuals diagnosed with a mutation for MTR genotype GG may be unable to synthesis methionine, this being so, SAMe (S-adenosyl methionine) may play a significant role in reducing symptoms of depression such individuals.
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