Review explores mounting science linking B vitamins and depression
“Vitamin B deficiency (B1, B2, B6, B12) is used by clinicians to recognize and treat psychiatric disorders,” they wrote in their review, published in the journal Maturitas. “It is clear that deficiency in B vitamins results in symptoms of depression, thus affecting health and well-being of individuals.”
The influence that a complex of B vitamins have on the immune and nervous systems is backed by a variety of scientific literature. The interactions are ‘intricate,’ the researchers argued, thus the review they prepared analyzed existing studies on B vitamins and their relation to mental health, in particular depression.
“Greater knowledge of how immune cells change in the presence of vitamin B derivatives could improve understanding of how immune changes may correlate with depression,” they added.
Study selection for analysis
For this review, the researchers looked at studies on PubMed that explored the role of B vitamins on the immune network in relation to depression.
They looked at various vitamin B types: Vitamin B1 (thiamine), vitamin B2 (riboflavin), and vitamin B3 (niacin), vitamin B5 (pantothenic acid), vitamin B6 (pyridoxine), vitamin B9 (folate or folic acid), and vitamin B12 (cobalamin). They also included the terms “depression” and “immune” in their searches.
Though there were no time restrictions placed on the search, most of the results from the search queries were published between 2008 and 2016, and they included meta-analyses as well as randomized, placebo-controlled trials.
Supplementation and depression
The researchers reviewed the pool of studies to reveal vitamin B complex’s link to depression (further breaking it down to the eight vitamin B types); the link between immune system and depression; link between inflammation and depression; and finally the modifications of immune cells in the presence of vitamin B.
Looking at each of the eight vitamin B types, the researchers found that three of them had clinical studies proposing benefits of vitamin B supplementation. Several clinical trials have been conducted on vitamin B1 (thiamin) supplementation where researchers found that, compared to placebo, the supplemented group experienced improvements in their depression symptoms.
Additionally, studies on supplementation of vitamin B6 (pyridoxine), showed reduction of blood plasma homocysteine levels—an indicator of neuropsychiatric disorders—in patients with schizophrenia. The vitamin also showed improvements of depressive symptoms among women when taken combined with estradiol in another study.
There has been a clinical trial conducted on vitamin B3 (niacin), though the researchers argued that “further studies are required to ascertain the effectiveness of niacin in depression.”
Deficiencies used to recognize psychiatric disorders
For the other B vitamins, the researchers did not elaborate (or didn’t find) studies on how supplementation may improve depression symptoms. However, the pooled studies showed “clear evidence” between deficiencies in B vitamins and depression.
In particular, vitamins B1, B3, B6, B9, and B12 “are essential for neuronal function and deficiencies have been linked to depression,” they wrote.
For example, with B12 (cobalamin), a deficiency of it is “quite often noted in patients presenting with depression and higher levels of B12 correlates with improved treatment outcomes,” they argued. However, “although there is a clear link between depression and vitamin B12, more studies are necessary to establish the direct effects of vitamin B12 in depression.”
They also found evidence of B vitamins playing a role in regulating immune responses and, in patients with depression, pro-inflammatory responses, “hence, there is an inter-linked relationship between vitamin B, the immune system, inflammation and depression.”
Source: Maturitas
Published online ahead of print, http://dx.doi.org/10.1016/j.maturitas.2016.11.012
The effects of vitamin B on the immune/cytokine network and theirinvolvement in depression
Authors: Kathleen Mikkelsen, et al
