According to clinical nutritionist Blake Graham, all vitamins and minerals are involved in one or more biochemical pathways and/or physiological actions which influence the function of the human brain. Most vitamin and mineral deficiencies result in psychiatric symptoms in a significant number of people, and in people with psychiatric diagnoses these deficiencies are often associated with more severe symptoms and poorer outcome from conventional treatment. Vitamin and mineral deficiencies may act as an exacerbating factor secondary to malnutrition, alcoholism, etc. or may be a primary causative factor. Either way, optimisation of nutrient levels is in each patients best interest.
Several named vitamin deficiency diseases may result from the lack of sufficient B-vitamins. Also, several unnamed, sub-clinical responses can result from B-vitamin deficiency.
Vitamin B12 (cobalamin).
Depression is a common early psychiatric manifestation of B12 deficiency. (Durand C. 2003 & Goodman KI. 1990 & Hector M. 1988) Other symptoms include mania and psychosis, (Hector M. 1988) and slowing of mental processes, confusion and memory defects. (Holmes JM. 1956) Of 1081 young men, those who were B12 deficient were significantly more anxious based on ratings from the Adjective checklist, although not more anxious based on the Frieburg personality inventory scale. (Heseker H. 1992)
B12 is a cofactor required for methionine synthase, which catalyses the conversion of homocysteine to methionine (Bottiglieri T. 1996), and is required for the production of energy from fatty acids and proteins. (Mann. 2000)
Methionine is the direct precursor of S-adenosylmethionine (SAMe), which is involved in methylation reactions including neurotransmitter synthesis. B12 deficiency also causes folate to be ‘trapped’ in a form not available to perform its function. (Mann. 2000) B-12 also aids in folate metabolism. A B-12 deficiency can result in a secondary folate deficiency.
In one study, 47 patients with depression underwent high-resolution magnetic resonance imaging scans and B12 levels assessment. (HickieI. 2005) Low B12 levels were found to be predictive of white matter lesions. Of 50 patients with B12 deficiency associated megaloblastic anaemia, 26% displayed organic mental changes and 16% had subacute combined degeneration of the spinal cord. (Shorvon SD. 1980) 8/9 patients with B12 deficiency and the absence of hematologic evidence of deficiency displayed abnormal evoked potential, evidence of electrophysiologic neurological impairment, while selected individuals had myelopathy, neuropathy and seizure disorders. (Karnaze DS. 1990) Low B12 status is associated with low RBC and WBC in psychiatric inpatients. (Carney MW. 1978) These haematological abnormalities are predictive of low B12, although their presence or absence does not confirm or rule out B12 deficiency. B12 deficiency has a major and well documented negative effect on neurological function.
A number of studies have investigated the presence of B12 deficiency in psychiatric populations. The discrepancy between different studies is likely explained by different diets (e.g. animal product consumption), laboratory techniques and reference ranges. The rate of deficiency varied between 3.7 and 26.1 %.
In psychiatric patients, low B12 levels correlate highly with depression rating scores (Levitt AJ. 2003) and, in healthy volunteers, those with chronically low B12 levels have significantly higher depression levels. (Heseker H. 1992) Other studies have not confirmed these associations. In a group of 5948 subjects aged 46 to 49 years, depression ratings, anxiety/depression ratings andB12 levels were assessed. No significant correlation was found between B12 levels and depression and anxiety. (BjellandI. 2003)
Another study of 412 persons aged 60-64 years also found no significant association between B12 levels and depression ratings. (SachdevPS. 2005) Several studies have confirmed depressive patients who also had symptoms of psychosis tend to have lower B12 levels than depressive patients with no psychotic symptoms. (Bell IR. 1991 & Bell IR. 1990) Of 84 patients with megaloblastic anaemia, 50 had B12 deficiency. Of these 50 patients 20% had an affective disorder. (Shorvon SD. 1980) In a case study, a patient with no previous history of mental illness was admitted to the hospital in an extremely agitated manic phase. When treatment with B-12 was started, the patient’s behavior normalized, his slow EEG normalized and he was able to return to full work duties. (Goggins, 1984) B-12 is involved in the synthesis of monoamine neurotransmitters. (Hutto, 1997) It also helps to maintain the nerves’ myelin sheaths.
In patients with major depression, higher B12 levels have been associated with improved treatment outcomes in one study (Hintikka J. 2003) while another using fluoxetine as the treatment agent found no association between B12 levels and treatment outcome. (Fava M. 1997)
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