Increased vitamin B12 levels can lead to several metabolic disorders that primarily affect cognitive functions leading to dementia. Excessive levels are often assumed to be due to supplementation prescribed by a health care professional. In nearly all cases, however, no action is taken upon discovering the irregularity. It is now clear that an unusually high concentrations of vitamin B12 reflects the production of significant amounts by the bacteria of the small intestine.
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Homocysteine and B12 Levels
Homocysteine is an amino acid derived from the diet and is converted by folate and vitamins B12 and B6 for biological functions. Homocysteine levels in the blood typically increase with age and with diminishing kidney function, but are largely determined by dietary intake and levels of vitamins B12, B6, and folate. Studies have shown that increased homocysteine levels might be a risk factor for vascular disease, brain atrophy, cognitive impairment, Alzheimer's disease, depression, and an assortment of psychiatric disorders.
Depression is a leading cause of disability worldwide and depressive symptoms are common in later life. The March 2010 issue of “Trials” cited evidence suggesting that depression is more prevalent among people with high plasma homocysteine through the supplementation of vitamins B6, B12 and folate. The authors designed a trial to determine whether treatment with these vitamins increases the efficacy of standard antidepressant treatment. The trial involved over 300 older adults with major depression and found a clinically significant improvement and remission of symptoms weeks after supplementation began. The results of this trial showed that the use of B vitamins improves the response of older adults to standard antidepressant treatment.
A study that appeared in the March 2010 issue of “Joint, Bone and Spine” detailed vitamin B12 benefits in treating adult-onset Still's disease, a blood disease in which red blood cells are destroyed by the body’s innate immune cells. The investigators reviewed patients' files for clinical data indicative of the disorder including fever, rash, sore throat, and arthritis. They conducted laboratory tests including complete blood count, serum iron, enzymes, serum triglyceride and vitamin B12 levels. The study found that elevated vitamin B12 levels seem to be a good diagnostic marker the complications associated with Still’s disease.
In the September 2010 issue of “Acta Neurology – Tiawan” a medical literature review was included that evaluated Alzheimer’s disease, AD, patients and investigated the relationship between cognition change and plasma homocysteine levels through supplementation by vitamin B12. The authors found that plasma homocysteine levels were associated with rapid cognitive decline as determined by magnetic resonance imaging, MRI. The authors found that levels of homocysteine are higher in AD, most likely caused by folate, vitamin B12, and possibly vitamin B6 levels during the progression of the disease. The authors further stated that increased homocysteine levels are a risk factor for atherosclerotic diseases and thromboembolic events. Increased homocysteine levels may lead to the earlier onset of clinical dementia and intensifies the severity of AD.