Vitamin B12 Deficiency and Cognitive Decline in Geriatric Population

Globally, 24 million people have some form of dementia, with 4.6 million new cases diagnosed each year (Ferri, MBrayne et al., 2005). Vitamin B12 deficiency is now known to be one of the causes of neuropsychiatric symptoms in elderly persons (Lachner, Steinle, Regenold et al. 2012). The malabsorption of vitamin B12 can account for the majority of deficiencies (Lachner, Steinle, Regenold et al. 2012). Vitamin B12 deficiency has been associated with neurologic, cognitive, psychotic, and mood symptoms, as well as resistance to treatment (Lachner, Steinle, Regenold et al. 2012). Clinician awareness should be raised in order to diagnose and treat early deficiencies which could help to prevent irreversible structural brain damage, because the current practice can be ineffective at identifying cases that lead to cognitive decline (Lachner, Steinle, Regenold et al. 2012). This research paper focuses on important aspects of the recognition and treatment of vitamin B12 deficiency and the neuropsychiatric manifestations of this preventable illness in elderly patients. This research paper will focus on whether supplementing vitamin B12 can slow down cognitive decline and prevent dementia and Alzheimer’s disease in the elderly population.

With the objective to determine the clinical utility of B12 testing in patients with suspected dementia or cognitive decline, a research paper based on a literature search was performed using MEDLINE, Embase, EBSCO Cumulative Index to Nursing & Allied Health Literature (CINAHL), the Cochrane Library, and the Centre for Reviews and Dissemination database, from January 2002 until August 2012 (Health Quality Ontario, 2013). Eighteen studies (7 systematic reviews and 11 observational studies) were used in order to address the association between B12 and the onset of dementia (Health Quality Ontario, 2013). Four systematic reviews were identified to address the question of the treatment of B12 on cognitive function (Health Quality Ontario, 2013). Finally, 3 randomized controlled trials were identified that compared oral B12 to intramuscular B12 (Health Quality Ontario, 2013). The reviews showed that based on very low quality evidence, there does appear to be an association between elevated plasma homocysteine levels (a by-product of B vitamins) and the onset of dementia (Health Quality Ontario, 2013). In addition, moderate evidence shows that with less than optimal duration of follow-up, treatment with B12 supplementation does not appreciably change cognitive function (Health Quality Ontario, 2013). Following, based on low to moderate quality of evidence, treatment with vitamin B12 and folate in patients showed that mild cognitive impairment decreased the rate of brain atrophy (Health Quality Ontario, 2013). Finally, based on moderate quality evidence, oral vitamin B12 is as effective as parenteral vitamin B12 in patients with confirmed B12 deficiency (Health Quality Ontario, 2013).

Vitamin B12 deficiency is often seen in those with neurocognitive disorders. This may have led to the thought that by supplementing vitamin B12, it may slow cognitive decline or may even prevent it. Some research suggest that there may be an association between increased plasma homocysteine levels and the onset of dementia (Health Quality Ontario, 2013). However, it is important to note that the evidence found for this association was of low quality. Current literature also strongly suggests that supplementation with vitamin B12 does not have an effect on cognitive function (Health Quality Ontario, 2013). In the same analysis, they also found a weak association between supplementation with vitamin B12 and folate in patients with mild cognitive impairment, to reduced rate of brain atrophy (Health Quality Ontario, 2013).

Furthermore, there have been many original studies that show conflicting results. There have only been a small amount of studies that show potential effects of vitamin B12 supplementation in preventing cognitive decline. However, majority of studies have showed conflicting results and suggest that vitamin B12 supplementation has no effect in decreasing or preventing cognitive decline which may lead to dementia or alzheimer's disease.

A random control trial investigating the relations between plasma concentrations of homocysteine and vitamins B12 and B6 and folate, and scores from a battery of cognitive tested 70 male subjects, between 54-81 years old (Riggs et al., 2006). The study found that lower concentrations of vitamin B-12 (P=0.04) and folate (P=0.003) and higher concentrations of homocysteine (P=0.0009 ) were associated with decreased spatial copying skills (Riggs et al., 2006). Plasma homocysteine levels were a stronger predictor of the spatial copying performance more than were vitamin B-12 or folate as predictors (Riggs et al., 2006). The higher concentrations of vitamin B-6 were related to better performance on two measures of memory (P=0.03 and P=0.05) (Riggs et al., 2006). The results suggest that vitamins (and homocysteine) may have differential effects on cognitive abilities (Riggs et al., 2006). Individual vitamins and homocysteine should be explored further as determinants of patterns of cognitive impairment (Riggs et al., 2006). In a double-blind randomized control trial by Aisen et al. (2008), the objective was to find out how effective and safe vitamin B12 supplementation would be for the treatment of alzheimer’s disease (AD). The study lasted for approximately four years, from March 2003 to February 2007. The 409 participants recruited had mild to moderate alzheimer’s disease based on the mini-mental status scores and had normal folic acid, B12 and homocysteine levels, where only 340 completed the trial. The subjects were randomly assigned to either receive a daily high-dose supplement with folate, vitamin b6, and vitamin b12 or an identical placebo. The main outcome measure they wanted to look at was the change in the cognitive subscale of the Alzheimer’s Disease Assessment scale (ADAS cog). The results showed that the supplement was effective in decreasing homocysteine levels, but had no helpful effect on the primary cognitive measure, the rate of change in ADAS cog, over the course of the 18 month treatment. The group with the vitamin supplements actually showed higher rates of adverse events involving depression. Overall, the results of this study suggest that high dosage of vitamin B supplements does not slow cognitive decline in people with mild to moderate AD.

Low levels of vitamin B12 have been shown to be associated with neurocognitive disorders (Kwok et al., 2006). Reviews of meta-analyses and random control trials have assessed the usefulness of serum vitamin B12 testing as it relates to brain function (Cho et al., 2018). This research paper found very low quality evidence that suggests there may be a connection between high plasma homocysteine levels (a by-product of B vitamin metabolism in the body) and the onset of dementia (Zhang et al., 2017). In addition, treatment with vitamin B12 does not improve brain function (Zhang et al., 2017). Finally, in terms of effectiveness of administration of B12, moderate quality of evidence also indicates treatment using oral vitamin B12 supplements is as effective as injections of vitamin B12 (Malouf, Grimley & Areosa, 2003). In conclusion, evidence suggests that vitamin B12 supplementation does not prevent dementia or Alzheimer’s disease yet it may slow cognitive decline in patients with AD or dementia (Balk, 2007). Further research in the decrease in rate of cognitive decline is needed to encourage supplementation in the elderly population.

References

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