Table of contents
- Low Vitamin B12 and Parkinson Disease – May 2019
- Taking B12 slowed the progression of PD March 2018
- Vitamin B12 and Parkinson's disease: What is the relationship? – Editorial March 2018
- Association of plasma homocysteine, vitamin B12 and folate levels with cognitive function in Parkinson's disease: A meta-analysis. – Jan 2017
- Associations between B Vitamins and Parkinson's Disease – Aug 2015
- See also VitaminDWiki
Potential Link to Reduced Cholinergic Transmission and Severity of Disease
Mayo Clinic COMMENTARY, ISSUE 5, P757-762, MAY 01, 2019 DOI:https://doi.org/10.1016/j.mayocp.2019.01.039
Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by prominent motor dysfunction including rest tremor, bradykinesia, and rigidity responsive to levodopa. However, postural instability, freezing of gait, and cognitive impairment are important non–levodopa-responsive symptoms of PD and are significant risk factors for falls, leading to hospitalization, disability, and death.1 Treatments for key nonmotor symptoms of PD that might improve cognitive decline and postural instability are currently a major gap in PD therapeutics.
Dysfunction of the cholinergic systems in PD is thought to possibly play a contributory role in postural instability and cognitive impairment. Therefore, modulation of cholinergic transmission could improve balance and cognition in these patients.1 Vitamin B12 is lower in patients with PD compared with controls, and low levels have been associated with peripheral neuropathy, cognitive impairment, and more rapid rate of disease progression in PD.2, 3, 4 Although this relationship does not necessarily mean causality, there are several hypothetical mechanisms by which reduced vitamin B12 may lead to reduced availability of choline as a substrate for cholinergic transmission. Here we will review the proposed pathophysiology of nonmotor symptoms in PD and the potential relationship between vitamin B12 and acetylcholine metabolism. We propose that vitamin B12 supplementation could be considered as an adjuvant approach to improve cholinergic transmission and, potentially, motor and cognitive function in patients with PD.
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Vitamin B12 and homocysteine levels predict different outcomes in early Parkinson's disease.
Mov Disord. 2018 Mar 6. doi: 10.1002/mds.27301. [Epub ahead of print]
Christine CW1, Auinger P2, Joslin A3, Yelpaala Y3, Green R3; Parkinson Study Group-DATATOP Investigators.
BACKGROUND: In moderately advanced Parkinson's disease (PD), low serum vitamin B12 levels are common and are associated with neuropathy and cognitive impairment. However, little is known about B12 in early PD.
OBJECTIVE: To determine the prevalence of low vitamin B12 status in early PD and whether it is associated with clinical progression.
We measured vitamin B12 and other B12 status determinants (methylmalonic acid, homocysteine, and holotranscobalamin) in 680 baseline and 456 follow-up serum samples collected from DATATOP participants with early, untreated PD. Borderline low B12 status was defined as serum B12 <184 pmol/L (250 pg/mL), and elevated homocysteine was defined as >15 µmol/L. Outcomes included the UPDRS, ambulatory capacity score (sum of UPDRS items 13-15, 29&30), and MMSE, calculated as annualized rates of change.
At baseline, 13% had borderline low B12 levels, 7% had elevated homocysteine, whereas 2% had both. Elevated homocysteine at baseline was associated with worse scores on the baseline MMSE. Analysis of study outcomes showed that compared with the other tertiles, participants in the low B12 tertile (<234 pmol/L; 317 pg/mL) developed greater morbidity as assessed by greater annualized worsening of the ambulatory capacity score. Elevated homocysteine was associated with greater annualized decline in MMSE (-1.96 vs. 0.06; P = 0001). Blood count indices were not associated with B12 or homocysteine status.
In this study of early PD, low B12 status was common. Low B12 at baseline predicted greater worsening of mobility whereas elevated homocysteine predicted greater cognitive decline. Given that low B12 and elevated homocysteine can improve with vitamin supplementation, future studies should test whether prevention or early correction of these nutritionally modifiable conditions slows development of disability. © 2018 International Parkinson and Movement Disorder Society.
PMID: 29508904 DOI: 10.1002/mds.27301
Mov Disord. 2018 Mar 6. doi: 10.1002/mds.27366. [Epub ahead of print]
Cardoso F1. PMID: 29508925 DOI: 10.1002/mds.27366
Association of plasma homocysteine, vitamin B12 and folate levels with cognitive function in Parkinson's disease: A meta-analysis. – Jan 2017
Neurosci Lett. 2017 Jan 1;636:190-195. doi: 10.1016/j.neulet.2016.11.007. Epub 2016 Nov 10.
Xie Y1, Feng H1, Peng S1, Xiao J1, Zhang J2.
1 Dept of Neurology, Zhongnan Hospital, Wuhan University, No. 169, Donghu Road, 430071 Hubei, China.
2 Dept of Neurology, Zhongnan Hospital, Wuhan University, No. 169, Donghu Road, 430071 Hubei, China. wdsjkx at 163.com.
Hyperhomocysteinemia has been associated with cognitive disorders such as mild cognitive impairment, Alzheimer's disease and vascular dementia. Previous studies showed that levodopa-treated Parkinson's disease (PD) patients were likely to have elevated homocysteine levels. In addition, epidemiological evidence found that cognitive impairment presented in the vast majority of PD patients. However, what role homocysteine played in cognitive function of PD patients remained debated. Therefore, we conducted this meta-analysis to investigate the possible correlations among cognitive function, homocysteine, folate and vitamin B12 levels in PD patients. A structured literature search was carried out on Pubmed, Springer, EMbase, Cochrane library, CNKI, VP and Wanfang database up to April 2016 using strict inclusion criteria. Data on demographic information, levodopa equivalent dosage, homocysteine, folate and vitamin B12 levels and Mini Mental Scale Examination scores were collected and pooled. The mean difference (MD) with 95% confidence intervals (CIs) was used as the effect size. Of 75 articles identified, 15 were eligible for inclusion.
The results suggested that PD patients with cognitive dysfunction were likely to have
- higher homocysteine levels( MD=5.05, 95%CI [4.03, 6.07]),
- lower folate (MD=-0.21, 95%CI [-0.34, -0.08]) and
- (lower) vitamin B12 levels(MD=-47.58, 95%CI [-72.07, -23.09]).
We again verified a close relationship between hyperhomocysteinemia and PD (MD=5.67, 95%CI [4.40, 6.94]). We concluded that hyperhomocysteinemia was related to cognitive impairment of PD patients, and further studies should focus on the intervention to lower homocysteine level, hopefully to provide useful advice for clinical practice.
PMID: 27840145 DOI: 10.1016/j.neulet.2016.11.007
Nutrients. 2015 Aug 27;7(9):7197-208. doi: 10.3390/nu7095333.
Shen L Shandong Provincial Research Center for Bioinformatic Engineering and Technique, School of Life Sciences, Shandong University of Technology, Zibo 255049, China. shen at sdut.edu.cn.
B vitamins may correlate with Parkinson's disease (PD) through regulating homocysteine level. However, there is no comprehensive assessment on the associations between PD and B vitamins. The present study was designed to perform a meta-analytic assessment of the associations between folate, vitamin B6, and vitamin B12 and PD, including the status of B vitamins in PD patients compared with controls, and associations of dietary intakes of B vitamins and risk of PD. A literature search using Medline database obtained 10 eligible studies included in the meta-analyses. Stata 12.0 statistical software was used to perform the meta-analysis. Pooled data revealed that there was no obvious difference in folate level between PD patients and healthy controls, and PD patients had lower level of vitamin B12 than controls. Available data suggested that higher dietary intake of vitamin B6 was associated with a decreased risk of PD (odds ratio (OR) = 0.65, 95% confidence intervals (CI) = (0.30, 1.01)), while no significant association was observed for dietary intake of folate and vitamin B12 and risk of PD. PD patients had lower level of vitamin B12 and similar level of folate compared with controls. Dietary intake of vitamin B6 exhibited preventive effect of developing PD based on the available data. As the number of included studies is limited, more studies are needed to confirm the findings and elucidate the underpinning underlying these associations.
PMID: 26343714 PMCID: PMC4586528 DOI: 10.3390/nu7095333
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Overview Parkinson's and Vitamin D contains the following summary
Parkinson's Disease proven to be TREATED by Vitamin D (Many Meta-analyses of trials)
- Parkinson's disease stabilized with just 1200 IU of vitamin D – RCT May 2013
First RCT to report results - +anticipate far better results when more vitamin D is used.
(Belief based on the results with vitamin D on MS and Diabetes)
Additonal proofs that vitamin D treats or prevents diseases
- 6 clinical trials for PD with vitamin D intervention as of Jan 2016
A person could wait a few years to get the results of the clinical trials, but
- Based on reading more than 4,000 studies of vitamin D at VitaminDWiki
- A (loading) dose of 20,000 IU of vitamin D daily for the 3 weeks should provide observable benefit
To avoid a rare reaction to Vitamin D
take 1,000 IU of vitamin D first, and stop if you you have an allergic reaction withiin 3 days
When continuing to take vitamin D you should also take cofactors
There is virtually no need have a vitamin D test in first 2 months
- Parkinson's category has
The articles in both Parkinson's and Meta-analysis
This page is in the following categories (# of items in each category)
- Parkinson’s disease 1.6X more likely if a poor Vitamin D Receptor – meta-analysis Jan 2020
- Parkinson’s disease 20 percent more likely in Asians if poor Vitamin D Receptor – meta-analysis April 2019
- Parkinson’s patients 50X less likely to get even a little sun– meta-analysis Jan 2019
- Parkinson's Disease 2.1 X more likely if low Vitamin D – Meta-analysis Nov 2018
- Parkinson’s Disease systematic review finds association with low vitamin D – Jan 2016
- 2X more Parkinson's disease if modified vitamin D receptor genes – meta-analysis Aug 2014
- Parkinson's and Alzheimer's: associations with vitamin D receptor genes and race – meta-analysis July 2014
- Parkinson’s Disease – no association found with changes in Vitamin D genes – meta-analysis June 2014
- Parkinson’s disease 2X more likely if low Vitamin D – meta-analysis May 2014
- Parkinson’s Disease and the “Sunshine” Vitamin (vitamin D) – July 2013
- Alzheimer’s and Parkinson’s diseases associated with low vitamin D – meta-analysis June 2013
- Hip fractures greatly reduced by sunshine, vitamin D, and vitamin K – meta-analysis Sept 2012