High intake of folic acid or complex of B vitamins provides anti-Parkinsonism effect: No role for serum level of homocysteine.


http://www.ncbi.nlm.nih.gov/pubmed/22610053


Abstract

Several lines of evidence show that homocysteine (Hcy) levels are increased in blood and CSF of patients with Parkinson's disease. B vitamins are necessary for Hcy metabolism and their deficiencies cause hyperhomocysteinemia and neurodegeneration. In present study, effect of B vitamin supplementation on the severity of 6-hydroxydopamine (6-OHDA)-induced Parkinsonism was investigated. Rats were nourished with B vitamin supplements from 1 month before of stereotaxic injection of 6-OHDA to the end of experiments. Total serum Hcy was measured at the end of experiments to identify its association with Parkinsonism. Both rotational and rotarod tests revealed that supplementation of folic acid, in a dose dependent manner, attenuates severity of Parkinsonism. Supplement of B complex also had beneficial effect and improved motor performance in rotarod test and decreased biased swings in elevated body swing test but had no effect on the apomorphine-induced rotational behavior. Supplement of B(6) attenuated rotational behavior but had no effect on the rotarod performance and swinging behavior. Supplement of B(12) or combination of folic acid with B(6) and B(12) had no effect on the behavioral symptoms of Parkinsonism. Except one group, the levels of Hcy in other vitamin B treated groups were near to that in control group. Surprisingly, Hcy in group of rats that received high intake of folic acid was significantly higher than that in control group. Our results indicate that high intake of folic acid or B complex provides anti-Parkinsonism effect but it is not mediated by lowering plasma Hcy.

....without realizing it. Several times, in fact, but I had dismissed it as a result of excessive bladder activity and dehydration since the Bs are water soluble. If it is more complex than that..... Well let's just say that I'm really going to be pi**ed off if PD turns out to be another vitamin deficiency. Meanwhile, I continue to take a daily B-complex. Maybe we all should since we don't retain them.

....but a monkey would not have a B-deficiency, now would he. And remember that they warn us away from some Bs since it might interfere with our sinemet.


1. Fortschr Neurol Psychiatr. 2007 Sep;75(9):515-27.

[Review of the role of hyperhomocysteinemia and B-vitamin deficiency in
neurological and psychiatric disorders--current evidence and preliminary
recommendations].

[Article in German]

Herrmann W, Lorenzl S, Obeid R.

Institut für Klinische Chemie und Laboratoriumsmedizin, Universitätsklinikum des
Saarlandes, Kirrberger Strasse, Gebaude 57, 66421 Homburg.
prof.wolfgang.herrmann@uni-klinikum-saarland.de

Elevated concentration of total homocysteine (Hcy) in plasma (> 12 micromol/l) is
a risk factor for several diseases of the central nervous system. Epidemiological
studies have shown a dose-dependent relationship between concentrations of Hcy
and the risk for neurodegenerative diseases. Hcy is a marker for B-vitamin
deficiency (folate, B12, B6). Hyperhomocysteinemia (HHcy) causes hypomethylation
which is an important mechanism that links Hcy to dementia. Supplementation with
vitamins B aims at reducing the risk of neurodegenerative diseases. Current
evidence suggests that Hcy-lowering treatment has a positive effect for the
secondary and primary prevention of stroke. HHcy is very common in patients with
Parkinson disease particularly those who receive L-dopa treatment. Furthermore, a
positive association has been reported between HHcy and multiple sclerosis.
Moreover, HHcy and vitamin B deficiency are reported to have a causal role in
depression, and epilepsy. In addition several anti-epileptic drugs cause
secondary HHcy. Therefore, sufficient intakes of the vitamins are recommended for
patients who have already developed neuropsychiatric diseases. Vitamin B
deficiency should be suspected in children with development disorders, failure to
thrive and unexplained neurological manifestations. Elderly people are also an
important at-risk group where vitamin B deficiency and HHcy have been linked to
neurodegenerative diseases. Treatment with folate, B12, and B6 can improve
cerebral function. Preventive vitamin B supplementation and sufficient intake
seem very important for secondary and primary prevention of neuropsychiatric
disorders, especially in subjects with a low intake or status of the vitamins.

PMID: 17729191 [PubMed - indexed for MEDLINE]

Many thanks Rick. As always, I read your posts, that are very useful and interesting. Now, I would to ask you, what's your daily amount of B vitamins. Is there a favourite moment, in a daytime, to take that product, for you ?

Thanks a lot.

Hi Sim00,

I like "NOW " brand of liposomal b12 ttaken 1st thing in the morning on empty stomach and no food intake for an hour afterwards - it doesn't make a difference everyd ay but if i stop taking it then start up again i notice increased energy level especially in the evening - takes the edge off if i feel stressed too.

md

http://neurotalk.psychcentral.com/sh...mrs+folic+acid

folic acid and B 12
there are a number of studies noting use of supplements Vitamin B 12 and folic acid in instances of B 12 deficiencies to decrease homocysteine levels that result from use of Levodopa. Levodopa reportedly interferes with folate metabolism and B 12 function.

Parkinsonism Relat Disord. 2008;14(4):321-5. Epub 2007 Dec 4.
Folate and vitamin B12 levels in levodopa-treated Parkinson's disease patients: their relationship to clinical manifestations, mood and cognition.

Abstract
We tested the hypothesis that mood, clinical manifestations and cognitive impairment of levodopa-treated Parkinson's disease (PD) patients are associated with vitamin B12 and folate deficiency...Levodopa-treated PD patients showed significantly lower serum levels of folate and vitamin B12 than neurological controls, while depressed patients had significantly lower serum folate levels as compared to non-depressed. Cognitively impaired PD patients exhibited significantly lower serum vitamin B12 levels as compared to cognitively non-impaired. In conclusion, lower folate levels were associated with depression, while lower vitamin B12 levels were associated with cognitive impairment. The effects of vitamin supplementation merit further attention and investigation.
PMID: 18055246 [PubMed - indexed for MEDLINE]


The influence of levodopa and the COMT inhibitor on serum vitamin B12 and folate levels in Parkinson's disease patients.
...Our findings show that levodopa-treated Parkinson's disease patients have low folate (p < 0.0007) and vitamin B12 levels (p < 0.0003). They also demonstrate that the addition of a COMT-i to levodopa + DDC-i treatment causes lower serum vitamin B12 (p < 0.03) and folate levels (p < 0.005) than levodopa + DDC-i treatment alone. We suggest supplementary treatment with vitamin B12 and folic acid in these situations.
http://www.ncbi.nlm.nih.gov/pubmed/17565222

Neurol Neurosurg Psychiatry 2003;74:549 doi:10.1136/jnnp.74.4.549
Correspondence
Benefit of folic acid supplementation in parkinsonian patients treated with levodopa
T Müller, D Woitalla, W Kuhn
+ Author Affiliations

Department of Neurology, St Josef Hospital, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany
Correspondence to:
 Dr T Müller; 
 thomas.mueller@ruhr-uni-bochum.de
We read with interest the recent excellent review by Reynolds on the role of folic acid and the risks and benefits of its supplementation in the nervous system.1 It emphasises the beneficial importance of folate on the numerous methylation processes in combination with S-adenosylmethionine (SAM), which donates its methyl group to prevent hyperhomocysteinaemia.1 However SAM deficiency, which is associated with, for example, cognitive decline and/or mood disturbances, and increased total homocysteine levels, which support onset of vascular disease, may also caused by drugs, for example, levodopa.2,3 Levodopa is administered with dopa decarboxylase inhibitors (DDI) to prevent its peripheral degradation. This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by the ubiquitious enzyme catechol-O-methyltransferase (COMT) in blood, peripheral tissues and in nigrostriatal neurons.2,3 COMT requires Mg2+ as cofactor and SAM as methyl donor. Thus O-methylation of levodopa to 3-OMD is associated with conversion of SAM to S-adenosylhomocysteine and subsequently homocysteine.

http://jnnp.bmj.com/content/74/4/549.1.full
.
For those individuals who have had DNA profiling, check for polymorphisms of the methylenetetrahydrofolate reductase (MTHFR C677T), methyltetrahydrofolate-homocysteine methyltransferase (MTR A2756G), and 5-methyltetrahydrofolate-homocysteine methyltransferase reductase both associated with folate metabolism and in addition, check (MTRR A1049G and C1783T) associated with processing of B12 in the bodY. If you have mutations in the MTHFR gene, must use a breakdown product of folic acid, methyl folate, and folinic acid if one has the other mutation. Mutations in MTRR requires a B 12 supplement.
__________________

sm00-
Nothing special on this one. Just a "B100 Complex" from the local Big Pharma Trading Post. I have been taking a single tablet first thing in the AM but I am thinking of adding a second at dinner in light of its water-wasting in order to cover the day better.
-Rick
PS- Glad you like the posts

Ok, this may be a long shot, but I can't help but wonder if a deficiency in follic acid and/or B vitamins, which cause homocysteine to rise, which in turn leads to vascular diseases per the above article....perhaps this is why close to 80% of Jannetta's PD group had vascular compression in the brain? I wonder if he did blood work for that group and if so, what it showed. Now that would be interesting!