Parkinson's Disease Tulip


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Old 01-27-2015, 04:00 PM #11
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if it sounds too good to be true it likely is. the placebo affect is very strong in pd'ers. in the first trial with 3 patients would have liked to have seen the patients getting thiamine or placebo a week apart.
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Old 01-27-2015, 05:35 PM #12
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I do believe B vitamins play a huge role in PD, particularly since it is estimated that at least 40% of the population has issues with methylation. Also, for a couple of years, we got PD relief from those 5-hour energy drinks, which are loaded with B vitamins. There are also studies on thiamine benefitting other nervous system maladies, one of the authors on the Italian study has written extensively on thiamin, you can check out his papers on a link in the article cited above.

So we are looking into this, but so far, I am having a heck of a time finding someone who will do a thiamine treatment. You can get B12 shots everywhere, but not B1. I have found wellness places that offer a "cocktail" IV push, but it is all the B vitamins and not just B1. We may give that a go, but they do not like to do it every day, which is how the patients in these studies received thiamin. I also am not clear on two things in these studies:

1. "parenteral" can mean IV or an injection into the muscle (or a number of other ways)-neither study cited above offers detail into which method of parenteral was used to deliver the thiamine;

2. which thiamine was used? the water soluble or fat soluble variety?

If anyone knows either answer, please share here, thanks.
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Old 01-27-2015, 05:52 PM #13
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Quote:
Originally Posted by lurkingforacure View Post
I do believe B vitamins play a huge role in PD, particularly since it is estimated that at least 40% of the population has issues with methylation. Also, for a couple of years, we got PD relief from those 5-hour energy drinks, which are loaded with B vitamins. There are also studies on thiamine benefitting other nervous system maladies, one of the authors on the Italian study has written extensively on thiamin, you can check out his papers on a link in the article cited above.

So we are looking into this, but so far, I am having a heck of a time finding someone who will do a thiamine treatment. You can get B12 shots everywhere, but not B1. I have found wellness places that offer a "cocktail" IV push, but it is all the B vitamins and not just B1. We may give that a go, but they do not like to do it every day, which is how the patients in these studies received thiamin. I also am not clear on two things in these studies:

1. "parenteral" can mean IV or an injection into the muscle (or a number of other ways)-neither study cited above offers detail into which method of parenteral was used to deliver the thiamine;

2. which thiamine was used? the water soluble or fat soluble variety?

If anyone knows either answer, please share here, thanks.

try contacting the author?
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Old 01-27-2015, 06:19 PM #14
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Quote:
Originally Posted by lurkingforacure View Post
I do believe B vitamins play a huge role in PD, particularly since it is estimated that at least 40% of the population has issues with methylation. Also, for a couple of years, we got PD relief from those 5-hour energy drinks, which are loaded with B vitamins. There are also studies on thiamine benefitting other nervous system maladies, one of the authors on the Italian study has written extensively on thiamin, you can check out his papers on a link in the article cited above.

So we are looking into this, but so far, I am having a heck of a time finding someone who will do a thiamine treatment. You can get B12 shots everywhere, but not B1. I have found wellness places that offer a "cocktail" IV push, but it is all the B vitamins and not just B1. We may give that a go, but they do not like to do it every day, which is how the patients in these studies received thiamin. I also am not clear on two things in these studies:

1. "parenteral" can mean IV or an injection into the muscle (or a number of other ways)-neither study cited above offers detail into which method of parenteral was used to deliver the thiamine;

2. which thiamine was used? the water soluble or fat soluble variety?

If anyone knows either answer, please share here, thanks.
Please let us know how this goes ok? I'm just taking water soluble thiamine 300mg twice a day for now till I can figure a better plan.
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Old 01-27-2015, 09:20 PM #15
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Originally Posted by soccertese View Post
try contacting the author?
on my list, already looked the phone number up will let everyone know what they say.

FWIT, the cocktail (they call it a "Myer's Cocktail") I was told about today at one wellness place has all the Bs in it, magnesium, I think C and perhaps some other nutrients...and even glutathione if you want to pay an extra $25.00. It's an IV push and costs $150.00 unless you sign up for a package of them and then it's less...not covered by insurance of course. They use them for cancer patients, Epstein-Barr, Lyme, a few other illnesses as well as people who just want a boost. They will give them once a week unless you have cancer in which case they will allow twice a week. We may give this a go if we cannot find anyone who will do straight thiamine.
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Old 01-27-2015, 10:30 PM #16
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Here are couple articles on B1. Because of the copyright I can only provide abstract.

Burke Medical Research Institute, Weil Medical College, Cornell University, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
Gary E. Gibson∗, Hui Zhang
Accepted 30 October 2001
Thiamine-dependent processes are diminished in brains of patients with several neurodegenerative diseases. The decline in thiamine-dependent enzymes can be readily linked to the symptoms and pathology of the disorders. Why the reductions in thiamine linked processes occur is an important experimental and clinical question. Oxidative stress (i.e. abnormal metabolism of free radicals) accompanies neurodegeneration and causes abnormalities in thiamine-dependent processes. The vulnerability of thiamine homeostasis to oxidative stress may explain deficits in thiamine homeostasis in numerous neurological disorders. The interactions of thiamine with oxidative processes may be part of a spiral of events that lead to neurodegeneration, because reductions in thiamine and tiamine-dependent processes promote neurodegeneration and cause oxidative stress. The reversal of the effects of thiamine deficiency by antioxidants, and amelioration of other forms of oxidative stress by thiamine, suggest that thiamine may act as a site-directed antioxidant. The data indicate that the interactions of thiamine-dependent processes with oxidative stress are critical in neurodegenerative processes. © 2002 Elsevier Science Ltd. All rights reserved
Keywords: Thiamine; Oxidative stress; Alzheimer’s disease; Parkinson’s disease; -Ketoglutarate dehydrogenase complex; Pyruvate dehydrogenase complex.

And, another article:

Modeling neurodegenerative disease pathophysiology in thiamine deficiency:
Consequences of impaired oxidative metabolism
Shivraj S. Jhala, Alan S. Hazell *
Department of Medicine, University of Montreal, Montreal, Quebec, Canada
ARTICLE INFO
Article history:
Received 20 September 2010 Received in revised form 18 November 2010 Accepted 25 November 2010 Available online 3 December 2010
ABSTRACT
Emerging evidence suggests that thiamine deficiency (TD), the cause of Wernicke’s encephalopathy, produces alterations in brain function and structural damage that closely model a number of maladies in which neurodegeneration is a characteristic feature, including Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, multiple sclerosis, along with alcoholic brain disease, stroke, and traumatic brain injury. Impaired oxidative metabolism in TD due to decreased activity of thiamine-dependent enzymes leads to a multifactorial cascade of events in the brain that include focal decreases in energy status, oxidative stress, lactic acidosis, blood–brain barrier disruption, astrocyte dysfunction, glutamate-mediated excitotoxicity, amyloid deposition, decreased glucose utilization, immediate-early induction, and inflammation. This review describes our current understanding of the basis of these processes in TD, their interrelationships, and why this disorder can be useful for our understanding of how decreased cerebral energy metabolism can give rise to cell death in different neurodegenerative disease states.
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Old 01-27-2015, 10:50 PM #17
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Default Bacteria Prevotella Aids In Creation Of Thiamine...

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Originally Posted by zanpar321 View Post
It's been said that Parkinsons is like Diabetes of the brain

http://neurotalk.psychcentral.com/ar.../t-210912.html

so if Thiamine is directly connected to the use of sugar/glucose to produce ATP energy then we may be onto something significant here! Let the research continue!
In Dr. Scheperjans’ study, the bacteria Prevotella was present at lower levels in the guts of people with Parkinson’s disease. This bacterium aids in the creation of the vitamins thiamine and folate and the maintenance of an intestinal barrier protecting against environmental toxins. If so, the replenishing of the bacteria may need to be considered at the same time of taking high dose thiamine, supposedly. This also implies that the cause(s) of low Prevotella in pwp may be one of the crucial areas that need more work on...

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Old 01-27-2015, 11:06 PM #18
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In Dr. Scheperjans’ study, the bacteria Prevotella was present at lower levels in the guts of people with Parkinson’s disease. This bacterium aids in the creation of the vitamins thiamine and folate and the maintenance of an intestinal barrier protecting against environmental toxins. If so, the replenishing of the bacteria may need to be considered at the same time of taking high dose thiamine, supposedly. This also implies that the cause(s) of low Prevotella in pwp may be one of the crucial areas that need more work on...
This Prevotella bacteria which aids in thiamine creation is very interesting indeed! The body needs only around 1mg of thiamine from food per day but if the gut isn't producing thiamine it sure seems like a deficit would develop. Thanks much
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Old 01-27-2015, 11:51 PM #19
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Quote:
Originally Posted by Bogusia View Post
Here are couple articles on B1. Because of the copyright I can only provide abstract.

Burke Medical Research Institute, Weil Medical College, Cornell University, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
Gary E. Gibson∗, Hui Zhang
Accepted 30 October 2001
Thiamine-dependent processes are diminished in brains of patients with several neurodegenerative diseases. The decline in thiamine-dependent enzymes can be readily linked to the symptoms and pathology of the disorders. Why the reductions in thiamine linked processes occur is an important experimental and clinical question. Oxidative stress (i.e. abnormal metabolism of free radicals) accompanies neurodegeneration and causes abnormalities in thiamine-dependent processes. The vulnerability of thiamine homeostasis to oxidative stress may explain deficits in thiamine homeostasis in numerous neurological disorders. The interactions of thiamine with oxidative processes may be part of a spiral of events that lead to neurodegeneration, because reductions in thiamine and tiamine-dependent processes promote neurodegeneration and cause oxidative stress. The reversal of the effects of thiamine deficiency by antioxidants, and amelioration of other forms of oxidative stress by thiamine, suggest that thiamine may act as a site-directed antioxidant. The data indicate that the interactions of thiamine-dependent processes with oxidative stress are critical in neurodegenerative processes. © 2002 Elsevier Science Ltd. All rights reserved
Keywords: Thiamine; Oxidative stress; Alzheimer’s disease; Parkinson’s disease; -Ketoglutarate dehydrogenase complex; Pyruvate dehydrogenase complex.

And, another article:

Modeling neurodegenerative disease pathophysiology in thiamine deficiency:
Consequences of impaired oxidative metabolism
Shivraj S. Jhala, Alan S. Hazell *
Department of Medicine, University of Montreal, Montreal, Quebec, Canada
ARTICLE INFO
Article history:
Received 20 September 2010 Received in revised form 18 November 2010 Accepted 25 November 2010 Available online 3 December 2010
ABSTRACT
Emerging evidence suggests that thiamine deficiency (TD), the cause of Wernicke’s encephalopathy, produces alterations in brain function and structural damage that closely model a number of maladies in which neurodegeneration is a characteristic feature, including Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, multiple sclerosis, along with alcoholic brain disease, stroke, and traumatic brain injury. Impaired oxidative metabolism in TD due to decreased activity of thiamine-dependent enzymes leads to a multifactorial cascade of events in the brain that include focal decreases in energy status, oxidative stress, lactic acidosis, blood–brain barrier disruption, astrocyte dysfunction, glutamate-mediated excitotoxicity, amyloid deposition, decreased glucose utilization, immediate-early induction, and inflammation. This review describes our current understanding of the basis of these processes in TD, their interrelationships, and why this disorder can be useful for our understanding of how decreased cerebral energy metabolism can give rise to cell death in different neurodegenerative disease states.
Please provide the link to articles

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Old 01-27-2015, 11:56 PM #20
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Quote:
Originally Posted by soccertese View Post
try contacting the author?

Only today I read the post. It is really very interesting, if it is confirmed it would be a great success. I'll find out by the authors, as soon as possible. The clinic is located about 1 hour drive from my house. I will let you know about the updates.
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