Exciting research breakthroughs are all well and good for future generations, but if you are reading this they probably aren't going to arrive in time to help you, today's PWP.

However, there are things available today that have enough research behind them to warrant consideration. I propose this thread as a sticky to keep track of these so that they are not lost.

The type of treatments I am talking about carry varying amounts of risk and no one should assume anything about these. This is serious stuff and the decisions you make about them will determine the course of your life. Even choosing to ignore them will be a momentous one.

This is the place for promises not of just borrowing time with neuroprotection but of putting things to rights with neurogenesis. But that is where risk comes in. Things that trigger regrowth of nervous tissue could also trigger overgrowth and resulting tumors for example.

This is not to say that one should avoid risk - one cannot. And bluntly put, doing nothing but the treatments offered by our neuros has a clear end - and it is not pleasent. Each of us must decide for ourselves with the best information available to us. I hope this thread will provide a place to gather that information.

Old drugs have been around long enough to let thier problems show. The risks are much lower and side effects are known. And every now and then we stumble upon a new use. Called "off label" use, they don't have to pass the FDA labyrinth and their use is a matter between patient and doctor.


A story from April 17, 2006 deals with unsuspected protective and regenerative powers of an old blood pressure medication.


<QUOTE>
A research team led by Riyi Shi (REE-yee SHEE) and Richard Borgens found that hydralazine, a medication that relaxes veins and arteries, may be an antidote for acrolein, a deadly toxin that is produced after a nerve cell is injured.

New findings based on research at the cellular level are detailed in two studies published in the Journal of Neuroscience Research today (Monday, April 17). In the first article, researchers examine how acrolein attacks and kills cells. In the second article, they demonstrate that cell death caused by acrolein (a-KRO-le-an), a byproduct of an injury, can be reversed when hydralazine is administered.

"This is probably the most important fundamental discovery we have made at the Center for Paralysis Research because we are saving nerve cells from death," said Borgens, Mari Hulman George Professor of Applied Neurology in the School of Veterinary Medicine and founder of the paralysis research center where the research was conducted.

"Initially we may use this discovery for spinal cord injury and stroke, but we can expect further studies will look at how it works against a whole spectrum of injury and disease," he said.


Purdue researchers collected data on acrolein from cell cultures and found that the potent toxin can destroy entire groups of cells in less than 12 hours. But they also determined that the cells would survive if the toxin were treated with hydralazine that acts very much like an antidote, Borgens said.

"We analyzed other natural toxins as well, and our success has been remarkable," Borgens said. "We found that more than 80 percent of the cells can be saved with hydralazine."

Acrolein stays in the body for days and is responsible for secondary damage that keeps injured cells from healing. The idea to use hydralazine against acrolein is a logical extension of research on the toxin, such as the use of a beta blocker against high blood pressure or chicken soup for a cold, Shi said.

"Acrolein is one of the causes of free radicals that are known to damage cells, so it makes sense to stop them from ever being produced," said Shi, who is associate professor of basic medical science in Purdue's School of Veterinary Medicine. "With hydralazine, we are attacking the root of the problem rather than the symptom."


Acrolein is a type of cell toxin called an aldehyde; and the drug, hydralazine, is effective because it has the ability to trap aldehydes and stick to them. Once hydralazine binds to the aldehyde, the toxin is neutralized, deactivated and secreted, Shi said.

The Purdue researchers started looking at alternative methods to save cells because other studies that had tried to use antioxidants to deactivate free radical molecules had failed in human clinical trials in traumatic brain injuries, strokes and spinal cord injuries.

"If we intervene early enough, we may have the ability to slow down the process of diseases, such as Alzheimer's and Parkinson's, which would be significant," Shi said. "If we can prevent these diseases from getting worse, we can give people a better quality of life."

Peishan Liu-Snyder, who graduated last summer and will be a post-doctoral fellow at Brown University in June, also was part of the Purdue research team. She became interested in research at the Center for Paralysis Research when it focused on the use of liquid polymers that prevent nerve cells from rupturing, enabling them to heal themselves.

"We found hydralazine works well after the initial injury period because it targets the secondary injury process," said Liu-Snyder. "It binds to the acrolein to inactivate its toxicity."
<END QUOTE>

Some things to note- 1) PD is purpotedly a constant cascade of dying cells, i.e. a slow rolling brain injury where one death triggers the next and 2) this drug works by causing the walls of blood vessels to relax and grow bigger - this allows more blood (and oxygen) to reach the brain.




1: J Neurosci Res. 2006 Jul;84(1):219-27.

Hydralazine rescues PC12 cells from acrolein-mediated death.

Liu-Snyder P, Borgens RB, Shi R.

Center for Paralysis Research, Department of Basic Medical Sciences, School of
Veterinary Medicine, Purdue University, West Lafayette, Indiana 47907-2096, USA.

Acrolein, a major lipid peroxidation product, has been associated with both CNS
trauma and neurodegenerative diseases. Because of its long half-life, acrolein
is a potent endogenous toxin capable of killing healthy cells during the
secondary injury process. Traditionally, attempts to intervene in the process of
progressive cell death after the primary injury have included scavenging
reactive oxygen species (so-called free radicals). The animal data supporting
such an approach have generally been positive, but all human clinical trials
attempting a similar outcome in human CNS injury have failed. New drugs that
might reduce toxicity by scavenging the products of lipid peroxidation present a
promising, and little investigated, therapeutic approach. Hydralazine, a
well-known treatment for hypertension, has been reported to react with acrolein,
forming hydrazone in cell-free systems. In the companion paper, we have
established an acrolein-mediated cell injury model using PC12 cells in vitro.
Here we test the hypothesis that the formation of hydrazone adducts with
acrolein is able to reduce acrolein toxicity and spare a significant percentage
of the population of PC12 cells from death. Concentrations of approximately 1 mM
of this aldehyde scavenger can rescue over 80% of the population of PC12 cells.
This study provides a basis for a new pharmacological treatment to reduce the
effects of secondary injury in the damaged and/or diseased nervous system. In
particular, we describe the need for new drugs that possess aldehyde scavenging
properties but do not interfere with the regulation of blood pressure. Copyright
2006 Wiley-Liss, Inc.

PMID: 16619236 [PubMed - indexed for MEDLINE]

Finally, the side effects of hydralazine are detailed at http://www.drugs.com/cons/hydralazine_systemic.html

ALL drugs have side effects.

...but lordy it's hard. In case you needed inspiration to exercise.

Exercise has dramatic effects on BDNF. And so does lack of it.


1: J Neurophysiol. 2002 Nov;88(5):2187-95.

Voluntary exercise induces a BDNF-mediated mechanism that promotes
neuroplasticity.

Gomez-Pinilla F, Ying Z, Roy RR, Molteni R, Edgerton VR.

Department of Physiological Science, Los Angeles, California 90095, USA.
fgomezpi@ucla.edu

We have investigated potential mechanisms by which exercise can promote changes
in neuronal plasticity via modulation of neurotrophins. Rodents were exposed to
voluntary wheel running for 3 or 7 days, and their lumbar spinal cord and soleus
muscle were assessed for changes in brain-derived neurotrophic factor (BDNF),
its signal transduction receptor (trkB), and downstream effectors for the action
of BDNF on synaptic plasticity. Exercise increased the expression of BDNF and
its receptor, synapsin I (mRNA and phosphorylated protein), growth-associated
protein (GAP-43) mRNA, and cyclic AMP response element-binding (CREB) mRNA in
the lumbar spinal cord. Synapsin I, a synaptic mediator for the action of BDNF
on neurotransmitter release, increased in proportion to GAP-43 and trkB mRNA
levels. CREB mRNA levels increased in proportion to BDNF mRNA levels. In
separate experiments, the soleus muscle was paralyzed unilaterally via
intramuscular botulinum toxin type A (BTX-A) injection to determine the effects
of reducing the neuromechanical output of a single muscle on the neurotrophin
response to motor activity. In sedentary BTX-A-treated rats, BDNF and synapsin I
mRNAs were reduced below control levels in the spinal cord and soleus muscle.
Exercise did not change the BDNF mRNA levels in the spinal cord of BTX-A-treated
rats but further reduced the BDNF mRNA levels in the paralyzed soleus relative
to the levels in sedentary BTX-A-treated rats. Exercise also restored synapsin I
to near control levels in the spinal cord. These results indicate that basal
levels of neuromuscular activity are required to maintain normal levels of BDNF
in the neuromuscular system and the potential for neuroplasticity.

PMID: 12424260 [PubMed - indexed for MEDLINE]

1: Neuroscience. 2004;124(4):985-92.

Voluntary exercise protects against stress-induced decreases in brain-derived
neurotrophic factor protein expression.

Adlard PA, Cotman CW.

Institute for Brain Aging and Dementia, 1113 Gillespie N.R.F., University of
California, Irvine, Irvine, CA 92697-4540, USA. padlard@uci.edu

Exercise is increasingly recognized as an intervention that can reduce CNS
dysfunctions such as cognitive decline, depression and stress. Previously we
have demonstrated that brain-derived neurotrophic factor (BDNF) is increased in
the hippocampus following exercise. In this study we tested the hypothesis that
exercise can counteract a reduction in hippocampal BDNF protein caused by acute
immobilization stress. Since BDNF expression is suppressed by corticosterone
(CORT), circulating CORT levels were also monitored. In animals subjected to 2 h
immobilization stress, CORT was elevated immediately following, and at 1 h after
the cessation of stress, but remained unchanged from baseline up to 24 h
post-stress. The stress protocol resulted in a reduction in BDNF protein at 5
and 10 h post-stress that returned to baseline at 24 h. To determine if exercise
could prevent this stress-induced reduction in BDNF protein, animals were given
voluntary access to running wheels for 3 weeks prior to the stress. Stressed
animals, in the absence of exercise, again demonstrated an initial elevation in
CORT (at 0 h) and a subsequent decrease in hippocampal BDNF at the 10 h time
point. Exercising animals, both non-stressed and stressed, demonstrated
circulating CORT and hippocampal BDNF protein levels that were significantly
elevated above control values at both time points examined (0 and 10 h
post-stress). Thus, the persistently high CORT levels in exercised animals did
not affect the induction of BDNF with exercise, and the effect of immobilization
stress on BDNF protein was overcome. To examine the role of CORT in the
stress-related regulation of BDNF protein, experiments were carried out in
adrenalectomized (ADX) animals. BDNF protein was not downregulated as a result
of immobilization stress in ADX animals, while there continued to be an
exercise-induced upregulation of BDNF. This study demonstrates that CORT
modulates stress-related alterations in BDNF protein. Further, exercise can
override the negative effects of stress and high levels of CORT on BDNF protein.
Voluntary physical activity may, therefore, represent a simple
non-pharmacological tool for the maintenance of neurotrophin levels in the
brain.

PMID: 15026138 [PubMed - indexed for MEDLINE]

1: Neuroscience. 2004;123(2):429-40.

Exercise reverses the harmful effects of consumption of a high-fat diet on
synaptic and behavioral plasticity associated to the action of brain-derived
neurotrophic factor.

Molteni R, Wu A, Vaynman S, Ying Z, Barnard RJ, Gomez-Pinilla F.

Department of Physiological Science, Brain Injury Research Center, University of
California at Los Angeles, 621 Charles E. Young Drive, Los Angeles, CA 90095,
USA.

A diet high in total fat (HF) reduces hippocampal levels of brain-derived
neurotrophic factor (BDNF), a crucial modulator of synaptic plasticity, and a
predictor of learning efficacy. We have evaluated the capacity of voluntary
exercise to interact with the effects of diet at the molecular level. Animal
groups were exposed to the HF diet for 2 months with and without access to
voluntary wheel running. Exercise reversed the decrease in BDNF and its
downstream effectors on plasticity such as synapsin I, a molecule with a key
role in the modulation of neurotransmitter release by BDNF, and the
transcription factor cyclic AMP response element binding protein (CREB),
important for learning and memory. Furthermore, we found that exercise
influenced the activational state of synapsin as well as of CREB, by increasing
the phosphorylation of these molecules. In addition, exercise prevented the
deficit in spatial learning induced by the diet, tested in the Morris water
maze. Furthermore, levels of reactive oxygen species increased by the effects of
the diet were decreased by exercise. Results indicate that exercise interacts
with the same molecular systems disrupted by the HF diet, reversing their
effects on neural function. Reactive oxygen species, and BDNF in conjunction
with its downstream effectors on synaptic and neuronal plasticity, are common
molecular targets for the action of the diet and exercise. Results unveil a
possible molecular mechanism by which lifestyle factors can interact at a
molecular level, and provide information for potential therapeutic applications
to decrease the risk imposed by certain lifestyles.

PMID: 14698750 [PubMed - indexed for MEDLINE]

1: Neuroscience. 2005;133(3):853-61.

Exercise primes a molecular memory for brain-derived neurotrophic factor protein
induction in the rat hippocampus.

Berchtold NC, Chinn G, Chou M, Kesslak JP, Cotman CW.

Institute for Brain Aging and Dementia, 1226 Gillespie Neuroscience Facility,
University of California, Irvine, CA 92697-4540, USA. nberchto@uci.edu

Exercise is an important facet of behavior that enhances brain health and
function. Increased expression of the plasticity molecule brain-derived
neurotrophic factor (BDNF) as a response to exercise may be a central factor in
exercise-derived benefits to brain function. In rodents, daily wheel-running
exercise increases BDNF gene and protein levels in the hippocampus. However, in
humans, exercise patterns are generally less rigorous, and rarely follow a daily
consistency. The benefit to the brain of intermittent exercise is unknown, and
the duration that exercise benefits endure after exercise has ended is
unexplored. In this study, BDNF protein expression was used as an index of the
hippocampal response to exercise. Both daily exercise and alternating days of
exercise increased BDNF protein, and levels progressively increased with longer
running duration, even after 3 months of daily exercise. Exercise on alternating
days was as effective as daily exercise, even though exercise took place only on
half as many days as in the daily regimen. In addition, BDNF protein remained
elevated for several days after exercise ceased. Further, after prior exercise
experience, a brief second exercise re-exposure insufficient to cause a BDNF
change in naive animals, rapidly reinduced BDNF protein to levels normally
requiring several weeks of exercise for induction. The protein reinduction
occurred with an intervening "rest" period as long as 2 weeks. The rapid
reinduction of BDNF by an exercise stimulation protocol that is normally
subthreshold in naive animals suggests that exercise primes a molecular memory
for BDNF induction. These findings are clinically important because they provide
guidelines for optimizing the design of exercise and rehabilitation programs, in
order to promote hippocampal function.

Intermittent fasting is eating every other day. The good news is that you can pork out to your little heart's content on the "eat" day. The results seem to be spectacular.

<BEGIN>
1: J Neurochem. 2003 Feb;84(3):417-31. Links
Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms.

* Mattson MP,
* Duan W,
* Guo Z.

Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, Baltimore, Maryland 21224, USA.

Although all cells in the body require energy to survive and function properly, excessive calorie intake over long time periods can compromise cell function and promote disorders such as cardiovascular disease, type-2 diabetes and cancers. Accordingly, dietary restriction (DR; either caloric restriction or intermittent fasting, with maintained vitamin and mineral intake) can extend lifespan and can increase disease resistance. Recent studies have shown that DR can have profound effects on brain function and vulnerability to injury and disease. DR can protect neurons against degeneration in animal models of Alzheimer's, Parkinson's and Huntington's diseases and stroke. Moreover, DR can stimulate the production of new neurons from stem cells (neurogenesis) and can enhance synaptic plasticity, which may increase the ability of the brain to resist aging and restore function following injury. Interestingly, increasing the time interval between meals can have beneficial effects on the brain and overall health of mice that are independent of cumulative calorie intake. The beneficial effects of DR, particularly those of intermittent fasting, appear to be the result of a cellular stress response that stimulates the production of proteins that enhance neuronal plasticity and resistance to oxidative and metabolic insults; they include neurotrophic factors such as brain-derived neurotrophic factor (BDNF), protein chaperones such as heat-shock proteins, and mitochondrial uncoupling proteins. Some beneficial effects of DR can be achieved by administering hormones that suppress appetite (leptin and ciliary neurotrophic factor) or by supplementing the diet with 2-deoxy-d-glucose, which may act as a calorie restriction mimetic. The profound influences of the quantity and timing of food intake on neuronal function and vulnerability to disease have revealed novel molecular and cellular mechanisms whereby diet affects the nervous system, and are leading to novel preventative and therapeutic approaches for neurodegenerative disorders.

PMID: 12558961 [PubMed - indexed for MEDLINE]

1: Ageing Res Rev. 2006 Aug;5(3):332-53. Epub 2006 Aug 8.Click here to read Links
Caloric restriction and intermittent fasting: Two potential diets for successful brain aging.

* Martin B,
* Mattson MP,
* Maudsley S.

Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, United States.

The vulnerability of the nervous system to advancing age is all too often manifest in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. In this review article we describe evidence suggesting that two dietary interventions, caloric restriction (CR) and intermittent fasting (IF), can prolong the health-span of the nervous system by impinging upon fundamental metabolic and cellular signaling pathways that regulate life-span. CR and IF affect energy and oxygen radical metabolism, and cellular stress response systems, in ways that protect neurons against genetic and environmental factors to which they would otherwise succumb during aging. There are multiple interactive pathways and molecular mechanisms by which CR and IF benefit neurons including those involving insulin-like signaling, FoxO transcription factors, sirtuins and peroxisome proliferator-activated receptors. These pathways stimulate the production of protein chaperones, neurotrophic factors and antioxidant enzymes, all of which help cells cope with stress and resist disease. A better understanding of the impact of CR and IF on the aging nervous system will likely lead to novel approaches for preventing and treating neurodegenerative disorders.

PMID: 16899414 [PubMed - in process]

1: Physiol Rev. 2002 Jul;82(3):637-72.Click here to read Links
Modification of brain aging and neurodegenerative disorders by genes, diet, and behavior.

* Mattson MP,
* Chan SL,
* Duan W.

Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA. mattsonm@grc.nia.nih.gov

Multiple molecular, cellular, structural, and functional changes occur in the brain during aging. Neural cells may respond to these changes adaptively, or they may succumb to neurodegenerative cascades that result in disorders such as Alzheimer's and Parkinson's diseases. Multiple mechanisms are employed to maintain the integrity of nerve cell circuits and to facilitate responses to environmental demands and promote recovery of function after injury. The mechanisms include production of neurotrophic factors and cytokines, expression of various cell survival-promoting proteins (e.g., protein chaperones, antioxidant enzymes, Bcl-2 and inhibitor of apoptosis proteins), preservation of genomic integrity by telomerase and DNA repair proteins, and mobilization of neural stem cells to replace damaged neurons and glia. The aging process challenges such neuroprotective and neurorestorative mechanisms. Genetic and environmental factors superimposed upon the aging process can determine whether brain aging is successful or unsuccessful. Mutations in genes that cause inherited forms of Alzheimer's disease (amyloid precursor protein and presenilins), Parkinson's disease (alpha-synuclein and Parkin), and trinucleotide repeat disorders (huntingtin, androgen receptor, ataxin, and others) overwhelm endogenous neuroprotective mechanisms; other genes, such as those encoding apolipoprotein E(4), have more subtle effects on brain aging. On the other hand, neuroprotective mechanisms can be bolstered by dietary (caloric restriction and folate and antioxidant supplementation) and behavioral (intellectual and physical activities) modifications. At the cellular and molecular levels, successful brain aging can be facilitated by activating a hormesis response in which neurons increase production of neurotrophic factors and stress proteins. Neural stem cells that reside in the adult brain are also responsive to environmental demands and appear capable of replacing lost or dysfunctional neurons and glial cells, perhaps even in the aging brain. The recent application of modern methods of molecular and cellular biology to the problem of brain aging is revealing a remarkable capacity within brain cells for adaptation to aging and resistance to disease.

PMID: 12087131 [PubMed - indexed for MEDLINE]

1: J Nutr Biochem. 2005 Mar;16(3):129-37.Click here to read Links
Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems.

* Mattson MP,
* Wan R.

Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. mattsonm@grc.nia.nih.gov

Intermittent fasting (IF; reduced meal frequency) and caloric restriction (CR) extend lifespan and increase resistance to age-related diseases in rodents and monkeys and improve the health of overweight humans. Both IF and CR enhance cardiovascular and brain functions and improve several risk factors for coronary artery disease and stroke including a reduction in blood pressure and increased insulin sensitivity. Cardiovascular stress adaptation is improved and heart rate variability is increased in rodents maintained on an IF or a CR diet. Moreover, rodents maintained on an IF regimen exhibit increased resistance of heart and brain cells to ischemic injury in experimental models of myocardial infarction and stroke. The beneficial effects of IF and CR result from at least two mechanisms--reduced oxidative damage and increased cellular stress resistance. Recent findings suggest that some of the beneficial effects of IF on both the cardiovascular system and the brain are mediated by brain-derived neurotrophic factor signaling in the brain. Interestingly, cellular and molecular effects of IF and CR on the cardiovascular system and the brain are similar to those of regular physical exercise, suggesting shared mechanisms. A better understanding of the cellular and molecular mechanisms by which IF and CR affect the blood vessels and heart and brain cells will likely lead to novel preventative and therapeutic strategies for extending health span.

PMID: 15741046 [PubMed - indexed for MEDLINE]

1: Annu Rev Nutr. 2005;25:237-60.Click here to read Links
Energy intake, meal frequency, and health: a neurobiological perspective.

* Mattson MP.

Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. mattsonm@grc.nia.nih.gov

The size and frequency of meals are fundamental aspects of nutrition that can have profound effects on the health and longevity of laboratory animals. In humans, excessive energy intake is associated with increased incidence of cardiovascular disease, diabetes, and certain cancers and is a major cause of disability and death in industrialized countries. On the other hand, the influence of meal frequency on human health and longevity is unclear. Both caloric (energy) restriction (CR) and reduced meal frequency/intermittent fasting can suppress the development of various diseases and can increase life span in rodents by mechanisms involving reduced oxidative damage and increased stress resistance. Many of the beneficial effects of CR and fasting appear to be mediated by the nervous system. For example, intermittent fasting results in increased production of brain-derived neurotrophic factor (BDNF), which increases the resistance of neurons in the brain to dysfunction and degeneration in animal models of neurodegenerative disorders; BDNF signaling may also mediate beneficial effects of intermittent fasting on glucose regulation and cardiovascular function. A better understanding of the neurobiological mechanisms by which meal size and frequency affect human health may lead to novel approaches for disease prevention and treatment.

PMID: 16011467 [PubMed - indexed for MEDLINE]



<END>

A good article about mucuna pruriens:

http://www.parkinson.org/site/pp.asp...JLPwB&b=184301

Zandopa (HP200) source:

http://mall.coimbatore.com/bnh/zandu/zandopa.htm

This was ordered 10/4 and arrived from India on 10/13.

Herbal Powers has their mucuna extract back in stock. It's 60% L-Dopa, and a couple of posters use it with great benefit:

http://herbalpowers.stores.yahoo.net...apruriens.html

This arrived within three days of ordering.

i've been using it for a year or so. some thoughts--

1- this is a real drug. treat it with respect.

2- the higher the level of ldopa the less mucuna. this is not necessarily a good thing since mp is a veritable chemical warehouse and our knowledge of its safety is based on the whole bean powder. herbal powers product is too good for me. i am currently using "dopabean" by solaray at 15% ldopa.

3- if you take it with sinemet and carbidopa enzyme inhibitor expect a different effect than if you don't.

4- don't take it if pregnant.

all that being said i still trust it more than sinemet.

I have residual of ICD (impulse control disorder) remaining...urge to eat pretty much when pramipexole in therapeutic range. Specifically crave the bad stuff : sugar,salt,fat...basically think fast food. Do you know of anyone who's actually tried this?

If it is solely fast food, it might be interesting to consider how an entire society came to be addicted

Thanks for this thread. I would like to add some material on simple things you can do to help brain repair.
1. Get a test for Helicobacter pylori and if positive get it eradicated asap. During eradication and after use probiotics (Bifidus and lactobacillus) to lessen the side effects of the antibiotic.
2. Take Ascorbyl palmitate. This is a fat soluble version of Vitamin C and is eight times more effective at reaching brain than standard Vit C.
I have done a study of the wide effects of H pylori and attach it here. Sorry for all the references but all the claims in it are backed up.
A review of Helicobacter pylori and what it may do to you

There should be great concern about the gap in time between research findings and the practical medical use of them in the treatment of patients. (A)

Eradication of Helicobacter pylori, a common stomach bacterium,
can greatly reduce your chances of suffering these diseases or in some cases, reduce the symptoms already noticed:
gastritis/ dyspepsia ( 1, 4 )
gastric / duodenal ulcer ( 2, 3, 4 )
gastric cancer ( 3, 4, 5, 6,7 )
high blood pressure ( 8, 9, 10, 11 )
resolution of Syndrome X (heart and chest pain) ( 12 )
altered lipid metabolism leads to obesity, heart attack and stroke (13, 14, 15 )
iron deficiency anaemia ( 16, 17 )
abnormal blood counts (neutrophils and monocytes) ( 18, 19)
neurological damage such as Parkinson's, Alzheimer's, MS, ME, optic nerve damage leading to blindness due to Vitamin B12 deficiency (20, 21, 22, 23 )
chronic sub-clinical vitamin deficiency of A, B6, B12, C, E (24,25,26,27,28,29 )
skin conditions such as itchy, flaky, hard skin ( 30, 31 )
rheumatoid arthritis ( 32 )
chronic cholecystitis ( 33 )
glaucoma ( 34, 35 )
insulin resistance ( 36 )
macular degeneration leading to blindness ( 37 )
periodontal disease, tooth loss, reservoir of Hp infection in mouth (38, 39, 40)
some sexually acquired infections of nipples, vulva (41 )

These are the subjects of a large number of peer-reviewed articles in learned journals over many years. ( reference list in numerical order is attached)
Now it is time to do something about it.
ALL medical and gastroenterology surgical patients should be tested for helicobacter species ( 42 ) and appropriate eradication commenced as a matter of routine using antibiotics if required. This should be in addition to dietary supplementation with probiotics, omega-3 oils and / or fish oils and supplements of Vitamins A, B6, B12 and E.
Together with these there are two food additives both widely used in the processed food industry and therefore already of proven safety for human consumption.
One of these, 6-O-palmitoyl-l-ascorbate, (E 304), is a fat-soluble variant of Vitamin C (ascorbic acid). It is already in use in anti-wrinkle creams, infant formula milk, beefburgers and is used by bodybuilders to add collagen to their intestinal and over-developed muscles. It also has the effect of reducing the formation of new blood vessels.
It is known to eradicate Helicobacter at least as efficiently as antibiotics, is a powerful anti-oxidant and can provide a source of ascorbate to replace the Vitamin C lost to the Helicobacter infestation. Ascorbate is essential for tissue repair and this lack of repair in subclinical chronic Vitamin C deficiency accounts for many of the disease effects listed above. It also provides a source of palmitoyl useful in the repair process. Concentrations of this Vitamin C ester are found up to 10 times that of 'ordinary' Vitamin C in the brain. The suggested daily intake of this powder is 250mg and it is intended to investigate the supply of suitable tablets or capsules as soon as possible in order to make this useful stuff available in the UK. A daily intake will cost about 10 pence. ( 43, 44, 45 )

The second additive is a modified form of fructose sold as Trehalose (trade name Ascend™) made by Cargill Inc. It acts as a fructose replacement and has been shown to assist with the unfolding of misfolded proteins such as those in Lewy bodies and amyloid plaques. It is in use by some Huntington's patients as a delaying measure and is taken in a dose of 10 –30 grams three times a day. It is available in 1350 Gram (3 pound) packs from the USA @ about £25 per pack including postage.The suggested daily intake is 30gm costing about 48pence ( 46, 47 )

Combination of these measures with the use of probiotics such as Danone Fruit Layer™ yoghurt and Actimel ™ lactobacillus drink and Omega-3 oils or alternative fish or plant oils can make significant positive differences to Parkinson's and the other diseases listed. They enable self-repair to take place using the body's own naturally occurring stem cells or cell repair mechanisms. Taken before hospital admission for surgery there could be a significant reduction in recovery time.


The use of Lactulose (prescribed by your GP) gives a further boost to the eradication of Helicobacter and assists with the reduction of the constipation so often a dreaded complication of Parkinsons.

By eradicating Helicobacter you will reduce the amount of antigen to it which circulates in your blood and which has been suggested as the cause of death of sensitive long-axon nerve cells possibly because it stimulates platelet activity. ( 48 )

All these measures are safe and proven to be useful but it must be remembered that your neurological condition may have taken years to develop so expect results in months rather than days.

















References re Helicobacter pylori eradication and food additives

A. The Translation of Helicobacter pylori Basic Research to Patient Care
Peter B. Ernst, David A Peura and Sheila E. Crowe
Gastroenterology Volume 130, Issue 1, January 2006, Pages 188 - 206

1. The bidirectional communication between neurons and mast cells within the gastrointestinal tract
Luc Van Nassauw, Dirk Adriaensen and Jean-Pierre Timmermans
Autonomic Neuroscience doi: 10.1016/j.autneu.2006.10.003

2. Critical role of an endogenous gastric peroxidase in controlling oxidative damage in H. pylori-mediated and non-mediated gastric ulcer
Mrinalini Bhattacharjee, Samir Bhattacharjee, Arnab Gupta and Ranajit K. Banerjee
Free Radical Biology and Medicine Volume 32, Issue 8, 15 April 2002, pages 731 – 743

3. Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa
John R. Goldblum M.D., Joel E. Richter M.D., Michael Vaezi M.D., Gary W. Falk M.D., Thomas W. Rice M.D. and Richard M. Peek M.D.
The American Journal of Gastroenterology Volume 97, Issue 2, February 2002, pages 302 – 311

4. Serum and plasma concentration of oxidant and antioxidants in patients of Helicobacter pylori gastritis and its correlation with gastric cancer
Shruti S. Khanzode, Suchet D. Khanzode and Ganesh N. Dakhale
Cancer Letters Volume 195, Issue 1, 30 May 2003, pages 27 – 31

5. Carcinogenic role of tumor necrosis factor-alpha inducing protein of Helicobacter pylori in human stomach
Suganuma, Masami; Kuzuhara, Takashi; Yamaguchi, Kensai; Fujiki, Hirota
Journal of Biochemistry and Molecular Biology Volume 39, Issue 1, January 31, 2006, Pages 1 – 8
6. Will eradication of Helicobacter pylori infection influence the risk of gastric cancer?
Richard H. Hunt FRCP, FRCP(C), FACG
American Journal of Medicine Supplement Volume 117, Issue 5, Supplement 1, 6 September 2004, pages 86 – 91

7. Can gastric cancer be prevented by Helicobacter pylori eradication?
Peter Malfertheiner, Professor, Lucia C Fry, Consultant and Klaus Munkenuller, Consultant
Best Practice and Research Clinical Gastroenterology Volume 20, Issue 4, 2006, pages 709 – 719

8. Eradication of Helicobacter pylori infection improves blood pressure values in patients affected by hypertension
Migneco, Alessio; Ojetti, Veronica; Specchia, Lucia; Franceschi, Francesco; Candelli, Marcello; Mettimano, Marco; Montebelli, Rita; Savi, Luigi; Gasbarrini, Giovanni
Helicobacter Volume 8, Issue 6, December 2003, pages 585 – 589

9. Prevalence of Helicobacter pylori infection in coronary artery disease and effect of its eradication on coronary lumen reduction after percutaneous coronary angioplasty
Kowalski M.; Konturek P.C.; Pieniazek P.; Karczewska E.; Kluczka A.; Grove R.; Kranig W.; Nasseri R.; Thale J.; Hahn E.G.; Konturek S.J.
Digestive and Liver Disease Volume 33, Issue 3, 2001, Pages 222 – 229

10. A link between Helicobacter pylori and/or Chlamydia spp. infections and atherosclerosis
Magdalena Chmiela, Magdalena Kowalewicz-Kulbat, Anita Miszczak, Monika Wisniewska, Tomas Rechcinski, Katarzyna Kolodziej, Jaroslaw Kasprzak, Torkel Wadstrom and Wieslawa Rudnicka
FEMS Immunology and Medical Microbiology Volume 36, Issue 3, 25 May 2003, pages 187 – 192

11. Helicobacter pylori (H. pylori) infection in coronary artery disease: influence of H. pylori eradication on coronary artery lumen after percutaneous transluminal coronary angioplasty. The detection of H. pylori specific DNA in human coronary atherosclerotic plaque
Kowalski, M
Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society Volume 52, Issue 1, Supplement 1, August 2001, pages 3 – 31

12. Resolution of Syndrome X after eradication of virulent CagA-positive Helicobacter pylori
Nocente, R; Gentiloni, N; Cremonini, F; Giorgi, A; Serricchio, M; Santoliquido, A; Gasbarrini, G; Gasbarrini, A
Southern Medical Journal Volume 93, Issue 10, October 2000, pages 1022 – 1023

13. Helicobacter pylori is associated with modified lipid profile: impact on lipoprotein(a)
G. Chimienti, F. Russo, B. L. Lamanuzzi, M. Nardulli, C. Messa, A. Di Leo, M. Correale, V. Gianuzzi and G. Pepe
Clinical Biochemistry Volume 36, Issue 5, July 2003, pages 359 – 365

14. Does eradication of Helicobacter pylori infection help normalise serum lipid and CRP levels?
Kanbay M.; Gur G.; Yucel M.; Yilmaz U.; Boyacioglu S.
Digestive Diseases and Sciences Volume 50, Issue 7, 2005, Pages 1228 – 1231

15. Association between chronic Helicobacter pylori infection and acute ischemic stroke: Fukuoka Harasanshin Atherosclerosis Trial (FHAT)
Yasunori Sawayama, Iwao Ariyama, Maki Hamada, Shigeru Otaguro, Takao Machi, Yuji Taira and Jun Hayashi
Atherosclerosis Volume 178, Issue 2, February 2005, Pages 303 – 309

16. A hematologist's view of unexplained iron deficiency anemia in males: Impact of Helicobacter pylori eradication
Chaim Hershko, Mara Ianculovich and Moshe Souroujou
Blood Cells, Molecules and Diseases doi 10.1016/j.bcmd.2006.09.006

17. The clinical importance of hypochlorhydria (a consequence of chronic Helicobacter infection): Its possible etiological role in mineral and amino acid malabsorption, depression, and other syndromes
R. E. Cater 11
Medical Hypotheses Volume 39, Issue 4, December 1992, Pages 375 – 383

18. Helicobacter pylori eradication decreases blood neutrophil and monocyte counts
Kondo Y.; Joh T.; Sasaki M.; Oshima T.; Itoh K.; Tanida S.; Kataoka H.; Ohara H.; Nomura T.; Itoh M.
Alimentary Pharmacology and Therapeutics, Supplement Volume 20, Issue1, 2004, pages 74 – 79

19. Effect of Helicobacter pylori eradication in patients with chronic idiopathic thrombocytopenic purpura – A randomised controlled trial
Suzuki T.; Matsushima M.; Masui A.; Watanabe K.-L; Takagi A.; Ogawa Y.; Shirai T.; Mine T.
American Journal of Gastroenterology Volume 100, Issue 6, 2005, Pages 1265 – 1270

20. Alzheimer's disease and Helicobacter pylori infection: Defective immune regulation and apoptosis as proposed common links
Jannis Kountouras, Emmanuel Gavalas, Christos Zavos, Christos Stergiopoulos, Dimitrios Chatzopolous, Nikolaos Kapetanakis and Dimitrios Gisakis
Medical Hypotheses Volume 68, Issue 2, 2007, Pages 378 – 388




21. Role of inflammation in gastrointestinal tract in aetiology and pathogenesis of idiopathic parkinsonism
Clive Weller, Norman Oxlade, Sylvia M. Dobbs, R. John Dobbs, Andre Charlett and Ingvar T. Bjarnason
FEMS Immunology and Medical Microbiology Volume 44, Issue 2, 1 May 2005, pp 129-135

22. Link between Helicobacter pylori infection and idiopathic parkinsonism
S.M. Dobbs, R.J. Dobbs, C. Weller and A. Charlett
Medical Hypotheses Volume 55, Issue 2, August 2000, pp93-98

23. Epidemic Optic and Peripheral Neuropathy in Cuba: A Unique Geopolitical Public Health Problem
Thomas R. Hedges 111, MD, Michio Hirano, MD, Katherine Tucker, PHD, and Benjamin Caballero, MD, PHD
Survey of Ophthalmology Volume 41, Number 4, January-February 1997

24. Plasma levels of antioxidant vitamins C and E are decreased in vascular parkinsonism
George P. Paraskevas, Elizabeth Kapaki, Olga Petropolou, Maria Anagnostouli, Vasileious Vagenas and Constantine Papageorgiou
Journal of The Neurological Sciences Volume 215, Issues 1-2, 15 November 2003, pages 51 – 55

25. Influence of gastric juice pH on the metabolism of vitamin C in gastric mucosa and juice
Safranow K, Korzonek M, Dziedziejko V, Jacubowska K, Sulzyc-Bielicka V, Domanski L, Ciechanowski K, Chlubek D.
Pol Merkur Lekarski, 2006 Feb; 20(116);168 –172

26. Relationship of Helicobacter pylori CagA(+) status to gastric juice vitamin C levels
Rokkas T.; Liatsos C.; Petridou E.; Karameris A.; Ladas S.D.; Raptis S.A.
European Journal of Clinical Investigation Volume 29, Issue 1, 1999, Pages 56-62
27. Omeprazole and dietary nitrate independently affect levels of Vitamin C and nitrite in gastric juice
Craig Mowat, Andrew Carswell, Angela Wirz and Kenneth E. L. McColl
Gastroenterology Volume 116, Issue 4, Pages 813 – 822

28. Investigation of Helicobacter pylori ascorbic acid oxidating activity
Lars Odum and Leif P. Andersen
FEMS Immunology and Medical Microbiology Volume 10, Issues 3-4, February 1995, Pages 289 – 294

29. Vitamin B12, demyelination, remyelination and repair in multiple sclerosis
Ariel Miller, Maya Korem, Ronit Almog and Yanina Galboiz
Journal of the Neurological Sciences Volume 233, Issues 1-2, 15 June 2005, Pages 93 – 97

30. Tumor initiating activity of Helicobacter pylori water extract on mouse skin carcinogenesis
Takeshi Ishikawa, Norimasa Yoshida, Harukuni Tokada, Eiichiro Ichiishi, Masashi Kuchide, Satoshi Kokura, Yuji Naito, Shinya Toyokuni, Hoyoko Nishino and Toshikazu Yoshikawa
Cancer Letters Volume 191, Issue 1, 28 February 2003, Pages 41 – 47

31. Therapeutic effects of the antibacterial treatment on intractable skin diseases in Helicobacter pylori-positive patients
Mikihisa Sakurane, Matsunaka Masahiro, Koji Uede, Akiko Shiotani, Shingo Nishioka
Department of Dermatology; Second Department of Internal Medicine, Wakayama Medical University, Japan (Poster Display P249)

32. Eradication of Helicobacter pylori may reduce disease severity in rheumatoid arthritis
Zentillin, P; Seriolo, B; Dulbecco, P; Caratto, E; Iiritano, E; Fasciolo, D; Bilardi, C; Mansi, C; Testa, E; Savarino, V
Alimentary Pharmacology and Therapeutics Volume 16, Issue 7, July 2002, Pages 1291 – 1299
33. Helicobacter pylori and other Helicobacter species in gallbladder and liver of patients with chronic cholecystitis detected by immunological and molecular methods
Apostolov E.; Abu Al-Soud W.; Nilsson I.; Kornilovska I.; Usenko V.; Lyzogubov V.; Gaydar Y.; Wadstrom T.; Ljungh A.
Scandinavian Journal of Gastroenterology Volume 40, Issue 1, 2005, Pages 96 – 102

34. Eradication of Helicobacter pylori may be beneficial in the management of chronic open-angle glaucoma
Kountouras J.; Mylopoulos N.; Chatzopoulos D.; Zavos C.; Boura P.; Konstas A.G.P.; Venizelos J.
Archives of Internal Medicine Volume 162, Issue 11, 10 June 2002, Pages 1237 – 1244

35. Induction of apoptosis as a proposed pathophysiological link between glaucoma and Helicobacter pylori infection
Jannis Kountouras, Christos Zavos and Dimitrios Chatzopoulos
Medical Hypotheses Volume 62, Issue 3, March 2004, Pages 378 – 381

36. The effect of Helicobacter pylori on insulin resistance
Aydemir S.; Bayraktaroglu T.; Sert M.; Sokmen C.; Atmaca H.; Mungan G.; Gun B.D.; Borazan A.; Ustundag Y.
Digestive Diseases and Sciences Volume 50, Issue 11, 2005, Pages 2090 – 2093

37. Association of Helicobacter pylori with central serous chorioretinopathy: hypotheses regarding pathogenesis
Christiano Giusti
Medical Hypotheses Volume 63, Issue 3, 2004, Pages 524 – 527

38. Are dental plaque, poor oral hygiene, and periodontal disease associated with Helicobacter pylori infection?
Anand P.S.; Nandakumar K.; Shenoy K.T.
Journal of Periodontology Volume 77, Issue 4, 2006, Pages 692 – 698
39. Expression cloning of a periodontitis-associated apoptotic effector, cagE homologue, in Actinobacillus actinomycetemcomitans
Yen-Tung A. Teng, and Wenqui Hu
Biochemical and Biophysical Research Communications Volume 303, Issue 4, 18 April 2003, Pages 1086 – 1094

40. Persistence of Helicobacter pylori in the oral cavity after systemic eradication therapy
Gebara E.C.E.; Faria C.M.; Pannuti C.; Chehter L.; Mayer M.P.A.; Lima L.A.;
Journal of Clinical Periodontology Volume 33, Issue 5, May 2006, Pages 329-333

41. Some fibrocystic breast change may be caused by sexually transmitted H. pylori during oral nipple contact: Supporting literature and case report of resolution after gut H. pylori eradication treatment
R.E.Kast
Medical Hypotheses doi:10.1016/j.mehy.2006.09.050 (article in press)

42. Helicobacter pylori "Test and Treat" or Endoscopy for Managing Dyspepsia: An Individual Patient Data Meta-analysis
Alexander C. Ford, Michelle Qume, Paul Moayyedi, Nicolas L.A. Arents, Annmarie T. Lassen, Richard F.A. Logan, Kenneth E.I. McColl, Paul Myres and Brendan C. Delaney
Gastroenterology Volume 128, Issue 7, June 2005, Pages 1838 – 1844

43. Palmitoyl ascorbate: Selective augmentation of procollagen mRNA expression compared with L-ascorbate in human intestinal smooth muscle cells
Rosenblat G.; Willey A.; Zhu Y.-N.; Jonas A.; Diegelmann R.F.; Neeman I.; Graham M.F.
Journal of Cellular Biochemistry Volume 73, Issue 3, 15 May 1999, Pages 312 - 320



44. Diverse effects of ascorbic acid and palmitoyl ascorbate on Helicobacter pylori survival and growth
M.Tabak, R.Armon, G. Rosenblat, E. Stermer and I. Neeman
FEMS Microbiology Letters Volume 224, Issue 2, 29 July 2003, Pages 247-253

45. Ascorbyl Palmitate as a Carrier of Ascorbate into Neural Tissues
Mieczyslaw Pokorski, Magdalena Marczak, Aneta Dymecka, Piotr Suchocki
Journal of Biomedical Science Volume 10, Issue 2, 2003

46. Multiple Effects of Trehalose on Protein Folding In Vitro and In Vivo
Mike A. Singer and Susan Lindquist
Molecular Cell Volume1, Issue 5, April 1998, Pages 639 – 648

47. Aggregation mechanism of polyglutamine diseases revealed using quantum chemical calculations, fragment molecular orbital calculations, molecular dynamics simulations, and binding free energy calculations
Koki Tsukamoto, Hideaki Shimizu, Takashi Ishida, Yutaka Akiyama and Noboyuki Nukina
Journal of Molecular Structure: THEOCHEM Volume 778, Issues 1-3, 11 December 2006, Pages 85 – 95

48. Cholesterol synthesis inhibitors protect against platelet-activating factor-induced neuronal damage
Clive Bate, Louis Rumbold and Alun Williams
Journal of Neuroinflammation Volume 4, Issue5, 18 January 2007


References 21, 22 are relevant to PD.

I totally agree regarding the value of exercise.
It definitely helps me feel less symptomatic and I wish I'd started it sooner.
Couldn't access the websites you mentioned though.
Like to know what EECP and blood modulation therapy is if you have time to reply.
Thanks,
Lee