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Possible Treatments for TODAY's PWP

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Old 09-23-2006, 03:04 PM   #1
reverett123
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Arrow Possible Treatments for TODAY's PWP

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.
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 09-23-2006, 04:57 PM   #2
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Default Hydralazine

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.
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.

Last edited by reverett123; 09-24-2006 at 08:35 PM. Reason: To meet "Fair Use" requirements
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Old 09-23-2006, 05:20 PM   #3
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Default Everyone talks about it...

...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.
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.

Last edited by reverett123; 09-24-2006 at 08:38 PM. Reason: corrected spelling
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Old 10-01-2006, 04:23 PM   #4
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Default INTERMITTENT fasting

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>
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 10-04-2006, 07:47 PM   #5
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Default

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.
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Old 10-04-2006, 09:00 PM   #6
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Default mucuna experience

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.
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 10-05-2006, 07:00 AM   #7
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Default Treatments of Parkinson's Disease

Treatments of Parkinson's Disease :

http://************/parkinsons.disease/treatments.htm
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Old 10-05-2006, 08:03 PM   #8
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Quote:
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.
Rick, thanks for that info. I agree with all of your points. I wondered about Dopabean. Glad to know it works well for you. Thanks for the heads up about Herbal Powers stuff being too strong for you. The Zandopa, HP200, is what they used in research trials and is approved by the Indian version of the FDA. It's been approved for use in trials here by our FDA:

"Recently the US FDA accepted their application for a new drug for Parkinson Disease - HP-200 and clinical trials are starting soon."

I plan to use it on an as needed basis, that is, as little as possible. Zandopa is only about 4% L-Dopa, but it contains other good mucuna ingredients that I have some blind faith in.

I'll start with a low dose. I can weigh it out precisely in my lab. I hope I can tolerate it. Supposedly, it dissolves in water.
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Old 10-17-2006, 06:11 PM   #9
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Bioavailability of L-DOPA from HP-200 : a formulation of seed powder of Mucuna pruriens (Bak) : a pharmacokinetic and pharmacodynamic study
Auteur(s) / Author(s)
MAHAJANI S. S. (1) ; DOSHI V. J. ; PARIKH K. M. (1) ; MANYAM B. V. ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Divisions of Pharmacology, The Zandu Pharmaceutical Works Ltd., Bombay, INDE
Résumé / Abstract


HP-200, a formulation made from the seed powder of Mucuna pruriens, contains among other constituents, about 4% L-DOPA. After five normal human volunteers were each given a single oral dose of 30 g of HP-200, plasma samples were obtained at 0, 20, 40, 60, 90, 120, 180, 240 and 360 min for assay of L-DOPA by HPLC technique using electrochemical detection. The supine systolic and diastolic blood pressures were recorded at each sampling time.

The results indicate that on oral administration, L-DOPA was absorbed from HP-200 with plasma peak levels (C[max]=1.56±0.163 μg/mL) achieved at T[max]=83±16.09 min. The plasma half life was 102±2 min and the auc was determined as 6.508±0.421 μg/h/mL. The pharmacokinetic profile of HP-200 exhibited characteristics similar to formulations of synthetic L-DOPA, except for the lack of a sharp peak. HP-200, a new herbal formulation, appears to be suitable for the treatment of Parkinson's disease.

***************

Mucuna pruriens in Parkinson’s disease: a double blind clinical and pharmacological study
R Katzenschlager1,2, A Evans1, A Manson3, P N Patsalos4, N Ratnaraj4, H Watt5, L Timmermann6, R Van der Giessen7 and A J Lees1

Journal of Neurology Neurosurgery and Psychiatry 2004;75:1672-1677

Background: The seed powder of the leguminous plant, Mucuna pruriens has long been used in traditional Ayurvedic Indian medicine for diseases including parkinsonism. We have assessed the clinical effects and levodopa (L-dopa) pharmacokinetics following two different doses of mucuna preparation and compared them with standard L-dopa/carbidopa (LD/CD).

Methods: Eight Parkinson’s disease patients with a short duration L-dopa response and on period dyskinesias completed a randomised, controlled, double blind crossover trial. Patients were challenged with single doses of 200/50 mg LD/CD, and 15 and 30 g of mucuna preparation in randomised order at weekly intervals. L-Dopa pharmacokinetics were determined, and Unified Parkinson’s Disease Rating Scale and tapping speed were obtained at baseline and repeatedly during the 4 h following drug ingestion. Dyskinesias were assessed using modified AIMS and Goetz scales.

Results: Compared with standard LD/CD, the 30 g mucuna preparation led to a considerably faster onset of effect (34.6 v 68.5 min; p = 0.021), reflected in shorter latencies to peak L-dopa plasma concentrations. Mean on time was 21.9% (37 min) longer with 30 g mucuna than with LD/CD (p = 0.021); peak L-dopa plasma concentrations were 110% higher and the area under the plasma concentration v time curve (area under curve) was 165.3% larger (p = 0.012). No significant differences in dyskinesias or tolerability occurred.

Conclusions: The rapid onset of action and longer on time without concomitant increase in dyskinesias on mucuna seed powder formulation suggest that this natural source of L-dopa might possess advantages over conventional L-dopa preparations in the long term management of PD. Assessment of long term efficacy and tolerability in a randomised, controlled study is warranted.

FULL ARTICLE:

http://jnnp.bmjjournals.com/cgi/content/full/75/12/1672
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Old 11-29-2006, 06:50 PM   #10
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Default Looking for something to maintain your mobility?

For anyone coming here for the first time, and needing some answers on self-help, especially with regard to maintaining flexibility John Argue's book 'Parkinson's Disease and the Art of Moving' is a good resource. Based on both western and eastern ideas on body work it takes you through a process of developing skills that will help you keep your independence, and minimise some of the movement difficulties that PD brings. In case you think I am giving this book some good advertising space, I have never had anything to do with John Argue, just recognise a good thing when I see it!

Tai Chi is also pretty good, and one of the forms of exercise that comes recommended for PD'ers. Look for a teacher who is non competitive and will take things at an easy pace........... A good teacher will help you get your stance right early on, and teach you to step out using a heel-toe movement, which helps with falls and poor balance, getting out of hesitation and freezes etc. It's relaxing and good fun, and helps maintain good memory too ....

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