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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. |
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. |
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. |
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> |
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. |
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. |
Treatments of Parkinson's Disease
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Quote:
"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. :cool: 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. |
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 |
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 .... Lindy |
The Big Three...
...at least for me. :)
There are supplements and there are supplements and one can go quite mad and poor trying to take all of them that show promise. Plus, it gets downright awful to be taking pills and pills and pills. But some of them do a lot of good and here are the best that I have tried. I suggest that newbies adopt a simple test to see if these or any others are worth taking. Stand on one foot as long as you can by making several attempts and then write down your time. Repeat on your other foot. This simple test gives you a baseline on half-a-dozen PD parameters. After trying a new supplement or therapy, repeat the testing. While it won't tell you much about longterm benefits, it helps tremendously with benefits to daily function. In my case the following pair TRIPLED my times in one week and there is some good research to back them up. Alpha Lipoic Acid (ALA) and Acetyl-L-Carnitine (ALC) work both together and seperately to address some core problems of PD. Inflammation, oxidation, and mitochondrial problems are very destructive processes at work in PWP. ALA is one of the most important anti-oxidants around for two reasons. It crosses the blood brain barrier for one. And it not only neutralizes the free radicals that damage nerve tissues, it also is critical to recycling other anti-oxidants like Vit E and Vit C. ALC has at least two things going for it. It boosts mitochondrial function for one. Secondly and even more interestingly, it increases the diameter of remaining neurons and makes them more efficient and able to partly compensate for the ones lost. The third and final part of the team is green tea extract. it has many benefits but one stands out for PWP. One of the things that kills our neurons is an over-reaction of our brain's immune system. The defenders are a cell-type called the microglia. In PD, when microglia are "activated" they just don't know when to quit and destroy neurons around themselves. The substantia nigra has the greatest microglial density in the brain. Green tea's ingredients calm down the microglial reaction and stop the slaughter. |
Alpha Lipoic Acid and Acetyl-L-Carnitine
From: Altern Med Rev. 2006 Sept;11(3):232-237.
Alpha-lipoic acid- Monograph. [No authors listed] Alpha-lipoic acid (ALA - also known as thioctic acid) was discovered in 1951 as a molecule that assists in acyl-group transfer and as a coenzyme in the Krebs cycle. In the 1980s, the scientific community realized alpha-lipoic acid is a powerful antioxidant. Several qualities distinguish alpha-lipoic acid from other antioxidants: ALA can be synthesized by animals and humans; it neutralizes free radicals in both the fatty and watery regions of cells, in contrast to vitamin C (water soluble) and vitamin E (fat soluble); and, ALA functions as an antioxidant in both its reduced and oxidized forms. Mechanisms of Action Alpha-lipoic acid is a potent antioxidant in both fat- and water-soluble mediums. Furthermore, its antioxi- dant activity extends to both its oxidized and reduced forms. DHLA is capable of directly regenerating ascorbic acid from dehydroascorbic acid and indirectly regenerating vitamin E. Researchers have also found ALA increases intracellular glutathione and coenzyme Q levels. Alpha-lipoic acid appears capable of chelating certain metals. It forms stable complexes with copper, man- ganese, and zinc. In animal studies, it has been found to protect against arsenic poisoning, and, in both animal and in vitro studies, ALA reduced cadmium-induced hepatotoxicity. In vitro, ALA chelated mercury from renal slices. 1: J Gerontol A Biol Sci Med Sci. 2003 Nov;58(11):970-4. Carnitine: a neuromodulator in aged rats. Juliet PA, Balasubramaniam D, Balasubramaniam N, Panneerselvam C. Department of Geriatrics, Nagoya University School of Medicine, Japan. A wide range of morphological and biochemical changes occur in the central nervous system with increasing age. L-carnitine, a naturally occurring compound, plays a vital role in fatty acid transport across the mitochondrial membrane. L-carnitine (300 mg/kg body wt/day) was administered intraperitoneally to young and old male Wistar rats for 7, 14, and 21 days. Carnitine, dopamine, epinephrine, and serotonin levels were assayed in discrete regions of the brain. Carnitine supplementation increased the levels of dopamine, epinephrine, and serotonin in the experimental animals in our study. Response to carnitine supplementation varied among the brain regions that have been studied. The regions rich in cholinergic neurons such as the cortex, hippocampus, and striatum showed more response after 21 days of carnitine treatment. The results of the present study suggest the role of L-carnitine as a neuromodulator and antiaging medication. PMID: 14630876 [PubMed - indexed for MEDLINE] |
iv glutathione
how much al do you take?
whoops! my neuologist prescribes iv glutathione for symptom reduction, neuro-protection of my pd. there is a published paper on this therapy, the experiment was conducted in italy. there is another study bbeing conducted in, i believe, miami fl, that should be published any time. i will try to find the italian study and then i,ll ask for help to post it here. has anyone tried intermittant fasting? |
Exercise, active and passive and PD
Dr, Lieberman's theoretical basis, at:
http://www.parkinsonresearchfoundati...349&Itemid=104 http://www.parkinsonresearchfoundati...d=79&Itemid=95 http://www.parkinsonresearchfoundati...=219&Itemid=83 examples of active exercise: Cycling: Inevergiveup.org, tandem bycicling, static byke. Examples of passive exercise: As mentioned by Dr. Lieberman: acceleration therapeutics, EECP,and found elsewhere, blood modulation therapy. |
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. |
Dear PDInfo
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 |
tested all three links and they all opened fine
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As regards the other options mentioned: oogle)eecp = enhanced external counterpulsation, a cardiac therapy which proved to improve pd symptoms: (Google)Acceleration therapeutics = back and forth moving bed (Google)Blood modulation therapy -BPM- = See-saw moving bed |
http://www.scielo.br/scielo.php?scri...lng=en&nrm=iso
High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson's disease patient Abstract Introduction Patients and Methods Results Discussion References Acknowledgments Correspondence and Footnotes Abstract Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson's disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12 patients who did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age ± SD = 66.2 ± 8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4 ± 34.9 to 179.2 ± 23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of treatment showed improved motor capacity during the first three months and most reached a plateau while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity increased from 44 to 71% after 6 months, increasing significantly every month compared with their own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for several days did not impair motor capacity and yellowish urine was the only side effect observed. The data show that the proposed treatment improves the clinical condition of PD patients. Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron metabolism. More studies are required to identify the mechanisms involved. |
Dr. Ulrich Werth Parkinson Implant Therapy
http://www.werththerapie.de/en/hintergruende.html
On these pages we inform you about an alternative treatment of Parkinson’s disease and the physiological background of peripheral stimulation of the brain. http://www.werththerapie.de/en/player.html |
Brain Gym
Hello,
I'm new to this group, not sure if I'm doing this posting right, anyway here it goes. "Brain Gym" I've been practicing it for about 4 years now. I don't do it every day, and it only takes about 15 minutes, but their's lots of different exercises so you can, so do as many as you like and do different ones each time. When I lived in Calgary, I belonged to the young onset pd group. Once of the facilitators put together a course on "Brain Gym". She told us that pd'ers practicing this have shown improvements. I don't remember where she got the following info, but it really sounded interesting: "By practicing Brain Gym, you will stimulate new areas of the brain to create dopamine" Sounds good enough for me, so I signed up for the course. So what is "Brain Gym" Info taken from: brainworksnaturally.com Brain Gym® consists of various combinations of 26 targeted movements. It grew out of clinical studies started in 1969 by Paul Dennison. In the more than thirty years since, research has shown that application of Brain Gym® provides significant improvement in concentration, memory, reading, organization skills, language and number skills, writing, speaking, athletic performance and more. It is used worldwide in more than 90 countries, in 40 different languages. In 1989, in response to "The Nation At Risk" study, The National Learning Foundation selected Brain Gym® as a recommended learning strategy, and continued to rate it highly throughout the 1990’s. Who Benefits ? Students with special needs, ADD, ADHD, autism, dyslexia, patients with Alzheimer's or Parkinson's disease, and people with learning disorders have all shown improvement using brain gym. Change may be remarkably immediate or take place in a period of days or weeks, according to the extent of the problem, but profound differences are usually noticed by the clients themselves. Check into research studies for more information. Anyone who wants to think better, clearer and faster can benefit. Academic, physical and personal goals are met using Brain Gym®. No matter what your age, it is never too late to activate! Learn simple ways to energize, meet challenges and optimize learning potential. The best book I found on "Brain Gym" is called: Brain Gym for Business by Gail & Paul Dennison cost around $18.00 at Amazon.com I couldn't find a book that specificallly for pd'ers These exercises are fun and easy to do. They are mostly cross-overs. Like an infant learning how to crawl, this is a cross over. You will be working both sides of the brain, creating new or strengthing the links between them. These exercises will improve your balance, concentration, problem solving, handwriting, reading, speaking, memory, writing skills, focus, improves posture, releases stress, etc. Here is an example of one of these exercises. Called: "The Cross Crawl" Taken from: Brain Gym for Business by Gail & Paul Dennison You will need to be standing. Start by marching in place, alternate touching each hand to the opposite knee. Continue during the course of 4 to 8 complete, relaxed breaths. A variation of this movement can be done sitting down. The Cross Crawl activates both brain hemispheres simultaneously. It engages the brain for coordinating visual, auditory, and kinesthetic abilities, thus improving such skills as lisitening, reading writing and memory. I've had pd for 7 years now, and something I'm doing has dramatically slowed down the progression. As the months go by, I've been getting better, maybe "Brain Gym" has something to do with it. Who knows. It couldn't hurt. I'm also taking mucuna. Been taking it for over a year now with excellent results. Sincerely. Max |
stem cell treatments
I'm new here and I dont know if you talked about it in the past - stem cell treatment.
what about treat PD with stem cells? I just start to read about it, and I find this success stories at the frc-family research council. what you think ? |
Could you give me the dosages you are suing with the current formulas?
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Just ordered Munuca for for the first time because I heard so much about it, all good. Can you give me some information on how you started and how much you took, you know, the details. I believe in taking natural drugs. I believe in exercise. I set up my own regime that works great for me. I too was getting better, until the Dystenesa set in and when I saw my doctor he said that I was being overdosed and reduced my Levocarb to half of what I was taking. 200 to 100 for 4 times a day. But I'm still not happy and I want to get off as many drugs as I can, that's why the Mucuna. thank you C |
Fasting and a vegetarian diet
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Parkinson ear implants
Hi
Any experiences in using dr Werth¨s ear implant acupuncture |
inplant acupuncture needle - Dr werth titanium needle
HI
I am new to this forum but would like to know if anyone has experiences about dr Werth inplant acupuncture implant. see Werth acupuncture for ever needle regards Seppo, Finland |
John Argue
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Am wondering if you proceeded with Werth's implant acupuncture? My friend Jan wants to learn about other's experiences. Kind regards, Trisha |
ICD and food
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?:cool:
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Being paranoid does not necessarily mean you are wrong
If it is solely fast food, it might be interesting to consider how an entire society came to be addicted
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Caffeine
I see a few good studies mentioned in this forum, but I haven't seen any mention of caffeine or adenosine blockers. Findings from a longitudinal study examining the effects of caffeine found that people who drink a moderate amount of caffeine (or more) per day were less likely to develop Parkinson's disease, or for it to develop later in life. In response to that, several studies were done which strongly suggest that caffeine does indeed slow the progression of Parkinson's disease. Since caffeine works as an adenosine blocker, several studies were done to test the effects of adenosine blockers to slow the progression of Parkinson's. I've read several of these studies, and they all lead to the conclusion that adenosine blockers in general can reduce the amount of l-dopa needed to control Parkinson's, and can slow progression of the disease. All the studies I read have copyrights which expressly forbid posting them to online forums, so I can't post them here. If you're interested, you can search for scholarly articles about adenosine, caffeine and Parkinson's disease.
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I think that adenosine blockers are a current target
For pharmaceutical companies, looking for further exploration of small molecule therapy for PD. but just enough already with the palliatives, what we need is cell replacement therapy. It it terrible that DBS is the neuro's last words. In today's worlds of biochemical knowledge it is a shame that we are not ten years ahead on this.
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I second your opinion.
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challenge conventional expectations about Parkinson's disease
To reverett123
i have read some of your 3600 posts -- and I agree with your basic attitude that its up to us to do waht we can rather than waiting for researchers to make the miracle breakthrough they keep telling us they will make if only we donate more to fund their research. In 1997 I was 41 years old when I was diagnosed wiith Parkinson's disease, in 2010 I began leading exercise classes for people with Parkinson's disease, and in 2013 I participated in my first masters slalom and giant slalom ski races. Vigorous exercise can enable us to beat expectations. David Quote:
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Zucchini Flower - Zandopa.
This ifo dates back to 2006 and indicates above helps PWP. 2013 and nobody has mentioned anything about it. what has gone wrong?
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What has gone wrong is that no one seems to know what really causes
PD. Dopamine deficiency certainly plays a big role, but it's something else that triggers everything. I am afraid it might be too late for us to hope for a cure. Stem cell research is probably the most promising lead. But Bush has pushed it back 10 or 20 years. Let's hope the Europeans can take over and help us all. |
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Also, another glimmer of hope discusses New research which: shows that, when properly manipulated, a population of support cells found in the brain called astrocytes could provide a new and promising approach to treat Parkinson's disease. These findings, which were made using an animal model of the disease, demonstrate that a single therapy could simultaneously repair the multiple types of neurological damage caused by Parkinson's, providing an overall benefit that has not been achieved in other approaches. http://www.sciencedaily.com/releases...0128184809.htm |
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