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    Psychedelics and neurodegenerative disorders 
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    Following is a digest of articles and reports that is constantly updated. Jump in!






    Ibogaine and Parkinson's Disease

    After Alzheimer's, Parkinson's Disease is the second most common neurodegenerative disease and is currently not curable. The disease manifests itself by the progressive loss of nerve cells, mainly of dopamine neurons in the Substantia Nigra (part of the mid-brain). This results in a lack of dopamine in the striatum (a subcortical part of the forebrain), as well as a dysfunction in motor functions, tremors, stiffening muscles, language problems and a general loss of balance and coordination.

    These physical symptoms are also accompanied by psychological effects like dementia and depression. It is thought that the neurodegenerative aspects of Parkinson's disease are caused by the body's immune system. Healthy nervous system tissue is attacked when the immune system is no longer able to distinguish between healthy and diseased cells, similar to autoimmune diseases such as multiple sclerosis, fibromyalgia and polyneuropathy.

    GDNF (glial cell line-derived neurotrophic factor) is a protein discovered in 1991 with an extraordinarily positive effect on nerve cell tissue. GDNF stimulates nerve cell growth, especially dopamine neurons. In addition to the ability to regenerate nerve cells in the brain, GDNF also appears to possess neuroprotective properties.

    In an animal experiment in which rats with Parkinson's disease had GDNF injected directly into the brain, a significant improvement in the symptoms was observed. After one year, there were still no undesirable side effects of GDNF administration. Initial studies have shown that GDNF significantly improves the overall condition of Parkinson's patients. The resulting data suggests that new nerve cells had formed.

    Ibogaine and its metabolite noribogaine lead to a substantial increase in GDNF levels in the brain. This indicates that ibogaine could provide a very effective treatment for neurodegenerative diseases, such as Parkinsons.

    Until now, it was not possible to introduce GDNF directly into the desired regions of the brain. But Ibogaine stimulates the glial cells and neurons to produce GDNF itself, increasing GDNF levels throughout the brain. Phytostan, a pharmaceutical company focused on developing ibogaine, has developed an ibogaine-based medicine called CK-BR-12 consisting of Ibogaine HCL and a cocktail composed of 12 vitamins.

    Patient D is a 69-year-old Parkinson's disease patient and until now the only human treated with Ibogaine for his condition. Patient D reported numerous positive changes regarding his illness: he could swallow again, speech and facial expressions improved noticeably, the control of the hands increased and he could write again legibly. Also, his general motor skills increased.

    He could dress again, eat independently and climb stairs, all activities which were not possible prior to his treatment. The Parkinson's symptomatology also improved after the treatment was completed. Patient D. was examined by various physicians as well as pharmacologist Dr. Susanne Cappendijk from Semper Clarus Consulting, who presented the promising results at the New York Academy of Sciences conference on April 27, 2015.


    The standard symptomatic treatment, is predominantly carried out with drugs with strong side effects. The quality of life of the patients is often characterised by significant suffering in the terminal phase. In contrast, treatment with ibogaine, in particular through the approach of microdosing, allows an increase in the GDNF levels in the brain, without the side effects of conventionally used medications.

    It was reported that 4mg Ibogaine HCL can increase GDNF levels in the brain by a factor of 12. The neuroplasticity increased by the growth of new neurons promotes the restoration and the construction of nerve tracts. Also, the challenge of introducing GDNF by injection into the brain is obviated. These results could help to redefine the position of Ibogaine in general research and, as unknown healing properties of the plant are discovered, open up new research areas and thereby achieve a wider social and regulatory acceptance.

    At the Ibogaine conference in 2016, Dr. Ignacio Carrera from the Universidad de la Republica Uruguay presented the research of an interdisciplinary group. Novel variations of the ibogaine molecular structure have been developed that enhance the production of GDNF. The group of N-indolylethyl isoquinuclidines appears to be most promising. The synthesis of these molecules is far less complex than that of Ibogaine and there are several promising derivatives. Some of the analogues cause an even higher GDNF-release in vitro than Ibogaine does, but can have cytotoxic effects depending on the structure. The research in this field is still nascent, but it has enormous potential.

    http://iboga.info/parkinsons-disease/

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    Ayahuasca stimulates brain cells and could treat Alzheimers


    By Olivia Lerche

    SCIENTISTS have discovered that a psychedelic substance from the Amazon stimulates the birth of new brains cells and could lead to treatment for neurodegenerative diseases such as Alzheimers disease. The tea called Ayahuasca, is also used as a traditional spiritual medicine in ceremonies in Peru, South America.

    The Sant Pau Hospital Barcelona, which worked in collaboration with the Beckley Foundation and Spanish National Research Council in Madrid, has released the findings from a study investigating the potential of ayahuasca to promote neurogenesis - which is the development of new brain cells. The investigators believe that these findings will open up a new avenue of research that may help develop drugs to treat diseases like Alzheimers, Parkinsons and addiction.

    Dr Jordi Riba, lead investigator, presented preliminary data, at the Interdisciplinary Conference on Psychedelic Research in Amsterdam at the weekend. Results showed that two compounds - harmine and tetrahydro harmine - which are found in the hallucinogenic tea, potently stimulated the transformation of stem cells into new neurons.

    Amanda Feilding, director of the Beckley Foundation said: The images from the Beckley/Sant Pau collaboration showing the birth of new neurons are very interesting and suggest that ayahuasca could lead to a new approach in the treatment of neurodegenerative conditions such as Alzheimers and Parkinsons, among others.?

    Experts have believed for years that the brain doesnt make neurons during adulthood. In the 1990s, research changed this finding, showing that new neurons are generated throughout adult life in two regions of the human brain: the area around the ventricles and in the hippocampus. The hippocampus, thought to be the center of emotion and autonomic nervous system, plays a key role in memory. Its function declines with age and in neurological disorders.

    Under normal conditions, the rate of the birth of new neurons is very low, and it cannot keep up with the rate of neural death that occurs in diseases such such as Alzheimers disease. In the study, neural stem cells were isolated from the hippocampus of adult mice. The stem cells were grown in the lab and substances that are present in ayahuasca were added to the cultures and compared with saline a placebo control.

    Scientists have described the results as impressive, with ayahuasca substances stimulating the transformation of stem cells into new neurons.

    Dr Riba has been studying ayahuasca for twenty years.

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    Is Ibogaine a promising new treatment for Parkinson's?

    There is reason to believe that ibogaine may be beneficial in Parkinson's treatment. Columbias two-year animal study represents the first time that researchers will probe for a direct link.

    The exact mechanisms of action of ibogaine are still obscure, but the theory for ibogaines benefit for Parkinsons rests on the fact that amongst its other effects, it has been shown to increase the production of a protein called glial cell-derived neurotrophic factor, or GDNF. This and other neurotrophic factors have been shown to stimulate the production of dopaminergic fibers throughout the brain, and some existing research shows that GDNF in particular improves the recovery of dopaminergic neurons and leads to an improvement of Parkinsons symptoms.

    Previous methods used to increase the expression of GDNF were limited gene therapy and direct brain infusion, but according the research abstract, the research team, led by Dr. Serge Przedborski, President of the World Parkinson Coalition, is exploring whether ibogaine could provide safer and more convenient means to enhance GDNF production in the brain.

    Dr. Jeffrey Kamlet, a Miami medical doctor and board certified addiction specialist has been researching ibogaine for over 20 years, and is a strong advocate for medical supervision. According to Dr. Kamlet, Ibogaine is the most important discovery in the field of opiate dependency in the history of addiction medicines, and I am confident that it will one day be a main stay treatment for many addictions.

    Even with this in mind, some advocates believe that ibogaine application as a treatment for Parkinson's may prove more straightforward for research. In the case of addiction therapy, ibogaine is most often administered in a single large dose, but there is anecdotal evidence that the repeated use of very low sub-perceptual doses, which are generally agreed to be well tolerated in patients, could be sufficient to reverse Parkinson's symptoms over time.

    Patient D was 69 years old in 2012 when he was diagnosed with Atypical Parkinsons, a Parkinson's-like syndrome that does not include the characteristic palsy. By last year Patient Ds symptoms had advanced to the point where his facial muscles felt frozen. He had difficulty finding his balance, talking or using his hands. As a writer and artist, he noted that emotionally it was the first time in his life he had lost his desire to do anything creative.

    Patient D was treated with CKBR-12, an experimental natural health product and ibogaine-derivative? at a medical center in Rosarito, Mexico. He took a small dosage twice a day for 30 days, and after the first two weeks began to notice that he could use his fingers to pick up objects again. After a month he had seen a gradual improvement in all of his symptoms to the point where he could carry on normal conversation, and coordinate previously impossible tasks such as buttoning his shirt.

    In a post-treatment interview that was published on YouTube, Patient D says, Its difficult to explain what Parkinson's is, but you lose your edge. And I have got my edge back in a few areas. It may be small things to some, but they are big things for me. I am anxious to see what happens next.

    When we spoke, to Patient D, he said that he had continued to have improvements with further treatment. His case has been reviewed by several doctors, including Dr. Susanne Cappendijk of Florida State University Medical Center, who relayed some of the results at a conference at the New York Academy of Sciences.

    -Jonathan Dickinson





    Psilocybin rebuilds damaged neurotransmitters


    Dr. Juan R. Sanchez-Ramos has discovered that using large doses of psilocybin allow the (hippocampus and cerebellum for this study) brain to create new brain cells. Dr. Ramos is actively seeking alternatives from mainstream medicine to cure Neurodegenerative diseases, Huntington's Disease and Parkinson's Disease.

    This is promising news for Alzheimer's patients who suffer with a sloughing of brain cells causing a disruption and permanent loss of memory, and also for people who suffer with depression because of the low serotonin levels. The magic mushrooms rebuild the neurotransmitters responsible for serotonin. Because at the root of many tragic massacres today are psychotropic (Prozac, Paxil, etc.) drugs with side effects like suicide, extreme depression and violence. It appears whenever a natural remedy is applied to alleviate a problem, it does not have these hazardous side effects.

    -Michael Erevna

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    Ayahuasca and ALS

    Male, 65, UK, diagnosed with ALS

    Q: What can you tell us in general about your medical condition, and to what degree has it affected you? (Prior to treatment using ayahuasca)

    A: My prognosis as of March 2013 was that of a one-year life expectancy, I did get a specific MND diagnosis confirmed by a consultant neurologist, on the back of which an insurance company paid up on my critical illness cover, there being a clear understanding that I would probably not last the year. I was very weak and trembly, had lost over 20 pounds in muscle mass, my knees were prone to swelling and I was racked by cramps and muscle twitching. I could barely manage stairs, and couldnt get out of the bath unassisted. I remember being a little challenged by a four inch step across the end of the room, choosing my best leg to step down.

    Q: Describe a typical experience with ayahuasca. What is it like during the immediate time the medicine is active in the body? What has been experienced afterwards?

    A: Initially a fair amount of retching, although I didnt actually vomit much. Then some spastic activity, after which a warmth spread throughout my chest cavity, and sensations from the connection between muscle tissue and skeletal bone. It left me exhausted, but it mellowed out? after a while into a contemplation state of mind where the concept of fear had a major part. Stressful emotions such as fear and anxiety seems to be a major vexation (in relation to neurological diseases), and the ayahuasca seemed to soothe that too. I didnt feel that much different immediately afterwards, I suppose I felt a little more relaxed, but the following weeks (after sessions) my massage therapist said the muscle twitching was much improved, and I continued to recover steadily.

    Q: Has this treatment relieved or improved your condition in any way so far?

    A: I have made essentially a full recovery, slow but persistent, and NHS consultants involved are mystified. Ayahuasca seems to me to have been instrumental in my recovery, which is fully documented. I am now fully healthy, I cycle to work. Now, after today doing a nine mile coastal walk for the pleasure it, I feel pretty much up to snuff, for a man of my age. A year after my diagnosis I held a party to express my gratitude to all the people who had helped me through, including T.H., the consultant neurologist (he didnt actually come). I was by that time much better, not up to full strength, but could party on and play the saxophone. I told my doctors about ayahuasca in August of 2013 I think, it was for a six monthly reassessment of my condition. T.H was frankly astonished, and when challenged said that the diagnosis was absolutely sound adding that the nerve conductivity tests were particularly unequivocal. It was then that I told him about the ayahuasca, and rather sheepishly, and mistakenly, he asked me if I had had a good trip? I replied that it had been unpleasant and that it was not a therapy for the faint-hearted. Since then T.H. has presented my case to some regional peer group, and a professor K.T. Their response was that perhaps I had a mimi?, which seems to be exactly the same as the disease except for the outcome; or that the condition might have been brought upon me by the cocktail of therapies I was taking? at the time. I have yet to make a measured response to this, but it was not until I had serious symptoms that were initially interpreted as Lyme disease or an atypical sero-negative rheumatoid arthritic condition, that I embarked on any kind of medical therapy at all. The history presents a persuasive argument. My family, friends and some of my patients are aware of my ayahuasca treatment and are generally supportive. My wife plays tennis with a number of retired GPs, and their general opinion is that whatever I did cant be too bad. Hell I am still walking about and they were initially supporting my wife and family on the clear expectation of my imminent demise.

    Q: Will you continue this treatment? If so, will you make any changes to your current regimen?

    A: I dont see any necessity to carry on being treated. I might do the ayahuasca again but that would really be just out of curiosity.

    Q: Have you been following any particular diet prior to, or during your treatment?

    A: Lots of organic fruit and vegetables, and I have a small holding so we have organic lamb and chicken too. I haven't eaten dairy for the past two years, and I seldom drink alcohol though I had a glass of cider the other day.

    Q: What made you try this alternative treatment?

    A: It was an inspired patient who in doing an art degree in Plymouth came across the (ayahuasca) visionary art, and drew my attention to its source. Curiously some members of the church group with whom I sit proved an unexpected source of interest and loaned me various books on the topic, including those of the late Alexander Shulgin.

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    Cannabis oil shown to mitigate the symptoms of Alzheimer's-induced dementia


    The administration of liquid cannabis extracts containing THC is associated with the mitigation of various symptoms of Alzheimer's-related agitation and dementia, according to observational trial data published online ahead of print in The Journal of Alzheimers Disease.

    Israeli investigators assessed the use of cannabis oil as an adjunct pharmacotherapy treatment in ten Alzheimer's disease patients over a period of several weeks. Researchers reported that drug administration was associated with a significant reduction in patients symptom severity scores. Specifically, cannabis oil ingestion corresponded with decreased levels of aggression, irritability, apathy, and delusions.

    Investigators concluded, Adding medical cannabis oil to Alzheimer's disease patients pharmacotherapy is safe and a promising treatment option.

    The administration of dronabinol (oral synthetic THC in pill form) has previously been reported to reduce Alzheimer's-induced agitation and improve weight gain, while preclinical studies have theorized that cannabinoids may be neuroprotective against the onset of the disease.


    Last edited by mr peabody; 18-09-2018 at 01:05.
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    Eduardo Schenberg


    Ayahuasca in the treatment of ALS


    This article is the culmination of six years work, having studied ethnobotanical medicine and the field of neurodisease, making connections between the two in the search for a viable
    alternative treatment option for ALS and similar neurological conditions.

    In south and central america, many tribes living along the amazon river have a long historical tradition of making and consuming a natural medicine/tea called ayahuasca. It is harvested and prepared mainly from the bark from a wild growing vine, its latin name being Banisteriopsis Caapi. Often, leaves from trees named Chacruna or Chaliponga (Psychotria Viridis and Diplopterys Cabrerana) are added to the tea.

    The rainforests of the earth are known to be an enormous resource and a necessity for upholding the ecosystem of the planet. It is estimated that a very great number of undiscovered plants of medicinal value, are yet to be explored within these forests. Many conventional pharmaceutical medicines originate from substances found in rainforest plants, or their synthesized variants. Ethnopharmacologists have long been aware that there is vast support for the medicinal value of ayahuasca in its use against a number of diseases, but until recently this has been limited to individual claims. Even if a great number of very in-depth and credible personal stories have been available, serious studies have been missing.

    This, however, has come to change the last few years. Natural substances extracted from the ayahuasca plants have been found to possess unique and strongly antioxidative properties on specific nerve cells in the brain, in areas controlling memory, muscle control and motor activity. This gives probable cause to the theory that ayahuasca could be an effective treatment against neurodegenerative diseases such as ALS, Alzheimers, and Parkinsons disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occurring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

    According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

    Eduardo E. Schenberg, Federal University of Sao Paulo:

    There are enough available evidence that the active substances in ayahuasca, especially dimethyltryptamine and harmine, has the positive effect of preventing cancer cells in cultures used for cancer research, and that these substances affect the biochemical processes that are crucial to the treatment of cancer in-vitro as well as in-vivo. The reports available about people with experience from ayahuasca in the treatment of cancer should be taken seriously. The hypothesis is that the combination of (beta-carboline) alkaloids and dimethyltryptamine present in ayahuasca blocks the transportation of nutrients to tumours, lessens the dividing process of cancer cells, and changes the unbalanced mutation-causing metabolism in cancer cells.

    What has previously been somewhat controversial about ayahuasca, is that the plants in question used to be thought of simply as hallucinogens by western science. In other words, these medicinal plants of great importance, were neglected by the scientific community and thought of simply as if they were natural drugs. A more correct term for these plants, with respect to the indigenous culture in which ayahuasca is a part of, would be entheogens, which means plants used in a context sacred to the native people, inducing spiritual experiences. In several countries, such as Peru, ayahuasca is fully legal and accepted as a complement to conventional medicine, and these last 10 years, western countries have to an increasing degree changed their former unfounded and faulty attitude towards entheogens such as ayahuasca, as more and more studies of entheogenic plants have been completed with positive outcome.

    Along with several other similar harmala-alkaloids that can be found in B. Caapi, harmaline is a mono amino oxidase inhibitor. Mono amino oxidase (MAO) is an enzyme in the body that breaks down signal substances (such as serotonin). The inhibition of MAO allows the signal substance to remain in the synapse for a longer period of time. Many antidepressants work in a similar way, as they stimulate receptors in a targeted area. However, the alkaloids present in ayahuasca should not be compared to antidepressants, as they are not the same though they both have the ability to affect the same receptors. A comparison is that Caapi alkaloids and antidepressants have the same type of delivery system, but different contents. The biochemical properties of plants used in ayahuasca, and the effects they cause on a multitude of bodily functions remain unique to these plants alone.

    Ayahuasca in itself is proven to be unharmful, as its compounds are non-toxic, though temporary side effects such as nausea and vertigo are common. However, combining certain medical drugs with MAO-inhibitors (such as the ones found in ayahuasca) is very dangerous, even lethal in some cases. This means that in order to safely consume ayahuasca, one must not combine it with any contraindicated medicinal drugs. The more or less uncomfortable side effects from ayahuasca, are greatly dose-dependent, and a smaller amount consumed for medicinal purpose can thus mean few, if any, side effects experienced.

    When searching for information regarding ayahuasca, a few negative articles can be found, emotionally angled (understandably so), since they tell stories of unfortunate tourists who on their own, or having been duped into doing so, drink something entirely else than ayahuasca, for instance the toxic plant Datura, with serious outcome to their health (including death in a few known cases). This leads to fear and misinformation, and is not only tragic for the diseased and their families, but also for the natural medicine community that is trying to promote the safe and responsible use of natural medicine for health benefits, and treatment of diseases that regular medical care fails to provide options for. Sensationalistic headlines making unfounded claims, written by people without any knowledge about ethnobotanical medicine, will definitely not help neither ALS patients or others seeking viable treatment options for their condition. In several countries, including Peru, Brazil and Costa Rica, established retreats offer ayahuasca treatment where the right plants are harvested (sometimes even organically grown on the property) and prepared by experienced botanists.

    One of the earliest studies on B. Caapi was done in the 1920s, and involved patients with Parkinsons Disease. The patients experienced great symptom relief in early trials, but unfortunately the research was discontinued due to lack of profit potential, as substances already present in natural plants could not be applicable for any patent useful to pharma companies.

    Ayahuasca as an alternative therapy is likely to gain further attention in coming years, but is already well established. Should the discoveries eventually lead to a therapeutic pharmaceutical drug, derived from these plants, to be produced, it lies many years ahead from now. The process from studies, through trials, to eventual launch of an approved drug made for use in the medical care system, is slow due to obvious reasons. The real interesting fact is that ayahuasca in its natural form is something that is available now, today, for those who live with a diagnose lacking options for other treatment. For those who want and can partake in alternative treatment using ayahuasca, there is, while not in any way guaranteed, the real possibility for improvement. As in many other cases, the individual results will vary, and there should be an emphasis on not overly stirring peoples hope up when questions and work remain. There is also the importance of emphasizing and thereby minimizing the risks involved concerning contraindicated medications. But while studies are ongoing, this information should be worth the attention of anyone suffering from a debilitating progressive disease such as ALS.

    My personal connection to this, was the passing of a close friends mother due to ALS a few years ago. The course of her disease was rapid, and unfortunately several of the now available studies, had not yet been published at the time. This led me into investigating the connection between any available natural medicine and the treatment of neurological disease.

    B. Caapi is legal to use much in the same way as other known herbal remedies, such as Ginkgo Biloba and Ginseng. However, just like with these potent natural supplements, it is up to the consumer to use and combine these in an informed and responsible way. Natural medicines should always be treated with respect, just like conventional medicinal drugs.

    The substance known as dimethyltryptamine, found in plants traditionally added to ayahuasca, is however regulated by law in some countries as a scheduled substance. (Questionably so, due to its medicinal value in multiple areas). It is these secondary added plants and this particular substance that induces an altered state of consciousness, a many times misunderstood and stigmatized phenomenon. A description of this altered state is that it is dreamlike, that it stimulates memory and the ability to think abstract, and that it has self-therapeutic qualities. Even though dimethyltryptamine is naturally occurring in the human body, thought to be produced by the pineal gland in the brain during the dream phases of sleep, it remains an illegal substance in some western countries since the 1960s, when lawmakers prematurely criminalized many substances suspected of having any effect on the mind, including natural ones, due to the widespread moral panic at the time, regardless of the fact that many of them, including dimethyltryptamine, has never been proven unhealthy in any way, and has in fact been used by indigenous people to successfully treat disease for centuries. Although, several European countries has redefined their policy regarding many formerly frowned upon medicinal plants in recent years, much due to an increasing awareness and access to new and unbiased information regarding these plants, as well as up-to-date research. In Scandinavia, Sami native Urbi Svonni from Sapmi, Sweden, was recently aquitted from all charges in the court of law, for having brought Peruvian medicinal cactus into the country. The court established that natural plant material cannot be defined as a scheduled substance, and that the therapeutic work Svonni was doing, which included Echinopsis Pachanoi cactus, was indeed not a criminal act, but served the purpose to help and heal people. Another similar case with the same outcome involved ayahuasca additive plants. Cacti from the Echinopsis and Lophophora species are known for their soothing and restorative effects on the central nervous system, and are used as such in ethnobotanical medicine.

    To be precise, the definition of Ayahuasca is any tea made from either the plant Banisteriopsis Caapi alone, or from B. Caapi + additional plants containing dimethyltryptamine. A tea made from B. Caapi alone does not have what is sometimes referred to as visionary qualities, as it is only the addition of dimethyltryptamine from the additive plants discussed, or actually the combination from the mao-inhibiting alkaloids in B. Caapi together with dimethyltryptamine-containing plants that induces a state of mind formerly mislabeled hallucinogenic. It needs to be clarified though, that this word brings up negative associations in many people, and is thus feared and misunderstood. Unlike what some people tend to think, one does not hallucinate things appearing out of thin air after having consumed ayahuasca, but rather there are sequences of inner dreamlike visions taking place while resting, while still awake and fully conscious, provided a significant amount of tea has been consumed. It is actually quite undramatic, aside from the side effect of vomiting which does affect many people.

    And herein lies the essence that is many times misunderstood: One does not have to take a great amount of ayahuasca for experiencing strictly its medicinal effects without the abstractions and visionary effects some people are wary of. (Or the nausea/vomiting for that matter). Also, several of the medicinal health benefits can be obtained by using B. Caapi alone without any additive plants, thereby ensuring no peculiar visionary effects experienced at all, should this be desired. It should be noted though, that the synergistic effect between the two plants used simultaneously will bring the best medicinal and bodily response. Exaggerations regarding ayahuasca is what made these medicinal plants overlooked for many years in the west to begin with, but its reputation has been steadily revised as more people with experience from these plants in a medicinal context have come forward, claiming the true medicinal value of ayahuasca relevant to medical conditions of different types, the field of neurological disease being the latest. Ayahuasca has already been effectively used for symptom relief from Multiple Sclerosis, by a growing number of people in Europe since at least 2006. ALS, Multiple Sclerosis, Alzheimers and Parkinsons disease all share a lot of common ground, being that they all involve nerve cell degeneration of some kind. It is thus likely that any type of natural broad spectrum medicine able to affect the process of nerve cell recreation, and that also has substantially antioxidative properties, could prevent and slow the progression of neurological disease in general.

    Whatever wild or strange stories about ayahuasca that may occasionally be found circulating, they stem mostly from people who went to live with native tribes during the late 80s and early 90s, taking part in traditional ceremonial use of ayahuasca, consuming exceptionally generous or concentrated amounts of the medicine, enfolding themselves in deep cleansing experiences not necessarily easily endured. This medicine, like any other, should most definitely be well respected, but not subjected to exaggeration or downright misrepresentation, causing people to dismiss what they are simply uneducated about. The vivid and fascinating visions induced by strong tea often seem to have a theme rooted in nature, as depicted quite beautifully by Peruvian artist Pablo Amaringo (1938-2009). They arise from the simple fact that the alkaloids and tryptamines dissolved in the tea, combine to affect receptors that in turn stimulate the processing of memory relating to images and words, noticeably of relevance to Alzheimers research.

    Ayahuasca is proven to be non-addictive, and is even used to aid people in breaking their drug dependencies, as ayahuasca has a detoxifying and documented effect of ridding the user of drug related abstinence issues.

    The MAO-inhibition does, among other things, ensure that the uptake of dimethyltryptamine can occur in the body, as it is otherwise (without MAO-inhibition) broken down in the stomach, unable to cause any effect. Dimethyltryptamine is molecularly near identical with the above mentioned psilocybin in Dr. Ramos research. It is theorized that the unique combination of various harmala-alkaloids from B. Caapi, and dimethyltryptamine from additional plant sources used in ayahuasca, work on a cellular level to repair and restore nerve cells and tissue, and to protect nerve cells and other cells from degenerative damage. This is without doubt valuable from both a neuromedical standpoint, as well as from a cancer research perspective.

    As the non regulated B. Caapi alone has proven to have very positive abilities, potentially effective against neuro and cancer diseases, it is thus something real that may be a valuable alternative treatment option. For someone who experiences positive results to whatever degree, but does not live in a state or country where the use of plants containing dimethyltryptamine is permitted, there is then the possibility to travel to one of the many countries (or states) which by law allows the use of added secondary plants with their combined medicinal properties for evalution of full ayahuasca treatment. In Europe, Spain is one of several countries where ayahuasca is becoming established as an alternative therapy, and Spain is also the chosen location for an international conference 2014, where ethnopharmacologists, psychologists and researchers from all over the world gather around the topics of ayahuasca and other entheogens.

    Among others, Ede Frecska, M.D., Ph.D, University of Debrecen, lectures on the possibilities of recreating brain cells and regulating the immune defense system through this plant-based medicine and others.

    Furthermore, besides their ability to aid and enhance the process of nerve cellular repair and the protection against cell oxidation, many of these entheogenic plants (and fungi), including ayahuasca, do possess psychotherapeutical qualities as well. Coping with degenerative illness is obviously stressful to patients, and a great deal of emotional relief, personal insight, and ability to better cope with ones personal situation is achievable through the single or repeated experience of entheogenic medicinal plants/mushrooms in a comfortable and supportive environment, according to renowned John Hopkins medical university.

    The fact that many of these medicinal plants are becoming revived as they receive scientific approval, is great news in many ways. Sustainability and environmental issues comes to mind, and so far the outlook is positive. Many organic farms have developed in south and central america, cultivating ayahuasca plants for both local use and for export, providing work and income for people in rural areas otherwise struggling with poverty. This also serves as a way for many locals to reconnect with their cultural past, as ayahuasca is declared a national heritage in Peru among other places.

    It used to be that this formerly unknown plant medicine was completely overlooked, but as we have begun to understand its potential, neglect has been replaced with knowledge, and the scientific groundwork on this matter is becoming firm. People should not be led into thinking this is some kind of natural miracle cure, but if anything it could provide a long-term aid in the restoration of body and mind function in people with certain neurological conditions. Together as a community we can all help to inform people in an unbiased, ethical and safe way about any viable alternative treatment options.

    Ayahuasca has been used for a very long time historically, and only recently for treatment of the conditions brought up in this article. Any substantial improvement would be likely to reveal itself long-term at first. Initial updates from people taking part in the ALS pilot project report a few things in common; the feeling of a somewhat wider range of movement, tension relief in muscles and slightly improved grip in affected limbs, though it should be noted that none of these had lost all of their muscle control prior to treatment, and that whether or not this effect will prove to be permanent is not known at this moment. Only time will tell what can, or cannot be achieved from this treatment.

    In due time, ayahuasca and other entheogens can and will gain the credibility and amends they truly deserve, and bring new possibilities to many out there living with diseases that lack conventional options for treatment. Meanwhile, these medicinal plants remain available for the personal evaluation of the individual who chooses to explore the option. In relation to the medical conditions brought up in this article, these plants may have a future role as a powerful tool for the reversal of the progression of ALS and related diseases. Hopefully, you found this information interesting.

    http://www.thisisms.com/forum/natura...opic25343.html
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    Low dose ibogaine therapy


    By Dr. Tom Grodski

    Parkinson’s disease, ALS and Alzheimer’s are chronic disorders with no known cure. Most neurodegenerative diseases require management with prescription medications that can have considerable side effects, which may cause a very poor quality of life for terminal sufferers. In turn, Ibogaine may be very beneficial to those with degenerative neurological diseases.

    Ibogaine is a naturally occurring psychoactive indole alkaloid derived from the roots of the African rain forest shrub Tabernanthe iboga. Ibogaine is part of the Apocynaceae family and traditionally used by the Bwiti, indigenous peoples of Western Africa; in low doses to combat fatigue, hunger and thirst.

    Ibogaine increases levels of glial cell line-derived neurotrophic factor (GDNF) in the brain (He & Ron 2006), and this appears to have neuroprotective properties that promote the survival of both dopaminergic and motor neurons (Bermingham et al.2004; He and Ron 2006). GDNF can also cause sprouting of dopaminergic fibers and clinical improvement in experimental animal and human studies in which the test subjects had Parkinson’s Disease, with the resultant clinical improvement in symptoms (Love et al. 2005). GDNF has been shown to have potent neurotrophic factor in both rodent and primate models of Parkinson’s disease (Gill et al. 2003).

    Direct brain infusion of GDNF into the brains of five Parkinson sufferers resulted in a 39% improvement in the off-medication motor sub-score of the Unite Parkinson’s Disease Rating Scale (UPDRS) and a 61% improvement in the activities of daily living sub score (Gill et al. 2003). Positron emission tomography (PET) scans of dopamine uptake showed a significant 28% increase in putamen dopamine storage after 18 months, indicating a direct effect of GDNF on dopamine function. Further, after one year, no serious clinical side effects were observed (Gill et al. 2003).

    The use of Iboga alkaloid extract or Ibogaine would provide a longer term and much less invasive method of GDNF administration than direct brain infusion. Thus, further research on Ibogaine and GDNF is certainly warranted. Ibogaine therapy may offer a non-invasive and low-toxicity method of treatment for sufferers of these disorders.

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    CBD oil may prolong life for those suffering with ALS


    Based on some exciting new anecdotal evidence, the use of cannabis oil to treat ALS may actually prolong the life of the patient in addition to relieving many of the diseases devastating day-to-day symptoms.

    ALS or Lou Gehrigs disease, named after the baseball legend, is a debilitating disorder that affects an estimated 30,000 people in the United States at any given time. You might remember ALS from that craze last summer when everyone decided to dump ice on their heads to raise awareness for the disease and to raise money for ALS research. Even Leafly hopped on the bandwagon for a good cause, and overall, the ALS Foundation received over $100 million in donations by the time the summer of the Ice Bucket Challenge was over.

    ALS is a degenerative neurological disorder that causes muscle weakness, wasting, and paralysis of the limbs, as well as those that control vital functions such as speech, swallowing, and breathing. It is often the deterioration of these crucial muscles that leads to respiratory failure; even with breathing aids or a tracheotomy, the risk of respiratory failure persists.

    Being diagnosed with ALS is devastating, and for many it can feel like a death sentence. The average life expectancy of a person with ALS is two to five years. However, more than half of all people with ALS live more than three years from diagnosis and there are definitely outliers, such as Stephen Hawking, one of the most iconic figures with ALS. Hawking was diagnosed in 1963, and now, more than 30 years later, he is among only 5% of those diagnosed with ALS who live more than 20 years after diagnosis.

    Cannabis has long been known as a viable treatment option to relieve symptoms of ALS, which was outlined in this handy chart created by the American Journal of Hospice and Palliative Medicine, but the most astonishing results have come from several ALS sufferers who have managed to slow the progression of the disease through regular, controlled doses of cannabis oil.

    Bob Strider began experiencing the symptoms of ALS in 1998, specifically the loss of function in his right arm and problems swallowing. An avid cannabis enthusiast, he had used cannabis heavily for decades, which he believes has kept the progression of his disease slow but steady. In 2012, Strider began manufacturing his own cannabis oils, dosing himself with approximately a gram a day for 60 days. Within 10 days of his regimen, he regained control of his right arm and was able to stop using opiates to manage his pain.

    Another remarkable case comes from Cathy Jordan, who was diagnosed with ALS in 1986 and given less than five years to live. In the winter of 1989, Jordan spent the holiday in Florida, preparing for the end of her life, when she made a crucial discovery. While walking on the beach one night, she smoked a joint of Myakka Gold and felt her symptoms cease, essentially experiencing the neuroprotective effects of cannabis before theyd been proven.

    Jordan never set out to be a cannabis activist, preferring instead to quietly continue treating her disease. She tried to tell her neurologist in 1989 that cannabis had helped her, and he tried to convince her husband to have her committed to a mental facility. In 1994, Jordan met a new doctor who was astonished by her progress. When he asked what shed been doing to stay alive, she informed him, and he advised her, Smoke all the cannabis you can and never tell a soul, because they will never believe you.

    Unfortunately, Donnie Clark, the grower of Myakka Gold (named for the Myakka region of Florida), was arrested and sent to prison for 12 years until his sentence was commuted by former President Clinton. The strain itself, which Jordan credits with stopping the progression of her ALS, has since been eradicated by the DEA.

    Cathy Jordan, however, ended up becoming the inspiration for Amendment 2, the medical marijuana initiative in Florida that was edged out last November. Ironically, on February 25, 2013, the same day that the Cathy Jordan Medical Cannabis Amendment was announced, Jordans home was raided and 23 plants were seized by local authorities, although charges were dropped when it became evident that she was using cannabis for medicinal purposes.

    Now, finally, years later, there has been more and more conclusive research indicating that these patients self-medicating regimen was beneficial, after all. Preclinical data shows that cannabis has powerful anti-oxidative, anti-inflammatory, and neuroprotective effects, and with regular applications, it may actually slow the progress of the disease and prolong the lives of the individuals affected by ALS.

    Amyotrophic Lateral Sclerosis is a qualifying condition for medical marijuana programs in Delaware, Washington, D.C., Georgia, Illinois, Maine, Massachusetts, Michigan, New Jersey, New Mexico, and New York. However, with more promising research emerging, other states medical marijuana programs need to follow suit and allow suffering patients the right to try and treat this horrible disease with cannabis if it can provide them with even a little bit of relief.

    https://www.leafly.com/news/science-...gression-of-al

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    Teri Heede and Multiple Sclerosis - Cannabis Saved My Life

    This is the story of Teri Heede, who went from being bedbound and pain racked to taking on the system with the help of medical marijuana. Its just one of the stories profiled in Resets new book Cannabis Saved My Life by award-winning journalist Elizabeth Limbach. The book features interviews and testimonies from 46 different patients who were able to reclaim their life after facing serious illnesses, everything from cancer to depression, thanks to the little herb that could.

    Active is the last word usually used to describe those with multiple sclerosis. A degenerative disease that affects over 2 million people worldwide, MS often causes paralysis, blindness, and cognitive dysfunction that worsens over time, as well as excruciating daily pain.

    The entire central nervous system of MS sufferers, including the brain, spinal cord, and optic nerves are under constant attack and the medical community still does not know exactly why.
    Nor do they have a cure.

    This is where medical marijuana comes in. For MS sufferers, cannabis offers immediate pain relief, although its benefits do not stop there. Far from it.

    I have a theory about MS, says Teri Heede, a Vietnam War veteran who was diagnosed with MS twenty years ago. Now a politically involved cannabis crusader in her community in Oahu, Hawaii, Teri is definitely active in every sense of the word.

    Its kind of like an electrical cord in your body, she tells Reset. If you went around and ripped off the cover of all the electrical cords in your house, what would happen?

    Short circuits, misfires, and everything goes wrong. I can have muscle spasms so bad it will pull a muscle.

    So my theory is that the THC receptors in the body can mediate this, Teri explains. When the nerve fires off and hits that lesion, and MS is local lesions, the THC circumvents the process.

    While there are dozens of studies that prove the efficacy of cannabis in treating the symptoms of MS, a 2012 study at the Queen Mary University in London that looked at the underpinning biology of cannabis-based medicines for MS shows that Teri is pretty spot on with her assessment of the mechanics of the medicine and how it works at a much deeper level than just suppression of the symptoms.

    MS results from disease that impairs neurotransmission and this is controlled by cannabinoid receptors and endogenous cannabinoid ligand, the study states. This can limit spasticity and may also influence the processes that drive the accumulation of progressive disability.

    The endocannabinoid system, for those who havent been paying attention to what is probably the most important biological discovery in recent history, interacts with the immune, nervous, and other systems in the human body though cannabinoid receptors in everything from the brain to connective tissue. While the interactions are complex and numerous, the purpose of the system is straightforward: homeostasis, the stabilization of the system involved.

    This is why cannabis, the plant for which the system is named after, is so effective in treating everything from cancer to insomnia, all conditions where something biological is out of balance.

    For multiple sclerosis, cannabis is like a miracle drug, correcting neurological misfiring, reversing inflammation, reducing pain, and returning muscle plasticity all at the same time.

    I feel like it has stopped the disease from progressing, Teri says. I am sixty years old and up and around.

    Proving Teri right once again, an Oxford University study found that cannabinoids are highly neuroprotective and can in fact slow the neurodegenerative processes that ultimately lead to chronic disability in multiple sclerosis.

    With the endocannabinoid system, we have to start educating not just the public but the doctors that there is a SYSTEM here. Teri emphasizes, Its not just a Cheech and Chong movie.

    What it is in fact, is a powerful biological system activated by marijuana that can dramatically turnaround the lives of those who are disabled by MS and scores of other diseases.

    I was down for a year, Teri tells us. I fell down at work and I couldnt get back up. I was like whao, what happened?!?

    I thought I cracked my tailbone, because thats how much it hurt, but six months later I wasnt getting better, I was getting worse. After I did everything they told me to do, including hot water therapy, which only made it worse, I found out I had a lesion along my entire spinal column.

    I went to the neurologist and she told me I had MS, Teri continues. I said, I am a widow with PTSD and you cant tell me that now I have MS too.

    Luckily my doctor was very open-minded. She said, try everything you can, as we have nothing more we can give to you. So I went to Humboldt County [in Northern California] and bought a quarter pound and took it home and sat on top of it.

    And I will tell you, within three weeks I was on my feet again.

    As soon as cannabis put Teri back in action, she began what has become a lifetime mission to spread the word and fight back against the stigma that marijuana is just a drug.

    If you have ever seen a child in seizures or in pain, you just want to help that child, and this Reefer Madness attitude is really not helping at all, she says.

    Active in the fight for safe access at the local level in Hawaii, one of the most restrictive states in the nation, she often shows up for important legislative meetings as a living testimony to the power of medical marijuana.

    Without this cannabis therapy I would have a basketful of old prescription medication. I actually used to walk in with the basket in front of the legislature just to show them, Terri tells us.

    I still have to take a stomach pill, because I have taken so many pharmaceuticals that I have whats called watermelon stomach, your stomach lining regrows every three days normally, but mine doesnt, she explains. Its because of all the pharmaceuticals, they just ate my stomach lining away.

    We need to make these herbal alternatives legal and available, these pharmaceutical are killing people.

    Teri is now the Female-at-Large for the Democratic Party for the county of Oahu, meaning she represents Democratic voters at the State Central Committee for Hawaii.

    I am also working heavily with the League of Women Voters, which is non-partisan, she tells us. Our main focus is registering voters.

    We have such a low voter turnout here in Hawaii that getting people to the polls to elect people that represent them is our goal.

    Full legalization of cannabis is only part of the plan though. In the larger picture, Teri knows that the movement must also ensure that access to the medicine remains in the hands of the people that need it the most, the patients.

    A lot of patients are afraid of legalization, they think that they will lose their medicine and only have access to a homogenized strain that is developed to make a profit off of. She muses, While I do see that as a possibility, if we as patients get together and preserve our strains for ourselves we will be ok.

    Part of that is ensuring that patients have the right to grow their own plants, as although Hawaii is one of the major cannabis producers in the United States, medical marijuana patients are currently limited to only seven personal plants. And even that may be in danger.

    We have these Democratic legislators who have told me as soon as it goes legal [they] want all patient grows to stop, Teri tells us.

    This is exactly what has happened in states like Pennsylvania, which just passed a large medical marijuana bill after several years of intense pressure from the public, including serious campaigning by former talk show host Montel Williams, himself an MS patient that found relief from pain and other symptoms through cannabis.

    This is an issue of compassion and that is it, Williams said at a rally for legalization last year.

    But while the PA bill opens up medical marijuana treatment for a wide variety of conditions, including MS, it also prohibits patients from growing their own herb. Legalization also means regulation, and there are powerful interests that would like to capitalize and monopolize on the fast growing medical marijuana market.

    With a shifting landscape in terms of access and legality, the future of medical marijuana is in the hands of those who take a stand for patients rights, like Teri Heede.

    I am there in the legislature when they have their hearings. I go door to door trying to spread the word about the many people who benefit from cannabis therapy, says Teri. There are believers out there now, huge believers.

    I just want more people to get active about this. We are coming out of a time of a lot of preconceived notions and we need to move forward with this medicine.

    Once crippled with pain and unable to walk, Teri is now one of the forerunners in the battle to make and keep medical marijuana accessible to all that need it. And thats as active as it gets.

    http://reset.me/story/cannabis-saved-my-life-multiple-sclerosis/

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    Is Ibogaine a promising new treatment for Parkinson's?

    There is reason to believe that ibogaine may be beneficial in Parkinson's treatment. Columbias two-year animal study represents the first time that researchers will probe for a direct link.

    The exact mechanisms of action of ibogaine are still obscure, but the theory for ibogaines benefit for Parkinsons rests on the fact that amongst its other effects, it has been shown to increase the production of a protein called glial cell-derived neurotrophic factor, or GDNF. This and other neurotrophic factors have been shown to stimulate the production of dopaminergic fibers throughout the brain, and some existing research shows that GDNF in particular improves the recovery of dopaminergic neurons and leads to an improvement of Parkinsons symptoms.

    Previous methods used to increase the expression of GDNF were limited gene therapy and direct brain infusion, but according the research abstract, the research team, led by Dr. Serge Przedborski, President of the World Parkinson Coalition, is exploring whether ibogaine could provide safer and more convenient means to enhance GDNF production in the brain.

    Dr. Jeffrey Kamlet, a Miami medical doctor and board certified addiction specialist has been researching ibogaine for over 20 years, and is a strong advocate for medical supervision. According to Dr. Kamlet, Ibogaine is the most important discovery in the field of opiate dependency in the history of addiction medicines, and I am confident that it will one day be a main stay treatment for many addictions.

    Even with this in mind, some advocates believe that ibogaine application as a treatment for Parkinson's may prove more straightforward for research. In the case of addiction therapy, ibogaine is most often administered in a single large dose, but there is anecdotal evidence that the repeated use of very low sub-perceptual doses, which are generally agreed to be well tolerated in patients, could be sufficient to reverse Parkinson's symptoms over time.

    Patient D was 69 years old in 2012 when he was diagnosed with Atypical Parkinsons, a Parkinson's-like syndrome that does not include the characteristic palsy. By last year Patient Ds symptoms had advanced to the point where his facial muscles felt frozen. He had difficulty finding his balance, talking or using his hands. As a writer and artist, he noted that emotionally it was the first time in his life he had lost his desire to do anything creative.

    Patient D was treated with CKBR-12, an experimental natural health product and ibogaine-derivative at a medical center in Rosarito, Mexico. He took a small dosage twice a day for 30 days, and after the first two weeks began to notice that he could use his fingers to pick up objects again. After a month he had seen a gradual improvement in all of his symptoms to the point where he could carry on normal conversation, and coordinate previously impossible tasks such as buttoning his shirt.

    In a post-treatment interview that was published on YouTube, Patient D says, Its difficult to explain what Parkinson's is, but you lose your edge. And I have got my edge back in a few areas. It may be small things to some, but they are big things for me. I am anxious to see what happens next.

    When we spoke, to Patient D, he said that he had continued to have improvements with further treatment. His case has been reviewed by several doctors, including Dr. Susanne Cappendijk of Florida State University Medical Center, who relayed some of the results at a conference at the New York Academy of Sciences.

    -Jonathan Dickinson
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    Parkinson's and MDMA


    By David Concar

    MDMA is being hailed as the key to better treatments for the Parkinson's disease, marking a complete turnaround from a few weeks ago when ecstasy was condemned for causing the disease.

    New animal studies have confirmed anecdotal reports that ecstasy can dramatically curb the uncontrollable arm and leg movements that plague so many people with Parkinson's. But the finding may be of little immediate help to sufferers.

    The researchers are not calling for patients to be given legal supplies of ecstasy (MDMA). Instead, they want to look for related drugs with the same beneficial effects. And patients are being warned against trying MDMA for themselves. Its impure, illegal and dangerous, says Robert Meadowcroft, policy director of Britain's Parkinson's Disease Society.

    Others are calling for further animal studies to establish the effective dose, followed by human trials. People who are suffering should have the right to decide carefully for themselves whether or not to take MDMA, says American drugs policy campaigner Rick Doblin. His organisation, MAPS, recently won approval from the Food and Drug Administration for a human trial of ecstasy for treating post-traumatic stress disorder.

    Regaining control

    The latest study was prompted by the experiences of a former stuntman, Tim Lawrence. He made headlines when he claimed in a BBC TV documentary that enabled him to regain control of his body for hours at a time.

    Parkinson's experts at the University of Manchester decided to test Lawrences claims. Concerns about the dangers of MDMA ruled out human trials, says team member Jonathan Brotchie, who now runs Manchester-based biotech company Motac. So the researchers turned to marmosets with a form of the disease.

    Parkinson's is caused by a loss of the dopamine-producing cells in the brain. Symptoms include rigidity and a shuffling gait. Since the late 1960s doctors have treated it with L-dopa, a chemical precursor to dopamine that can unfreeze patients.

    The downside is that patients develop uncontrollable movements after taking L-dopa for a while. Their condition tends to oscillates between flailing limbs while on the drug and immobility off it.

    To mimic Parkinson's, they gave six marmosets a chemical that kills dopamine neurons. Then, over the next few months, the monkeys had daily doses of L-dopa until they developed the usual side effect of uncontrolled movements. At this point the animals were given MDMA.

    Dramatic effects

    The effects were dramatic. Normally, monkeys on L-dopa move their arms and legs around in a repetitive and uncontrolled way virtually all the time. But in the six hours after a dose of MDMA, these movements happened no more than 15 per cent of the time. MDMA somehow reduces the debilitating side effects of L-dopa without blocking its beneficial effects.

    The magnitude and quality of the effect took us by surprise, says Brotchie, whose teams findings were unveiled this week at the conference of the Society for Neuroscience in Florida. It was always possible that Tims response to ecstasy was unusual.

    The researchers suspect the finding reflects MDMAs ability to stimulate the release of the neurotransmitter serotonin in the brain. That might make up for a lack of serotonin caused by taking L-dopa for prolonged periods, says Brotchie. However, there are fears that MDMA can damage serotonin-producing cells.

    And last month the journal Science published a paper claiming that MDMA can actually cause the type of damage to dopamine cells that can lead to Parkinson's. But the evidence was far from conclusive.

    https://www.newscientist.com/article...sons-symptoms/

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    Cannabis may prevent the onset of Alzheimers


    by Steve Elliott

    Early use of cannabis apparently delays and might even prevent the onset of Alzheimers disease, according to a leading scientist in the field. But the work of longtime researcher Gary Wenk of Ohio State University has come to a halt, despite the promising results.

    We found out that people who smoked cannabis in the 1960s were not getting Alzheimers, Wenk explained, reports KJ Hiramoto at the Seattle PI. These 90-year-olds without dementia were telling us things like, Well, I drank whiskey and smoked cannabis, and these are the things they remember. They dont remember habits like how often they ate broccoli.

    Maddeningly, Wenk's research ground to a halt due to political, legal and financial reasons.

    The evidence in animals is clear but making the leap to humans means that you have to find a drug company willing to handle the lawsuits and the money, Wenk said.

    He faced other hurdles, as well. Scientists who wish to research marijuana have to compete for approval and grants from the National Institute on Drug Abuse (NIDA), for which The University of Mississippi is the only source of cannabis. Ole Miss has the only federally legal, grant-funded cannabis garden in the U.S.A.

    What makes the situation even worse is that, as admitted even by NIDA Director Nora D. Valkow, M.D., is that the agency is only interested in studying the potential harms of cannabis, not the medicinal benefits.

    A spokesperson for the NIDA told the New York Times in 2010 that the agency does not fund research focused on the potential medical benefits of cannabis.

    As the National Institute on Drug Abuse, our focus is primarily on the negative consequences of cannabis use, NIDA spokeswoman Shirley Simson told the Times.

    And under federal law, the NIDA must approve all clinical research involving cannabis. It tightly controls which investigators are allowed access to the federal government's Ole Miss cannabis supply, which is grown (and then stored, for years) at the research facility in Oxford, Mississippi.

    I am not funded to do marijuana research, Wenk said. It cost me about $100,000 to do a whole experiment, $10,000 just to buy the molecule, and every old rat is $150. You can see how it adds up, and individuals cant afford it.

    British researchers find corroborating evidence

    A paper published in the British Journal of Pharmacology suggests that the cannabinoids in cannabis are likely not only to prevent the onset of Alzheimers, but also of Parkinsons disease, Huntingtons disease, and age-related dementia, reports Brandon Isaak at the Marijuana Policy Project.

    Chronic brain inflammation, oxidative stress, and intra-cellular dysfunction are the primary reasons people develop these debilitating neurological diseases, and the study found that both THC and CBD, found in marijuana, help protect nerve cell function in users, significant reducing these harmful conditions.

    The cannabinoids tap into the endocannabinoid system, reducing inflammation, protecting brain cells from oxidative damage, and promoting cellular health on multiple levels, according to the researchers.

    Showing promise: Old people are going to win

    Wenks research, before it was halted, anyway, was showing promise to middle-aged and older Americans. Cannabinoids found in marijuana may delay the onset of Alzheimers so effectively that people are more likely to die of old age before showing any signs of dementia.

    In the study, Wenk dosed rats in his lab at Ohio State a dosage equivalent to one puff of marijuana every day. In old rats that had impaired memory due to brain inflammation, that single puff a day was making them smarter. Not only were they more intelligent, but some of the pathological changes in the rats brains, due to aging, were being reversed.

    Essentially, what we found was that we know that as people get older, their neurogenesis drops to zero, Wenk said, referring to the process through which new brain cells are created. And thats part of the reason old people have a problem with their memory and depression. What we found was that not only did the single puff a day reverse the memory impairment but also restarted neurogenesis.

    According to Wenk, delaying the end of neurogenesis (regeneration of neurons) helps middle-aged Americans and their families in a very easy-to-measure way: in their pocketbooks.

    If we can keep a person out of a nursing home for five years, weve saved that family and their insurance companies an awful lot of money, Wenk said. No matter how we spin this, old people are going to win.

    I am incredibly excited about it, because this is the first time we have ever had a compound that actually works in the old brain, Wenk said. Everything works in the young brain, but this is working in old brains. So this means if you are, 60, 70, and you are having problems with mental decline? We might have a mechanism that could target that.

    Very low doses are effective, Wenk saidk even just one puff of marijuana a day helps, according to his research. This is just the beginning of what we believe we will uncover as we investigate this line of research, he said.

    Blocking endocannabinoids may trigger early Alzheimers

    Another study from a team of investigators at the Stanford University School of Medicine led by Daniel Madison has implicated the blocking of endocannabinoids, the brains own internal versions of the active compounds in cannabis, in the early pathology of Alzheimers.

    It seems a substance called A-beta, suspected to play a key role in Alzheimers because it is the main part of clumps which dot the brains of Alzheimers patients, may, in the early stages of the disease, impair learning and memory by blocking the beneficial action of endocannabinoids.

    The group at Stanford is now trying to suss out the molecular details of how this occurs. Pinning down the details could pave the path to new ways to stave off the learning disabilities and memory deficits that characterize Alzheimers and could also help explain how smoking marijuana helps to delay or even prevent its onset.

    In the study, published in the June 28, 2014 issue of the scientific journal Neuron, the researchers detail how pyramidal cells in the brain underpin learning and memory. This assures, they learned, that high-intensity input such as falling down or burning your finger tends to stick in your memory, thus presumably help avoid such mishaps in the future.

    Pyramidal cells are encouraged to ignore noise signals, they constantly receive random signals from upstream nerve cells by a sort of wet blanket nerve cells called interneurons.
    These secret an inhibitory substance, the molecular equivalent of an indifferent shrug or yawn, signaling that the input is not really very important.

    But when the news actually is significant, pyramidal cells secrete their own Now just you wait a minute, these are important chemicals. And guess what? Those chemicals which signal the importance of incoming information are none other than the endocannabinoids.

    Madison speculates that when we smoke marijuana, the phytocannabinoids from the plant have the effect of enhancing the perceived importance of events that happen while we are under the influence of cannabis.

    And another likely effect is inhibiting the wet blanket effect of interneurons which, in Alzheimers, needs reducing to increase the ability to learn and remember.

    Increasing tolerance

    The federal Schedule I illegality of marijuana, under which it is officially considered to have no medical uses and a high danger of abuse, has stymied Wenk's research. But the scientist has noticed a refreshing trend, a major shift in the cultural tolerance of cannabis, particularly from young people, including his students.

    Ive really seen a shift in 10 years of increased marijuana tolerance, Wenk said. In my class, people are more than willing to discuss their marijuana use. But they would be embarrassed to mention that they smoke cigarettes.

    With Alzheimers ranking as the sixth leading cause of death in the United States, and with more than five million Americans currently struggling with the disease, which has no known cure, you would think that lab results as promising as Wenk's would have attracted major funding by now. But that is not the case, because, as we have pointed out, the NIDA is not really interested in knowing about the medical benefits of marijuana, just its dangers.

    Wenk, who has researched the effects of Alzheimers on animals for about 40 years, has shared his findings in his book, Your Brain On Food.

    https://tokesignals.com/marijuana-sh...ch-is-stalled/
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    CBD and Multiple Sclerosis

    As a blog concerned with new developments in CBD science, we tend to do a lot of writing about future treatments, or new scientific developments that may eventually lead to treatments.

    Part of the issue is that large-scale, clinical testing of new cannabinoid based medicine is still years away in a lot of areas, particularly in cancer-related fields. That’s why reading a good, new large-scale study is always exhilarating. In this case, a recent study from the University of Bari in Italy took a look at a large scale, real-world application of a THC/CBD oral spray in treating adults with treatment-resistant Multiple Sclerosis (MS). In the past, we’ve written about treating MS models via lab mice with THC and CBD, and also the theory behind that treatment. So being able to finally see how things play out in real life with real patients is particularly rewarding for us and is yet another confirmation of the efficacy of cannabis based treatments.

    To review, MS is an auto-immune disease in which the body’s immune system is confused into turning against the body and attacking cells. In particular, MS is caused by the immune system stripping neurons of their outer protective linings, which normally prevent “signals” from being crossed or lost in the brain, both for conscious and unconscious tasks. This stripping eventually results in loss of physical mobility and function and can prevent patients from fulfilling active, healthy lives. Spasticity, which affects about 2/3rds of patients, is particularly problematic. Unfortunately, at this time not many treatments are available that are effective. Aside from instructing patients to try to avoid seizure triggers, doctors often prescribe anti-spastic pharmaceuticals and muscle relaxers as a method of decreasing seizure rate. However, these medications, specifically benzodiazepines, are sedative and hypnotic, and come with risk of physical dependence and withdrawal. Additionally, many patients’ conditions are treatment resistant, meaning these medications make no difference in the first place.

    As a result, the medical community has been searching for more effective treatments. Enter cannabis. Cannabis is a well-established anti-inflammatory agent and has been shown to help dampen immune system over-stimulation in a multitude of conditions. Initial lab tests also confirmed that THC and CBD were helpful in animal models of MS. As a result, the authors of this study decided to conduct a large-scale human trial. At the time being, Sativex, produced by GW Pharmaceuticals, is one of the most respected and convenient cannabinoid based treatments for conducting such a trial. Currently available in 15 countries, Sativex is a 1:1 preparation of THC:CBD which can be sprayed orally multiple times daily. Realistically, Sativex faces a much easier time acquiring approval than cannabis in many countries, both because cannabis is more difficult to standardize, and also because cannabis itself carries a lot of cultural baggage as a recreational drug.

    The MOVE 2 EU study is a multi-institution, non-interventional study of patients in Europe with MS spasticity receiving THC:CBD oral spray in an outpatient setting. Non-interventional means that patients’ current treatment plans are not altered, rather Sativex is added to their treatment to see what changes. The MOVE 2 EU study specifically aims to “determine the effectiveness of THC:CBD, collect data on tolerability/safety, determine patient satisfaction with THC:CBD, and determine resource use by patients over a 3-month period after adjustment” to the spray. The set up, of course, is straight-forward. Patients are prescribed Sativex and data is collected three times: once at the beginning of the study, once one month later, and finally three months later at the conclusion of the study. Data collection consists of not only patient surveys, which answer questions about patient satisfaction and usage, but also two tests known as the Modified Ashworth Scale (MAS) and the Numerical Rating Scale (NRS), which rank spasticity severity and spasticity numerically in a more objective manner. Other scales are used in addition to establish mobility and pain and fatigue symptoms.

    While the study will eventually expand to multiple countries, Italy was the first to reach the initial target of 300 enrolled patients, with a total of 322 patients responding and 203 patients following the study through to completion. In this case, the trial population was mostly female with an average age of around 50.

    The results are that spasticity dropped significantly in both cases after three months of treatment, proving that in a large population, Sativex appears to be capable of making a significant difference! Of course, you’ll also notice that the “n” number under each bar, which stands for the number of patients data was available for, decreases with each successive data point. This occurs as patients drop out of the study for various reasons, mostly due to lack of impact or inability to tolerate the side effects of Sativex (although in some cases due to pregnancy). Assuming those patients were to be factored in, the drop in spasticity would be lower. What that means is that Sativex is helpful to a little under 70% of patients, with another 30% either seeing no real change or being unable to tolerate treatment. For the rest, a roughly 20% improvement is observed on average, indicating that the treatment “works” in a clinical sense. In fact, after three months’ treatment, over half of the original population “were deriving sufficient benefit in the opinion of their treating physicians to warrant continued use”. However, beyond asking if Sativex simply works, researchers sought to understand how practical the treatment is for MS patients and how likely they are to adhere to using it. In this particular study, patients averaged between only 6-7 sprays a day, which combined with the portable, quick method of administration, makes it a very reasonable treatment.

    As the study spreads to other countries, we’ll keep you posted on new developments. However, we already expect to see more real-life studies based on the outcomes here, particularly in America. In the meantime, patients with treatment-resistant MS may benefit from discussing cannabinoid preparations with their physicians.

    https://cornerstonecollective.com/re...ple-sclerosis/


    Last edited by mr peabody; 20-09-2018 at 10:07.
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    Ibogaine and neurodegenerative diseases

    This is a summary on existing research looking at the influence of Ibogaine on glial cell line-derived neurotrophic factor (GDNF) levels in the brain, and the beneficial impact that an increase in this protein can have. While existing studies have examined these areas, few have identified a possible link between Ibogaine, GDNF expression and neurodegenerative diseases.

    Both Parkinsons disease and Motor neuron disease are chronic disorders with no known cure, and require management with drugs that can have considerable side effects, causing a very poor quality of life for terminal stage sufferers of these diseases. By contrast, a low dose regime of Ibogaine or Iboga alkaloid extract would be of low toxicity and free of serious side effects.

    GDNF has been shown to have potent neurotrophic factor in both rodent and primate models of Parkinsons disease (Gill et al. 2003). Direct brain infusion of GDNF into the brains of five Parkinson sufferers resulted in a 39% improvement in the off-medication motor sub-score of the Unite Parkinsons Disease Rating Scale (UPDRS) and a 61% improvement in the activities of daily living sub score (Gill et al. 2003). Positron emission tomography (PET) scans of dopamine uptake showed a significant 28% increase in putamen dopamine storage after 18 months, indicating a direct effect of GDNF on dopamine function. Furthermore, after one year, no serious clinical side effects were observed (Gill et al. 2003). The use of Iboga alkaloid extract or Ibogaine would provide a longer term and much less invasive method of GDNF administration than direct brain infusion. Thus, further research on Ibogaine and GDNF is certainly warranted.

    Regarding motor neuron disease, the little research that has occurred in this area, such as gene transfer of neurotrophic factors, suggests potential in the treatment of motor neuron disease (Haase et al. 1997). Again, Ibogaine therapy may offer a straightforward, non-invasive, cheap, low-toxicity method of treatment for sufferers of this disease.

    -Bancopuma

    -----

    Ayahuasca shows potential for treating ALS


    Could ayahuasca be the key to combating destructive neurodegenerative diseases like ALS? That’s the focus of an article by Daniel Gustafsson, who is studying the connections between ethnobotanical medicine and neurodisease.

    While native people in the Amazon have been using ayahuasca for centuries, and its popularity has grown over the last few decades, science has not caught up to the legend. Researchers
    are trying to remedy the gaps in our knowledge, however. One informal study currently underway is looking at how ayahuasca can be used to treat people suffering from ALS, or amyotrophic lateral sclerosis. According to initial updates, some are experiencing a wider range of movement, tension relief in their muscles and improved grip strength after taking ayahuasca.

    There is science behind the hypothesis that ayahusaca could be useful. “Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system,” Gustafsson writes, “controlling neurotransmission, muscle/motor activity, memory and coordination.”

    That means it could be effective against diseases like ALS, which currently has no known cure, as well as other neurodegenerative conditions like Multiple Sclerosis, Alzheimer’s and Parkinson’s disease. Initial studies have suggested that ayahuasca might actually stimulate new cell growth in areas where these diseases have ravaged the brain.

    In addition to the possible physiological benefits for patients with ALS, ayahuasca and other psychedelics can be useful in a psychotherapeutic role as well by helping patients mentally come
    to grips with their illness.

    Other research suggests that ayahuasca could be useful in treating conditions such as spinal chord injuries, diabetes and cancer. Yet scientific studies are still few and far between, because the substance is considered a Schedule I controlled substance with no medical value by the United States government, making it difficult for researchers to get permission to work with it.

    There is a ray of hope, however. Banisteriopsis Caapi, one of the plants from which ayahuasca brews are concocted, does not contain any dimethyltryptamine, or DMT. That means that when consumed on its own it doesn’t invoke the psychedelic visions for which ayahuasca is famous, and therefore is not banned in the United States and most other countries. While B. Caapi on its own doesn’t boast the full medicinal portfolio of the true ayahuasca drink, it might still be helpful for people facing ALS and other diseases who can’t find relief anywhere else.

    One big step, Gustafsson argues, would be to stop calling plant-based psychedelics “drugs,” and lumping them in with more harmful substances that are tied to public health problems. “A more correct term for these plants, with respect to the indigenous culture in which ayahuasca is a part of, would be ‘entheogens’,” he writes, “which means plants used in a context sacred to the native people, inducing spiritual experiences.”

    http://reset.me/story/ayahuasca-show...-to-treat-als/

    -----

    Zaki Jackson and epilepsy - Cannabis saved my son's life

    This is the story of 12-year old Zaki Jackson, who was diagnosed with Doose Syndrome, a rare form of epilepsy characterized by frequent and severe seizures, when he was 15 months old. With the help of cannabis, he has gone from having hundreds of seizures a day, to being virtually seizure free.

    The first thing Heather Jackson did each day for much of her son Zakis life was make sure he was still alive.

    It all started in September of 2003, when Zaki was just 4 months old. The infant began having strange episodes that baffled his parents. His body would clench up, and he would throw his
    head back. If he was holding a rattle, it was often flicked up into the air. Sometimes it occurred in response to loud noises, leading Heather to believe her son was easily startled.

    But it was happening quite a bit by the time Zaki was 6 months old, when doctors took his first electroencephalogram (EEG), a diagnostic test for epilepsy.

    When the doctor's office called, it was the doctor, not the nurse or the receptionist, recalls Heather. So I figured it was bad. He said it was seizures.

    Around 15 months old, Zaki was diagnosed with Doose Syndrome, a rare, little-understood and grave form of early child-onset epilepsy that is often not responsive to medication.

    The condition progressed to the point, in 2011, where Zaki was having hundreds of brief, violent seizures a day. His brain was under constant assault for the better part of a decade.

    They never knew when the spell would break. Years of seizures translated into significant delays and collateral damage that put Zaki at 28 to 41 months old developmentally. A parade of weekly occupational, speech and physical therapies helped some, but any progress could be washed away by a single episode.

    It would set him back months developmentally and all of the hard work we did every day was just gone, Heather says. I would crumble, and then I would get up, brush myself off and say, because of Zaki we need to carry on.

    In 2011, Zaki began having chronic seizures called tonics where he would cease breathing. Every time, Heather feared it was the end. She awoke every day and looked over at him, where he slept in his parents bed or nearby on a makeshift bed on the floor. As 2011 came to a close, it seemed that Zakis young life would, as well. The family took a Make-a-Wish trip to Disneyworld, and tried to cherish the time they had left together.

    We were doing our best, says Heather. We were enjoying him. We weren't focused on death. We were focused on living and trying to be happy. But its hard when the first thing you do in the morning is check your kid to see if he still has a pulse. Its a really difficult way to live.

    After 17 pharmaceuticals were tried, and failed, Zaki's doctors didn't have anything left in their bag of tricks.

    Our option was to recycle through the drugs we had tried, which was definitely not something I was interested in doing, says Heather. Every pharmaceutical has side effects, and the drugs they use to control epilepsy are really heavy hitting.

    Some drugs cut Zaki's appetite; others made him eat too much. Some caused him to lose sleep; others forced him to sleep all day. The most successful, long-term therapy he tried was steroids. Zaki has bone loss and cataracts. He was like an old man because of these pharmaceuticals.

    Zaki's initial diagnosis provoked Heather to investigate every possible treatment and proposed medication. And as each failed to bring her little boy out of the dark, one unexplored option flickered promisingly in the distance. Swinging her researchers spotlight onto cannabis, though, meant overcoming her personal hang-ups. Like many others who grew up in the 1980s, the no-nonsense message delivered as an egg sizzling in a frying pan informed Heather's views on marijuana. I thought cannabis can't be good for you, she says.

    Heather was concerned about what her family and friends might think. No more concerned than I was for my son's health, she says. Which is why, after I dug into the research, I accepted
    that it was an anti-convulsant.

    We didn't have anything to lose at this point, she adds.

    Fortunately, the Jackson family lived in Colorado Springs, a mecca of cannabis treatment for pediatric epilepsy. It is just outside of this 440,000-person city that Charlottes Web is grown, a high-CBD strain that has become particularly popular for addressing epilepsy. Hundreds, 400 by Heather's estimation, of other families have fled their home states and flocked to Colorado, particularly Colorado Springs, in a quest for safe, legal access to this medicine. The Jacksons needed to drive just 10 minutes from their home to pick up Zaki's Charlottes Web.

    Heather was still skeptical when in July, 2012, they gave it a try for the first time. Following the nightly bedtime routine, she filled a syringe with a low dose of the viscous amber honey-based medicine, and squirted it into his mouth. Then she waited, staring at the time on her phone, counting the minutes as they passed. Suddenly, it was morning, she awoke startled, only to realize that Zaki did not have a seizure all night.

    Her hope grew when an unheard of 48 hours passed without a seizure. She slowly raised Zaki's dose over the coming months, and the seizures were sporadic.

    Zaki had his last big seizure on Oct. 3, 2012.

    It has literally put his condition into remission, Heather says, speaking just after the 30-month seizure-free mark.

    Without seizures standing in his way, Zaki has made leaps and bounds developmentally. Before trying cannabis he was still, in most ways, a toddler: he had to wear pull-up diapers. He didn't know his colors or how to write his name. Today, now 12 years old, he's mastered colors and his name, and is working on the alphabet and numbers.

    He's learning concepts he hadn't been able to grasp before, Heather says. What is even more exciting is the social aspect; he used to have severe autistic tendencies. Now he has friends and plays and rides a bike. These might be little things to other families, but to us, its huge. He is living life.

    No longer hampered by his suffering, Zaki's spirit has burst forth in full force.

    Zaki has the greatest sense of humor, says Heather. He's funny. He'ss very sensitive, very sweet, he's extremely active. He's constantly playing, wants to go outside, climb a tree, ride a bike. He's amazing.

    The improvements Zaki has made because of cannabis have also been life-changing for his parents, who have been together since high school, and his older brother, Zarek, all of whom were also hostages of the condition. His healing is allowing the family to heal.

    But Heather didn't rest on her laurels. Along with Paige Figi, whose daughter Charlotte was the inspiration and impetus behind the famous Charlottes Web strain, Heather started the nonprofit Realm of Caring in 2012 to connect families with information and resources.

    Heather tells Zaki's story to the press and through advocacy, in hopes of sparing other families the pain they endured. You do a news interview then you read the comments, and people are mean and ignorant and come from a place of misunderstanding, she says. But they haven't walked in my shoes, and I would challenge them to hold their child in their arms while they are not breathing, after exhausting all other options, and tell me what they would do.

    One of Heather's goals is to encourage better research, because as wonderful and healing as Zaki's story is, it is still considered anecdotal evidence. It's time an appropriate amount of funding and research was put into understanding marijuana as medicine, she says.

    This isnt a political issue, she adds. This is a human rights issue. I want us to stop making political decisions that could literally be life or death for a family.

    http://reset.me/story/cannabis-saved...atic-epilepsy/
    Last edited by mr peabody; 27-08-2018 at 02:57.
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    Ayahuasca and ALS

    Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system controlling neurotransmission, muscle/motor activity, memory and coordination. This gives probable cause to the theory that ayahuasca could be an effective treatment for neurodegenerative diseases such as ALS, Alzheimers, and Parkinsons disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occuring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

    According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. There is also a growing interest in exploring the cell regenerative properties of these plants within the spinal chord injury support communities. Should people with this background eventually try and find the results of this treatment useful, medical science would be bound to take note. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

    Summary

    Ayahuasca could effectively be used in treatment of ALS and other motor neuron diseases based on the fact that studies suggest uniquely antioxidative effects that seem to protect brain/nerve cells, targeting motor neurons through a unique biochemical transport system, and that it and other molecularly similar substances, also naturally occurring, stimulate neurogenesis, the development of new brain/nerve cells, and the communicative capacity between these. In studies it has been found to reduce symptoms in Parkinsons patients; all neurodegenerative diseases share common ground, thus making it likely that something that improves a given neurological condition could also be beneficial to other conditions nearly related. Also based on credible personal accounts from people having used ayahuasca for symptom relief from their multiple sclerosis (the common ground of neurodegenerative diseases), documented in books about ayahuasca, and from descriptions of early stage minor improvement by those with various types of ALS now participating in the treatment project, already having used this medicine for a period of time. Studies also indicate the ability to normalize metabolism in mitochondria, crucial to motor neuron survival, and to regulate and decrease levels of excitotoxicity in the central nervous system.

    -Daniel Gustafsson

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    Psychedelics may help the brain repair itself, study finds


    A new study in Cell Reports has found that psychedelics promote structural and functional neural plasticity.

    In recent years, psychedelic party drugs such as LSD and MDMA have been studied by scientists for their potential ability to treat mental health problems like depression and anxiety—often in microdoses much smaller than the what a person would take to trip. But while the research into these drugs is promising, there’s still a lot we don’t understand about how they affect the brain. A new study, published Tuesday in Cell Reports, seems to offer the strongest evidence yet that they can actually help repair the brain’s circuitry and function.

    The researchers, primarily from the University of California, Davis, exposed lab-cultured neurons from humans, rats, and other animals to various psychedelics. Drugs from different classes were used, including the amphetamine MDMA, the tryptamine psilocin, and the ergoline LSD. The neurons were taken from the prefrontal cortex, an area of the brain thought to be crucial in the development of certain mental illnesses.

    Most of the psychedelics tested, the researchers found, promoted the growth of new dendrites from a neuron cell, which help transmit information from other neurons to the cell, as well as increased the density of small protrusions on these dendrites, known as dendritic spines. They also jumpstarted the growth of new connections, or synapses, between individual neurons. Similar effects were also seen in the brains of living test animals.

    The net result of these changes, the authors say, is that they improve the brain’s plasticity, which includes its ability to repair itself from damage caused by things like stress or trauma. These changes, the researchers noted, are the reverse of what seems to happen in the brains of people living with chronic depression, post-traumatic stress disorder, or addiction. And they resemble the changes seen in people who take ketamine, an anesthetic and recreational drug that has been retooled in recent years as a fast-acting, if still experimental, antidepressant that some research has found can quickly tamp down suicidal thoughts.

    “People have long assumed that psychedelics are capable of altering neuronal structure, but this is the first study that clearly and unambiguously supports that hypothesis,” said lead author David Olson, an assistant professor in the Departments of Chemistry and of Biochemistry and Molecular Medicine, in a statement. “What is really exciting is that psychedelics seem to mirror the effects produced by ketamine.”

    It’s exciting, the authors say, because it means there’s more than one way for drugs to quickly improve a person’s brain plasticity. And the more options available, the better the chances someone can benefit from treatment, especially if other current drugs haven’t worked. Ultimately, it also provides researchers like Olson that many more avenues to pursue in developing more palatable versions of the psychedelic drugs we have available (i.e., versions that don’t cause long, mind-bending trips). The team even wants to rebrand these drugs as “psychoplastogens.”

    “Ketamine is no longer our only option,” Olson said. “Our work demonstrates that there are a number of distinct chemical scaffolds capable of promoting plasticity like ketamine, providing additional opportunities for medicinal chemists to develop safer and more effective alternatives.”

    Olson’s team is already studying whether non-hallucinogenic analogs of these psychedelics can still improve brain plasticity, and they note that researchers elsewhere are in the middle of developing safer analogs of ketamine, which has some potential for addiction and abuse.

    https://www.cell.com/cell-reports/fulltext/
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    Treating neurodegenerative disorders with cannabinoids

    Neuroinflammation is known to play a significant role in essentially all neurodegenerative processes. Diseases such as Alzheimer’s, Multiple Sclerosis (MS), Huntington’s Disease, and Parkinson’s Disease all involve hyperactive microglia, which are the live-in macrophages of the brain, spinal cord, and central nervous system. Macrophages are immune cells that capture and dissolve foreign substances, germs, and cancer cells within the body. The microglia in the brain and spinal cord form the first line of immune defense in the central nervous system. Unfortunately, in the case of aforementioned diseases, these cells have become overactive causing them to secrete excess substances, such as cytokines (cell signals that regulate cell group growth and response), glutamate, and harmful free radicals. This excessive production of chemicals causes inflammation, which leads to further cell death.

    Cannabis and the family of chemicals it produces are known to act on two major cell receptor types named CB1 and CB2 respectively. The CB1 receptor is most commonly found in neurons throughout the brain. The psychedelic effects of cannabis come from this receptor’s function, which re-wires the way neurons signal each other. The CB2 receptor on the other hand, is found throughout the body, especially within the immune system cells. The effects of activating the CB2 receptor are more myriad, but within the immune system specifically four groups of effects have been identified:

    1. Induction of apoptosis or forced cell death

    2. Suppression of cell proliferation

    3. Induction of regulatory T cells

    4. Inhibition of pro-inflammatory cytokine/chemokine production and increase in anti-inflammatory cytokines

    The last of these effects is the basis upon exploring using cannabinoids to halt the progress of neurodegenerative disorders. The idea is that if cannabinoids can prevent excess production of cytokine, inflammation will decrease, and the resultant cell death around that inflammation will not occur. This would go a long measure toward slowing progression of neuro-inflammatory diseases. However, it is important to note that tempering inflammation would still not allow the brain to recover to its pre-disease state and slow neural damage would inevitably continue to occur. Likewise, modern medicine currently utilizes a variety of treatments in these diseases as more or less palliative care.

    Based on these observations, research groups worldwide have been testing specific cannabinoids and other CB2 agonists with various models of neuro-inflammatory disease, generally in rodents.

    The following is a general review of effects noticed, grouped by disease:

    Alzheimer’s Disease – In Alzheimer’s cannabidiol has been shown to “reduce the transcription and expression of pro-inflammatory molecules in the hippocampus of an in-vivo model of induced neuroinflammation”. The hippocampus is the part of the brain that controls conversion of memory from short to long-term and controls spatial navigation. In Alzheimer’s, it’s one of the first areas of the brain to suffer damage and why patients have memory problems. Another agonist, which has the name SR141716A, also prevents amnesia induced by certain peptides, so these both promise a future in treating the disease.

    Parkinson’s Disease – In this disease, the agonist WIN55,212-2 has been shown to protect mouse neurons from the neurotoxin MPTP, which is the chemical which leads to the death of dopaminergic neurons and causes Parkinson’s Disease.

    Multiple Sclerosis (MS) – Although the cause of MS is unclear, researchers have determined that both genetic susceptibility and environmental trigger play a role. Some patients develop their symptoms of MS after contracting a virus. Likewise, testing rodents injected with a virus that intentionally lead to animal models of MS provided ground to investigate the effects that CB2 agonists might have on MS in humans. As is, cannabis concentrate is already prescribed under the name Sativex to alleviate neuropathic pain, spasticity, and overactive bladder symptoms associated with MS. Although some agonists did increase symptoms, several, including THC, delayed onset and reduced severity of symptoms. Three agonists, WIN55,212-2, ACEA, and JWH-015 were shown to improve motor function by attenuating microglia and immune cell infiltration into the spinal cord.

    Exactly how these effects are achieved is still unknown. Although it is presumed that the effects of the CB2 agonists (any molecules that can activate CB2 receptors, including cannabinoids) stem from CB2 receptor activation, other theories have been proposed. One research group at the University of Bari has explored the extra-cannabinoid receptor binding activity of cannabidiol (CBD). Researchers there found that CBD can surprisingly communicate with the nucleus of the cell directly through interaction with nuclear hormone receptors. There are several possible chemical pathways through which cannabinoids can achieve their effects, beyond CB2 receptors. Further research will illuminate these pathways.

    https://cornerstonecollective.com/ho...der-treatment/


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    Repurposing ketamine for Parkinson’s

    The best-known treatment for Parkinson’s disease isn’t perfect. Named Levodopa, the drug can treat the stiffness and slowness of movement associated with the debilitating disease.

    “The problem is levodopa works great for a few years — we call that the ‘honeymoon’ period — but then you start getting these side effects,” says Scott Sherman, MD, PhD, a neurologist at the University of Arizona College of Medicine – Tucson.

    Forty percent of patients on levodopa eventually will experience dyskinesia — uncontrollable and involuntary movements of the arms, legs, head or entire body. Severity can range from small, fidget-like motions to larger continuous bursts of movement.

    Unless patients stop levodopa treatment altogether, these movements do not go away.

    Now, UA researchers will repurpose ketamine, a drug currently used to treat pain and depression, to try to reduce and control these involuntary movements brought on by levodopa.

    Led by Dr. Sherman and Torsten Falk, PhD, a neuroscientist in the UA Department of Neurology, the two will launch a small phase I clinical trial this summer at the UA College of Medicine – Tucson. The trial is supported by a three-year $750,000 grant from the Arizona Biomedical Research Commission (ABRC).

    Drs. Sherman and Falk first got a glimpse of ketamine’s potential in Parkinson’s disease treatment more than five years ago.

    The two were using ketamine to relieve pain in five hospitalized patients with Parkinson’s disease. The treatment worked as expected, but the researchers noticed an unintended side effect: the patients’ uncontrolled movements while on levodopa were noticeably reduced. One patient experienced complete resolution of these movements for a period of several weeks.

    Intrigued, the researchers continued investigating and have since shown similar results in rodents with Parkinson’s disease.

    Ketamine has been known to raise blood pressure and cause a feeling of disassociation in humans.

    “Disassociation is a sort of ‘out-of-body’ experience,” Dr. Sherman explains. “When people describe it, they have told me that they feel like they are in fish bowl.”

    In the past, ketamine has been abused by partygoers for this psychedelic effect, but Dr. Sherman is hopeful these side effects will not affect the clinical trial.

    “We are going to monitor blood pressure closely to make sure it doesn’t get high,” he says. “And we know at what dosage ketamine causes this disassociation; we expect that the dosage needed in Parkinson’s disease will stay well below that level.”

    Using 10 patients, this first clinical trial will verify that Dr. Sherman’s hunch holds true — that ketamine is tolerable and effective for treating dyskinesia.

    In addition to supporting the clinical trial, grant funding from the ABRC will back a separate rodent study that examines exactly how ketamine affects the brain and reduces dyskinesia triggered by levodopa.

    “We want to find out exactly what ketamine is doing to have this effect,” Dr. Sherman explains.

    If the team achieves positive results in both the human and rodent studies, Drs. Sherman and Falk will be one step closer to their goal: establishing that ketamine can help patients with Parkinson’s disease.

    Dr. Sherman says, “Ketamine has been long overlooked. Now it could prove very useful for Parkinson’s patients.”

    http://uahs.arizona.edu/news/ua-clin...nsons-patients

    -----

    Ibogaine and Parkinson's Disease

    After Alzheimer's, Parkinson's Disease is the second most common neurodegenerative disease and is currently not curable. The disease manifests itself by the progressive loss of nerve cells, mainly of dopamine neurons in the Substantia Nigra (part of the mid-brain). This results in a lack of dopamine in the striatum (a subcortical part of the forebrain), as well as a dysfunction in motor functions, tremors, stiffening muscles, language problems and a general loss of balance and coordination.

    These physical symptoms are also accompanied by psychological effects like dementia and depression. It is thought that the neurodegenerative aspects of Parkinson's disease are caused by the body's immune system. Healthy nervous system tissue is attacked when the immune system is no longer able to distinguish between healthy and diseased cells, similar to autoimmune diseases such as multiple sclerosis, fibromyalgia and polyneuropathy.

    GDNF (glial cell line-derived neurotrophic factor) is a protein discovered in 1991 with an extraordinarily positive effect on nerve cell tissue. GDNF stimulates nerve cell growth, especially dopamine neurons. In addition to the ability to regenerate nerve cells in the brain, GDNF also appears to possess neuroprotective properties.

    In an animal experiment in which rats with Parkinson's disease had GDNF injected directly into the brain, a significant improvement in the symptoms was observed. After one year, there were still no undesirable side effects of GDNF administration. Initial studies have shown that GDNF significantly improves the overall condition of Parkinson's patients. The resulting data suggests that new nerve cells had formed.

    Ibogaine and its metabolite noribogaine lead to a substantial increase in GDNF levels in the brain. This indicates that ibogaine could provide a very effective treatment for neurodegenerative diseases, such as Parkinsons.

    Until now, it was not possible to introduce GDNF directly into the desired regions of the brain. But Ibogaine stimulates the glial cells and neurons to produce GDNF itself, increasing GDNF levels throughout the brain. Phytostan, a pharmaceutical company focused on developing ibogaine, has developed an ibogaine-based medicine called CK-BR-12 consisting of Ibogaine HCL and a cocktail composed of 12 vitamins.

    Patient D is a 69-year-old Parkinson's disease patient and until now the only human treated with Ibogaine for his condition. Patient D reported numerous positive changes regarding his illness: he could swallow again, speech and facial expressions improved noticeably, the control of the hands increased and he could write again legibly. Also, his general motor skills increased.

    He could dress again, eat independently and climb stairs, all activities which were not possible prior to his treatment. The Parkinson's symptomatology also improved after the treatment was completed. Patient D. was examined by various physicians as well as pharmacologist Dr. Susanne Cappendijk from Semper Clarus Consulting, who presented the promising results at the New York Academy of Sciences conference in April of 2015.

    The standard symptomatic treatment, is predominantly carried out with drugs with strong side effects. The quality of life of the patients is often characterised by significant suffering in the terminal phase. In contrast, treatment with ibogaine, in particular through the approach of microdosing, allows an increase in the GDNF levels in the brain, without the side effects of conventionally used medications.

    It was reported that 4mg Ibogaine HCL can increase GDNF levels in the brain by a factor of 12. The neuroplasticity increased by the growth of new neurons promotes the restoration and the construction of nerve tracts. Also, the challenge of introducing GDNF by injection into the brain is obviated. These results could help to redefine the position of Ibogaine in general research and, as unknown healing properties of the plant are discovered, open up new research areas and thereby achieve a wider social and regulatory acceptance.

    At the Ibogaine conference in 2016, Dr. Ignacio Carrera from the Universidad de la Republica Uruguay presented the research of an interdisciplinary group. Novel variations of the ibogaine molecular structure have been developed that enhance the production of GDNF. The group of N-indolylethyl isoquinuclidines appears to be most promising. The synthesis of these molecules is far less complex than that of Ibogaine and there are several promising derivatives. Some of the analogues cause an even higher GDNF-release in vitro than Ibogaine does, but can have cytotoxic effects depending on the structure. The research in this field is still nascent, but it has enormous potential.

    http://iboga.info/parkinsons-disease/

    -----

    Ibogaine component CKBR-12 for treating Parkinson's Disease

    CKBR-12, an Ibogaine derivative medicine is currently being investigated to treat Parkinson's disease. It has been found to upregulate Glial cell line-Derived Neurotrophic Factor expression in the mid brain, increase GDNF secretion 6, and may represent a powerful new method to upregulate GDNF in the treatment of PD and other neurodegenerative disorders.

    REDUCTION OF PD SYMPTOMS In Patients With CKBR-12

    1. Decreased or elimination of Saliva and drooling. No problems in swallowing
    2. Loss of any depression or anxiety.
    3. Improvement in his speech, diction, and tongue control.
    4. Increased facial activity, muscles coming alive. Loss of facial rigidity.
    5. Regaining hand movement and use.
    6. Free flowing handwriting.
    7. Motor Skills: 50% or 75% better within 30 days.
    8. Return of self dressing and dexterity with fingers
    9. Naturally eating, cutting own food, dont need assistance. Able to hold a fork and knife differently .
    10. Balance: Standing up for long periods of time and regaining a sense of balance. Loss of feeling of falling.
    11. Walking: Able to walk up and down stairs much faster and longer distances.
    12. Loss of tremors.

    Parkinson's Disease, Motor Neuron Disease and Alzheimer's Disease are chronic disorders that are normally treated with prescription medications that can have considerable side effects which may cause a very poor quality of life for terminal sufferers. In turn, Ibogaine may be very beneficial to those with degenerative neurological diseases.

    -GIC





    Parkinson's and MDMA


    By David Concar

    MDMA is being hailed as the key to better treatments for the Parkinson's disease, marking a complete turnaround from a few weeks ago when ecstasy was condemned for causing the disease.

    New animal studies have confirmed anecdotal reports that ecstasy can dramatically curb the uncontrollable arm and leg movements that plague so many people with Parkinson's. But the finding may be of little immediate help to sufferers.

    The researchers are not calling for patients to be given legal supplies of ecstasy (MDMA). Instead, they want to look for related drugs with the same beneficial effects. And patients are being warned against trying MDMA for themselves. Its impure, illegal and dangerous, says Robert Meadowcroft, policy director of Britain's Parkinson's Disease Society.

    Others are calling for further animal studies to establish the effective dose, followed by human trials. People who are suffering should have the right to decide carefully for themselves whether or not to take MDMA, says American drugs policy campaigner Rick Doblin. His organisation, MAPS, recently won approval from the Food and Drug Administration for a human trial of ecstasy for treating post-traumatic stress disorder.

    Regaining control

    The latest study was prompted by the experiences of a former stuntman, Tim Lawrence. He made headlines when he claimed in a BBC TV documentary that enabled him to regain control of his body for hours at a time.

    Parkinson's experts at the University of Manchester decided to test Lawrences claims. Concerns about the dangers of MDMA ruled out human trials, says team member Jonathan Brotchie, who now runs Manchester-based biotech company Motac. So the researchers turned to marmosets with a form of the disease.

    Parkinson's is caused by a loss of the dopamine-producing cells in the brain. Symptoms include rigidity and a shuffling gait. Since the late 1960s doctors have treated it with L-dopa, a chemical precursor to dopamine that can unfreeze patients.

    The downside is that patients develop uncontrollable movements after taking L-dopa for a while. Their condition tends to oscillates between flailing limbs while on the drug and immobility off it.

    To mimic Parkinson's, they gave six marmosets a chemical that kills dopamine neurons. Then, over the next few months, the monkeys had daily doses of L-dopa until they developed the usual side effect of uncontrolled movements. At this point the animals were given MDMA.

    Dramatic effects

    The effects were dramatic. Normally, monkeys on L-dopa move their arms and legs around in a repetitive and uncontrolled way virtually all the time. But in the six hours after a dose of MDMA, these movements happened no more than 15 per cent of the time. MDMA somehow reduces the debilitating side effects of L-dopa without blocking its beneficial effects.

    The magnitude and quality of the effect took us by surprise, says Brotchie, whose teams findings were unveiled this week at the conference of the Society for Neuroscience in Florida. It was always possible that Tims response to ecstasy was unusual.

    The researchers suspect the finding reflects MDMAs ability to stimulate the release of the neurotransmitter serotonin in the brain. That might make up for a lack of serotonin caused by taking L-dopa for prolonged periods, says Brotchie. However, there are fears that MDMA can damage serotonin-producing cells.

    And last month the journal Science published a paper claiming that MDMA can actually cause the type of damage to dopamine cells that can lead to Parkinson's. But the evidence was far from conclusive.

    https://www.newscientist.com/article...sons-symptoms/
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    Cannabis shown to reverse cognitive decline and fight Alzheimer’s



    Cannabis has the reputation of impairing memory, attention and motivation, especially in young people. But what if it could actually protect the brain and prevent neurodegenerative disorders like Alzheimer’s and other types of dementia from developing?

    Although cannabis has been used for its medicinal properties for many thousands of years, scientific research into the plant and its derivatives (pioneered by the Beckley Foundation and others) has only recently started to acknowledge and investigate some of its health benefits. Among many therapeutic applications, results gathered over the last decade have unveiled some extremely promising brain-protective and restorative properties.

    The effects of cannabis are caused by chemical compounds produced by the plant known as cannabinoids. These include tetrahydrocannabinol (THC) and cannabidiol (CBD). Cannabinoid-like molecules – called endocannabinoids – occur naturally in the brain, and are involved in a diverse range of processes including appetite, energy regulation, and sleep. Indeed, cannabinoid receptors are some of the most abundant receptors found in the body.

    The endocannabinoid system develops gradually throughout childhood and is most active during adolescence, but as we age, its activity declines. Compelling evidence suggests this may be one of the root causes of some of the detrimental aspects of normal and pathological aging. One possibility seems particularly worth exploring – that supplementing the aging endocannabinoid system with exogenous plant cannabinoids may mitigate some of the damage that occurs in the brain as we grow older.

    Recent experimental research seems to support this notion. In a study published last year, THC – the molecule in cannabis responsible for its psychoactive effects – was found to reverse age-related cognitive decline in old mice. The study also found that THC increased the number of connections between brain cells in the hippocampus, a brain region which plays a key role in memory.


    THC, administered on consecutive days, significantly increased the speed at which
    mature and old mice completed a maze task


    This is not an isolated report; several other studies have found that THC-like substances improve memory and cognition in rodents. The positive effects of cannabis and cannabinoids on sleep and appetite, and on reducing stress and anxiety, may constitute other indirect ways in which these substances can ward off cognitive decline.

    Perhaps even more profound is the implication that cannabinoids may treat more serious age-related disorders such as Alzheimer’s Disease. Despite the diagnosis of Alzheimer’s in millions of people every year, there is yet no definitive treatment for the condition. The disease involves accumulation of the toxic protein amyloid-beta (Aβ) in the brain. The insoluble Aβ plaques also cause further damage when the bodies own inflammatory response attacks cells in an attempt to clear them, leading to further death of brain tissue.

    The idea that a component of cannabis – a natural, easily-grown substance with a known, positive safety profile – could be used to treat a disease which is afflicting more and more people in an aging population is a very attractive one.

    Though the science is still at an early stage, pre-clinical research is promising. A study using neuronal cell cultures that had been genetically altered to over-produce Aβ – effectively a test-tube model of Alzheimer’s Disease – found that by adding increasing doses of THC, less of the toxic protein accumulated, and cells were less likely to die. These findings are also reflected in animal studies, which found that cannabinoids similar to THC and CBD improved cognition and decreased cellular damage in a mouse model of the disease.


    THC increased survival of Aβ-producing neurones (left), and decreased the
    accumulation of Aβ (right) in a dose-dependent manner


    There are various proposed mechanisms for the neuroprotective effect of cannabinoids in degenerative disorders such as Alzheimer’s. Symptoms of these diseases are partially a result of the body’s own immune system overreacting to diseased neurones. In chronic brain diseases, excessive immune response to neurones can further damage them, a process known as pathological neuroinflammation. The endocannabinoid system is involved in regulating the inflammatory response by inducing changes in pro-inflammatory proteins, limiting possible damage caused by their over-activation.

    Another potential mechanism via which cannabinoids may exert their neuroprotective effects could be through inhibiting excitotoxicity. If neurones activate for too long and too often (excitation), they become damaged (toxicity). Damaged neurones then release chemicals that further activate and damage neurones near them, creating a positive feedback loop of spreading cellular damage. Activation of the cannabinoid system by endocannabinoids decreases the release of these potentially harmful molecules, limiting the spread of damage from an initial injury. By introducing plant cannabinoids in addition to those naturally produced by the body, it may be possible to boost these effects and further minimise brain damage.

    Cannabis derivatives hold great medical potential – not only for the treatment of neurodegenerative diseases such as Alzheimer’s, but for epilepsy, addiction, pain, and a host of other conditions. Unfortunately, this potential is limited by anti-scientific laws and policies. Cannabis is currently on Schedule I of the UN’s global drug conventions; of ‘little or no therapeutic value’, despite the overwhelming amount of evidence to the contrary. This strict legal scheduling means that research into the plant is severely underfunded and limited by bureaucratic restrictions which do little to quell recreational use of cannabis, but which do prevent doctors prescribing it to patients.

    We are actively campaigning to reform the current system of drug legislation, and hope that both UK and global policy will soon change to reflect the scientific evidence. The Beckley Foundation and other research groups are dedicated to fully unravelling the therapeutic benefits of cannabis and other psychoactive compounds – something that everyone will benefit from.

    http://beckleyfoundation.org/2018/06...ne-alzheimers/
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    Ayahuasca stimulates neurogenesis and could treat Alzheimer’s

    By Olivia Lerche

    SCIENTISTS have discovered that a hallucinogenic substance from the Amazon stimulates the birth of new brains cells and could lead to treatment for neurodegenerative diseases
    such as Alzheimer’s disease. The tea called Ayahuasca, is also used as a traditional spiritual medicine in ceremonies in Peru, South America.

    The Sant Pau Hospital Barcelona, which worked in collaboration with the Beckley Foundation and Spanish National Research Council in Madrid, has released the findings from a study investigating the potential of ayahuasca to promote neurogenesis - which is the development of new brain cells. The investigators believe that these findings will open up a new avenue of research that may help develop drugs to treat diseases like Alzheimer’s, Parkinson’s and addiction.

    Dr Jordi Riba, lead investigator, presented preliminary data, at the Interdisciplinary Conference on Psychedelic Research in Amsterdam at the weekend. Results showed that two compounds - harmine and tetrahydro harmine - which are found in the hallucinogenic tea, potently stimulated the transformation of stem cells into new neurons.

    Amanda Feilding, director of the Beckley Foundation said: “The images from the Beckley/Sant Pau collaboration showing the birth of new neurons are very interesting and suggest that ayahuasca could lead to a new approach in the treatment of neurodegenerative conditions such as Alzheimer’s and Parkinson’s, among others.”

    Experts have believed for years that the brain doesn’t make neurons during adulthood. In the 1990s, research changed this finding, showing that new neurons are generated throughout adult life in two regions of the human brain: the area around the ventricles and in the hippocampus. The hippocampus, thought to be the center of emotion and autonomic nervous system, plays a key role in memory. Its function declines with age and in neurological disorders.

    Under normal conditions, the rate of the birth of new neurons is very low, and it cannot keep up with the rate of neural death that occurs in diseases such such as Alzheimer’s disease. In the study, neural stem cells were isolated from the hippocampus of adult mice. The stem cells were grown in the lab and substances that are present in ayahuasca were added to the cultures and compared with saline a placebo control.

    Scientists have described the results as ‘impressive’, with ayahuasca substances stimulating the transformation of stem cells into new neurons.

    Dr Riba has been studying ayahuasca for twenty years.

    -----

    The ability of psychedelics such as LSD to interact with receptors for endogenous neurotransmitters such as GABA, serotonin and glutamate is significant. LSD and other psychedelics can modulate activity in the Default Mode Network. This is a distinct network of brain regions providing the neurologic basis for “self.” Abnormal function in this network may be responsible for disorders such as autism, Alzheimer’s, PTSD, chronic pain and certain depressive disorders. In addition to providing possible mechanisms explaining microdosing’s clinical actions in regulating mood, these findings point to important research possibilities.

    -Dr. Bruce Heischober

    -----

    Ergoloid mesylates, trade name Hydergine, is a mixture of the methanesulfonate salts of three dihydrogenated ergot alkaloids. It was developed by Albert Hofmann for Sandoz. Hydergine has been used to treat dementia and age-related cognitive impairment (such as Alzheimer disease). It stimulates dopaminergic and serotonergic receptors and blocks alpha-adrenoreceptors.

    The drug works within the central nervous system to reduce the vascular tone of blood vessels supplying the brain. Consequently, the cerebrovascular is relaxed leading to an increase in the amount of oxygen that is delivered to the neurons. Increased oxygen in the brain is thought to increase neural metabolism hence function.

    Hydergine, an extract of a fungus that grows on rye, was the first drug believed to show some promise in treating Alzheimer's. A year after UC San Diego neurologist Robert Katzman wrote his editorial calling for an increase in research, the FDA approved its use in Alzheimer's patients sixty and older in 1977.

    Although it was originally created to treat hypertension, because it dilates blood vessels in the brain, it wasn't very effective at lowering blood pressure. However, some patients reported that it did improve their memory and mood, which led to its use as a treatment for dementia.

    -Niki Kapsambelis

    -----

    Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system – controlling neurotransmission, muscle/motor activity, memory and coordination. This gives probable cause to the theory that ayahuasca could be an effective treatment for neurodegenerative diseases such as ALS, Alzheimer’s, and Parkinson’s disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occuring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

    According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. There is also a growing interest in exploring the cell regenerative properties of these plants within the spinal chord injury support communities. Should people with this background eventually try and find the results of this treatment useful, medical science would be bound to take note. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

    Summary

    Ayahuasca could effectively be used in treatment of ALS and other motor neuron diseases based on the fact that studies suggest uniquely antioxidative effects that seem to protect brain/nerve cells, targeting motor neurons through a unique biochemical transport system, and that it and other molecularly similar substances, also naturally occurring, stimulate neurogenesis – the development of new brain/nerve cells, and the communicative capacity between these. In studies it has been found to reduce symptoms in Parkinson’s patients – all neurodegenerative diseases share common ground, thus making it likely that something that improves a given neurological condition could also be beneficial to other conditions nearly related. Also based on credible personal accounts from people having used ayahuasca for symptom relief from their multiple sclerosis (once again – the common ground of neurodegenerative diseases), documented in books about ayahuasca, and from descriptions of early stage minor improvement by those with various types of ALS now participating in the treatment project, already having used this medicine for a period of time. Studies also indicate ability to normalize metabolism in mitochondria, crucial to motor neuron survival, and to regulate and decrease levels of excitotoxicity in the central nervous system.

    -Daniel Gustafsson

    -----

    Ibogaine and Parkinson’s Disease – case study

    By Trevor Millar

    It’s been recently discovered that Ibogaine may work to reverse the debilitating effects of Parkinson’s Disease (PD). A recent article published on the Global Ibogaine Therapy Alliance website prompted a PD sufferer to contact Liberty Root to see if we might be able to help him follow a protocol to work on his disease. Having heard that the study at Columbia University was using a low-dose protocol, a mere 4 mg of ibogaine a couple of times a day, which is sub-perceptual, and very low-risk dose, we were excited to provide this gentleman with some medicine and see what the effects might be.

    Bill is a 52 year old male who was diagnosed with PD more than two years ago, but had early signs four years ago. He’s been very proactive since his diagnosis in trying to mitigate the onset of the symptoms of the disease, which include tremors, slow movement, rigid muscles, impaired posture and balance, loss of automatic movements; speech and writing impairment. Bill has changed his lifestyle so as to include daily exercise (yoga, cycling, PD specific exercises) as well as switched to a clean diet, avoiding processed food, and including organic vegetables and other nutrient dense foods. He’s been taking Apo-Levocarb daily, which is a dopamine medicine that helps reduce the symptoms of PD, but as Bill told me, it has diminishing returns – the more you take, the less effective it is.

    Bill has been spending the winters in Tucson, Arizona, as it’s got a large community of PD patients, and specifically the Parkinson’s Wellness Recovery, which Bill speaks very highly of. When I first met him, he had just finished driving from AZ to BC, and stopped by our facility on the last leg of his journey to pick up some tablets that contain Ibogaine prior to heading to his home on Vancouver Island. Meeting Bill it was obvious he suffered from PD, especially after that long drive. He was bent over, had a hard time walking, was shaky, his speech was slurred, with a slight facial paralysis. During our initial consultation he needed to sit, and had a hard time getting up afterward. Some other symptoms he described to me were a loss of movements that had been automatic, like with using the turn signal on his car he needed to be very conscious when making that happen, or once he finished urinating in the toilet, that first step backing up afterward needed to be very consciously thought out; it didn’t just happen automatically anymore.

    Initially we gave Bill a supply of tablets each containing 4 milligrams of Ibogaine HCL and once we saw there was no adverse reaction, with plenty of improvement, some 10 mg doses were compounded. As mentioned, this is a very low dose of Ibogaine compared to what we would give to a person so as to interrupt an addiction (we might use a gram and a half or more of ibogaine for addiction therapy). Bill started by taking one of these in the morning, along with his dopamine med, and then one in the afternoon. Here are some comments relating to his couple of months with low-dose protocol and its effects:

    10 mgs or less of Ibogaine twice daily:
    – Feeling of looseness in my arms neck, shoulders and chest
    – Able to shoulder check when driving
    – More power in left arm while driving
    – Able to back up easier when driving with left-handed steering
    – Easier exiting car
    – Easier doing up seatbelt (reaching and clasping)
    – More torque in left hand when turning on water taps and door knobs
    – Opening jars much easier
    – Sweeping and raking much easier
    – Able to let go of objects without thinking about it first (left hand)
    – Dopamine medicine much more effective, works faster lasts a little longer
    – Fewer left hand cramps
    – Less restless arm and legs at night
    – Stronger voice
    – Way less need to stretch during the day and morning
    – Just more coordination in left hand and right hand as well
    – Walking gate improved, less clop in left foot longer steps
    – Late night and early morning walking more steady (getting up to pee in the night and waking up in the morning )
    – Don’t feel a sense of depression on off days and haven’t cried since starting Ibogaine

    Once we started seeing such great improvements in Bill’s condition, we upped the dosage and compounded some 20 mg caplets of Ibogaine, which is still a very low dose; he continued to experience zero psychedelic effects.

    20 mgs of Ibogaine twice daily:
    – All of the above with more vigour, speed, and strength
    – Knocked 10 minutes off time for regular 34 km bike ride; way stronger on hills and head winds
    – Less fatigue when walking and more improvements in gate
    – Grades less noticeable when walking uphill
    – Stepping backwards easier with larger steps
    – Less shaking on exertion with left arm (lifting weights)
    – Much easier pulling up spandex cycling shorts
    – Reduction of getting stuck (less often and shorter duration)

    As a general rule, with Ibogaine and addiction interruption, the more you take, the better it works, to a point at least. So we figured we’d bring Bill into our facility for a larger dose. After clearing it with his doctor, and having the standard tests we have done prior to a larger dose (ECG, blood work) we welcomed Bill to Liberty Root for him to go on a little ‘journey’ with the medicine. After two days of larger dosing (>250 mgs) Bill had this to report:

    – Feel no need for dopamine, moving better than even with dopamine supplement
    – Left hand no longer hyper-extended at rest and has stopped “locking” open
    – Using left hand in more spontaneous fashion, no self-correction
    – Washing easier, dressing easier, tying shoes easier
    – Improved sense of smell and taste
    – Haven’t been stuck since last dosage

    It’s only been a few days since Bill left our facility. In speaking with him today, he mentioned that his left hand has become a bit more stiff than it was upon his departure. There is obviously a lot more research and experimentation that needs be done, but the preliminary findings are very encouraging, and have offered Bill a degree of liberty he hasn’t seen in years.


    Last edited by mr peabody; 20-09-2018 at 07:45.
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    PATIENT REPORT: Ayahuasca and ALS

    Male, 65, UK, diagnosed with ALS

    Q: What can you tell us in general about your medical condition, and to what degree has it affected you? (At the point prior to treatment using ayahuasca)

    A: My prognosis as of March 2013 was that of a one-year life expectancy, I did get a specific MND diagnosis confirmed by a consultant neurologist, on the back of which an insurance company paid up on my critical illness cover, there being a clear understanding that I would probably not last the year. I was very weak and trembly, had lost over 20 pounds in muscle mass, my knees were prone to swelling and I was racked by cramps and muscle twitching. I could barely manage stairs, and couldn’t get out of the bath unassisted. I remember being a little challenged by a four inch step across the end of the room, choosing my best leg to step down.

    Q: Describe a typical experience with ayahuasca. What is it like during the immediate time the medicine is active in the body? What has been experienced afterwards?

    A: Initially a fair amount of retching, although I didn’t actually vomit much. Then some spastic activity, after which a warmth spread throughout my chest cavity, and sensations from the connection between muscle tissue and skeletal bone. It left me exhausted, but it “mellowed out” after a while into a contemplation state of mind where the concept of fear had a major part. Stressful emotions such as fear and anxiety seems to be a major vexation (in relation to neurological diseases), and the ayahuasca seemed to soothe that too. I didn’t feel that much different immediately afterwards, I suppose I felt a little more relaxed, but the following weeks (after sessions) my massage therapist said the muscle twitching was much improved, and I continued to recover steadily.

    Q: Has this treatment relieved or improved your condition in any way so far?

    A: I have made essentially a full recovery, slow but persistent, and NHS consultants involved are mystified. Ayahuasca seems to me to have been instrumental in my recovery, which is fully documented. I am now fully healthy, I cycle to work. Now, after today doing a nine mile coastal walk for the pleasure it, I feel pretty much up to snuff, for a man of my age. A year after my diagnosis I held a party to express my gratitude to all the people who had helped me through, including T.H., the consultant neurologist (he didn’t actually come). I was by that time much better, not up to full strength, but could party on and play the saxophone. I told my doctors about ayahuasca in August of 2013 I think, it was for a six monthly reassessment of my condition. T.H was frankly astonished, and when challenged said that the diagnosis was absolutely sound adding that the nerve conductivity tests were particularly unequivocal. It was then that I told him about the ayahuasca, and rather sheepishly, and mistakenly, he asked me if I had had a “good trip?” I replied that it had been unpleasant and that it was not a therapy for the faint hearted. Since then T.H has presented my case to some regional peer group, and a professor K.T. Their response was that perhaps I had a “mimic”, which seems to be exactly the same as the disease except for the outcome; or that the condition might have been brought upon me by the “cocktail of therapies I was taking” at the time. I have yet to make a measured response to this, but it was not until I had serious symptoms that were initially interpreted as Lyme’s disease or an atypical sero-negative rheumatoid arthritic condition, that I embarked on any kind of medical therapy at all. The history presents a persuasive argument. My family, friends and some of my patients are aware of my ayahuasca treatment and are generally supportive. My wife plays tennis with a number of retired GPs – their general opinion is that whatever I did can’t be too bad. Hell I’m still walking about and they were initially supporting my wife and family on the clear expectation of my imminent demise.

    Q: Will you continue this treatment? If so, will you make any changes to your current regimen?

    A: I don’t see any necessity to carry on being treated. I might do the ayahuasca again but that would really be just out of curiosity.

    Q: Have you been following any particular diet prior to, or during your treatment?

    A: Lots of organic fruit and vegetables, and I have a small holding so we have organic lamb and chicken too. I haven’t eaten dairy for the past two years, and I seldom drink alcohol though I had a glass of cider the other day.

    Q: What made you try this alternative treatment?

    A: It was an inspired patient who in doing an art degree in Plymouth came across the (ayahuasca) visionary art, and drew my attention to its source. Curiously some members of the church group with whom I sit proved an unexpected source of interest and loaned me various books on the topic, including those of the late Alexander T. Shulgin.



    San Luis Obispo
    Last edited by mr peabody; 04-09-2018 at 23:28.
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    Psychedelic tea from the Amazon stimulates brain cells and could treat Alzheimer’s

    By Olivia Lerche

    SCIENTISTS have discovered that a hallucinogenic substance from the Amazon stimulates the birth of new brains cells and could lead to treatment for neurodegenerative diseases
    such as Alzheimer’s disease. The tea called Ayahuasca, is also used as a traditional spiritual medicine in ceremonies in Peru, South America.

    The Sant Pau Hospital Barcelona, which worked in collaboration with the Beckley Foundation and Spanish National Research Council in Madrid, has released the findings from a study investigating the potential of ayahuasca to promote neurogenesis - which is the development of new brain cells. The investigators believe that these findings will open up a new avenue of research that may help develop drugs to treat diseases like Alzheimer’s, Parkinson’s and addiction.

    Dr Jordi Riba, lead investigator, presented preliminary data, at the Interdisciplinary Conference on Psychedelic Research in Amsterdam at the weekend. Results showed that two compounds - harmine and tetrahydro harmine - which are found in the hallucinogenic tea, potently stimulated the transformation of stem cells into new neurons.

    Amanda Feilding, director of the Beckley Foundation said: “The images from the Beckley/Sant Pau collaboration showing the birth of new neurons are very interesting and suggest that ayahuasca could lead to a new approach in the treatment of neurodegenerative conditions such as Alzheimer’s and Parkinson’s, among others.”

    Experts have believed for years that the brain doesn’t make neurons during adulthood. In the 1990s, research changed this finding, showing that new neurons are generated throughout adult life in two regions of the human brain: the area around the ventricles and in the hippocampus. The hippocampus, thought to be the center of emotion and autonomic nervous system, plays a key role in memory. Its function declines with age and in neurological disorders.

    Under normal conditions, the rate of the birth of new neurons is very low, and it cannot keep up with the rate of neural death that occurs in diseases such such as Alzheimer’s disease. In the study, neural stem cells were isolated from the hippocampus of adult mice. The stem cells were grown in the lab and substances that are present in ayahuasca were added to the cultures and compared with saline a placebo control.

    Scientists have described the results as ‘impressive’, with ayahuasca substances stimulating the transformation of stem cells into new neurons.

    Dr Riba has been studying ayahuasca for twenty years.

    -----

    The ability of psychedelics such as LSD to interact with receptors for endogenous neurotransmitters such as GABA, serotonin and glutamate is significant. LSD and other psychedelics can modulate activity in the Default Mode Network. This is a distinct network of brain regions providing the neurologic basis for “self.” Abnormal function in this network may be responsible for disorders such as autism, Alzheimer’s, PTSD, chronic pain and certain depressive disorders. In addition to providing possible mechanisms explaining microdosing’s clinical actions in regulating mood, these findings point to important research possibilities.

    -Dr. Bruce Heischober

    -----

    Ergoloid mesylates, trade name Hydergine, is a mixture of the methanesulfonate salts of three dihydrogenated ergot alkaloids. It was developed by Albert Hofmann for Sandoz. Hydergine has been used to treat dementia and age-related cognitive impairment (such as Alzheimer disease). It stimulates dopaminergic and serotonergic receptors and blocks alpha-adrenoreceptors.

    The drug works within the central nervous system to reduce the vascular tone of blood vessels supplying the brain. Consequently, the cerebrovascular is relaxed leading to an increase in the amount of oxygen that is delivered to the neurons. Increased oxygen in the brain is thought to increase neural metabolism hence function.

    Hydergine, an extract of a fungus that grows on rye, was the first drug believed to show some promise in treating Alzheimer's. A year after UC San Diego neurologist Robert Katzman wrote his editorial calling for an increase in research, the FDA approved its use in Alzheimer's patients sixty and older in 1977.

    Although it was originally created to treat hypertension, because it dilates blood vessels in the brain, it wasn't very effective at lowering blood pressure. However, some patients reported that it did improve their memory and mood, which led to its use as a treatment for dementia.

    -Niki Kapsambelis

    -----

    Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system – controlling neurotransmission, muscle/motor activity, memory and coordination. This gives probable cause to the theory that ayahuasca could be an effective treatment for neurodegenerative diseases such as ALS, Alzheimer’s, and Parkinson’s disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occuring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

    According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. There is also a growing interest in exploring the cell regenerative properties of these plants within the spinal chord injury support communities. Should people with this background eventually try and find the results of this treatment useful, medical science would be bound to take note. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

    Ayahuasca could effectively be used in treatment of ALS and other motor neuron diseases based on the fact that studies suggest uniquely antioxidative effects that seem to protect brain/nerve cells, targeting motor neurons through a unique biochemical transport system, and that it and other molecularly similar substances, also naturally occurring, stimulate neurogenesis – the development of new brain/nerve cells, and the communicative capacity between these. In studies it has been found to reduce symptoms in Parkinson’s patients – all neurodegenerative diseases share common ground, thus making it likely that something that improves a given neurological condition could also be beneficial to other conditions nearly related. Also based on credible personal accounts from people having used ayahuasca for symptom relief from their multiple sclerosis (once again – the common ground of neurodegenerative diseases), documented in books about ayahuasca, and from descriptions of early stage minor improvement by those with various types of ALS now participating in the treatment project, already having used this medicine for a period of time. Studies also indicate ability to normalize metabolism in mitochondria, crucial to motor neuron survival, and to regulate and decrease levels of excitotoxicity in the central nervous system.

    -Daniel Gustafsson
    Last edited by mr peabody; 27-08-2018 at 05:42.
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    Psychedelics and MS


    I was recently introduced to an alternative health care clinic in Mexico. I was shocked to find out they've treated over 750 patients suffering from MS using ibogaine!

    I spoke with a 43 year old women who takes a flood dose of ibogaine immediately after feeling the onset of an exacerbation. She says it stops her relapses dead in their tracks,
    and she's taken ibogaine at least once a year for the last 22 years.

    Another man claims to have thrown his wheel chair in the garbage after his first time using 5-MEO-DMT. He says the psychedelic trip taught him a new way to use his legs.

    Again.. 750+ patients have used this, just in this one clinic in Mexico.

    The clinic's chief of staff says he's used COCKTAILS of several different psychedelic medicines for treatment of not just multiple sclerosis, but on a myriad of different neurological
    diseases with great results. They regularly use - ibogaine, DMT, ayahuasca, peyote, magic mushrooms, and occasionally LSD.

    -WarmOutToday

    http://www.thisisms.com/forum/natura...opic24133.html

    -----

    Clare Hodges, also known as Elizabeth Brice, was an English activist who advanced the medical understanding of cannabis and campaigned for its widespread benefit as a therapeutic medicine in the United Kingdom. Clare Hodges is the pseudonym that Elizabeth Brice used, Clare being her middle name and Hodges her mother's maiden name.

    She was diagnosed with multiple sclerosis (MS) at age 26 but it was nearly 10 years before she tried cannabis to alleviate the symptoms. Hodges found that cannabis greatly alleviated
    her condition. It was this that motivated her to become an avid cannabis rights campaigner.

    Consequently, Hodges founded the Alliance for Cannabis Therapeutics (ACT) in 1992 with two other patients. The ACT worked to provide advice and assistance to other MS suffers and individuals with other medical conditions which might benefit from the use of cannabis.

    Hodges took the matter to the House of Lords in 1998 where she spoke about the benefits she had found from the therapeutic use of this illicit drug. She stated "Cannabis helps my body relax. I function and move much easier. The physical effects are very clear. It is not just a vague feeling of well-being".

    Despite the backing of several members of the House of Lords, and Austin Mitchell MP, the ACT was unable to change the law in the UK with regards to the use of cannabis. Hodges later went on to join the Board of Directors of the International Association for Cannabinoid Medicines (IACM) as a patient representative.

    Nonetheless, Hodges worked with Dr William Notcutt to ensure GW Pharmaceuticals took up the issue and as a result Sativex is now available as an alternative.

    She also addressed the European Parliament in Brussels following which the law was change in Belgium.

    Due to deteriorating health as a result of her MS, Hodges handed over the articles and patient transcripts to the Wellcome Trust in 2009.

    "https://en.wikipedia.org/wiki/Clare_Hodges"

    -----

    There are numerous reports that people with multiple sclerosis (MS) have for many years been self-medicating with illegal street cannabis or more recently medicinal cannabis to alleviate the symptoms associated with MS and also amyotrophic lateral sclerosis (ALS). These anecdotal reports have been confirmed by data from animal models and more recently clinical trials on the ability of cannabinoids to alleviate limb spasticity, a common feature of progressive MS (and also ALS) and neurodegeneration. Experimental studies into the biology of the endocannabinoid system have revealed that cannabinoids have efficacy, not only in symptom relief but also as neuroprotective agents which may slow disease progression and thus delay the onset of symptoms. This review discusses what we now know about the endocannabinoid system as it relates to MS and ALS and also the therapeutic potential of cannabinoid therapeutics as disease-modifying or symptom control agents, as well as future therapeutic strategies including the potential for slowing disease progression in MS and ALS.

    https://www.ncbi.nlm.nih.gov/pubmed/26408162

    -----

    I took a small amount MDMA and I could do things I couldn’t before. For about 5 hours I could stand long enough to have a conversation without having to find a seat. I could dance for
    an entire song. It was rather amazing. I checked out the side effects and they list possible neurological impairment which I have ALL THE TIME!!

    I had [some] fears about trying [MDMA], but after 23 years of every activity in my life being hard I said f*** it! And I am glad I did. I decided life is so short and I don’t know how long I will be walking around on my own. This year I got my first wheel chair and although it is wonderful for getting around it is still a wheel chair! It is not legal and I know the person well that gets me the drug so not a lot of fear of getting crap. I have been getting the same effect every time but have only been using it for about 6-8 months two to three times a week. This stuff is amazing, I can walk up a fight of stairs, better yet I can run! Personally unless someone tells me that it is going to kill me, I am going to keep taking 5 hours vacations from this crappy disease.

    -angela351

    https://shift.ms/forums/topic/mdma-m...ay-for-5-hours

    -----

    I was diagnosed with RRMS Christmas 2013 and you wouldn't believe how difficult it has been to get the medicine that I chose to use to manage my symptoms. That is cannabis, and man, it works every time. But how much better would it be if I could get access to particular strains which will alleviate specific symptoms. So I'm rambling now, what I really wanted to say was that personally I love LSD for many purposes! Including, but not limited to, expanded, layered thinking! The torrents of creativity that fall from the mind like rain from the clouds! The glimpses beyond the veil of Maya, and just like your reasons, the way it makes me feel. Which is kinda like superman. And aside, man I've been using LSD since I was 16, and I wouldn't change it for the world! It helps one to find clarity in the chaos that we call home today! In my opinion it should not be illegal, moreover it should be an obligatory right of passage into adulthood.

    -K3el

    -----

    I too have MS, and I can tell you from personal experiences that there are times when you feel like you're at death's door. There are also times when you just can't function. That's frustrating enough if you're on disability, living with excellent caretakers, and free of responsibility. But what about those who have children? What about those who have demanding jobs and refuse to let MS take that away from them? What about those of us who are graduate students? Many of the FDA-approved medications available for treating the debilitating symptoms of MS come with dangerous side effects, sometimes far more dangerous than the side effects of illegal drugs.

    I am a neuropharmacology and cognitive neuroscience researcher. There is absolutely no definitive evidence that drug use causes MS. And there is no definitive evidence that using illegal drugs can exacerbate MS. I don't think it's a good idea for anyone to regularly use illegal drugs (except of course, marijuana, and only if you have a condition for which its efficacy has been scientifically demonstrated). But, come on! MS SUCKS. If you can get a few hours of relief from this living hell now and again, I certainly won't judge you. I think the scientific community needs to broaden their minds and think outside the box where MS treatments are concerned.

    https://ehealthforum.com/health/ille...177245_20.html

    -----

    Some evidence suggests that the neurodegeneration in Parkinson’s may be caused by the body’s own immune system losing the ability to determine between healthy and unhealthy cells, as is the case with autoimmune diseases such as Fibromyalgia, Multiple Sclerosis and others, in which much of the body’s organs and cell tissue deteriorate because of misdirected attack by the immune system.

    Although the theory is still untested, there is anecdotal evidence and a theoretical framework that suggests ibogaine may have therapeutic benefits in the treatment of Parkinson, and possibly other disorders that cause the degeneration of brain and cell tissues.

    Ibogaine therapy, especially low-dose regimens, may facilitate the expression of GDNF without the side effects of other medications or the difficulty of other avenues of administering neurotrophic factor. Anecdotal reports suggest that at least several people with Fibromyalgia, Multiple Sclerosis, and Parkinson’s who have been treated with ibogaine have seen an extended remission of symptoms.

    https://www.ibogainealliance.org/ibo...py/parkinsons/

    -----

    Endocannabinoids in Multiple Sclerosis and Amyotrophic Lateral Sclerosis

    There are numerous reports that people with multiple sclerosis (MS) have for many years been self-medicating with illegal street cannabis or more recently medicinal cannabis to alleviate the symptoms associated with MS and also amyotrophic lateral sclerosis (ALS). These anecdotal reports have been confirmed by data from animal models and more recently clinical trials on the ability of cannabinoids to alleviate limb spasticity, a common feature of progressive MS (and also ALS) and neurodegeneration. Experimental studies into the biology of the endocannabinoid system have revealed that cannabinoids have efficacy, not only in symptom relief but also as neuroprotective agents which may slow disease progression and thus delay the onset of symptoms. This review discusses what we now know about the endocannabinoid system as it relates to MS and ALS and also the therapeutic potential of cannabinoid therapeutics as disease-modifying or symptom control agents, as well as future therapeutic strategies including the potential for slowing disease progression in MS and ALS.

    https://www.ncbi.nlm.nih.gov/pubmed/26408162
    Last edited by mr peabody; 27-08-2018 at 23:15.
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    B. caapi and neurodegenerative disorders


    Volodymyr Samoylenko, Md. Mostafizur Rahman, Babu Tekwani, Lalit Tripathi, Yan-Hong Wang, Shabana Khan, Ikhlas Khan, Loren Miller, Vaishali C. Joshi, Ilias Muhammad

    Parkinson’s disease is a neurological disorder effecting the elderly. Currently there is no definitive treatment or cure for this disease. Therefore, in this study the composition and constituents of B. caapi for monoamine oxidases inhibitory and antioxidant activities were assessed, relevant to the prevention of neurological disorders, including Parkinsonism.

    Banisteriopsis is a tropical South American genus with 92 species distributed mainly in Brazil, Bolivia, Colombia, Ecuador, and Peru. B. caapi is an ingredient of the popular sacred and psychoactive drinks Ayahuasca, also known as Caapi, Pinde, Natema or Yaje, which is widely used for prophecy, divination, and as a sacrament in the northern part of South America. However, to the best of our knowledge, no traditional drink prepared only from B. caapi has been consumed for such uses. Earlier chemical investigation have reported the presence of B-carboline alkaloids (B-CA) harmine, harmaline and tetrahydroharmine (THH) as the principal MAO inhibitors, together with other B-CA’s, from B. caapi. In addition, two pyrrolidines, shihunine and (S)-(+)-dihydroshihunine, and terpenoids were also reported. The alkaloid content of B. caapi was determined previously by GC/MS, LC/MS, and HPLC, suggesting the content of harmine is highest among B-CA’s, followed by THH and harmaline.

    Parkinson’s disease (PD) is caused by a loss of neurons from substantia nigra of the brain. Once damaged, these neurons stop producing dopamine and compromise the brain's ability to control movement. It is not known what damages certain neurons in PD patients. One reason is that free radicals/ toxic particles normally deactivated in the body are responsible, which can be controlled by antioxidants as adjuvant with dopamine agonist or MAO inhibitors. The usefulness of B. caapi was established for alleviating symptoms of PD, which contains MAO inhibitor harmine as active constituent used in PD treatment. A double-blind, randomized placebo-controlled trial of B. caapi, using a single dose, revealed a significant improvement in motor function of PD patients. Tests for MAO inhibition using liver homogenate showed that B. caapi stem extract and harmine showed a concentration-dependent inhibition of MAO-A, and an increase in release of dopamine from rat striatal slices.

    During the course of chemical and biological standardization of B. caapi, an extract of B. caapi cultivar Da Vine, collected in Oahu, Hawaii, demonstrated potent in vitro MAO-A inhibitory and antioxidant activities. This led to the bioassay guided isolation of two new B-carboline alkaloidal glycosides, banistenoside A, a new tetrahydronorharmine, four known B-carbolines harmol , using regular and RP silica gel chromatography. In this paper, we report the isolation, characterization and bioactivities of isolated compounds, and HPLC analysis of B. caapi cultivar Da Vine and two regular/ commercial samples of B. caapi.

    Conclusion

    Inhibition of MAO-B activity by B-carbolines harmine and harmaline, in addition to potent MAO-A inhibition responsible for antidepressant activity, provide protection against neurodegeneration, and has a potential therapeutic value for the treatment of Parkinson's diseases. In addition, oxidative stress induced by ROS has been strongly associated with the pathogenesis of neurodegenerative disorders, including Parkinson’s and Alzheimer’s. Therefore, the presence of two potent antioxidants, epicatechin and procyanidin, have significant added value for the protection of neuronal cells damage by oxidative free radicals. Their selective MAO-B inhibitory activity benefits them even more. Collectively, these results give additional basis to the existing claim of B. caapi stem extract for the treatment of Parkinsonism, including other neurodegenerative disorders.

    https://www.ncbi.nlm.nih.gov/pmc/art...ihms156585.pdf
    Last edited by mr peabody; 09-09-2018 at 23:59.
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    Ibogaine and Parkinson’s Disease

    Parkinson’s Disease is classified as a neurodegenerative disorder, one characterized by the progressive atrophy of the central and peripheral nervous system. However, some evidence suggests that the neurodegeneration in Parkinson’s subjects may be caused by the body’s own immune system losing the ability to determine between healthy and unhealthy cells, as is the case with autoimmune diseases such as Fibromyalgia, Multiple Sclerosis and others, in which much of the body’s organs and cell tissue deteriorate because of misdirected attack by the immune system.

    Although the theory is still untested, there is anecdotal evidence and a theoretical framework that suggests ibogaine may have therapeutic benefits in the treatment of Parkinson, and possibly other disorders that cause the degeneration of brain and cell tissues.

    The theoretical case is based on the fact that both ibogaine and its metabolite noribogaine have been shown to lead to an increase in levels of glial cell line-derived neurotrophic factor (GDNF) in the brain. It has also been shown to have neuroprotective qualities promoting the survival of both dopaminergic and motor neurons.

    In other research, neutrophic factors, specifically GDNF, have been shown to cause sprouting of dopaminergic fibers, with a resulting improvement of clinical symptoms of Parkinson’s in experimental animal models and humans. However, there is little research available using neutrophic factors in the treatment of other neurodegenerative disorders, particularly because administration is usually limited by toxicity or poor bioavailability. Various other methods of administration such as direct brain infusion of GDNF and gene therapy that promotes the expression of neurotrophic factors have been explored.

    The direct brain infusion of GDNF into the brains of five rats induced with Parkinson’s disease showed a 39% improvement in off-medication motor sub-score of the Unite Parkinson’s Disease Rating Scale (UPDRS), and a 61% improvement in the activities of daily living sub score. After one year, no side effects from the treatment were observed.

    In addition to Parkinson’s, one study using gene therapy that promotes the expression of neurotrophic factors, showed a 50% increase in life span, reduced loss of motor axons and improved neuromuscular function in animal models representing Motor Neuron Diseases. The study suggested further research into neurotrophic factor as a treatment for MND.

    Parkinson’s and similar diseases have no known cure, and these conditions often require management with drugs that have considerable side effects, causing a very poor quality of life for terminal stage sufferers of these diseases.

    Ibogaine therapy, especially low-dose regimens, may facilitate the expression of GDNF without the side effects of other medications or the difficulty of other avenues of administering neurotrophic factor. Anecdotal reports suggest that at least several people with Fibromyalgia, Multiple Sclerosis, and Parkinson’s who have been treated with ibogaine have seen an extended remission of symptoms.

    Although there is little clinical research into this particular application, one of the first studies to assess ibogaine efficacy, specifically in the treatment of Parkinson disease in animal models, is currently underway at Columbia University.

    https://www.ibogainealliance.org/ibo...py/parkinsons/
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    Voacanga Africana found to protect brain cells from Alzheimer’s, Parkinson’s and the neurodegeneration

    Salk scientists find that a plant used for centuries by healers of Sao Tome e Principe holds lessons for modern medicine.

    For hundreds of years, healers in Sao Tome e Principe—an island off the western coast of Africa—have prescribed cata-manginga leaves and bark to their patients. These pickings from the Voacanga africana tree are said to decrease inflammation and ease the symptoms of mental disorders.

    Now, scientists at the Salk Institute for Biological Studies have discovered that the power of the plant isn’t just folklore: a compound isolated from Voacanga africana protects cells from altered molecular pathways linked to Alzheimer’s disease, Parkinson’s disease and the neurodegeneration that often follows a stroke.

    “What this provides us with is a source of potential new drug targets,” says senior author Pamela Maher, a senior staff scientist in Salk’s Cellular Neurobiology Laboratory. The results were published this week in the Journal of Ethnopharmacology.

    Antonio Currais, a research associate, was visiting family in his native Portugal when he crossed paths with Maria do Ceu Madureira, an ethnopharmacology researcher at the University of Coimbra. For the past twenty years, Madureira has been surveying the use of herbal medicine on the island. Currais and Maher had developed a series of tests to screen compounds for their potential use in treating neurodegenerative disorders and Currais saw the perfect chance to put the assay to the test. He began a collaboration with Madureira’s team.

    “There was already a lot of descriptive information of particular plants that have potential effects on the nervous system,” Currais says. “We took that further to quantitatively document the real neuroprotective action of the compounds in these plants.”

    Currais and Maher began studying seven different extracts collected from five species of plants in Sao Tome e Principe. Three of the five had been reported by local healers to have effects on the nervous system and two were used as controls. The Salk research team put each sample through different assays—all conducted in living human and mouse cells—designed to test their potential impact against neurodegeneration.

    One assay tested the ability of the plant extracts to protect cells against oxidative stress, a byproduct of metabolism that can cause DNA damage and has been linked to age-related neurodegeneration. Another tested anti-inflammatory properties of the compounds. A third test measured whether the samples could block the build-up of beta-amyloid peptides in neurons, which has been linked to Alzheimer’s disease.

    “I was surprised at how potent they were,” says Maher. “I thought maybe we’d see a little bit of activity in some of the assays and then have to separate out individual components to see a more profound effect.” But one sample in particular—Voacanga africana—performed exceptionally on all assays, even in its most dilute form.

    When Currais and Maher isolated different components of the plant, they found that the anti-inflammatory and neuroprotective effects of the plant were mostly due to one molecule, called voacamine. The compound hasn’t yet been tested in animal models but its performance in the assays suggests that it may have pharmaceutical potential for treating Alzheimer’s, Parkinson’s or stroke.

    “There are still a lot of potential sources of drugs in plants that are native to countries around the world and most of them haven’t been tested to any extent,” says Maher. “You can’t test everything, so the best way to approach plant research for drugs is to use the knowledge that’s been around for thousands of years to help you pick and choose what to study with modern techniques. That way you’re not just shooting in the dark.”

    Maher, Currais and Madureira are planning more follow up studies on voacamaine and also hope to apply their assays to more plants of interest.

    Other researchers on the study were Chandramouli Chiruta and Marie Goujon-Svrzic of the Salk Institute for Biological Studies; Gustavo Costa, Tania Santos, Maria Teresa Batista, Jorge Paiva, and Maria do Ceu Madureira of the University of Coimbra.

    Both the Portuguese and American researchers worked in full partnership with local institutions, traditional healers and communities in order to respectfully conduct research in the area of indigenous knowledge, assuring the intellectual property rights and the sharing of benefits that may arise as a result of the study of these local medicinal plants.

    https://www.salk.edu/news-release/analysis-of-african-plant-reveals-possible-treatment-for-aging-brain/



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    Multiple sclerosis patient calls medical cannabis trial 'a miracle'

    The Montreal study, now in Phase 2, will try to determine if cannabis can be used as a less-dangerous substitute for opiate-based painkillers

    By the time she decided to try cannabis pills, Joanne Fiorito was in dire straits.

    Fiorito could barely lift her feet when she walked and sometimes used an electric wheelchair to get around. Occasionally she’d wake up in the middle of the night, riddled with pain from her tensing muscles.

    The 61 year old has lived with multiple sclerosis for most of her life and, despite her use of heavy doses of painkillers and muscle relaxants, the symptoms were only getting worse.

    Last winter her neurologist suggested she take a chance and participate in a clinical trial on medical cannabis.

    “I had nothing to lose,” Fiorito said. “The cannabis was like a miracle. Within three days my legs were less stiff, they didn’t feel as heavy."

    “At physiotherapy, they time me for six minutes to see how far I can walk. In October I did 89 meters. This week, it was 251 meters. I’m not joking when I say it’s like a miracle.”

    Fiorito is one of 70 Montreal-area patients participating in a clinical trial for medicinal cannabis capsules. The study, which entered its second phase last April, will try to determine if cannabis can be used as a less-dangerous substitute for opiate-based painkillers.

    If it’s successful — and the capsules are approved by Health Canada’s Office of Controlled Substances — cannabis could be sold in pharmacies and covered by provincial health insurance.

    The study is a partnership between Montreal’s Sante Cannabis clinic and the Ottawa-based Tetra Pharma Bio. It mainly focuses on people with chronic pain and cancer pain who have never tried medical cannabis before.

    “This is about giving people like Joanne (Fiorito) a chance to access medicine that is quality-controlled and affordable,” said Erin Prosk, the co-founder of Sante Cannabis. “The medical cannabis system we have now is not enough. It’s a Band-Aid, it’s a temporary solution.”

    Canada’s medical cannabis system has existed under its current form for only four years. Each of the roughly 250,000 patients with prescriptions can order weed online from one of 115 producers licensed by the federal government.

    But unlike with the vast majority of medicines, cannabis isn’t covered by health insurance. In fact, patients have to pay sales tax on it.

    Adding to patients’ financial burden, the Cannabis Act — which will legalize the sale of recreational pot starting Oct. 17 — actually adds a 10-per-cent excise tax for medical cannabis users.

    “The Cannabis Act is causing collateral damage in our world,” said Prosk. “Some people think that with legalization, patients can just go to the store and buy cannabis. But the people who use medical cannabis need a specific pharmaceutical-grade product to treat specific symptoms.”

    In the study, patients are either given a placebo or capsules that contain a high concentration of two cannabinoids; tetrahydrocannabinol (THC) — which has a psychoactive and pain-numbing affect — and cannabidiol (CBD) — which can be used as an anti-inflammatory, a muscle relaxant and to treat epilepsy.

    Thus far, only one of the 70 patients recruited has reported experiencing severe side effects from the drug.

    “Except for that one case, where the patient wasn’t able to tolerate it, everyone has been tolerating it quite well,” said Dr. Antonio Vigano, who is leading the trial. “I was surprised at how tolerable it was, at how safe it was. That’s the main concern, when you do these trials, is to make sure the product is safe.”

    For the first phase of the study, patients were given a low dose of the CBD and THC pills so their bodies could adjust to the drug. Vigano says that, for some, it was enough to notice a difference in pain management.

    Gradually, the doctors increase patient doses until they reach a point where the medicine takes affect.

    “Our theory was that starting low and increasing slowly is really important to increase that tolerability,” said Vigano, an associate professor of oncology at McGill University. “That’s what we’re seeing in practice. It’s encouraging.”

    Prosk has been on the forefront of the fight to increase access to medical marijuana for years and says cannabis research is still in its infancy.

    As her clinic’s study is underway, the University of British Columbia is leading a trial on the use of medicinal pot for people who struggle with post-traumatic stress disorder.

    “Considering where we were four years ago — just getting the system to license cannabis producers off the ground — it’s unreal how far we’ve come,” said Prosk. “We’re global leaders in cannabis research and we’re getting interest from international companies. Countries like Germany and Australia are looking to Canada for leadership."

    “There’s huge potential here and the right people are finally taking notice.”

    Sante Cannabis and Tetra Pharma Bio still have reams of data to study and there are many more roadblocks on the way to having their product approved. But Prosk says the future looks promising.

    For Fiorito, the clinical trial has been a lifesaver.

    “I used to wake up in the night, screaming in pain,” she said. “I’m not waking up at night anymore. I’d say 80 per cent of the pain is gone."

    “Last year, I felt like the wheelchair was pretty close to my ass if I may say so. I felt like, ‘Oh she’s really gaining on me, I’ll be stuck in that wheelchair for the rest of my life.’ Last week, my neurologist said he hadn’t seen me move like that in years. It’s a miracle.”

    https://montrealgazette.com/news/mul...rial-a-miracle
    Last edited by mr peabody; 20-09-2018 at 10:03.
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