Below is a brief clip of an interview with Compounding Pharmacist Randy Mentzer who discusses Mucuna is a “medicine” and also highlights the potential value of taking NADH as a supplement.
Below is a brief interview clip with Seven Fowkes who discusses the potential value of NADH for addressing tremors and other symptoms. He is a researcher, not a medical doctor, so be sure and check with your doctor before taking action on any of his recommendations.
We present a 48-year-old woman with Parkinson’s disease in whom carbidopa was added to Mucuna pruriens, resulting in marked motor improvement (documented on video and using MDS-UPDRS motor scores). This case report shows that adding a dopa-decarboxylase inhibitor (DDCI) to Mucuna pruriens coud fit well in a personalized approach for patients who are reluctant to start levodopa. Meanwhile, larger trials with a longer follow-up are needed to establish the true effects and tolerability of Mucuna pruriens plus a DDCI.
Parkinson’s disease (PD) as the second leading neurodegenerative disease, imposes a heavy burden among individuals as well as economies worldwide. The main characteristics of PD is a progressive loss of dopaminergic neurons resulting in the loss of motor function, the occurrence of non-motor symptoms, and cognitive decline. Similar to many other chronic diseases, complementary and alternative therapies (CAT) are very popular for the treatment of this disease. This review evaluates six plants, three each from European and Asian traditional medicinal systems: (1) Atropa belladonna, (2) Hyoscyamus niger, (3) Lepidium meyenii, (4) Aspargus racemosus, (5) Mucunapruriens L., and (6) Gingko biloba. Atropa belladonna, and Hyoscyamus niger in particular, are better known for their poisonous and narcotic effects than as potentially effective plants for the treatment of neurodegenerative diseases. Ginkgo biloba is one of the most widely cultured plants in Traditional Chinese Medicine with high antioxidant potential which contributes to its neuroprotective/ anti-apoptotic activity. The bioactive compounds, anti-neurodegenerative effects and other neuroprotective effects of all six plants are discussed herein.
Parkinson’s disease (PD) is a multifactorial disorder of the nervous system in which there is a progressive loss of dopaminergic neurons. There is a disturbance in the movement in PD and these include resting tremors, rigidity, bradykinesia or akinesia, disturbance, posture and freezing (motor block). The substantia nigra and other parts of the brain are commonly affected. The disorder could be related to oxidative stress and there is an important role of reactive oxygen species (ROS). A number of herbal products contain active components which are known to possess antioxidant action. Hence, the potential role of herbal products in treating PD cannot be undermined. In the present narrative review, the main aim is to discuss the pathogenesis of PD, define the role of different potential herbal extracts on its pathogenesis which may form the basis of treatment. We also discuss in detail the active chemical compounds present each herb which are effective in the treatment of PD. These herbs include Baicalei, Erythrina velutin, Resveratrol, Peganum Harmal, Curcuma longa (Zingiberaceae), Carthamus tinctorius L. (Safflower), Pueraria lobate, Juglandis Semen (Walnut), Tianma Gouteng Yin (TGY), Lycium barbarum L fruit, Mucuna pruriens (Velvet bean), Chunghyuldan (CHD), Paeoniae Alba Radix. The present review may be beneficial for designing future drugs for effective treatment of PD.
Thousands of individuals with Parkinson’s disease (PD) in low-income countries have limited access to marketed levodopa preparations. Mucuna pruriens (MP), a levodopa-containing leguminous plant growing in tropical areas, may be a sustainable alternative therapy for indigent patients. Single-dose intake of MP proved noninferior to marketed levodopa preparations.
Fourteen PD patients with motor fluctuations and dyskinesias received MP powder (obtained from roasted seeds) and marketed levodopa/carbidopa (LD/CD) in a randomized order and crossover design over a 16-week period. Efficacy measures were changes in quality of life, motor and non-motor symptoms, and time with good mobility without troublesome dyskinesias. Safety measures included tolerability, frequency of adverse events, changes in laboratory indices and electrocardiogram.
Daily intake of MP was associated with a variable clinical response, especially in terms of tolerability. Seven patients (50%) discontinued MP prematurely due to either gastrointestinal side-effects (n = 4) or progressive worsening of motor performance (n = 3), while nobody discontinued during the LD/CD phase. In those who tolerated MP, clinical response to MP was similar to LD/CD on all efficacy outcome measures. Patients who dropped out entered a study extension using MP supernatant water (median[IQR], 16 [7-20] weeks), which was well tolerated.
The overall benefit provided by MP on the clinical outcome was limited by tolerability issues, as one could expect by the relatively rapid switch from LD/CD to levodopa alone in advanced PD. Larger parallel-group studies are needed to identify appropriate MP formulation (e.g. supernatant water), titration scheme and maintenance dose to minimize side-effects in the long-term. CLINICAL TRIALS.
To investigate whether Mucuna pruriens (MP), a levodopa-containing leguminous plant growing in all tropical areas worldwide, may be used as alternative source of levodopa for indigent individuals with Parkinson disease (PD) who cannot afford long-term therapy with marketed levodopa preparations.
We investigated efficacy and safety of single-dose intake of MP powder from roasted seeds obtained without any pharmacologic processing. Eighteen patients with advanced PD received the following treatments, whose sequence was randomized: (1) dispersible levodopa at 3.5 mg/kg combined with the dopa-decarboxylase inhibitor benserazide (LD+DDCI; the reference treatment); (2) high-dose MP (MP-Hd; 17.5 mg/kg); (3) low-dose MP (MP-Ld; 12.5 mg/kg); (4) pharmaceutical preparation of LD without DDCI (LD-DDCI; 17.5 mg/kg); (5) MP plus benserazide (MP+DDCI; 3.5 mg/kg); (6) placebo. Efficacy outcomes were the change in motor response at 90 and 180 minutes and the duration of on state. Safety measures included any adverse event (AE), changes in blood pressure and heart rate, and the severity of dyskinesias.
When compared to LD+DDCI, MP-Ld showed similar motor response with fewer dyskinesias and AEs, while MP-Hd induced greater motor improvement at 90 and 180 minutes, longer ON duration, and fewer dyskinesias. MP-Hd induced less AEs than LD+DDCI and LD-DDCI. No differences in cardiovascular response were recorded.
Single-dose MP intake met all noninferiority efficacy and safety outcome measures in comparison to dispersible levodopa/benserazide. Clinical effects of high-dose MP were similar to levodopa alone at the same dose, with a more favorable tolerability profile.
Here is the scoop on Mucuna Pruriens for Parkinson’s and a detailed description of Michael’s experience with it. Some people use it as an adjunct to medication like Sinemet in order to reduce the amount of medication, and then there are people like Michael who either want a more natural approach or have too many side effects with sinemet that use mucuna exclusively. Michael was never able to tolerate any of the medications and all natural strategies had failed up until what I describe below.
Michael had tried mucuna pruriens years ago – we bought some on Amazon.
What we didn’t realize was that Michael needed a much higher extract of mucuna.
The extract you can get from mucuna is L Dopa. The stuff we bought on amazon was only 15% L Dopa. Eventually we befriended a woman in the Netherlands that was getting great results with a 98% L Dopa extract of Mucuna that she was buying from someone in Australia (who got his supply from China). The 2 main source countries are India and China.
At the point that we learned this information, Michael was in very dire straits.
This was the winter of 2016. He was 97% dependent- he needed help dressing, eating, turning over in bed, covering himself with the sheet, bathing and even wiping his butt. He was considered Stage IV Tremor Dominant Parkinson’s by his neurologist. He could walk a little, falling forward and grabbing the walls for support. He could barely speak at an audible level and his diction was terrible.
He would have to whisper in my ear and I would decipher it. He also had constant tremendous pain due to muscle stiffening in his arms and legs. I had started interviewing 24/7 care because it was quickly becoming more than me and our friend who lived with us could handle.
I bought some of the 98% L Dopa and within 3 weeks of starting it Michael could go outside and walk. All pain left and all neurological symptoms improved. By 6 weeks he was 100% independent and he remained 100% independent until his death in July 2018 from a flu that progressed quickly into double pneumonia. His body had desperately needed L Dopa and this high potency mucuna gave it to him. He still had some tremor and low energy but everything was better. Even skin problems cleared up.
Eventually I found a source in the US that sells 99% extract and actually charges less than anyone else. Michael started with a dose of 300 mg just to see if he could tolerate it. He was always very sensitive. The effects initially lasted 3-4 hrs. This was January 2017.
Slowly we raised the dose to 700 mg 4-5x/day and eventually 850 mg 5x/day. Over time he did require more mucuna as well as more often – every 2-3 hours. He and got up to 1200 mg 5-6x/day this past year. Most people using mucuna don’t get the horrible side effect of dyskinesias (uncontrollable movements) that many people get from the drugs. At about 1200 mg mucuna, Michael did have some dyskinesia and he cut back to 1100 mg which reduced them. I know a woman that manages with 650 mg 4x/day for many years and a woman who uses a large dose of 5000 mg 3x/day for many years. Neither experience dyskinesias.
Everyone is different in terms of dose. You just start low and experiment.
I’ve also wondered about it being even more beneficial to add in some non-L-Dopa extract version of mucuna since the entire plant has many desirable healing properties. Places like Banyan Botanicals carry good quality organic whole plant mucuna if you want to try that along with the 98-99% L Dopa extract of Mucuna.
As a reference point – at Michael’s high dose of 1100-1200 mg 6x/day, a kg that costs $185 would last 2-3 months.
Many people who take Parkinson’s medications have to contend with nausea from the drug. It’s the L Dopa/ levodopa causing nausea. Michael did get nausea when he started on mucuna, but eventually we discovered that taking about 1000-2000mg of straight Vitamin C from ascorbic acid at the same time as the mucuna worked perfectly and he never had nausea again.
This is also working to prevent nausea for some friends who are also taking mucuna. It can’t be buffered C- it needs to be ascorbic acid, which thankfully is very inexpensive. (You can get ascorbic acid at a great price at the same place that sells the mucuna).
Candied ginger can also work for nausea but then you’re also getting a lot of sugar so we were really happy to discover the Vit C worked. Mucuna extract is a tasteless white to off-white powder. I mixed it along with the Vit C into some room temp herbal tea sweetened with honey (preferably raw honey that has more healing properties). Honey always helped Michael swallow.
Here is the US based company I bought mucuna from at a good price. We’ve also referred a number of people to this source and the mucuna is helping them, too.
(I’m not an affiliate and I get no financial benefit if you buy here).
https://www.nutrivitashop.com/l-dopa-100-pure-levodopa-mucuna-pruriens-dopamine/
You’ll also need a good mg scale so you can be exact in your dose. Here’s a link to a scale that has worked well for me.
Scale: there are similar ones on Amazon that have even better reviews, but this one has always worked for me and has not needed recalibration even after 18 months of frequent use. https://amzn.to/2BbNr0l
One more thing to mention that may help your readers.There is a Chinese Herbal Formula that has helped many people with tremors. A friend of Michael’s has used it for many months with great benefit. Michael had barely started it when he died so I can’t comment on his experience.
Here’s one place that sells it. If you email me I can tell you more about dosage. This place seems to have the best price and you can get 10% off using code: Wholesale https://www.maxnature.com/plumflower-tian-ma-gou-teng-san.html
Please feel free to post my email address of dovidagoodman@gmail.com I’m happy to answer questions about anything I’ve written here.
Warmest regards,
Dovida
Cannabidiol (CBD) is one of at least 85 active cannabinoids. Scientific studies are reporting a wide variety of positive health benefits. CBD has been found to be helpful to the endocannabinoid system. Many scientific discoveries link poor health to endocannabinoid deficiencies.
Studies have found positive effects for the use of CBD on anxiety, stress and PTSD. You can find these studies listed at : pubmed.com (the US government’s index of scientific studies). Search and the terms “CBD and anxiety.”
Below are listed three abstracts from recent studies that have studied the effects of CBD on subjects who currently experience Parkinson’s symptoms.
J Psychopharmacol. 2014 Nov;28(11):1088-98. doi: 10.1177/0269881114550355. Epub 2014 Sep 18.
Chagas MH, Zuardi AW, Tumas V, Pena-Pereira MA, Sobreira ET, Bergamaschi MM, dos Santos AC, Teixeira AL, Hallak JE, Crippa JA.
Twenty one (21) subjects were assigned to three groups of seven subjects each who were treated with placebo, cannabidiol (CBD) 75 mg/day or CBD 300 mg/day. One week before the trial and in the last week of treatment subjects were evaluated with respect to motor and general symptoms score (UPDRS) and well-being and quality of life (PDQ-39).
No statistically significant differences were found in UPDRS scores. Despite the very small sample size, groups treated with placebo and CBD 300 mg/day had significantly different mean total scores in the PDQ-39 (p = 0.05). Significance is very much a factor of sample size, so this result is striking in itself. Findings suggest a possible effect of CBD in improving quality of life measures in PD patients with no psychiatric comorbidities.
Clin Neuropharmacol. 2014 Mar-Apr;37(2):41-4. doi: 10.1097/WNF.0000000000000016.
Inhaling whole-plant cannabis provides symptomatic relief in patients with Parkinson’s disease (PD), according to a scientific article published in the March/April edition of the journal Clinical Neuropharmacology. Investigators at Tel Aviv University, Department of Neurology evaluated Parkinson’s disease symptoms in 22 patients at baseline and 30-minutes after inhaling cannabis.
Researchers reported that inhaled cannabis was associated with “significant improvement after treatment in tremor, rigidity, and bradykinsea (slowness of movement). There was also significant improvement of sleep and pain scores. No significant adverse effects of the drug were observed.”
The researchers concluded that their study is “the first to report an amelioration of both motor and non–motor symptoms in patients with PD treated with cannabis. The study opens new venues for treatment strategies in PD especially in patients refractory to current medications.”
J Clin Pharm Ther. 2014 Oct;39(5):564-6. doi: 10.1111/jcpt.12179. Epub 2014 May 21
Chagas MH, Eckeli AL, Zuardi AW, Pena-Pereira MA, Sobreira-Neto MA, Sobreira ET, Camilo MR, Bergamaschi MM, Schenck CH, Hallak JE, Tumas V, Crippa JA.
The administration of cannabidiol (CBD) was found to control sleep disorders in patients who currently experience the symptoms of Parkinson’s disease as reported in the Journal of Clinical Pharmacy and Therapeutics. An international team of researchers from the University of Sao Paulo in Brazil and the University of Minnesota Medical School USA evaluated the ingestion of CBD by four Parkinson’s disease patients with REM sleep behavior disorder (RBD). This condition is characterized by nightmares and active behavior during dreaming.
Cannabidiol treatment reduced symptoms in each of the four subjects. Symptoms returned with the same frequency and intensity following subjects’ discontinuation of the cannabinoid.
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease, characterized by the loss of dopaminergic neurons from substantia nigra pars compacta of basal ganglia caused due to gene mutation, misfolded protein aggregation, reactive oxygen species generation and inflammatory stress. Degeneration of dopaminergic neurons results in muscle stiffness, uncoordinated body movements, sleep disturbance, fatigue, amnesia and impaired voice. Currently, levodopa (L-DOPA) administration is the most widely used therapy for PD. But prolonged administration of L-DOPA is associated with the symptoms of dyskinesia. However, emerging evidences suggest the role of cannabinoid receptors (CBRs) in curtailing the progression of PD by activating neuroprotective pathways. Hence, cannabinoid therapy could be a promising alternative to combat PD in future. In the present review we have discussed the potential role of CBRs in attenuating the key mechanisms of PD and how the existing research gaps needs to be bridged in order to understand the molecular mechanism of CBRs in detail.
Neurological therapeutics have been hampered by its inability to advance beyond symptomatic treatment of neurodegenerative disorders into the realm of actual palliation, arrest or reversal of the attendant pathological processes. While cannabis-based medicines have demonstrated safety, efficacy and consistency sufficient for regulatory approval in spasticity in multiple sclerosis (MS), and in Dravet and Lennox-Gastaut Syndromes (LGS), many therapeutic challenges remain. This review will examine the intriguing promise that recent discoveries regarding cannabis-based medicines offer to neurological therapeutics by incorporating the neutral phytocannabinoids tetrahydrocannabinol (THC), cannabidiol (CBD), their acidic precursors, tetrahydrocannabinolic acid (THCA) and cannabidiolic acid (CBDA), and cannabis terpenoids in the putative treatment of five syndromes, currently labeled recalcitrant to therapeutic success, and wherein improved pharmacological intervention is required: intractable epilepsy, brain tumors, Parkinson disease (PD), Alzheimer disease (AD) and traumatic brain injury (TBI)/chronic traumatic encephalopathy (CTE). Current basic science and clinical investigations support the safety and efficacy of such interventions in treatment of these currently intractable conditions, that in some cases share pathological processes, and the plausibility of interventions that harness endocannabinoid mechanisms, whether mediated via direct activity on CB1 and CB2 (tetrahydrocannabinol, THC, caryophyllene), peroxisome proliferator-activated receptor-gamma (PPARγ; THCA), 5-HT1A (CBD, CBDA) or even nutritional approaches utilizing prebiotics and probiotics. The inherent polypharmaceutical properties of cannabis botanicals offer distinct advantages over the current single-target pharmaceutical model and portend to revolutionize neurological treatment into a new reality of effective interventional and even preventative treatment.
Cannabinoid receptors, endocannabinoids and the enzymes responsible for their biosynthesis and degradation constitute the endocannabinoid system. In recent decades, the endocannabinoid system has attracted considerable interest as a potential therapeutic target in numerous pathological conditions. Its involvement in several physiological processes is well known, such as in energy balance, appetite stimulation, blood pressure, pain modulation, embryogenesis, nausea and vomiting control, memory, learning and immune response, among others, as well as in pathological conditions where it exerts a protective role in the development of certain disorders. As a result, it has been reported that changes in endocannabinoid levels may be related to neurological diseases such as Parkinson’s disease, Huntington’s disease, Alzheimer’s disease and multiple sclerosis, as well as anorexia and irritable bowel syndrome. Alterations in the endocannabinoid system have also been associated with cancer, affecting the growth, migration and invasion of some tumours. Cannabinoids have been tested in several cancer types, including brain, breast and prostate cancers. Cannabinoids have shown promise as analgesics for the treatment of both inflammatory and neuropathic pain. There is also evidence for a role of the endocannabinoid system in the control of emotional states, and cannabinoids could prove useful in decreasing and palliating post-traumatic stress disorder symptoms and anxiolytic disorders. The role of the endocannabinoid system in addictions has also been examined, and cannabinoids have been postulated as alternative and co-adjuvant treatments in some abuse syndromes, mainly in ethanol and opioid abuses. The expression of the endocannabinoid system in the eye suggests that it could be a potential therapeutic target for eye diseases. Considering the importance of the endocannabinoid system and the therapeutic potential of cannabinoids in this vast number of medical conditions, several clinical studies with cannabinoid-based medications are ongoing. In addition, some cannabinoid-based medications have already been approved in various countries, including nabilone and dronabinol capsules for the treatment of nausea and vomiting associated with chemotherapy, dronabinol capsules for anorexia, an oral solution of dronabinol for both vomiting associated with chemotherapy and anorexia, a Δ9-tetrahydrocannabinol/cannabidiol oromucosal spray for pain related to cancer and for spasticity and pain associated with multiple sclerosis, and an oral solution of cannabidiol for Dravet and Lennox-Gastaut syndromes. Here, we review the available efficacy, safety and tolerability data for cannabinoids in a range of medical conditions.
Cannabis sativa active compounds are extensively studied for their therapeutic effects, beyond the well-known psychotropic activity. C. Sativais used to treat different medical indications, such as multiple sclerosis, spasticity, epilepsy, ulcerative colitis and pain. Simultaneously, basic research is discovering new constituents of cannabis-derived compounds and their receptors capable of neuroprotection and neuronal activity modulation. The function of the various phytochemicals in different therapeutic processes is not fully understood, but their significant role is starting to emerge and be appreciated. In this review, we will consider the structure-activity relationship (SAR) of cannabinoidcompounds able to bind to cannabinoid receptors and act as therapeutic agents in neuronal diseases, e.g., Parkinson’s disease.
Movement disorders such as Parkinson’s disease and dyskinesia are highly debilitating conditions linked to oxidative stress and neurodegeneration. When available, the pharmacological therapies for these disorders are still mainly symptomatic, do not benefit all patients and induce severe side effects. Cannabidiol is a non-psychotomimetic compound from Cannabis sativa that presents antipsychotic, anxiolytic, anti-inflammatory, and neuroprotective effects. Although the studies that investigate the effects of this compound on movement disorders are surprisingly few, cannabidiol emerges as a promising compound to treat and/or prevent them. Here, we review these clinical and pre-clinical studies and draw attention to the potential of cannabidiol in this field.
The CBD treatment options seems to be a good one to consider, especially if you are have significant challenges with functioning on a day to day basis. There is research on the use of CBD that address problems related to trauma, anxiety post traumatic stress – all of which lie at the core cause of neurological difficulties.
As with any natural treatment option, be sure to check with your doctor to insure that use of CBD will not interfere with any treatments your doctor has prescribed for you.
Robert Rodgers PhD
Parkinsons Recovery
robert@parkinsonsrecovery.com
What follows is a replay of a session I had with John O’Dwyer who helped me release trapped emotions connected to an anxiety issue I was experiencing using Bradley Nelson’s Emotion Code.
Robert Rodgers PhD
Founder 2004
Parkinsons Recovery
You may be pondering what art therapy is really all about. It opens up the opportunity to connect deeply with colors that convey precisely the frequencies that your body needs to be replenished. In effect – you are getting color therapy and getting it in an enjoyable fashion.
Jessie Lyle demonstrates her version of art therapy which she demonstrated at the Vancouver Parkinsons Recovery Summit.
Art therapy is fun to do and simple to learn. Anyone can do it. The therapeutic effects are powerful. If you are looking for novel ways to get relief from your symptoms, why not give color therapy a trial run?
Robert
Oxygen is a gateway to reducing anxiety. When cells are starved of oxygen, our body becomes very anxious understandably. After all, its primary function is to insure our survival. When your breathing becomes shallow, you set into motion a frantic anxiety within every cell of the body which manifests itself in all of the symptoms associated with a diagnosis of Parkinson’s Disease.
The following video was taken at the Vancouver Parkinsons Recovery Summit where Deborah explains a simple way to enhance and support breathing.
Do it along with us while you watch. You will then know it really does help.
Robert
The following is a video shot at the Santa Fe Parkinsons Recovery Summit. The initial 30 minutes of the presentation by Sharry Edwards previews various factors she has determined which cause Parkinson’s symptoms using her BioAcoustic System of Voice Profiling.
The presentation also presents examples of Voice Profiling.
Robert
This presentation was recorded at the Parkinsons Recovery Summit in Vancouver. Judith devoted her time during the Summit offering toning services to participants. Each chakra resonates as a very specific note (or tone). Judith would sound the tone for each chakra as they cleared and opened during her treatments. It was all really remarkable to watch.
I like this demonstration because you use whatever sounds that cry out as your most needed tonal therapy. You do not actually have to even know what note coincides with which chakra!
Robert
One of the least accessed therapies that offer an instant boost to energy and overall well being is sound. No one knows this better than Judith who experiences symptoms of Parkinson’s. She knows about the effect of sound on healing because she is an opera singer!
Here is a simple exercise that works wonders. Do it at least once every day.
Judith demonstrated this at the Parkinsons Recovery Summit in Vancouver.
Robert