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Integrative Parkinson’s Disease Care Part Two

July 29, 2015 Written by JP    [Font too small?]

In part one of this column, I mentioned that Parkinson’s disease (PD) is in the news on a weekly basis. Since writing that first piece, several articles about PD have appeared in various publications. Time magazine reports that diabetes drugs “may offer hope for Parkinson’s disease treatment”. EurekAlert, an influential science news resource, describes mounting evidence supporting the use of low-dose lithium to reduce involuntary muscle movements – a common side-effect of carbi- and levo-dopa treatment. There’s even a story about how some PD patients are literally fighting back against the disease by taking part in non-contact boxing.

There is no question that Parkinson’s disease is now a major area of interest both in our modern culture and in the field of scientific research. The majority of the research on PD is taking place in conventional medical circles. Medical devices, medications and surgical procedures top the list of avenues that allopathic researchers are investigating. On the holistic side of the equation, diet, mind-body therapies and supplements are most often explored.

The importance of diet in relation to PD is often overlooked by conventional physicians. If anything, the most prevalent recommendation is to avoid high protein diets which can negatively influence the efficacy of levodopa. It’s unfortunate, but quite possible, that many doctors are unaware of numerous studies suggesting that food choices can influence the course of Parkinson’s disease.

From my perspective, a healthy diet for PD patients should emphasize naturally occurring antioxidants and nutrient-density. There appears to be a connection between blood sugar irregularities, including metabolic syndrome and type 2 diabetes and PD risk. Therefore, a diet rich in fiber, healthy fat and moderate amounts of high quality protein is advisable. Opting for low-glycemic fruits and vegetables containing flavonoids, such as berries and peppers, seems to confer a protective effect as well.

A recent trial reports that higher intakes of dietary cholesterol and monounsaturated fat is linked to a statistically lower incidence of PD. If you do drink alcohol, beer or red wine are the best choices. However, moderation is key – no more than two alcoholic drinks daily. Lastly, preliminary research indicates that a ketogenic diet, very high in fat, low in carbohydrates with modest amounts of protein, may improve brain function and PD symptoms. This finding may be due to increased antioxidant (glutathione) activity in the brain that minimizes neurotoxicity.

Several supplements show promise in limiting PD progression and symptomatology. Topping the list is CoQ10. To be clear, the data on this fat-soluble antioxidant is mixed. But, the information currently available suggests that taking it in one of two ways may yield the best results: 1) 100 mg of CoQ along with 5 grams of creatine monohydrate, thrice-daily; 2) 300 mg/day of ubiquinol-10, an oxidized or “reduced” form of CoQ10. Creatine monohydrate is a supplemental form of a chemical naturally found in fish, meat and in our muscles. When taken in large quantities, creatine can promote cellular energy. There is some evidence that it works synergistically with CoQ10.

Mucuna pruriens aka velvet bean is a natural source of L-dopa. A few studies show that it effectively manages PD more safely than the standard of care (L-dopa/carbidopa). M. pruriens may also benefit PD patients because of its antioxidant content and metal chelating properties. Some research points to excess heavy metals, including iron, as a contributing factor in PD development and progression. While promising, it’s important to note that M. pruriens is best utilized under the supervision of a health care professional familiar with this bean extract and L-dopa therapy in general. Part of the reason is that some M. pruriens supplements may contain degraded L-dopa which could result in unreliable outcomes.

Two additional supplements worth considering are fenugreek and Vitamin D3. A substantial amount of data links low Vitamin D, measured as 25(OH)D, and Parkinson’s disease. PD patients frequently present inadequate 25(OH)D concentrations of <50 nmol/l. Such deficiencies have been found to more than double the risk of PD. The good news is that supplementing with Vitamin D3 may stabilize PD, even after it’s been diagnosed. Fenugreek, a culinary herb used in traditional Indian (Ayurvedic) medicine, is also showing potential as an adjunct to conventional PD care. A study appearing in the February 2014 issue of Phytotherapy Research reveals that taking 300 mg of fenugreek twice-daily improves the efficacy of L-dopa without any added safety concerns. What’s more, a 2013 study discovered that fenugreek “showed reversal of motor symptoms in an animal model of PD probably through neuroprotective properties”.

There is a great deal of on-going research on natural remedies that I didn’t discuss today. The truth is, much of the up-and-coming data is the form of animal and/or in-vitro studies. Many of the findings are encouraging to be sure. However, it remains to be seen if similar results will eventually be found in a real world setting i.e. in humans. I’ll keep an eye out for such developments. If and when I find something intriguing, I’ll certainly report it in the “Comments & Updates” section at the bottom of this page.

Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!

To learn more about the studies referenced in today’s column, please click on the following links:

Study 1 – Diabetes Drugs May Offer Hope for Parkinson’s Disease Treatment (link)

Study 2 – Low-Dose Lithium Reduces Side Effects from Most Common (link)

Study 3 – Parkinson’s Patients Fight Back — with Boxing(link)

Study 4 – Complementary & Alternative Management of Parkinson’s Disease (link)

Study 5 – Dietary Factors in the Etiology of Parkinson’s Disease (link)

Study 6 – Diabetes and Risk of Parkinson’s Disease: A Systematic Review (link)

Study 7 – Metabolic Syndrome: An Important Risk Factor for Parkinson’s (link)

Study 8 – Protein Intake, Nitrogen Balance and Nutritional Status (link)

Study 9 – Dietary Cholesterol, Fats and Risk of Parkinson’s Disease in the (link)

Study 10 – Flavonoid-Based Therapies in the Early Management of (link)

Study 11 – Habitual Intake of Dietary Flavonoids and Risk of Parkinson (link)

Study 12 – Nicotine from Edible Solanaceae and Risk of Parkinson Disease (link)

Study 13 – Alcohol Intake and Risk of Parkinson’s Disease: A Meta-Analysis (link)

Study 14 – Alcohol Consumption, Types of Alcohol, and Parkinson’s Disease (link)

Study 15 – Association Between Oxidative Stress and Nutritional Status in the (link)

Study 16 – Ketogenic Diet in Neuromuscular and Neurodegenerative Diseases (link)

Study 17 – Treatment of Parkinson Disease with Diet-Induced Hyperketonemia (link)

Study 18 – Ketogenic Diet Protects Dopaminergic Neurons Against 6-OHDA (link)

Study 19 – A Randomized Clinical Trial of High-Dosage Coenzyme Q10 … (link)

Study 20 – Randomized, Double-Blind, Placebo-Controlled Pilot Trial of (link)

Study 21 – The Effect of Creatine and Coenzyme Q10 Combination Therapy on (link)

Study 22 – Does High-Dose Coenzyme Q10 Improve Oxidative Damage and (link)

Study 23 – Coenzyme Q10 Deficiency in Patients with Parkinson’s Disease (link)

Study 24 – Combination Therapy with Coenzyme Q10 and Creatine Produces (link)

Study 25 – Mucuna Pruriens in Parkinson’s Disease: A Double Blind Clinical (link)

Study 26 – An Alternative Medicine Treatment for Parkinson’s Disease: Results (link)

Study 27 – Antiparkinson Drug – Mucuna Pruriens Shows Antioxidant & Metal (link)

Study 28 – The Role of Iron in Brain Aging and Neurodegenerative Disorders (link)

Study 29 – Levodopa in Mucuna Pruriens and its Degradation (link)

Study 30 – Associations Between Vitamin D Status, Supplementation, Outdoor (link)

Study 31 – Surprising Prevalence of Unrecognized Vitamin D3 Deficiency in Fall (link)

Study 32 – Vitamin D Status and Parkinson’s Disease: A Systematic Review and … (link)

Study 33 – Randomized, Double-Blind, Placebo-Controlled Trial of Vitamin D (link)

Study 34 – Efficacy and Safety of Standardized Extract of Trigonella Foenum- (link)

Study 35 – Neurobehavioral Assessment of Hydroalcoholic Extract of Trigonella (link)

Parkinson’s Disease Patients Often Have Low Vitamin D Levels

Source: Neurology. 2013 Oct 22;81(17):1531-7. (link)

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Posted in Alternative Therapies, Nutrition, Nutritional Supplements

6 Comments & Updates to “Integrative Parkinson’s Disease Care Part Two”

  1. JP Says:

    Updated 07/29/15:


    Evid Based Complement Alternat Med. 2015;2015:874849.

    Self-reported efficacy of cannabis and other complementary medicine modalities by Parkinson’s disease patients in colorado.

    Introduction. Complementary and alternative medicine (CAM) is frequently used by Parkinson’s disease (PD) patients. We sought to provide information on CAM use and efficacy in PD patients in the Denver metro area with particular attention to cannabis use given its recent change in legal status. Methods. Self-administered surveys on CAM use and efficacy were completed by PD patients identified in clinics and support groups across the Denver metro area between 2012 and 2013. Results. 207 patients (age 69 ± 11; 60% male) completed the survey. Responses to individual CAMtherapy items showed that 85% of respondents used at least one form of CAM. The most frequently reported CAMs were vitamins (66%), prayer (59%), massage (45%), and relaxation (32%). Self-reported improvement related to the use of CAM was highest for massage, art therapy, music therapy, and cannabis. While only 4.3% of our survey responders reported use of cannabis, it ranked among the most effective CAM therapies. Conclusions. Overall, our cross-sectional study was notable for a high rate of CAM utilization amongst PD patients and high rates of self-reported efficacy across most CAM modalities. Cannabis was rarely used in our population but users reported high efficacy, mainly for nonmotor symptoms.

    Be well!


  2. JP Says:

    Updated 07/29/15:


    Neural Regen Res. 2014 Feb 15;9(4):407-12. doi: 10.4103/1673-5374.128246.

    Compound Formula Rehmannia alleviates levodopa-induced dyskinesia in Parkinson’s disease.

    Compound Formula Rehmannia has been shown to be clinically effective in treating Parkinson’s disease and levodopa-induced dyskinesia; however, the mechanisms remain unclear. In this study, we established a model of Parkinson’s disease dyskinesia in rats, and treated these animals with Compound Formula Rehmannia. Compound Formula Rehmannia inhibited the increase in mRNA expression of N-methyl-D-aspartate receptor subunits 1 and 2 and excitatory amino acid neurotransmitter genes, and it inhibited the reduction in expression of γ-aminobutyric acid receptor B1, an inhibitory amino acid neurotransmitter gene, in the corpus striatum. In addition, Compound Formula Rehmannia alleviated dyskinesia symptoms in theParkinson’s disease rats. These experimental findings indicate that Compound Formula Rehmannia alleviates levodopa-induced dyskinesia inParkinson’s disease by modulating neurotransmitter signaling in the corpus striatum.

    Be well!


  3. JP Says:

    Updated 07/29/15:


    Glob Adv Health Med. 2014 Jul;3(4):43-4. doi: 10.7453/gahmj.2013.096.

    Is Ginkgo biloba and/or a Multivitamin-multimineral Supplement a Therapeutic Option for Parkinson’s Disease? A Case Report.

    For a number of years, there has been speculation about the potential benefit of Parkinson’s disease by treatment with Ginkgo biloba. In this case report, my grandfather, who had a known history of Parkinson’s, had dramatic improvement after supplementation with ginkgo and a multivitamin-multimineral supplement. Human studies are needed for confirmation.

    Be well!


  4. JP Says:

    Updated 09/10/15:


    Nutrients. 2015 Aug 27;7(9):7197-208.

    Associations between B Vitamins and Parkinson’s Disease.

    B vitamins may correlate with Parkinson’s disease (PD) through regulating homocysteine level. However, there is no comprehensive assessment on the associations between PD and B vitamins. The present study was designed to perform a meta-analytic assessment of the associations between folate, vitamin B6, and vitamin B12 and PD, including the status of B vitamins in PD patients compared with controls, and associations of dietary intakes of B vitamins and risk of PD. A literature search using Medline database obtained 10 eligible studies included in the meta-analyses. Stata 12.0 statistical software was used to perform the meta-analysis. Pooled data revealed that there was no obvious difference in folate level between PD patients and healthy controls, and PD patients had lower level of vitamin B12 than controls. Available data suggested that higher dietary intake of vitamin B6 was associated with a decreased risk of PD (odds ratio (OR) = 0.65, 95% confidence intervals (CI) = (0.30, 1.01)), while no significant association was observed for dietary intake of folate and vitamin B12 and risk of PD. PD patients had lower level of vitamin B12 and similar level of folate compared with controls. Dietary intake of vitamin B6 exhibited preventive effect of developing PD based on the available data. As the number of included studies is limited, more studies are needed to confirm the findings and elucidate the underpinning underlying these associations.

    Be well!


  5. JP Says:

    Updated 11/11/15:


    J Altern Complement Med. 2015 Oct 27.

    Long-Term Treatment with High-Dose Thiamine in Parkinson Disease: An Open-Label Pilot Study.

    OBJECTIVES: To investigate the potential clinical, restorative, and neuroprotective effects of long-term treatment with thiamine in Parkinson disease (PD).

    DESIGN: Observational open-label pilot study.

    SETTING: Outpatient neurologic rehabilitation clinic.

    PATIENTS AND METHODS: Starting in June 2012, we have recruited 50 patients with PD (33 men and 17 women; mean age, 70.4 ± 12.9 years; mean disease duration, 7.3 ± 6.7 years). All the patients were assessed at baseline with the Unified Parkinson’s Disease Rating Scale (UPDRS) and the Fatigue Severity Scale (FSS) and began treatment with 100 mg of thiamine administered intramuscularly twice a week, without any change to personal therapy. All the patients were re-evaluated after 1 month and then every 3 months during treatment.

    RESULTS: Thiamine treatment led to significant improvement of motor and nonmotor symptoms: mean UPDRS scores (parts I-IV) improved from 38.55 ± 15.24 to 18.16 ± 15.08 (p = 2.4 × 10-14, t test for paired data) within 3 months and remained stable over time; motor UPDRS part III score improved from 22.01 ± 8.57 to 9.92 ± 8.66 (p = 3.1 × 10-22). Some patients with a milder phenotype had complete clinical recovery. FSS scores, in six patients who had fatigue, improved from 53.00 ± 8.17 to 23.60 ± 7.77 (p < 0.0001, t test for paired data). Follow-up duration ranged from 95 to 831 days (mean, 291.6 ± 207.2 days). CONCLUSIONS: Administration of parenteral high-dose thiamine was effective in reversing PD motor and nonmotor symptoms. The clinical improvement was stable over time in all the patients. From our clinical evidence, we hypothesize that a dysfunction of thiamine-dependent metabolic processes could cause selective neural damage in the centers typically affected by this disease and might be a fundamental molecular event provoking neurodegeneration. Thiamine could have both restorative and neuroprotective action in PD. Be well! JP

  6. JP Says:

    Updated 07/07/17:


    Neurology. 2017 Jul 5.

    Mucuna pruriens in Parkinson disease: A double-blind, randomized, controlled, crossover study.

    OBJECTIVE: 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.

    METHODS: 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.

    RESULTS: 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.

    CONCLUSION: 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.

    Be well!


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