Adequate Vitamin B12 and low Homocysteine Levels may slow  progression of PD

Source: Vitamin B12 and Homocysteine Levels Predict Different Outcomes in Early Parkinson’s Disease

Background: In moderately advanced Parkinson’s disease (PD), low serum vitamin B12 levels are common and are associated with neuropathy and cognitive impairment. However, little is known about B12 in early PD.

Objective: To determine the prevalence of low vitamin B12 status in early PD and whether it is associated with clinical progression.

Methods: We measured vitamin B12 and other B12 status determinants (methylmalonic acid, , and holotranscobalamin) in 680 baseline and 456 follow-up serum samples collected from DATATOP participants with early, untreated PD. Borderline low B12 status was defined as serum B12 <184 pmol/L (250 pg/mL), and elevated homocysteine was defined as >15 µmol/L. Outcomes included the UPDRS, ambulatory capacity score (sum of UPDRS items 13-15, 29&30), and MMSE, calculated as annualized rates of change.

Results: At baseline, 13% had borderline low B12 levels, 7% had elevated homocysteine, whereas 2% had both. Elevated homocysteine at baseline was associated with worse scores on the baseline MMSE. Analysis of study outcomes showed that compared with the other tertiles, participants in the low B12 tertile (<234 pmol/L; 317 pg/mL) developed greater morbidity as assessed by greater annualized worsening of the ambulatory capacity score. Elevated homocysteine was associated with greater annualized decline in MMSE (−1.96 vs. 0.06; P = 0001). Blood count indices were not associated with B12 or homocysteine status. Conclusions: In this study of early PD, low B12 status was common. Low B12 at baseline predicted greater worsening of mobility whereas elevated homocysteine predicted greater cognitive decline. Given that low B12 and elevated homocysteine can improve with vitamin supplementation, future studies should test whether prevention or early correction of these nutritionally modifiable conditions slows development of disability. © 2018 International Parkinson and Movement Disorder Society Supporting Informatio

Vitamin D | Linus Pauling Institute | Oregon State University

n a randomized, double-blind, placebo-controlled study, 112 PD patients (mean age, 72 years) on standard PD treatment were supplemented with 1,200 IU/day of vitamin D or a placebo for 12 months. Vitamin D supplementation nearly doubled serum 25-hydroxyvitamin D concentration (from mean of 22.5 ng/mL to 41.7 ng/mL) in supplemented subjects and limited the progression of PD, as indicated by a greater proportion of patients who showed no worsening (as assessed by the Hoehn and Yahr stage and the United Parkinson Disease Rating Scale part II) in the supplemented group compared to the placebo group (243). It is not known whether vitamin D insufficiency has a role in the pathogenesis of the disease, but the repletion of vitamin D may provide health benefits that go beyond the prevention and/or the treatment of PD. For example, vitamin D deficiency may contribute to the increased risk of osteoporosis and bone fracture in individuals with neurologic disorders, including PD and multiple sclerosis (244-246). Interestingly, sunlight exposure was found to be associated with improved vitamin D status, higher bone mineral density of the second metacarpal bone, and lower incidence of hip fracture in a prospective study conducted in 324 elderly people with PD (247).

Source: Vitamin D | Linus Pauling Institute | Oregon State University

Stem Cell – Repairing the Brain: Cell Replacement Using Stem Cell-Based Technologies – IOS Press

Current approaches to cell replacement therapy in Parkinson’s disease are strongly focused on the dopamine system, with the view that restoring dopaminergic inputs in a localized and physiologic manner will provide superior benefits in terms of effec

Source: Repairing the Brain: Cell Replacement Using Stem Cell-Based Technologies – IOS Press

Fetal tissue implant – Wikipedia

Source: Fetal tissue implant – Wikipedia

…In 1982, seven people in Santa Clara County, California were diagnosed with Parkinsonism after having used MPPP contaminated with MPTP. In 1992, two of the seven patients were successfully treated at Lund University Hospital in Sweden with neural grafts of fetal tissue. One patient, who had been essentially paralyzed, regained enough motor function to ride a bicycle.[1]

NLY01 halts PD

Similar drugs to NLY01 already approved by the Food and Drug Administration for the treatment of type 2 diabetes include exenatide, lixisenatide, liraglutide and dulaglutide, each of which can cost approximately $2,000 for a 90-day supply. NLY01 is a long-acting drug with improved the brain penetration compared to these approved drugs for diabetes.

www.sciencedaily.com/releases/2018/07/180702120505.htm

afforable:
dir.indiamart.com/impcat/liraglutide.html

MS-The Wahls protocol

דר’ טרי ואלס הצליחה לרפא את עצמה מMS (או לפחות להפוך את מהלך המחלה)

היא פרסמה ספר המפרט את הפרוטוקול (מעל 1,000 ביקורות חיוביות באמזון)

האם זה עובד?

מחקר על 20 נבדקים, מראה שכן, בשלבים מוקדמים של המחלה
www.ncbi.nlm.nih.gov/pubmed/30050380

תקציר הדיאטה של ואלס
www.stfm.org/Portals/49/Documents/FMPDF/FamilyMedicineVol49Issue2Scherger149.pdf

 
ואלס מציגה את הפרוטוקול בטד

 
סיכום באחת התגובות:
Continue reading “MS-The Wahls protocol”

Ketogenic Diet and LGIT diet vs plant based Atkins

plant based low carb diet -EcO Atkins…Some 31% of the calories in the diet came from plant proteins, 43% from vegetable oils, and 26% from carbs.

improve motor function full text
from the review:
The classic ketogenic therapy is based on a diet providing 90% of calories from long-chain fatty acids, a restricted protein portion (1 g/kg/day), and minimal carbohydrates. Traditionally, the diet is comprised of four parts fat, mainly LCTs, for one part carbohydrates and proteins. The ratio can be modified to 3:1, 2:1, or 1:1, respectively, similar to the modified Atkins diet (Kossoff et al., 2003). The MCTs diet is also proposed with 60% of calories from octanoate and decanoate that are more ketogenic than LCTs (Huttenlocher, 1976). The last alternative to a ketogenic therapy is the low glycemic index diet characterized by higher amounts of carbohydrates with low glycemic index (Coppola et al., 2011).

Autophagy works, see reference link in entry

blood lipids rise – see www.seizure-journal.com/article/S1059-1311(13)00339-7/fulltext#sec0040

Keto vs LGIT

www.massgeneral.org/childhood-epilepsy/assets/images/medical/i_treatment_diet-l.gif

www.massgeneral.org/childhood-epilepsy/medical/treatment.aspx

charliefoundation.org/low-glycemic-index-treatment/

 

Ketonemeter – see appendix