Action items that may improve PD status
- evidence-based
- Root causes may play a role in many conditions, in all causes listed below, a link to PD was found
- Key items in the list include: Keto, Fasting, Intermittent fasting, FMD, mitochondria support, micronutrient optimization/supplementation, macro’s, pathogens, poisons, mind-body, motor learning, masticking, vibration therapy, diet, exercise, EMF radiation dysbiosis & licky gut. cold/ heat exposure, hormetic stressors, sleep optimization.
- The goal of the list is to map causes and available treatments relevant to the condition.
- This is a work in progress, adding new items all the time (sign up for updates)
- Visit https://healthlinks.cc/list/meds/pd-meds/ for the meds related
High Prevalence of Undiagnosed Insulin Resistance in Non-Diabetic Subjects with Parkinson’s Disease – IOS Press
Background: Reduced glucose tolerance has been long recognized as a potential risk factor for Parkinson’s disease (PD), and increasing scrutiny is currently being placed on insulin resistance (IR) as a pathologic driver of neurodegeneration. However,
for comparison, prevalence of Diabetes in the general population:
its high – 20% suggesting much higher prevalence of IR, not sure if IR in PD is that much above normal
Whole body vibration: Neuro-rehab applications
2-deoxy-D-glucose is noeroprotective
www.ncbi.nlm.nih.gov/pubmed/10398297
2-deoxy-D-glucose (2-DG; a nonmetabolizable analogue of glucose) to mice fed ad libitum. Mice receiving 2-DG exhibited reduced damage to dopaminergic neurons in the SN and improved behavioral outcome following MPTP treatment.
Increased intestinal permeability and Parkinson disease patients
Herbal Antibiotics
Herbal Antivirals
Functional Neurological Disorders
postpone (vegan source) protein intake until evening
N-hexacosanol and fisetin
Hydroxysafflor yellow A promotes α-synuclein clearance via regulating autophagy
Corynoxine, isolated from Uncaria rhynchophylla, promotes the clearance of alpha-synuclein
Corynoxine, isolated from Uncaria rhynchophylla, promotes the clearance of alpha-synuclein
www.ncbi.nlm.nih.gov/pubmed/24522518
Corynoxine, isolated from Uncaria rhynchophylla, promotes the clearance of alpha-synuclein via mTOR pathway [R].
use of Uncaria rhynchophylla, known as “Gou-teng” herb extract
examine.com/supplements/uncaria-rhynchophylla/
www.ncbi.nlm.nih.gov/pubmed/29940559
buy uncaria-rhynchophylla:
buy Corynoxine:
www.alibaba.com/trade/search?fsb=y&IndexArea=product_en&CatId=&SearchText=Corynoxine
Q10
Action item:
q10 1200mg/day
Creatine
Mucuna pruriens – Levedopa
Type 2 diabetes is associated with an increased risk of PD
type 2 diabetes is associated with an increased risk of Parkinson’s disease. Surveillance bias might account for higher rates in diabetes. The mechanism behind this association between diabetes and disease is not known
care.diabetesjournals.org/content/early/2007/01/24/dc06-2011.short
Low LDL Colesterol – risk factor for PD
mutant (A53T) α-synuclein exhibit impaired autonomic regulation of heart rate characterized by elevated resting heart rate
Mutations in α-synuclein cause some cases of familial PD. Several lines of transgenic mice that overexpress wild type or mutant human α-synuclein exhibit progressive accumulation of α-synuclein in neurons, motor dysfunction and death (Crabtree and Zhang, 2012). Mice expressing mutant (A53T) α-synuclein exhibit impaired autonomic regulation of heart rate characterized by elevated resting heart rate associated with accumulation of α-synuclein aggregates in the brainstem and reduced parasympa-thetic (cardiovagal) tone (Griffioen et al., 2013). Maintenance of the α-synuclein mutant mice on ADF reversed the autonomic deficit, whereas a high fat diet exacerbated the autonomic deficit (Griffioen et al., 2013). Consistent with the latter findings, a high fat diet hastened the onset of motor dysfunction and brainstem pathology in another line of α-synuclein mutant mice, which was associated with reduced activity of kinases known to be involved in neurotrophic factor signaling (Rotermund et al., 2014). In addition to enhancement of neurotrophic factor/BDNF signaling, IF may counteract PD-related pathogenic processes by stimulating autophagy. Indeed, inhibition of mTOR with rapamycin, which stimulates autophagy, reduced oxidative stress and synaptic damage, and improved motor function in a α-synuclein accumulation-based mouse model of PD (Bai et al., 2015).
Rapamycin
Toxicology tests
for MPTP or similar drag exposure