SelfDecode 2.0 The blueprint to your body Better health recommendations based on your DNA & lab tests. GET ACCESS Trustpilot The problem Generic strategies aren’t fixing your health issues. The solution Targeted remedies tailored specifically for your body. SelfDecode 2.0 is taking your health to the next level by analyzing more genetic variants (SNPs), providing […]
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The need for therapies that change the course of Parkinson’s disease is considerable. Several contenders are in development.
We reviewed computerized tomograms (CT) for basal ganglia and dentate nucleus calcifications in 79 patients with Parkinson’s disease (PD), 54 patients with Alzheimer’s disease (AD) and 109 controls aged 50 or more. When it was determined, no patient had disturbances in calcium metabolism. We found: …
Gluten ataxia
File:Gluten ataxia eng.ogv
en.wikipedia.org/wiki/Gluten
Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten.[75] With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing, with loss of Purkinje cells. People with gluten ataxia usually present gait abnormality or incoordination and tremor of the upper limbs. Gaze-evoked nystagmus and other ocular signs of cerebellar dysfunction are common. Myoclonus, palatal tremor, and opsoclonus-myoclonus may also appear.[76]
Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible.[76][77]
Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of all ataxias.[76][78] Less than 10% of people with gluten ataxia present any gastrointestinal symptom, yet about 40% have intestinal damage.[76]
Other neurological disorders
In addition to gluten ataxia, gluten sensitivity can cause a wide spectrum of neurological disorders, which develop with or without the presence of digestive symptoms or intestinal damage.[13] These include peripheral neuropathy, epilepsy, headache, encephalopathy, vascular dementia, and various movement disorders (restless legs syndrome, chorea, parkinsonism, Tourette syndrome, palatal tremor, myoclonus, dystonia, opsoclonus myoclonus syndrome, paroxysms, dyskinesia, myorhythmia, myokymia).[13][79]
The diagnosis of underlying gluten sensitivity is complicated and delayed when there are no digestive symptoms. People who do experience gastrointestinal problems are more likely to receive a correct diagnosis and treatment. A strict gluten-free diet is the first-line treatment, which should be started as soon as possible. It is effective in most of these disorders. When dementia has progressed to an advanced degree, the diet has no beneficial effect. Cortical myoclonus appears to be treatment-resistant on both gluten-free diet and immunosuppression.[13]
(2021). The therapeutic potential of ketone bodies in Parkinson’s disease. Expert Review of Neurotherapeutics: Vol. 21, No. 3, pp. 255-257.
Source: The therapeutic potential of ketone bodies in Parkinson’s disease
…Ketone supplementation combined with a regular carbohydrate-rich diet creates an unphysiological metabolic state that could undermine efficacy. A more promising approach may be to maintain a steady state of ketosis with a KD, while periodically boosting ketone concentration with supplementation. Progress will need to be made in developing a regimen that can be sustained for years, identifying individuals most likely to respond to ketone therapy, determining the threshold concentration for therapeutic ketosis, and managing other pharmacological treatments and social constraints. However, the bioenergetic potential of ketones and their wide-ranging pleiotropic effects indicate that ketone therapy holds considerable promise in PD and warrants further investigation.
detox guides by Jonn Barrom –
www.jonbarron.org/program/full-body-detox-program
Glutamine effectively increases circulating GLP-1, GIP and insulin levels in vivo and may represent a novel therapeutic approach to stimulating insulin secretion in obesity and type 2 diabetes.
Keywords: GLP-1, GIP, glucagon, insulin secretion, glutamine
This clip is by Swiss medica clinic
youtu.be/n6yxkFl0olk
#q1 how this works with downers
they treat aa range of auto-immune conditions
say they helped 145 people
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
