I've recently been diagnosed with Parkinsons and have been prescribed LevaDopa -1/2 tablet (125mg) 4 times per day.
I understand that there are complimentary drugs such MAO-B Inhibitors (such as Selegiline, Rasagiline, and Safinamide)
I've done some cursory reseach which indicates that MAO-B inhibitors are neuroprotective, may delay alpha-synuclein aggregation and therefore may have disease modifying effects. (see link below).
This being the case, is there any reason why an MAO-B inhibitor isn't prescribed along with LevaDopa when one is first diagnosed? Why delay!?
Hi I don't believe any pharmaceuticals have any significant neuroprotection. I was originally in 2017 told that Rasagaline was neuroprotective. Last year the same people said it wasn't.I'd suggest exercise the best you can, yoga or tai çhi, walking, destress where possible and think positive.
I'm sorry to have to tell you this but, THERE IS NO DRUG ON THE MARKET THAT CAN CURE PD!!!!
SO! WHERE DO YOU GO FROM HERE?
You take the matter into your own hands and start to do as I suggest here-----------------------
WALK AS FAST AS YOU CAN, FOR A MAXIMUM OF ONE HOUR, EVERY SECOND DAY!
If you are only able to walk for one minute, as fast as you can, then that is FINE!
It takes six or more momths to get up to one hour, but when you get there you will have noticed that your PD is already a lot better! After two years you will not have a sign of PD, but, if you stop the walking, the PD will return.
I am now 89 years old and I was diagnosed at the age of 52. YES! I have had PD for 37 years and only took medication for the first year, which did NOTHING!
I still walk, with a walker, every second day and I still show no sign of PD!
Hi John, Thanks for your reply. Brilliant to hear this works for you!
I'm not hanging around! 4-5 days per week I do the following:
BIKE: 25-30 minutes at 90-100 RPM, including a few sprints at high resistance to get my heart rate up to 85% of max.
WALK: 15 minutes on treadmill at 6.8-7.3 Km/hr pace, swinging arms so my hands touch the front bars. I focus on standing straight and looking straight ahead.
ROW: 4min:30 to cover 1000 metres
NORDIC SKI: 2min:30 to cover around 500 metres
SWIM: 250metres, casual.
WEIGHTS: 10 minutes of resistance training.
I also walk everywhere, if practical, rather than take the car.
There's no question that this all helps me, it improves my mood and sense of well being and energy levels, and I'm sure it helps with a myriad of other health markers (BMI, Blood Sugar etc) - but my PD hasn't gone away.
I'm hoping that my exercise regime will slow down progression but so far it has not reversed it!
I am now adding dietary protocols, restricting sugary carbs and using Ketone supplements (MCT oil and Esters). There's some very interesting science about this - I'm particular interested in the work of Stephen Cunnane having seen his talk on how Ketones improve the brain.
- Cognitive impairment in PD, Alzheimers, is due in part to an 'brain energy gap'. Young, healthy brains use around 98% Glucose, and 2% Ketones. However, as we age, and with the advent of cognitive impairment the brain is unable to use glucose so effectively and this then causes a deficit of energy to the brain, which starts to accelerate the decline.
= This 'energy deficit' can be partially restored by taking Ketone supplements - using MCT oil that is composed of Caprilic Acid (C8) and Capric Acid (C10) and/or by the use of Ketone esters and salts. Scans show that the parts of the brain which can't utilise glucose can use Ketones.
- His research shows a clinical improvement in the cognitive ability of Alzheimer patients, indicating a reduction in progression of the disease by 2 years.
- Exercise remains an important part of the equation. Exercise helps the body/brain to take up both glucose and ketones and helps reduce insulin resistance.
- Insulin resistance (high blood sugar) is prevalent in those who have PD which impacts the ability of the brain to utilise glucose efficiently. (Note: It is interesting to see that GLP-1 agonists such as Lixisenatide, which increase insulin and reduce blood sugar, appear to arrest PD symptoms in recent human trials).
Hope you find this interesting. I will post up the information about Stephen Cunnane's work as a separate note for others to also comment.
I am not a doctor so, please excuse my plain speaking.
The only exercise that has been proven to affect the area of the brain which has been damaged by PD is "FAST WALKING' THAT COMES FROM THE MAYO CLINIC AND. I THINK THEY KNOW WHAT THEY ARE TALKING ABOUT!
Hi John. Do you have a link. I’ve searched the Mayo clinic and there is nothing to suggest that fast walking is a cure or the only type of exercise recommended.
Many thanks for the link - which answers the question very well, and not a surprise - it would be astonishing if walking was the only exercise that produced results.
It appears that Parkinsons is partly a metabolic disease where the mitochondria fail to function. HIIT exercise is known to improve the efficiency of mitochondria, so this is good to know that it has a postive impact in PD. Longer exercise of less intensity is known to increase the number of mitochondria, so it would be interesting to know if this is also improves PD.
The initial studies in 2002 with Rasagiline already showed an inexplicable effect where 1 mg per day had an effect and 2 mg did not. Because of this discrepancy, the FDA did not approve rasagiline as a neuroprotective, disease-modifying therapy. However, my first neurologist, from the old school, prescribed Rasagiline immediately after the first C/L medication. On my own initiative, I stopped taking it due to side effects (headache and insomnia) and lack of noticeable effectiveness. Only 20 years later, 2021, a new study evaluating rasagiline for neuroprotective effect found no signs of disease-modifying effect over one year of treatment with rasagiline.
My new younger neurologist says he no longer prescribes the medication for new patients. For existing users, he still does so due to a lack of alternatives…
As mentioned in the research you provided, however, there are new and very promising developments underway with a new generation of MAO-B inhibitors in development. One of them seems to be Tavapadon, for which a recent update was posted by nednedned.
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