COULD BE VITAMIN B2 ONE OF THE KEYS TO ENDING PARKINSON'S?


Riboflavin or vitamin B2 is essential in human health, and therefore in Parkinson's. But one hundred, one thousand times more than I imagined.

The usual: water-soluble vitamin (the excess is eliminated through the urine) of the B group, essential functions in the metabolism of hydrates (energy), proteins (amino acids, neurotransmitters) and fats (cell membranes, nerves, energy). This is not insignificant.

Something else: Two of its coenzymes are essential: FAD and FMN. Almost as important as the pyridoxal phosphate of vitamin B6 or the NADH of vitamin B3 (I would bet that in these last three sentences is summarized more than 50% of the original Parkinson, before medication).
FMN is necessary for the conversion of pyridoxine (vitamin B6) into its functional form, pyridoxal phosphate. Without it there is no dopamine.
FAD is necessary for the biosynthesis of niacin - or vitamin B3 or vitamin PP - from the amino acid tryptophan. So important in Parkinson's, that Walther Birkmayer, the father neurologist and heretic of levodopa, proposed NADH - vitamin B3 co-enzyme - to stimulate the internal production of dopamine instead of providing it from outside, in synthetic form (the precursor levodopa).

Foods rich in it are milk and cheese, beef liver and chicken and pork, eggs, brewer's yeast, whole grains and green vegetables, asparagus and broccoli.

BUT HERE'S WHAT'S REALLY INTERESTING TO US:

When the amazing Coimbra and Junquiera study came out in 2003, the results were either ignored or relativised. But the exact question is not whether the study met the sometimes "draconian" standards of patentable products of a pharmaceutical industry that has billions to spend on whatever is needed. The right question is how it took so long to do so and how it might not have those results BEING THE B2 OR RIBOFLAVIN IMPRESSIBLE TO PRODUCE DOPAMINE, GLUTATHION AND ATP (THE MOLECULE OF ENERGY).

Its role in neuroprotection is already demonstrated (Marashly 2017) and it crosses the protective blood-brain barrier, reaching the neurons and astrocytes (Moriyama 2011).

It reduces the risk of developing Parkinson's by 51 % (McCormick 1988). And it produces a motor improvement in all cases in the study of 44-71 % at six months. As the months progress, the benefits are greater (Coimbra 2003). It plays a decisive role in complexes I and II of mitochondrial respiration, as well as being essential in the synthesis of glutathione and its recovery once oxidised (Powers 1999).
And if anything is missing, it has epigenetic potential (so far 90 genes are known to be encoded).

COIMBRA AND JUNQUEIRA 2003: I finally had time to read the entire 2003 Coimbra and Junqueira study. They were given 30 mg of riboflavin three times a day (every 8 hours, total: 90 mg daily). They eliminated red meat from their diet. All 31 patients were in advanced stages of Parkinson's. The level of vitamin B2 was deficient in all at the start. After 6 months, the motor capacity of all of them had improved between 44 and 71 % (according to the Hoehn and Yahr scale) with improvements in the difficult Parkinsonian night, sleep, reasoning, motivation and depression. And the improvement was correlated with the level of B2 in the blood.

I thought they went crazy using 90 mg a day. But in migraine studies, 400 mg daily was used without any problem (Schoenen 1994, 1999).

---

The video of the significant recovery of one of the 31 patients who benefited from Dr. Cicero Coimbra's study in 2003, using doses of 90 mg per day of vitamin B2 (riboflavin) In the video he talks about three months, but the maximum benefit was 6 months after the study started: 44 to 71% improvement in mobility (also in sleep, mood, etc.). It is likely that the improvement continued (after the video was recorded 17 years ago).

Parkinson Paciente se recupera. - YouTube

---

Sometimes we keep looking for legendary "unicorns" when the keys to preventing and curing Parkinson's are right in front of our eyes, at our fingertips. All it takes is the right information, a change of mentality and the prudence to consult the specialist.

Vitamin B2, vitamin D, vitamin C (tb, its oxidized form, dehydroascorbic acid, which crosses the barriers as if it were glucose to help the neurons and mitochondria, being restored already inside by glutathione), oral NAC or intranasal glutathione, polyphenol extract from green tea such as Teavigo, vitamin B9 for homocysteine toxicity (possibly responsible for alpha-synuclein craziness and much of the damage to mitochondria), milk thistle (silymarin, silibilin)?

Is there anyone in the world who dares to tell me that this would not greatly improve the lives of patients and their families, especially in the early stages of the disease, when the treatments have not yet done much damage? What would produce in patients before treatment an effect so similar to a cure that no one could distinguish it from a significant improvement?

They led us to frightening dead ends, not surprising now that the revolution is triumphing... from thousands of studies that continue to appear every year as a liberating flood.

If after reading this, you don't get a big smile on your face and don't feel like dancing for joy, you have to read it again and again, until it pierces the thick layer of indoctrination we have received throughout our lives in this Matrix that controls almost everything. It took me 26 years, so it's no wonder I'm telling you this.

ill read later...i do shake but no health care

https://www.mayoclinicproceedings.or...177-6/fulltext



Vitamin B12 is lower in patients with PD compared with controls, and low levels have been associated with peripheral neuropathy, cognitive impairment, and more rapid rate of disease progression in PD.vitamin B12 may lead to reduced availability of choline as a substrate for cholinergic transmission. Here we will review the proposed pathophysiology of nonmotor symptoms in PD and the potential relationship between vitamin B12 and acetylcholine metabolism. We propose that vitamin B12 supplementation could be considered as an adjuvant approach to improve cholinergic transmission and, potentially, motor and cognitive function in patients with PD.