Parkinson’s may be due to B vitamin deficiencies, riboflavin (B2) and biotin (B7) may treat
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Yet another study, which not only points to the gut/endotoxin as a major cause of many chronic, degenerative diseases, but also corroborates again the role that energy production plays in pathologies such as Parkinson Disease (PD). Namely, the study below found that “gut dysbiosis” can cause deficiencies of vitamins B2 and B7, which results in the classic symptoms (e.g. muscle weakness, tremors, and poor coordination) seen in PD and that correcting those deficiencies through supplementation can be a viable therapeutic strategy. The study cites a human trial (first link below) done more than 20 years ago, showing that riboflavin supplementation (90mg daily) significantly reduced the symptoms of PD patients. While the new study does not mentioned it, there have already been several human studies with biotin for treating multiple sclerosis (MS) and Huntington disease (HD), and the mechanism of action for the benefit biotin displayed in these trials was improving mitochondrial function and OXPHOS. Riboflavin does not even need an introduction as an “energy remedy” given its main role as a precursor to the crucial energy co-factor FAD, analogous to niacinamide as a precursor to NAD+. Moreover, several studies have suggested that riboflavin is an antagonist of the endotoxin receptor TLR4, which would further validate its role in treating PD, as well as the role of endotoxin/LPS in this condition. Thus, it is quite reasonable to conclude that B2 and B7 work through correcting the energy deficiency in PD caused by the gut dysbiosis and endotoxin/LPS. Now, the new study says that the vitamin supplementation is likely to help only the subset of PD patients who have gut dysbiosis. Well, that’s a rather evasive way to saying that the B vitamin therapy may work for most PD patients since the study itself states that most PD patients experience changes in the microbiome and poor digestion decades before their official diagnosis. Finally, since it does seem that PD is yet another condition driven by energy deficiency, I don’t see why adding niacinamide (a precursor to NAD+) won’t further increase the effectiveness of this vitamin therapy.
https://www.scielo.br/j/bjmbr/a/BM4WLJBtjxF8Cx3wFsjFhKb/?lang=en
https://www.nature.com/articles/s41531-024-00724-z
https://www.sciencealert.com/parkinsons-link-to-gut-bacteria-suggests-unexpected-simple-treatment
“…Researchers have suspected for some time that the link between our gut and brain plays a role in the development of Parkinson’s disease. A new study just identified gut microbes likely to be involved and linked them with decreased riboflavin ( vitamin B2) and biotin (vitamin B7), pointing the way to an unexpectedly simple treatment that may help: B vitamins.”
“…”Supplementation of riboflavin and/or biotin is likely to be beneficial in a subset of Parkinson’s disease patients, in which gut dysbiosis plays pivotal roles,” Nagoya University medical researcher Hiroshi Nishiwaki and colleagues write in their published paper. Previous research found people with Parkinson’s disease also experience changes in their microbiome long before other signs appear.”
“…Such toxins lead to the overproduction of α-synuclein fibrils – molecules known to amass in dopamine-producing cells in the substantia nigra part of our brains, and increased nervous system inflammation, eventually leading to the more debilitating motor and dementia symptoms of Parkinson’s. A 2003 study found high doses of riboflavin can assist in recovering some motor functions in patients who also eliminated red meat from their diets. So it’s possible that high doses of vitamin B may prevent some of the damage, Nishiwaki and team propose.”
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@haidut said in Parkinson’s may be due to B vitamin deficiencies, riboflavin (B2) and biotin (B7) may treat:
Yet another study, which not only points to the gut/endotoxin as a major cause of many chronic, degenerative diseases, but also corroborates again the role that energy production plays in pathologies such as Parkinson Disease (PD).
Very interesting. Thanks for sharing.
For the other readers:
I’d first deal with bacterial overgrowth (endotoxins LPS) and be sure to evacuate twice a day the stools (to avoid stagnation and proliferation of bacteria that have nothing to do in the second part of the colon, especially when eating starches, particularly potatoes). Thus, MMC must be optimal (motility of the intestines in the resting periods)
MMC= Migrating Motor Complex.
First calming before adding a layer.
Afterwards, we can manage to optimize useful nutrients.
More to say is needed but not now. -
@haidut
I had also read your previous post on that 300mg-biotin-per-day study and can attest by my own experience that there really are things opening up at thrice daily doses of about 100mg B7.
Practically, however, I ran into a few issues. What are your opinions on these?Biotin:
- I don't understand how study participants could cope for so long with such high doses, since B7 competes with B5 for uptake? Especially with regard to restoration of myelin sheaths, cell membranes and endogenous fatty acid synthesis they are both interdependent. I kept running into deficiency of one or the other and had to alternate both at least once every few days.
- I felt that at such high doses, purity and fillers really become a significant issue. I've tried different brands because of this and they ranged from awful (with excessively much MCC) to something-is-still-off. Pharmaceutical quality in general is only >97.5% purity which by itself I consistently find totally inadequate in many cases.
- Perhaps related to 2). My GI system and BMs became unbearably upset by high biotin doses. I suspect biotin exhibits inhibiting effects on aminooxidases similar to thiamin (thiamin metabolites) through displacement of enzymatic flavoproteins? I'm convinced much of the beneficial effects in Antonio Costantini's high-dose-thiamin therapy stems from MAO inhibition in the ganglions.
Riboflavin:
- Are such high bolus doses really sensible in people who are unaffected by that recognized genetic riboflavin transporter defect?
.1) I have noticed much better effects and tolerability from single digit mg doses continually (3-4x) throughout the day instead of higher doses twice or once daily.
.2) Someone on the forums reported to have had his actual serum/blood FAD and FMN levels tested with different amounts of B2 and that their ratio and the absolute value of FAD totally plumetted from high doses of B2, whereas FAD and also his symptoms improved with low doses.
Side note: I have used B2 in amounts up to 2grs for clostridioides prophylaxis because of the studies on its redox effects and the aerobic-anaerobic gradient of the intestinal lining and its microbes. While such amounts are probably really not harmful, they made for purging and very awful BMs.
Hope you are doing well! And thanks for all the work!
