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Parkinson's disease may start in the gut


PR activist
First MS, now Parkinson's...

The so-called Braak's hypothesis proposes that the disease process begins in the digestive tract and in the brain's center of smell. The theory is supported by the fact that symptoms associated with digestion and smell occur very early on in the disease.

Researchers at Lund University have previously mapped the spread of Parkinson's in the brain. The disease progression is believed to be driven by a misfolded protein that clumps together and "infects" neighboring cells.

Professor Jia-Yi Li's research team has now been able to track this process further, from the gut to the brain in rat models. The experiment shows how the toxic protein, alpha-synuclein, is transported from one cell to another before ultimately reaching the brain's movement center, giving rise to the characteristic movement disorders in Parkinson's disease.


Senior Member
England (south coast)
The folded protein (implicated by the hypothesis) seems to act like a prion, as far as my very basic understanding of the research goes. A prion is, by definition, infectious, and Parkinson's isn't usually considered infectious, but perhaps this hypothesis would change our understanding of the disease.

Interestingly, and perhaps significantly, Wikipedia says that: "All known prion diseases in mammals affect the structure of the brain or other neural tissue."

I don't understand it all, but the hypothesis is that these folded proteins spread via the vagal nerve, from gut to nervous system:
Holmqvist et al. said:
Direct evidence of Parkinson pathology spread from the gastrointestinal tract to the brain in rats
Holmqvist et al.
Acta Neuropathologica
9 Oct 2014
Braak and coworkers hypothesized that Lewy pathology primes in the enteric nervous system and spreads to the brain, suggesting an active retrograde transport of α-synuclein (the key protein component in Lewy bodies), via the vagal nerve.

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Senior Member

Study about Parkinson and SIBO:

The aim of this study was to investigate whether small intestinal bacterial overgrowth contributes to the pathophysiology of motor fluctuations. Thirty-three patients and 30 controls underwent glucose, lactulose, and urea breath tests to detect small intestinal bacterial overgrowth and Helicobacter pylori infection.

The prevalence of small intestinal bacterial overgrowth was significantly higher in patients than in controls (54.5% vs. 20.0%; P = .01), whereas the prevalence of Helicobacter pylori infection was not (33.3% vs. 26.7%). Compared with patients without any infection, the prevalence of unpredictable fluctuations was significantly higher in patients with both infections (8.3% vs. 87.5%; P = .008).

The eradication of small intestinal bacterial overgrowth resulted in improvement in motor fluctuations without affecting the pharmacokinetics of levodopa. The relapse rate of small intestinal bacterial overgrowth at 6 months was 43


Senior Member
Chris Kresser about parkinson:

We know that Parkinson’s patients have significantly greater intestinal permeability, i.e. their guts are more leaky than patients without Parkinson’s. We know that intestinal permeability in Parkinson’s patients is correlated with markers of oxidative stress and endotoxin exposure, like exposure to lipopolysaccharide.

SIBO is making Parkinson’s worse or contributing to Parkinson’s, but Parkinson’s is probably contributing to SIBO as well via perhaps a reduction in gut motility. So when you put all that together, it’s a pretty strong relationship between digestive and gut function and the risk of developing Parkinson’s disease, and also just exacerbating it if it’s already present.

I’m looking at the gut, I’m looking at the HPA axis, I’m looking at oxygen deliverability and blood sugar regulation, I’m looking at methylation. These are all the underlying mechanisms that tend to be at the root of most modern disease, regardless of whether we’re talking about diabetes, cardiovascular disease, autoimmunity or neurodegenerative conditions like Parkinson’s and Alzheimer’s.

He also suggests as treatment:

- ketogenic diet
- liposomal curcumin, to reduce oxidative damage and CNS inflammation
- reducing iron, as parkinson´s disease is often correlated with iron overloading (only little Vit. C and HCL Betain, as both increase iron intake)
- removing gluten from the diet