In the 1800s and early 20th century, physicians observed the phenomenon of Parkinson’s patients improving, sometimes into full remission, when their bowel health was optimized (Parkinson, 1817).


19th century physician Dr. Hermann Senator, a Prussian internal medicine specialist, speculated that latent intestinal bacteria could cause “self-infection” and eventual disease, and Dr. Ludwig Brieger, a German physician, described “ptomaines”, waste products of protein metabolism putrefying the entire system, causing disease.

French physician Dr. Charles Bouchard theorized the mechanism of degenerative illness as the autointoxication syndrome, whereby bowel toxins that failed to exit the body with adequate motility would poison the bloodstream, tissues, and brain, leading to pathologies such as Parkinsonian symptoms.

These concepts, tentative and vague, were later adopted mainly by naturopaths in the 21st century, and as a generalization were ridiculed by “skeptics” in the “evidence-based” mainstream medicine world, but there is now rapidly accumulating and substantial evidence that this intestinal influence is central to human pathology.

One of the prototype patients by which Dr. James Parkinson based his conception of the “shaking palsy” (Parkinson’s Disease) went into full remission after being given laxatives and (temporary) opium to regulate his bowels. Dr. Parkinson and the attending physician remarked at the rapid improvement of the patient, a child whose hands had been in “continual agitation” for weeks; “in three or four days the shaking had nearly left him.” Parkinson summarized, “by pursuing this plan, the medicine proving a vermifuge, he could soon walk, and was restored to perfect health.”

Dr. Parkinson also described the case of a 54 year old man suffering from weakness and hand-trembling who, when treated with laxatives (calomel and Epsom salts), recovered in ten days. Why have these observations been ignored, or scrubbed, from the modern medical understanding of Parkinson’s and other neurodegenerative and movement disorders? 

“It may be proper to observe once more, that an important object proposed to be obtained by them is, the leading of the attention of those who humanely employ anatomical examination in detecting the causes and nature of diseases, particularly to this malady. By their benevolent labours its real nature may be ascertained, and appropriate modes of relief, or even of cure, pointed out.”
—James Parkinson, An Essay on the Shaking Palsy (1817)

In searching for more information on the case of that 54 year old patient, I found a coincidental case study of a modern equivalent, a different 54 year old man diagnosed with Parkinson’s in 2004. He had similar symptoms, but was simply placed on “usual medications (trihexyphenidyl and selegiline)”, which actually increased his muscular spasming and abnormal posture, and his overall state continued to worsen. His condition is explained as a rare, inborn genetic defect of amino acid metabolism, and he died before his gene isoforms could be analyzed (Owens and Okun, 2004). The contrast is striking between so-called archaic thinking of classical physicians vs. the sterilized, robotic protocols of modern neurology.

In 2001, a study in the American Academy of Neurology’s journal linked constipation with the development of Parkinson’s (Abbott, et al., 2001), as if unearthing a fossil of truth, but concluded that the “clinical applications of the findings are not yet clear”, since the idea that intestinal health influences brain health wasn’t in the biomedical conceptual vocabulary, at least not in the field of neurology. Interestingly, the opposite possibility was considered by commenting neurogeriatric physician, Dr. Robert Friedland, that early brain-degeneration from Parkinson’s caused the constipation. He was correct, in that once the brain is malfunctioning, the cross-talk between the enteric (intestinal) nervous system and central nervous system breaks down, so a vicious circle ensues whereby brain damage impairs the intestine, and intestinal toxicity exposes the blood and brain to further damage (Charbonneau, HealthDayNews). 

The modern neglect of considering the gut as a potential origin of brain degeneration, which had been discussed as early as Hippocrates in 400 BC, seems to be a result of the Cartesian dualism that separates the brain and body in some abstract hierarchical thinking.


The fact that the emerging research is elucidating the central role of the intestine and its microbiome in Parkinson’s Disease after that connection was already empirically discovered a century ago and has been so long overlooked is especially shameful. It’s encouraging that truth will remain truth regardless of consensus, but the fact that truths can be unearthed and then dismissed and forgotten, to the detriment of the health of hundreds of millions of people is why an attitude of dissent towards established dogma can be so important. 

The authoritarian medical culture that we know today, starting around the 1970s, especially with the gastroenterologists, ridiculed and “debunked” the “quackery” of autointoxication, and reassured the public that of course, diseases like Parkinson’s are genetic, and that there is nothing one can do to cure such illnesses, but instead should focus on “management” and complacent-acceptance as the best one can hope for.

In the past decade, with the explosive trend in microbiome research implicating our digestive system and its bacteria in almost every pathology imaginable, you wouldn’t expect figures in the medical industry to possibly continue to deny the connection, although some of them still do, with almost psychotically delusional, or just extremely lazy, mental gymnastics (Odenwald, 2013). 

The two small purple circles inside the neuron are lewy bodies, first discovered by Dr. Frederic Lewy in 1912, who studied with Dr. Alois Alzheimer.

The evidence of the relationship continues mounting. In Parkinson’s and Lewy body-dementia, there is an observed aggregation of misshapen proteins: the 140 amino acids meant to be built into alpha-synuclein proteins fold incorrectly and aggregate in the brain and retina as an abnormal clumps, partly consisting of phosphorylated alpha-synuclein, an indication that something seriously wrong is occurring in the organism’s ability to regulate its own structure. In marmosets with inflamed colons, the neurons along their intestinal linings had the same aggregation of phosphorylated alpha-synuclein (Resnikoff, et al., 2019).

Since the intestine has an embedded nervous system, called the enteric nervous system, with a demonstrated proliferation of lewy bodies caused by inflammation, the implication is that as a general rule, prolonged inflammation may lead to Parkinsonian artifacts, for example from equivalent inflammation in the brain and central nervous system. In elderly men, it was observed that those with the most frequent bowel movements had the lowest occurrence of lewy bodies in their brains (Abbott, et al., 2007).

Heavy metals and pesticides also demonstrably induce the aggregation of misfolded alpha-synuclein (Rokad, et al., 2017). My article, Parkinson’s Pathology as a Manifestation of Mercury Toxicity, expands on the mechanisms by which the heavy metal mercury causes Parkinson’s Disease.

The vagus nerve is a nerve complex that connects the intestine and brain, enabling communication between them. In 15,000 patients who underwent vagotomies, meaning they had their vagus nerves severed, there was a 50% lower Parkinson’s Disease incidence after 20 years, compared to controls (Svensson, et al., 2015). By cutting off communication between the enteric and central nervous systems, the misfolded alpha-synucleins originating in the gut cannot be transported up the vagus nerve into the brain’s substantia nigra, the central location of damage in Parkinson’s. In rats with severed vagus nerves, none of the brain pathology of Parkinson’s occurred even after the rats had misfolded alpha-synuclein injected into their intestinal neurons. In rats with functioning vagus nerves, this same treatment induced Parkinson’s (Kim, et al., 2019). This goes further than demonstrating a mere gut-brain relationship; it absolutely confirms the possibility of neurodegenerative disease originating in the intestine.

Vagotomies to prevent brain disease aren’t ideal in the same way that mastectomies to avoid breast cancer aren’t ideal. Instead, the discovery is a clue and an indication to further explore and manipulate holistic mechanisms by which we can nourish and protect our guts, and by consequence, save our minds. 


Works Cited

Abbott, R. D., et al. “Frequency of Bowel Movements and the Future Risk of Parkinson’s Disease.” Neurology, vol. 57, no. 3, 2001, pp. 456–462., doi:10.1212/wnl.57.3.456.

Abbott, Robert D., et al. “Bowel Movement Frequency in Late-Life and Incidental Lewy Bodies.” Movement Disorders, vol. 22, no. 11, 2007, pp. 1581–1586., doi:10.1002/mds.21560.

Borghammer, Per, and Clement Hamani. “Preventing Parkinson Disease by Vagotomy.” Neurology, vol. 88, no. 21, 2017, pp. 1982–1983., doi:10.1212/wnl.0000000000003969.

Charbonneau, Nicolle. “Constipation Raises Risk of Parkinson’s.” Consumer HealthDay, 13 Aug. 2001,

Chen, Qian-Qian, et al. “Gut Inflammation in Association With Pathogenesis of Parkinson’s Disease.” Frontiers in Molecular Neuroscience, vol. 12, 2019, doi:10.3389/fnmol.2019.00218.

Kaufmann, Horacio. “Cutting the Vagal Highway Blocks One Point of Entry for Prion-like Alpha-Synuclein.” Annals of Neurology, vol. 78, no. 4, 2015, pp. 520–521., doi:10.1002/ana.24492.

Kim, Sangjune, et al. “Transneuronal Propagation of Pathologic α-Synuclein from the Gut to the Brain Models Parkinson’s Disease.” Neuron, vol. 103, no. 4, 2019, doi:10.1016/j.neuron.2019.05.035.

Lesser, G. T., et al. “Frequency of Bowel Movements and Future Risk of Parkinson’s Disease.” Neurology, vol. 58, no. 5, 2002, pp. 838–839., doi:10.1212/wnl.58.5.838-a.

Owens, W E. “Dystonia, Tremor, and Parkinsonism in a 54 Year Old Man with 2-Hydroxyglutaric Aciduria.” Journal of Neurology, Neurosurgery & Psychiatry, vol. 75, no. 9, 2004, pp. 1362–1363., doi:10.1136/jnnp.2003.033571.

Resnikoff, Henry, et al. “Colonic Inflammation Affects Myenteric Alpha-Synuclein in Nonhuman Primates.” Journal of Inflammation Research, Volume 12, 2019, pp. 113–126., doi:10.2147/jir.s196552.

Rokad, Dharmin, et al. “Role of Neurotoxicants and Traumatic Brain Injury in α-Synuclein Protein Misfolding and Aggregation.” Brain Research Bulletin, vol. 133, 2017, pp. 60–70., doi:10.1016/j.brainresbull.2016.12.003.

Svensson, Elisabeth, et al. “Vagotomy and Subsequent Risk of Parkinson’s Disease.” Annals of Neurology, vol. 78, no. 4, 2015, pp. 522–529., doi:10.1002/ana.24448.

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