A Parkinsonian gastrointestinal tract
29th of November 2018
Years before I am diagnosed with Parkinson’s disease, my intestines are playing out. Stinging pains, abdominal distention. The GP suspects sensitive intestines and sends me to the hospital for an endoscopy, a look in the intestines with a tube, light and camera. That does not shed any light on the matter and the pain remains.
After my diagnosis I dive into the scientific literature and I learn that many Parkinson’s patients have been plagued by gastrointestinal problems such as stomach ulcer and constipation for years before the official diagnosis. Chronic inflammation of the gastro-intestinal region could – in a certain subtype of Parkinson’s – even be a link in the cascade that causes or worsens Parkinson’s disease (1,2).
One of the most common non-motor symptoms in Parkinson’s Disease is GI dysfunction, with a prevalence of 70-80%. GI symptoms are identified as bloating, constipation, nausea, delayed gastric emptying and prolonged intestinal transit time | Paula Pérez Pardo (3)
I learn that people with Parkinson’s Disease have a different composition of the intestinal bacteria than healthy people (4) and that this is not innocent. For example, PD patients have less prevotella bacteria. Prevotellas are known to make building blocks for a solid intestinal wall. If there are fewer prevotella bacteria, this can lead to a so-called leaky gut. Substances and bacteria – that do not belong to the other side of the intestinal wall – can then seep through such a permeable bowel. And chronic inflammation may be the result.
It is not possible to determine whether the changes are a cause or consequence of Parkinson’s disease. But allowing chronic inflammation to persist can possibly speed up the process. The question that gives hope is therefore:
Would it be possible to break the vicious circle in the gastrointestinal tract?
You can, for example, influence the composition of your bacteria, and possibly also the inflammation, with:
- a poo transplant. In patients with MS they are already investigating this intervention.
But … then you should first of all know whether this type of chronic inflammation plays a role in ‘your Parkinson’s’.
I decide to start an experiment to see how far the gastroenterologists are in their line of thinking. I have two goals:
- A personal goal
I want to get rid of my pain. Based on my complaints, I ask my neurologist for a referral. He indicates that such a referral is not standard for Parkinson’s Disease, but he makes one for me anyway.
- An experimental goal
I want to know to what extent the gastroenterologists already believe that a leaky gut leads to chronic inflammation in the intestines, with all possible consequences. And if so, whether they want to test whether my subtype has such a chronic inflammation.
Armed with a poster, I make my appearance at gastroenterologist’s.
The reaction of the gastroenterologist is twofold:
- For me personally
The doctor finds that my complaints are more like stomach problems than intestinal complaints. She sends me home with omeprazole. On my second visit we conclude that this did not help sufficiently and that I could suffer from gastroparesis: a delayed gastric emptying. Very simplified this means that the muscles that have to contract to digest your food, listen less well. Subsequently, that means that food stays in your stomach longer with pain as a result. The gastroenterologist can determine whether I have gastroparesis with a gastric depletion test. But I do not want that. First, I want to find out what I can do myself in order to speed up gastric emptying. The doctor indicates that I can start with not eating anything anymore after dinner. The reason being that at night, even gravity does not help anymore with digesting your food, which aggravates the pain. If that does help enough, she could prescribe a stomach motility enhancer (an improver of the mobility of the stomach) such as domperidom.
- For the experiment
The doctor indicates that she can not test whether I have a leaky gut because with the determination of a leaky gut alone there is no solution to prevent it. Understandable. I will have to find other ways to continue the experiment.
In the meantime .. my pain has gone away
- Chew well;
- Stay upright for at least an hour after eating (or even better: go for a walk);
- Do not eat too much fat (fat from the diet slows gastric emptying);
- Eat more cooked and less raw vegetables (cooked vegetables more easily passes the stomach).
With these advices I am now almost pain free. I find it remarkable that I had to proactively go through several doors of healthcare to find such a seemingly simple solution to my pain. Maybe doctors start prescribing before they truly understand the problem?
And my experiment? That will continue. As a next step, I will interview Prof. Dr. Aletta Kraneveld. My main question: How can we bring science and healthcare closer together?
(1) Braak H., Del Tredici K., Rüb U., de Vos R.A.I., Steur E.N.H.J, Braak E. (2003) Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol Aging 24:197–211. https://doi.org/10.1016/S0197-4580(02)00065-9
(2) Rietdijk, C. D., Perez-Pardo, P., Garssen, J., van Wezel, R. J., & Kraneveld, A. D. (2017). Exploring Braak’s Hypothesis of Parkinson’s Disease. Frontiers in neurology, 8, 37. Retrieved from https://doi:10.3389/fneur.2017.00037
(3) Paula Pérez Pardo. Targeting the Gut-Brain axis in Parkinson’s disease. (2017). [THESIS]. Retrieved from https://dspace.library.uu.nl/bitstream/handle/1874/354242/Perez_Pardo.pdf?sequence=1&isAllowed=y
(4) Scheperjans, F., Aho V., Pereira P.A., Koskinen K., Paulin L., Pekkonen E., Haapaniemi E., Kaakkola S., Eerola-Rautio J., Pohja M., Kinnunen E., Murros K., Auvinen P. (2015) Gut microbiota are related to Parkinson’s disease and clinical phenotype. Mov Disord. Mar;30(3):350-8. Retrieved from http://www.wilson-disease.org/Editor/eWebeditor/uploadfile/20150831170701195.pdf.