Understanding the Relationship Between Constipation and Parkinson’s
As technology progresses, understanding about the intensive dialogue between the gut and the brain is also getting better. It is now understood that if things go wrong with this exchange, it is terrible for both of them. Changes in the activity of the gut may worsen the functioning of the brain, while if anything disturbs the brain than it would affect the movement of the gut.
When it comes to Parkinson’s, it has been long known that constipation is an early, non-motor symptom of the disease. In fact, in the vast majority of cases, chronic constipation can be regarded as of the initial signs. Constipation is when a person fails to defecate for more than three days. In Parkinson’s this issue of sluggish bowel movements can arise 10 to 20 years before the appearance of motor symptoms and is present in 60-80% of the cases.
The vagal nerve is the most vital mediator in communication between the gut and brain. Pathological studies have indicated that in the early stages for Parkinson’s, the formation of Lewy bodies in the dorsal nucleus of vagal nerve is the hallmark of the disease, with substantia nigra affected only in the later stages. Studies have also indicated that working of vagal nerve is altered in the earliest stage of the Parkinson’s, thus causing the slowdown in the intestinal movement. Though, how and why it happens is poorly understood. There is even a hypothesis that some intestinal toxins are absorbed via the intestines and assimilated into the terminal part of the vagal nerve axon, and further, they are transported to the vagal nucleus in a retrograde manner.
On the other hand, it is entirely possible that certain lifestyle habits like inadequate water intake, intake of food poor in dietary fibers, could be one of the reasons behind chronic constipation, which, if not taken care of over an extended period, may increase the risk of Parkinson’s. Thus, in one of the clinical studies done in Japan, it was found that people with an early stage of Parkinson’s had decreased bowel movement along with markedly reduced water intake. It was a study that involved 90 individuals, who were starting to show the signs of Parkinson’s. Though the nutrition status in these individuals does not differ much from the control group, but higher consumption of animal fat and low water intake was more common in the group being studied. The study also found the interesting fact that those who have Parkinson’s had a low desire to drink water for most of their life, and more than 70% had chronic constipation for years before being diagnosed with Parkinson’s. On average constipation started around 18 years before the motor symptoms of Parkinson’s. Some early studies found that a coffee drinking habit may also have a protective role in Parkinson’s, but it is not clear on whether it happens due to caffeine or merely due to better fluid intake.
In one of the meta-analysis by Adams-Carr et al., it was found that those with constipation were at 2.28-time higher risk of developing Parkinson’s later in the life.
So what is the exact nature of constipation in Parkinson’s disease? To answer these questions, researchers carried out a detailed bowel movement study in 22 Parkinson's patients , and compared their bowel movement with 15 healthy subjects (control group). In the study, researchers measured the gastric, small intestine, cecum, ascending colon transit times, along with the colonic motility at the time of defecation. In the study they found that those who have Parkinson’s had a much longer small intestine, cecum, and ascending colon transit time, indicating slower bowel movement. Research also found that gastric emptying was unaffected by Parkinson’s. It also found that in Parkinson’s propagation of colonic movement was much quieter. Thus the study showed that in Parkinson’s although the movement of the stomach is preserved, but the movement of small and large intestine in much-slowed down.
Does constipation cause Parkinson’s or is it the other way around?
Though the various studies undoubtedly indicate the relationship between constipation and Parkinson’s, they do not answer one of the most critical questions. Is constipation just an early sign of Parkinson’s or is constipation itself is something that increases the risk of developing Parkinson’s later in life? The complexity of the question is evident from the fact that constipation ensues much earlier than motor symptoms, in fact in many cases a couple of decades before.
It is entirely possible that constipation is just one of the earliest symptoms of Parkinson’s. It makes sense if we consider the fact that Parkinson’s is not an acute condition, it is something that develops over an extended period of time. In fact, there is no way to say precisely the beginning of Parkinson’s, until the typical motor symptoms develop. Yet, we know very well that constipation is quite common in many neurological diseases, and this is even true about those with motor and neurological issues like stroke victims and spinal disorders. Therefore, Parkinson’s is not an exception to this as it is a disease of motor function. So, it is entirely possible that in the very early stages of development of Parkinson’s, there are specific changes in the control of bowel movements, though other movement disorders like stiffness and rigidity are still not evident. If this is the case, it is entirely possible that constipation may help in identifying Parkinson’s in the future.
On the other hand, some theories say Parkinson’s is instead a result of chronic, poorly managed constipation. Adherent to this theory state that those with chronic constipation have the persistent gut inflammatory syndrome. This chronic inflammation of the gut over an extended period leads to changes in the immune responses leading to the Parkinson’s disease. This triggering of Parkinson’s could be both via vagal communication and direct penetration of neuro-inflammatory substances via blood-brain barrier.
Well, whatever the truth is, it undoubtedly remains as a chicken and egg type question. With the present evidence, it is not possible to conclude whether it is chronic constipation that causes Parkinson’s or if it is just an early sign of it. But what can be said with absolute confidence is that there is an association between the two, with constipation seen decades before motor symptoms of Parkinson's develop.
Whatever the cause, constipation is an unpleasant condition that worsens the quality of life and thus, must be managed in the best possible way. In the early stages, it is best to start with dietary modifications like increasing the fluid intake by 6-8 glasses of water a day, eating plenty of fresh fruits and vegetables, eating more of whole grains and other food items rich in dietary fiber. Adding bran to increase the bulk may be a good idea. Exercise is known not only to help with constipation, but also to slow down the symptoms of Parkinson’s. As the disease advances, patients may need to take medications like milk of magnesia, Mosapride, Cisapride, suppositories, enemas, and stool softeners like lactulose6.
References
1. Ueki A, Otsuka M. Life style risks of Parkinson’s disease: Association between decreased water intake and constipation. J Neurol. 2004;251 Suppl 7:vII18-23. doi:10.1007/s00415-004-1706-3.
2. Adams-Carr K, Schrag A, Shribman S, Bestwick J, Lees A, Noyce A. Constipation Preceding Parkinson’s Disease–Meta-Analysis. J Neurol Neurosurg Psychiatry. 2015;86(11):e4-e4. doi:10.1136/jnnp-2015-312379.98.
3. Knudsen K, Haase A-M, Fedorova TD, et al. Gastrointestinal Transit Time in Parkinson’s Disease Using a Magnetic Tracking System. J Park Dis. 2017;7(3):471-479. doi:10.3233/JPD-171131.
4. Winge K, Rasmussen D, Werdelin LM. Constipation in neurological diseases. J Neurol Neurosurg Psychiatry. 2003;74(1):13-19. doi:10.1136/jnnp.74.1.13.
5. Houser MC, Tansey MG. The gut-brain axis: is intestinal inflammation a silent driver of Parkinson’s disease pathogenesis? Npj Park Dis. 2017;3(1):3. doi:10.1038/s41531-016-0002-0.
6. Constipation in Parkinson’s disease. Ann Indian Acad Neurol. 2011;14(Suppl1): S15-S16.
