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General practitioner
The gut is a key factor in our overall health and has a significant impact on the risk of chronic diseases such as heart disease, obesity, sleep problems and depression.
Parkinson's is a disease of the central nervous system. Common symptoms are tremors and balance problems. The disease is idiopathic, which means that it has no (yet) known cause.
Some scientists published their research findings in the specialist journal "Neuron". They believe that Parkinson's may originate in intestinal cells and travel to the brain via the vagus nerve. The vagus nerve is the tenth cranial nerve, which extends from the brain stem to the abdomen.
If this is the case, completely new ways of prevention and treatment open up, starting with strengthening intestinal health. Of course, other factors that contribute to the development of Parkinson's disease should not be ignored.
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Alpha-synuclein is a protein that is naturally present in the human body. If proteins are folded incorrectly, they can clump together and damage nerve cells. This results in so-called Lewy bodies - areas of dead brain matter. These lead to Parkinson's symptoms such as movement and speech disorders.
In 2003, research by German neuroanalyst Dr. Heiko Braak suggested for the first time that Parkinson's could have its origins in the gastrointestinal tract.
The study presented was conducted on mice and provides "the first experimental evidence that Parkinson's begins in the gut and spreads via the vagus nerve," study author Dr. Ted Dawson, professor of neurology at Johns Hopkins University School of Medicine, told the Guardian.
Researchers injected misfolded alpha-synuclein into the intestines of healthy mice and then tracked its path through the body. One month later, it was detected in the brain stem, and after three months it had reached the amygdala and midbrain. Within seven to ten months, it had appeared in other regions of the brain.
Next, the researchers injected the misfolded proteins into the intestines of mice with a severed vagus nerve. After seven months, there were no signs of cell death in the brains of the mice. Apparently, the proteins were unable to reach the brain. The study also examined behavioral changes in the individual groups of mice, such as their nest-building abilities.
After seven months, it was found that the mice that had received the misfolded proteins and had an intact vagus nerve built smaller, messier nests - a sign of problems with movement control. Mice that did not receive the injection, as well as the mice that received the injection but had their vagus nerve severed, consistently scored higher in nest-building activity.
Mice with an intact vagus nerve that received the proteins showed memory difficulties and anxiety. The scientists were unable to detect these symptoms in mice in control groups. "Our study supports the Braak hypothesis in the genesis of idiopathic Parkinson's disease," the researchers concluded.
Dawson added to Medical News Today: "In this model, the disease originated in the gut. This allows scientists to study the full spectrum and time course of Parkinson's pathogenesis" and potentially find ways to halt the progression of symptoms.
Further evidence that Parkinson's originates in the intestine and can reach the brain via the vagus nerve was provided by a study with test subjects from whom part of the vagus nerve had previously been removed. This is often done in patients with ulcers to reduce the amount of acid secretion and reduce the risk of stomach ulcers.
Using the national registry in Sweden, researchers compared the data of 9,430 people who had a vagotomy with the data of more than 377,200 people who did not have this operation. Although the scientists found no difference in the total number of people who developed Parkinson's over time, after further analysis they discovered an interesting correlation.
People who had a truncal vagotomy - in which the trunk of the nerve was completely removed as opposed to a selective vagotomy - had a 40 percent lower risk of developing Parkinson's disease.
Further research published in 2016 also established a functional link between specific gut bacteria and the onset of Parkinson's disease. Using mice in which overexpression of alpha-synuclein was initiated, the researchers found that "gut microbial flora is required for motor deficits, microglial activation and αSyn[protein α-synuclein] pathology."
Furthermore, the researchers came to the following conclusion: "Antibiotic treatment improves while microbial recolonization promotes pathophysiology in adult animals. This suggests that postnatal signaling between the gut and brain leads to modulations of the disease." Other compounds were also found in the study, including:
The researchers came to the following conclusion: "These results show that gut bacteria can regulate movement disorders in mice and suggest that changes in the human microbiome are a risk factor for Parkinson's disease." This link makes perfect sense, as symptoms in the digestive tract such as constipation occur decades before other Parkinson's symptoms.
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The gut is a fascinating area of research that should definitely be pursued further in relation to Parkinson's. Other factors are also likely to play a role, including exposure to external toxins such as pesticides. Pesticide exposure is closely linked to Parkinson's and can increase the risk by 80 percent in some cases.
It is assumed that pesticides can contribute to dopaminergic neuron death. Even low levels of exposure can lead to mutations that cause Parkinson's disease. In one study, researchers exposed dopamine-producing neurons to two pesticides. This prevented the mitochondria from moving properly, which led to a loss of energy within the neurons.
"People who are exposed to these chemicals have an approximately 250 percent higher risk of Parkinson's disease - in contrast to the rest of the population," reports study author Scott Ryan from the University of Guelph in a press release.
"Until now, the established link between pesticides and Parkinson's was primarily based on animal studies and epidemiological studies that showed that farmers and other people exposed to agricultural chemicals are at increased risk. We are one of the first to study what happens in human cells."
In addition, people with a genetic predisposition to Parkinson's may be more affected by exposure to pesticides and may be at risk from lower levels. "People with a predisposition to Parkinson's are more affected by this low-level exposure to agricultural chemicals and are therefore more likely to develop the disease," Ryan explains. "That's one of the reasons why some people near agricultural areas are at higher risk."
Avoid the use of pesticides by not using them in your home or garden and eating as much organic or biodynamically grown food as possible. By doing so, you can reduce your own risk of Parkinson's. Improve your gut health with the following tips:
Eat plenty of fermented foods - healthy products include lassi, fermented kefir made from pasture milk, natto (fermented soy) and fermented vegetables.
Take probiotic supplements - Even if you're not a big proponent of taking many supplements, probiotics are an exception, especially if you don't regularly consume fermented foods.
Increase your intake of soluble and insoluble fiber and focus on vegetables, nuts and seeds, including sprouted seeds.
Get your hands dirty in the garden - Exposure to bacteria and viruses can help boost your immune system and ensure long-lasting immunity to disease.
Ventilate! - Scientific research shows that ventilation can improve natural airflow and the diversity and health of microbes in the home, which in turn benefits your health.
Wash your dishes by hand instead of in the dishwasher. - Research has shown that washing dishes by hand leaves more bacteria on the dishes than dishwashers. Eating from these less sterile dishes can reduce your risk of allergies by stimulating your immune system.
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Antibiotics unless absolutely necessary. If you do use antibiotics, make sure you colonize your gut with fermented foods and/or a high-quality probiotic supplement with good bacteria.
Conventionally farmed meat and other animal products, as such animals are routinely given low doses of antibiotics.
Chlorinated and/or fluoridated water - especially when bathing or showering, which is even worse than drinking such water.
Processed foods usually contain a lot of sugar, salt and artificial additives. Refined wheat and sugar, for example, have a negative effect on the gut.
Glyphosate (Roundup) in particular is a known antibiotic and has the potential to kill many beneficial gut bacteria if you eat food contaminated with it.
As it kills both good and bad bacteria and contributes to the development of antibiotic resistance
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Sources (in English):
Braak, H., Rüb, U., Gai, W. P. & Del Tredici, K. (2003, May). Idiopathic Parkinson's disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen. Journal of Neural Transmission, 110(5):517-36, doi: 10.1007/s00702-002-0808-2
Kim, S., Kwon, S. H., Kam, T. I., Dawson, V. L., Dawson, T. M. & Ko, H. S. (2019, August). Transneuronal Propagation of Pathologic α-Synuclein from the Gut to the Brain Models Parkinson’s Disease. Neuron, Volume 103, Issue 4, P627-641.E7, doi: 10.1016/j.neuron.2019.05.035
Wang, Z., Klipfell, E., Bennett, B. J., Koeth, R., Levison, B. S., Dugar, B., et al. (2011, April). Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature, 472(7341):57-63, doi: 10.1038/nature09922.
Karlsson, C. L., Molin, G., Fak, F., Johansson Hagslätt, M. L., Jakesevic, M., Hakansson, A., Jeppsson, B. et al. (2011, September). Effects on weight gain and gut microbiota in rats given bacterial supplements and a high-energy-dense diet from fetal life through to 6 months of age. The British Journal of Nutrition, 106(6):887-95, doi: 10.1017/S0007114511001036
Anderson, J. R., Carroll, I., Azcarate-Peril, M. A., Rochette, A. D., Heinberg, L. J., Peat, C. et al. (2017, October). A preliminary examination of gut microbiota, sleep, and cognitive flexibility in healthy older adults. Sleep Medicine, 38:104-107, doi: 10.1016/j.sleep.2017.07.018
Suez, J., Korem, T., Zilberman-Schapira, G., Segal, E. & Elinav, E. (2015, April). Non-caloric artificial sweeteners and the microbiome: findings and challenges. Gut Microbes, 6(2): 149–155, doi: 10.1080/19490976.2015.1017700
Kembel, S. W., Jones, E., Kline, J., Northcutt, D., Stenson, J., Womack, A. M., et al. (2012, August). Architectural design influences the diversity and structure of the built environment microbiome. The ISME Journal, 6(8):1469-79, doi: 10.1038/ismej.2011.211
Pinto-Sanchez, M. I., Hall, G. B., Ghajar, K., Nardelli, A., Bolino, C., Lau, J. T. (2017, August). Probiotic Bifidobacterium longum NCC3001 Reduces Depression Scores and Alters Brain Activity: A Pilot Study in Patients With Irritable Bowel Syndrome. Gastroenterology, Volume 153, Issue 2, doi: 10.1053/j.gastro.2017.05.003
Liu, B., Fang, F., Pedersen, N. L., Tillander, A., Ludvigsson, J. F., Ekbom, A. et al. (2017, May). Vagotomy and Parkinson disease. Neurology, 88 (21), doi: 10.1212/WNL.0000000000003961
Sampson, T. R., Debelius, J. W., Thron, T., Wittung-Stafshede, P., Knight, R. & Mazmanian, S. K. (2016, December). Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease. Cell, Volume 167, Issue 6, P1469-1480.E12, doi: 10.1016/j.cell.2016.11.018
Perez-Pardo, P., Dodiya, H., B., Engen, P. A., Forsyth, C. B., Huschens, A. M., Shaikh, M. (2018, December). Role of TLR4 in the gut-brain axis in Parkinson’s disease: a translational study from men to mice. BMJ Journals, 68:829-843, doi: 10.1136/gutjnl-2018-316844.
Wang, A., Costello, S., Cockburn, M., Zhang, X., Bronstein, J. & Ritz, B. (2011, July). Parkinson’s disease risk from ambient exposure to pesticides. European Journal of Epidemiology, 26: 547, Volume 26, Issue 7, pp 547–555, doi: 10.1007/s10654-011-9574-5
Stykel., M. G., Humphries, K., Kirby, M. P., Czaniecki, C., Wang, T. et al. (2018, September). Nitration of microtubules blocks axonal mitochondrial transport in a human pluripotent stem cell model of Parkinson’s disease. The FASEB Journal, Vol. 32, No. 10, doi: 10.1096/fj.201700759RR
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