By Yehudis Kundin, Staff Writer
Although bacteria are typically perceived as harmful, some actually play a crucial role in our health. The gut microbiome is a prime example of this, referring to the distinct ecosystem in your gut in which thousands of species of bacteria thrive. Your “gut” roughly refers to your gastrointestinal tract, or digestive tract, which is a tube from the mouth to the anus responsible for digesting food, absorbing nutrients and eliminating waste. However, it is colloquially used to mean the intestines, and it is specifically in the large intestines (colon) where the gut microbiome resides.
We have a symbiotic relationship with our gut bacteria, providing them with food and shelter while they perform several essential functions for our body. For example, they help the body break down complex carbohydrates and dietary fibers that our body can’t break down on its own. They also provide the enzymes necessary to synthesize important vitamins such as B1, B9, B12 and K. The gut microbiome also affects the nervous system, stimulating the production of neurotransmitters in the gut that then send chemical signals to the brain.
This link between the gut and the brain has been subject to suspicion by many researchers regarding the onset of Parkinson’s disease (PD). PD is a neurodegenerative disorder that affects 10 million people worldwide. It is a disease in which dopaminergic (dopamine-producing) neurons are damaged in an area of the brain known as the substantia nigra, which is primarily responsible for movement control. Symptoms generally develop slowly over the years, varying slightly from person to person. Some motor-related symptoms include tremor, slowness and paucity of movement, muscle stiffness and balance problems, but PD patients often experience symptoms unrelated to motor control as well, including depression, anxiety, sleep disorders, constipation and a variety of cognitive impairments. With the cause largely unknown, available treatments primarily alleviate singular symptoms, without actually slowing the disease progression.
Previous studies sought to determine whether changes in the body outside of the brain can be found before PD onset and perhaps contribute to its development. Since REM sleep behavior disorder (RBD) is a prodromal marker of PD, emerging up to 20 years before patients develop PD, researchers from China and Germany compared fecal samples of PD patients with those of patients experiencing RBD to ascertain whether any deficiencies in the body appear before PD onset. They found that both had a similar deficiency in the bacteria that produce short-chain fatty acids (SCFAs). SCFAs are essential for the maintenance of the gut barrier, the wall that separates the intestines from the bloodstream. A lack of SCFAs leads to higher permeability in the intestines, allowing a build-up of alpha-synuclein proteins, which are known to lead to motor impairment in PD. This discovery demonstrated a strong connection between gut deficiencies and PD.
A different study performed in 2003, also investigating possible roots of PD, discovered a similar connection. It found that despite adequate dietary intake, individuals with PD were found to have suboptimal levels of riboflavin (vitamin B2), which is largely synthesized by the gut bacteria. When patients were treated with supplemental riboflavin, complemented by the elimination of red meat (a known risk factor for neurodegenerative diseases) from their diets, motor capacity was improved.
Medical researchers Hiroshi Nishiwaki and Jun Ueyama from Nagoya University in Japan sought to determine the mechanisms underlying these gut deficiencies with the hopes of creating an effective treatment for alleviating PD symptoms and slowing the progression of the disease. Nishiwaki and Ueyama analyzed fecal samples of 94 patients with PD and 73 relatively healthy controls from Japan and then compared them with data from China, Taiwan, Germany and the United States. They used shotgun sequencing, a tool for determining the DNA sequence of a genome, to identify the genes in the samples. While bacterial types varied in different countries, the commonality among PD patients was the decrease in bacterial genes responsible for synthesizing riboflavin and biotin (vitamin B7). They showed that this lack of vitamins was what was causing the decrease in SCFAs found in previous research, which resulted in the thinning of the intestinal mucus layer. This weakened protection exposes the intestinal tract to toxins we encounter regularly in our environment, including herbicides, pesticides and cleaning chemicals. These toxins are the cause of the abnormal aggregation of alpha-synuclein proteins found in previous research, which activate immune cells in the brain and trigger neuroinflammation. This inflammation is what causes the muscle impairment characteristic of PD.
Based on this research, supplementing the diets of PD patients with riboflavin and biotin is a promising avenue for effective non-invasive therapeutic treatment to alleviate PD symptoms and slow the disease’s progression. These results also highlight the importance of analyzing the complex relationship between the gut microbiome and neurodegeneration. Identifying the unique microbiome profile of each patient can allow doctors to address patient-specific deficiencies and create personalized treatments to alter their bacterial levels, alleviating and potentially delaying the onset of symptoms.
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