Intestinal Barrier, Vitamin B Deficiencies Linked to Parkinson’s

An association between gut microbes and Parkinson’s disease (PD) has been shown in a recent study. Researchers discovered that PD patients have fewer genes that synthesize vital B vitamins, which could weaken the intestinal barrier and cause inflammation in the brain. According to this research, B vitamin supplements may provide PD patients with a therapeutic option.

Important Details:

• PD sufferers’ stomachs contain fewer microbes that produce B vitamins.
• Brain inflammation may result from a B vitamin deficiency’s weakened gut barrier.
• Supplementing with B vitamins may be one way to treat Parkinson’s disease.

Source: University of Nagoya

According to research conducted by the Graduate School of Medicine at Nagoya University in Japan, there is a connection between Parkinson’s disease (PD) and gut flora. The genes in the gut flora that synthesize the vital B vitamins B2 and B7 were found to be less prevalent.

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They also discovered a connection between low concentrations of substances that support intestinal barrier integrity and the absence of these genes. Toxins that induce the inflammation associated with Parkinson’s disease (PD) are kept out of circulation by this barrier.

According to their research published in npj Parkinson’s Disease, PD may be treated by administering B vitamin supplements to correct these deficiencies. 

Many physical symptoms, including stiffness, delayed movement, shaking, and balance issues, are indicative of Parkinson’s disease (PD) and can make daily tasks and mobility difficult. Although the prevalence of Parkinson’s disease (PD) varies throughout populations, it is thought to impact 1% to 2% of people 55 years of age or older.

The microorganisms known as gut microbiota, which are located in the gut, have a significant impact on several physiological processes. Under ideal circumstances, the intestinal barrier that keeps toxins out of circulation is maintained by the gut microbiota’s production of polyamines and SCFAs.

Blood toxins can go to the brain, where they impair neurotransmission processes that are essential for preserving mental health and induce inflammation. 

Hiroshi Nishiwaki and Jun Ueyama of the Nagoya University Graduate School of Medicine performed a metanalysis of stool samples from PD patients in Taiwan, Germany, China, Japan, and the United States to gain a better understanding of the relationship between the microbial characteristics of the gut in the disease.

Shotgun sequencing is a method that they employ to sequence every genetic molecule in a sample. Because it gives researchers a greater understanding of the microbial population and genetic makeup of the sample, this is an advantageous technique. 

In PD patients, they found a reduction in the bacterial genes that produce the vitamins B2 and B7, riboflavin and biotin, respectively. Food and gut microbiota-derived riboflavin and biotin have anti-inflammatory qualities that may mitigate the neuroinflammation associated with Parkinson’s disease (PD).

Short-chain fatty acids (SCFAs) and polyamines are two substances that support the integrity of the intestinal barrier and keep toxins out of the bloodstream. B vitamins are essential for these metabolic activities. Patients with Parkinson’s disease (PD) showed reductions in both when fecal metabolites were examined.  

The findings indicate a potential explanation for the progression of PD. “Deficiencies in polyamines and SCFAs could lead to thinning of the intestinal mucus layer, increasing intestinal permeability, both of which have been observed in PD,” Nishiwaki explained.

“This higher permeability exposes nerves to toxins, contributing to abnormal aggregation of alpha-synuclein, activating the immune cells in the brain, and leading to long-term inflammation.”  

He added, “Supplementation therapy targeting riboflavin and biotin holds promise as a potential therapeutic avenue for alleviating PD symptoms and slowing disease progression.” 

The findings indicate a potential explanation for the progression of PD. “Deficiencies in polyamines and SCFAs could lead to thinning of the intestinal mucus layer, increasing intestinal permeability, both of which have been observed in PD,” Nishiwaki explained.

“This higher permeability exposes nerves to toxins, contributing to abnormal aggregation of alpha-synuclein, activating the immune cells in the brain, and leading to long-term inflammation.”  

He added, “Supplementation therapy targeting riboflavin and biotin holds promise as a potential therapeutic avenue for alleviating PD symptoms and slowing disease progression.” 

The study’s findings emphasize how crucial it is to comprehend the intricate connection between neurodegeneration, metabolic pathways, and gut flora. In the upcoming years, treatment plans may be tailored to each patient’s microbiome profile. Through manipulation of the microbiome’s bacterial composition, medical professionals may be able to postpone the manifestation of Parkinson’s disease symptoms.

“We could perform gut microbiota analysis on patients or conduct fecal metabolite analysis,” Nishiwaki said.

“Using these findings, we could identify individuals with specific deficiencies and administer oral riboflavin and biotin supplements to those with decreased levels, potentially creating an effective treatment.” 

For more information: Meta-analysis of shotgun sequencing of gut microbiota in Parkinson’s disease, npj Parkinson’s disease, https://doi.org/10.1038/s41531-024-00724-z