Diet's impact on gut bacteria offers new clues in Parkinson's disease management

By Dr. Priyom Bose, Ph.D.

A recent Npj Parkinson’s Disease study investigates the association between diet and gut microbiome composition in an effort to identify the functional pathways that affect patients with Parkinson’s disease (PD).

Diet’s impact on gut bacteria offers new clues in Parkinson’s disease management

Study: Diet and the gut microbiome in patients with Parkinson’s disease. Image Credit: Chinnapong / Shutterstock.com

Diet and PD risk

PD is one of the most common neurodegenerative diseases associated with aging. Some common symptoms associated with PD include progressive motor impairment, as well as non-motor symptoms, such as gastrointestinal (GI) dysfunction, depression, constipation, and cognitive impairment. Specific non-motor symptoms may manifest decades before clinical diagnosis during its prodromal stages.

Previous studies have shown that diet plays a critical role in PD incidence and progression. For example, those who adhere to a high-quality diet measured by the alternate Mediterranean Diet Score (aMED) and Alternative Healthy Eating Index (AHEI) are at a lower risk of PD, whereas lower Healthy Eating Index (HEI) —2015 scores have been associated with chronic constipation and hyposmia in PD patients.

Previously, a correlation between cognitive impairment and low fiber intake was established. Additionally, many patients diagnosed with PD at a relatively younger age have reported greater sugar consumption habits.

Poor diet and aging modify the composition of the gut microbiome, in which the concentration of beneficial bacteria decreases and harmful bacteria increases. The gut microbiome’s inadequate synthesis of essential nutrients and elevated levels of toxins could result in neurodegeneration and neuroinflammation.

PD patients typically exhibit lower levels of putative short-chain fatty acid (SCFA)- producing bacteria, such as Coprococcus and Butyricicicoccus, as well as higher levels of Akkermansia, pro-inflammatory bacteria. Importantly, SCFAs have anti-inflammatory properties that influence the enteric nervous system, modulate inflammation in the central nervous system, and support normal microglia development.

To date, few studies have examined the role of diet in the development and progression of PD. Therefore, additional research is needed to explore this relationship and ultimately use these findings to develop suitable interventions to alleviate GI symptoms in PD.

About the study

The current study investigated the association between diet and gut microbial diversity, composition, abundance, and its predicted metagenome in PD patients. To this end, a cross-sectional analysis was performed using a subgroup of PD patients from the Parkinson’s Environment and Gene (PEG) study that recruited 832 PD patients between 2001-2007 (PEG1) and 2011-2017 (PEG2).

Patients diagnosed with PD in the last three to five years, were residents of California for at least five years, and did not have other neurological conditions or a terminal illness were recruited. Fecal samples were collected from patients who were re-contacted between 2017-2020 (PEG-Gut).

A total of 85 participants fulfilled all eligibility criteria and were considered in the current analysis. The study cohort completed the Diet History Questionnaire II (DHQ II) for dietary assessments. Diet quality was measured using the HEI-2015, with total scores ranging between zero and 100 points.

Study findings

Most of the study participants were men of European ancestry, non-smokers, overweight, and well-educated. Interestingly, most PD patients developed constipation in the lowest HEI score tertile.

Consistent with previous reports, the current study confirmed the benefits of a high-quality diet in maintaining a healthy gut in PD patients. A healthy diet leads to reduced putative pro-inflammatory bacteria, which are abundantly found in PD patients as compared to healthy individuals.

Adherence to a high-quality diet with a high HEI score increased the abundance of SCFA-producing bacteria, such as Coprococcus1, Ruminococcaceae, Butyricicoccus, NK4A214 group, Hydrogenoanaerobacterium, Romboutsia, Negativibacillus, and Ruminococcaceae UCG-003 in PD patients. These bacteria synthesize butyrate that reduces inflammation, thereby providing energy for intestinal epithelial cells and strengthening the intestinal epithelium.

Those who reported greater consumption of added sugar exhibited decreased levels of Romboutsia Butyricicoccus and Coprococcus 1. Increased levels of amyloid-producing bacteria, Klebsiella, were also observed.

PD patients often exhibit increased levels of pro-inflammatory cytokines in the serum and colon, which reflects systemic inflammation that could ultimately activate microglia. The activation of microglia is inherently associated with the progression of PD.

Mechanistically, a healthy diet decreases taurine degradation, lipopolysaccharide biosynthesis, as well as the number of circulating lipopolysaccharides and systemic inflammation in PD. A healthy diet in PD patients also increases the Ruminococcaceae family genera in the gut, which supports taurine metabolism and reduces taurine degradation.

Conclusions

The current study indicated that a healthy diet could be extremely beneficial for PD patients, as it could reduce both motor and non-motor symptoms, as well as delay disease progression. Furthermore, a healthy diet increases the levels of putative anti-inflammatory butyrate-producing bacteria and decreases putative pro-inflammatory bacteria in PD patients.

Thus, the study findings emphasize the importance of adhering to a high-quality diet from the initial diagnosis of PD, as it could help maintain a healthy microbiome and delay disease progression. Nevertheless, it should be noted that the ability to maintain a healthy diet can become increasingly difficult as the disease progresses.

Journal reference:

• Kwon, D., Zhang, K., Paul, K. C., et al. (2024) Diet and the gut microbiome in patients with Parkinson’s disease. Npj Parkinson’s Disease 10(1); 1-9. doi:10.1038/s41531-024-00681-7