I feel pretty good about eating a no gluten or lectin diet.
Gut-brain axis: Review on the association between Parkinson’s disease and plant lectins 2022 clinicalcases.eu/index.php/...
"Gastrointestinal (GI) involvement in the pathogenesis of Parkinson’s Disease (PD) has been widely recognized and supported in recent literature. Prospective and retrospective studies found non-motor symptoms within the GI, specifically constipation, precede cardinal signs and cognitive decline by almost 20 years. In 2002, Braak et al. were the first to propose that PD is a six-stage propagating neuropathological process originating from the GI tract (GIT). Aggregated a-synuclein (a-syn) protein from the GIT is pathognomonic for the development of PD.
This article reviews the current literature from the past 10 years as well as original research found in PubMed on the combined effects of enteric glial cells and lectins on the development of Parkinson’s Disease. Studies have found that these aggregated and phosphorylated proteins gain access to the brain via retrograde transport through fast and slow fibers of intestinal neurons. Plant lectins, commonly found within plant-based diets, have been found to induce Leaky Gut Syndrome and can activate enteric glial cells, causing the release of pro-inflammatory cytokines. Oxidative stress on the enteric neurons, caused by a chronic neuro-inflammatory state, can cause a-syn aggregation and lead to Lewy Body formation, a hallmark finding in PD. Although the current literature provides a connection between the consumption of plant lectins and the pathophysiology of PD, further research is required to evaluate confounding variables such as food antigen mimicry and other harmful substances found in our diets.
It is hypothesized that plant lectins have emerged and become more widely distributed due to their ability to defend against microorganisms (bacteria, viruses, and fungi), insects, and plant-eating animals [46].
This hypothesis has been linked to the carbohydrate-binding properties of lectins. For example, it has been found that extracellular lectins found in the roots of plants have a role in defense against bacteria by immobilizing copious quantities via carbohydrate residue recognition and agglutination [47].
In addition to their agglutinin properties, plant lectins are resistant to proteolysis both in vitro and in vivo and have been stable through a wide range of pH [40]. These characteristics help explain the mechanism in which plant lectins survive the gastric pH of plant-eating animals and cause deleterious systemic and gastrointestinal effects [48].
One of the most prominent effects that plant lectins have on the GIT is the induction of a phenomenon called leaky gut syndrome (LGS). LGS is a condition in which TJs are disrupted and gaps are formed in the intestinal wall, causing paracellular hyperpermeability [49]. This enables various hostile antigens or toxins to invade directly into the lamina propria, bloodstream, and plexus [50].
An animal study involving mammalian rats showed that when phytohemag-glutinin (PHA), a plant lectin derived from kidney bean (Phaseolus vulgaris) seeds, was ingested, there was increased mucosal epithelial cell turnover and TJ disruption, leading to increased intestinal permeability [51]. This observation is explained by lectin’s ability to bind to glycosylated residues on the gut epithelial cell surface [52].
Since carbohydrate residues on epithelial surfaces are similar between mammals, these findings suggest that lectins may also increase gut permeability in humans [53]."
(hamburger).
Recent gut-microbiome paper: Metagenomics of Parkinson’s disease implicates the gut microbiome in multiple disease mechanisms (Nov 2022)
Perspective on the Gut and Parkinson's Disase
Could there be a link between the enteric neurons, gut microbiome and ALS?
