Low Sulfur Diet?

So I was reading this Martha's Quest blog post: Desulfovibrio bacteria, Parkinson's and diet https://www.marthasquest.com/post/desulfovibrio-bacteria-parkinson-s-and-diet
She was talking about Desulfovibrio Bacteria being associated with Parkinson’s Disease. In fact, she linked to a paper from 2021 “Desulfovibrio Bacteria Are Associated With Parkinson’s Disease” https://www.frontiersin.org/articles/10.3389/fcimb.2021.652617/full and offered this quote from the paper “Desulfovibrio bacteria produce hydrogen sulfide and lipopolysaccharide, and several strains synthesize magnetite, all of which likely induce the oligomerization and aggregation of α-synuclein protein”.
Martha then went on to discuss hearing Dr. Michael Ruscio and Heidi Turner speak about the low sulfur diet and the many health conditions a low sulfur diet can address.

So then I looked up the low sulfur diet. It is like the exact opposite of my diet. Here is a great web site listing various low sulfur diets: The Most Popular Low Sulfur Diets By Andrew Day, ND https://www.lowsulfurdoctor.com/popular-low-sulfur-diets/

I'm going to come out and say it is very unlikely I will ever try a low sulfur diet. I eat an onion a day. Broccoli is high in sulfur. Check out this list. I can't even have well water (I live in the country. I have a well): https://www.lowsulfurdoctor.com/low-sulfur-diet/

So why am I posting on this subject? Because, as irritating as the subject is to me, there is a lot there, and it is fresh:

Here is another paper on this topic, from Jan 2022: Hydrogen Sulfide Produced by Gut Bacteria May Induce Parkinson’s Disease https://www.mdpi.com/2073-4409/11/6/978

"Conclusions: Considerable amounts of evidence support the view that an overgrowth of H2S-producing bacteria takes place in the gut microbiome of PD patients. It is plausible that by inhibiting acetyl-CoA synthesis, H2S decreases the amount of butyrate-producing gut bacteria. Furthemore, H2S can diffuse easily to gut cells and the vascular compartment. In blood circulation, some part of the bacterially produced H2S may end up at the brain level. When the gut cells are exposed to unphysiologically high concentrations of H2S, the release of Cyt c from the mitochondria will likely begin. In addition, H2S increases the iron content in the labile iron pool of the cell cytosol and the ROS content. In case the cell expresses aSyn, in the way that EECs and enteric neurons do, a development of aSyn oligomers and fibrils may start in the presence of Cyt c and increased ROS. The toxic oligomers and fibrils may spread to the lower brainstem via the vagal nerve and some oligomers will likely end up in the blood circulation. As to H2S producers, species of the genera Desulfovibrio, Escherichia, Bilophila, Porhyromonas, Prevotella, Corynebacterium, Veillonella, Helicobacter, and Clostridium invite particular attention when identifying the role of different bacterial genera in the etiology of PD. The bacterial composition of the microbiome in duodenum require special attention in PD as it is likely that the quantities and characteristics of the small intestinal bacteria, including the H2S-producing bacteria, differ significantly from those of the colon. Notably, studies on the bacterial composition of duodenal microbiome in PD are lacking. In future, microbiological and metabolomics-based studies on duodenal aspirates combined with the corresponding analyses of fecal samples may offer key information on the pathogenesis of PD. In case H2S plays a substantial role in the pathogenesis of PD, several strategies are already available to counteract its actions. In 2003, Braak and his colleagues proposed that PD is caused by an intestinal pathogen [107]. H2S could be that ”pathogen”. "

Maybe I will circle back to this topic. I will definitely circle back if somebody else starts having success with a low sulfur diet :)