Yes, I know it's targeting T1D, but I'm wondering if they would need to change very much if they were to run a similar trial for PD?
"Changes in gut microbiota composition, function, and immune profile following six weeks of HAMSAB supplementation were associated with increased SCFAs in stools and plasma. The persistence of these effects suggests that targeting dietary SCFAs may be a mechanism to alter immune profiles, promote immune tolerance and improve glycemic control for the treatment of T1D."
Kirstine J. Bell et al., Metabolite-based dietary supplementation in human type 1 diabetes is associated with microbiota and immune modulation, medRxiv pre-print, September 2021.
Wow! Results HAMSAB supplement was administered for six weeks with follow-up at 12 weeks in adults with long-standing T1D. Increased concentrations of SCFA acetate, propionate, and butyrate in stools and plasma were in concert with a shift in the composition and function of the gut microbiota. While glucose control and insulin requirements did not change, subjects with the highest SCFA concentrations exhibited the best glycemic control. Bifidobacterium longum, Bifidobacterium adolescentis, and vitamin B7 production correlated with lower HbA1c and basal insulin requirements. Circulating B and T cells developed a more regulatory phenotype post-intervention.
We have developed a high-SCFA-yielding dietary supplements that ameliorates gut infection, improves chemotherapy efficacy and protects mice against T1D via regulating the immune system [5, 10, 15]. The SCFA-based supplement is a type 2 resistant starch consisting of a high amylose (70%) maize starch (HAMS) that has been modified by bonding the acetate and butyrate (HAMSAB). It is resistant to digestion in the upper gastrointestinal tract, delivers a very high yield of SCFAs in the colon, and is a powerful tool to assess the effects of SCFAs on intestinal biology [5, 10, 15, 16]. The HAMSAB diet prevented beta-cell destruction by T cells and protected against T1D in 90% of NOD mice. Protection against T1D was associated with microbiota composition changes. The mechanism behind this SCFA-induced T1D protection involved synergistic effects of acetate and butyrate; expansion of regulatory T cells (Treg) was butyrate-dependent and a decrease in pathogenic B cells, CD4+ and CD8+ T cells was acetate-dependent [5]. Therefore, this dietary intervention targets microbiota-host interactions, nutrition, and phylogeny.
If you search on HAMS starch you will find plenty of studies and plenty of people we could contact to source the stuff.
I just ran out of butyrate. Time to order more I guess. And I guess I need acetate.
But what kind of butyrate and what type of acetate?
The HAMSAB supplement is a high amylose corn starch acetylated and butyrylated (Ingredion Incorporated, Bridgewater, NJ). To improve tolerability, participants commenced with 10g/day and increased the dose in 10g increments every 48h until 40g per day was reached. If the increased dose was not tolerated, the participant was to remain on the previous dose for an additional 48h before attempting the increased dose again. If that dose was not tolerated after the third attempt, (or on the judgement of the investigators), they were to remain on the previous dose for the remainder of the intervention. Participants were asked to return any unused HAMSAB supplement at the next visit.
This "might" be the maize they used: HI-MAIZE 260 - 22000B00
Bydureon (a.k.a., Exenatide), a repurposed Type 2 Diabetes drug is now in third-stage trials in UK for stopping Parkinson’s in its tracks — results expected 2023. Testing — mice, open label, double blind — has been going on since 2010 and it has been positive every time.
According to a very sensitive test, Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), 2/3 of Parkinson’s patients are supposed to be insulin resistant. IR may be treated with Bydureon (Exanatide). Just an angle that might get us one step closer to getting Bydureon.
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