A 2024 preprint published results of feasibility trial NCT03878368:

“High glucosinolate broccoli soup is a novel approach to managing osteoarthritis (OA) that is widely accessible and can be used on a large scale. This study shows that it is an acceptable way of delivering dietary bioactives and has potential for therapeutic benefit.

Limitations of the study:

1. COVID-19 curtailed data collection and restricted sample size below that originally planned, however we remained able to derive meaningful interpretation and meet our original study aims.

2. The study had a short time scale (12 weeks). A longer study would be useful to understand how a long-term intervention might be accepted, important for chronic conditions such as OA.

3. The full sample size fell short of the number anticipated, therefore we were unable to use the data to provide a reliable estimate of sample size for a full trial.

4. Participants were excluded if they did not like broccoli to maximise compliance and retention, and so a food intervention should account for this in future developments. While most patients tolerated the soups well, two patients withdrew because they did not like the soup.”

https://www.medrxiv.org/content/10.1101/2024.06.20.24309233v1.full-text “The BRoccoli In Osteoarthritis (BRIO study) – A randomised controlled feasibility trial to examine the potential protective effect of broccoli bioactives, (specifically sulforaphane), on osteoarthritis”

The glucoraphanin dose used was the highest of three tested in 2017 via NCT02300324:

“This study seeks to quantify the exposure of human tissues to glucoraphanin and sulforaphane following consumption of broccoli with contrasting Myb28 genotypes. Myrosinases are intentionally denatured during soup manufacture. Threefold and fivefold higher levels of sulforaphane occur in the circulation following consumption of Myb28^V/B and Myb28^V/V broccoli soups, respectively.

Myb28^V/V and Myb28^B/V broccoli soups contained 452 ± 10.6 μmoles glucoraphanin per 300 mL portion and 280 ± 8.8 μmoles glucoraphanin per 300 mL portion respectively, approximately five- and threefold greater glucoraphanin levels compared to Myb28^B/B broccoli soup that contained 84 ± 2.8 μmoles glucoraphanin per 300 mL.

The percentage of sulforaphane excreted in 24 h relative to the amount of glucoraphanin consumed varies among volunteers from 2 to 15%, but does not depend on the broccoli genotype.”

https://onlinelibrary.wiley.com/doi/10.1002/mnfr.201700911 “Bioavailability of Glucoraphanin and Sulforaphane from High-Glucoraphanin Broccoli”

Unlike these two papers, I don’t depend primarily on my gut microbiota for results. Microwaving 3-day-old broccoli sprouts to 60°C to create 80% bioavailable sulforaphane then immediately eating it is way more efficient. If depending on an individual’s gut microbiota to convert glucoraphanin into sulforaphane, the best that can be expected is 15% bioavailability.

Don’t think an osteoarthritis clinical trial that depends on a person’s gut microbiota could have steady, predictable results when there could be more than 700% variability (2% to 15%) among subjects’ sulforaphane conversions. If a treatment subject doesn’t have relief from knee pain, there would have to be additional methods to detect that subject’s effective sulforaphane dose based on their gut microbiota conversion ability. Would these researchers suggest that subject change their gut microbiota? What study has reliable results for that?