Broccoli sprout compounds and gut microbiota

Two 2021 reviews from one institution, with this first focused on aliphatic glucosinolates’ (GLS) metabolism to isothiocyanates (ITCs) like sulforaphane:

“Human clinical trials examining efficacy of whole food interventions on cancer prevention targets have shown high levels of inter-individual variation in both absorption and excretion of ITCs. We discuss how consumption of cruciferous vegetables may alter the microbiome, and in turn, influence ITC absorption.

Bioavailability of ITCs from GLS has been shown to be greatly impacted by processing before ingestion. When ITCs are given preformed, they possess the greatest level of bioavailability and are readily absorbed by humans.

Studies have indicated that without plant-derived myrosinase, the gut microbiome is essential for conversion of GLS to ITCs. Without conversion to ITCs, GLS are biologically inert.

There are two different intervals in time when GLS metabolism occurs in the large intestine:

  1. Metabolism of GLS directly following consumption when GLS are not absorbed in the small intestine; and
  2. When GLS are absorbed in the small intestine and go through enterohepatic circulation, returning as GLS in the gut where factors influencing microbial metabolism (such as food matrix, pH, and other compounds present) may be different from the first interval.

This list of bacterial genera altered by cruciferous vegetable consumption focuses on studies completed in healthy individuals and animal models:

Metabolic Fate of Dietary Glucosinolates and Their Metabolites:

Clinical trials have shown that consumption of a diet rich in cruciferous vegetables, compared to a cruciferous vegetable devoid diet, significantly alters composition of the gut microbiome. Each individual responded uniquely to cruciferous vegetable consumption, suggesting that basal microbiome composition may impact outcome.

Understanding the gut microbiome’s role in GLS metabolism, specifically GLS conversion to ITCs, is important to understanding drivers of inter-individual variation . Translating chemopreventative properties of cruciferous vegetables from the lab bench to the clinic requires addressing factors that drive high variability in ITC absorption and excretion observed in clinical trials.”

https://www.frontiersin.org/articles/10.3389/fnut.2021.748433/full “Metabolic Fate of Dietary Glucosinolates and Their Metabolites: A Role for the Microbiome”


Discussion of indole-3-carbinol (I3C) and 3,3′-diindolylmethane (DIM) was passed over to this second review:

“Hydrolysis of glucobrassicin GLS by plant or bacterial myrosinase produces multiple indoles, predominantly I3C. Yield of I3C from glucobrassicin is about 20%.

In the stomach, I3C undergoes extensive condensation to yield predominately DIM. Ingestion of I3C results in 20–40% conversion to DIM.

DIM has multiple mechanisms of action, the most well-characterized is modulation of aryl hydrocarbon receptor (AHR) signaling. The DIM-intestinal AHR-microbiome axis is an important component for future development of a personalized nutraceutical approach to achieving optimal health.”

https://www.frontiersin.org/articles/10.3389/fnut.2021.734334/full “Indoles Derived From Glucobrassicin: Cancer Chemoprevention by Indole-3-Carbinol and 3,3′-Diindolylmethane”


DIM estimates in this second review were too high with respect to clinical trial findings of Eat broccoli sprouts for DIM. Using the trial’s 21.61 μmol of average glucobrassicin intake, this review’s 20% I3C yield would be 4.32 μmol. This review’s lowest 20% DIM yield from I3C would be 0.86 μmol, representing a 4.0% DIM bioavailability from glucobrassicin intake.

The trial’s lowest average DIM (in postmenopausal women) after 35 days of eating broccoli sprouts measured 0.5544 μmol, representing an average 2.57% DIM bioavailability from glucobrassicin intake. One of the trial’s coauthors officially reviewed this second review, but he didn’t insist on better human in vivo estimates, although 4.0 / 2.57 is more than 50% too high for the review’s lowest DIM estimate.

The trial and its parent trial also weren’t cited by either review. Aren’t human clinical trials measuring sulforaphane, sulforaphane metabolites, and DIM bioavailability relevant to “Metabolic Fate of Dietary Glucosinolates and Their Metabolites” and “Indoles Derived From Glucobrassicin”?

Something else was missing from both papers. They had academic suggestions for future studies, but neither one continued on to say “and here’s what we’re sponsored to do to fill these gaps.”

PXL_20211023_111303363

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