A flawed broccoli sprouts clinical trial

This 2023 human study investigated commercially available broccoli sprouts’ effects on platelets. I’ll provide details of some procedures, but not of findings, as there were several issues:

“Administration of intervention (sulforaphane/placebo) was followed in 90 min by administration of standardized caloric challenge PhenFlex. Urine samples were classified into three groups: (A) baseline, green line, (B) after intervention or placebo, blue lines, and (C) after PhenFlex challenge, red lines. Samples were divided into 5 timepoints: (0) baseline, (1) <60 min after intervention or placebo, (2) >60 min after intervention or placebo, (3) <60 min after PhenFlex challenge, and (4) >60 min after PhenFlex challenge.

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Shortly (maximum of 3 min) before administration, sprouts were cut approximately 1 cm below the leaves, weighed, and mashed with a small amount of tap water (approximately 13°C) in a kitchen blender for 30s at room temperature. Subsequently, tap water was added to a total amount of 250 mL and participants were instructed to drink the entire mixture.

Commercially available pea sprouts (Affilla Cress®) were used as placebo in this study since pea sprouts do not contain glucoraphanin/sulforaphane. Affilla Cress (16 g) was prepared and administered in a similar fashion. Blinding of participants was ensured by the even appearance of both drinks and the use of nasal plugs during consumption of the investigational products. 🙂

Ninety minutes after administration of investigational products, participants were asked to drink PhenFlex, a high-fat, high-glucose, high-caloric product. PhenFlex mixtures were freshly prepared, and participants were instructed to consume the drink within 5 min.”

https://www.frontiersin.org/articles/10.3389/fnut.2023.1204561/full “The beneficial effect of sulforaphane on platelet responsiveness during caloric load: a single-intake, double-blind, placebo-controlled, crossover trial in healthy participants”


Two main issues were:

1. It was stated throughout that sulforaphane did or could do this and that. None of this was supported by sulforaphane intake measurements / estimates, although measuring equipment was available.

Researchers couldn’t assume that blending 16 grams of broccoli sprouts of unknown age creates x amount of sulforaphane. 3-day-old broccoli sprouts have the optimal yields measured 6 broccoli varieties’ sulforaphane content over 3, 5, and 7-day ages, and published 15 different answers.

Sulforaphane and two metabolites’ urinary output was measured. Supposing that only output measurements were adequate leads to the second main issue.

2. Genes were asserted for certain effects. Plausible alternate explanations such as individual differences in gut microbiota composition, excretion, and metabolism weren’t explored.

These researchers knew or should have known about the 2016 https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201600766 “Stabilized Sulforaphane for Clinical Use: Phytochemical Delivery Efficiency” (not freely available). That study measured two known sulforaphane inputs, and in ten people each, blood plasma and urinary outputs.

The first sulforaphane input had sulforaphane bioavailability from 19.5% to 86.9% of dose. The second input ranged from 48% to 96% of dose. Widely different responses to sulforaphane intake prompted those researchers to state:

“These differences in SF bioavailability may be due to differences in gut microbial metabolism, in the levels of drug metabolizing enzymes (e.g. well-known polymorphisms of glutathione S-transferases that catalyze the conjugation of SF with glutathione), and in excretion kinetics. Innate metabolic differences must not be discounted when assessing the metabolism of SF.”

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