The broccoli seed tea experiment

The results of eight coordinated (n=1) studies, designed and executed entirely by People with Parkinson’s, reveal that non-motor symptoms were strongly attenuated by a broccoli seed tea, whereas motor symptoms remained unchanged over the 6-week program.

For a complete report of the results and their interpretation please download the article entitled “Broccoli tea experiment results and interpretation” on the “Documents” page.

These results imply that the mechanisms involved in generating and attenuating non-motor symptoms differ from those for motor symptoms. They are fully consistent with the hypothesis that the first step of Parkinson’s disease is oxidative-stress damage to mitochondria. This automatically leads to an energy deficit in dopaminergic neurons, a condition that progressively enforces a decline in their dopamine production. This in turn leads to the well-known and debilitating motor symptoms of the the disease such as slowness, stiffness and tremor.i

If you would like to know more about the scientific justification for this experiment, please read “Resetting the Redox Balance to fight Parkinson’s disease.

The Protocol

Experimtnts and observations made by the author Dr Albert Wright, enabled a protocol to be defined for the preparation and dosing of Brassica seed extracts and a checklist for following up the evolution of symptoms over a period of weeks or months. This protocol, was made available to a group of Parkinson’s disease sufferers in October 2020. A small number of them decided to commit to a program of self-experimentation, making their own broccoli tea and pooling their data for analysis.

Making sulforaphane from Brassica seeds

To get a good yield of sulforaphane from broccoli seeds or sprouts, the basic chemistry of the phytochemicals and enzymes in broccoli seeds must be taken into account. The seeds or sprouts contain three separate substances, glucoraphanin (a glucosinolate precursor of sulforaphane), myrosinase (an enzyme which catalyses the conversion of glucoraphanin to sulforaphane) and a co-enzyme ESP (epithiospecifier protein), which modifies the conversion of glucoraphanin to make an inactive byproduct. A high yield of sulforaphane can only be obtained when ESP is inactivated and the conditions are optimised to enable myrosinase to work efficiently. The conditions present in the gastrointestinal tract (temperature, pH), lead to low bioavailability of sulforaphane. At high temperatures the myrosinase enzyme is destroyed which totally blocks any production of sulforaphane. For these reasons, cooked broccoli contains very little sulforaphane. White mustard or daikon radish seeds contain versions of myrosinase which are more efficient than that in broccoli seed and can be used as replacement catalysts. Optimised hydrolysis conditions produce a cloudy yellow suspension which can be which filtered through a fine-mesh tea strainer to remove inactive particulate matter. This suspension contains highly bioavailable sulforaphane which will calm down Keap1 and let Nrf2 do its work.

Results

The results of this pioneering experiment were quite remarkable. They clearly show that a specific group of symptoms, collectively called non-motor symptoms respond strongly to this treatment over a period of just a few weeks, whereas motor symptoms remain practically unchanged over this short timescale.

These results are both encouraging and instructive. Encouraging, because they provide the first evidence that activating Nrf2 has an immediate and powerful impact on a subset of Parkinson’s disease symptoms. Instructive, because the distinction between non-motor and motor symptoms provides guidance about the mechanisms in action when Nrf2 impacts the health of neurons. This result was achieved by Parkinson’s patients taking coordinated action to improve their knowledge of the disease. They did it entirely on their own, in just 3 months and with no external funding. These Patients took action to become researchers and have succeeded where others dared not try. These results make two important statements:

• A broccoli tea, rich in sulforaphane rapidly attenuates a subset of Parkinson’s disease symptoms,

• There was a clear distinction in the response of non-motor compared to motor symptoms. This implies that at least 2 different mechanisms are involved in the genesis and/or resolution of Parkinson’s disease symptoms.

What more can we learn from the results of this patient-driven study?

The three symptoms which responded most strongly and progressively to the treatment were “fatigue, sleep quality and lack of motivation”. These symptoms have a strong association with energy production. This implies that the first direct impact of upregulating Nrf2 is to improve energy production in neurons, most likely by reducing ROS damage to mitochondria. If so, this could also break the vicious circle whereby mitochondrial damage, once established is self-sustaining because ROS damage to mitochondria creates more ROS which sustains more mitochondrial damage etc. In extreme cases it can get out of control. We can infer from this that oxidative stress is likely to be the dominant mechanism in the genesis of the process that leads to these non-motor symptoms. If confirmed, this mechanistic pathway should be the primary target to be investigated in any therapeutic plan to fight Parkinson’s disease.

Urinary incontinence and night time urinary frequency were also considerably improved. These are symptoms that strongly impact the quality of life of PwP.

Another important conclusion is that the natural isothiocyanates found in Brassica seeds have more than enough potency to reduce oxidative stress and rapidly attenuate non-motor Parkinson’s disease symptoms.