How it started and hopefully, where it’s going
How it started
I was diagnosed with Parkinson’s disease in 2018, but had many of its symptoms years before that. The first was loss of the sense of smell, but the symptoms that most affected my quality of life came in the 5 years before diagnosis: fatigue, daytime sleepiness, poor sleep, confusion, urinary urgency.
I am a professional research scientist, trained as a chemist, but for most of my life I worked as a physicist. Research scientists learn how to do research in different fields. It is not easy to change fields and it takes time, but I know many people who have done it successfully.
As soon as I was told that the causes of Parkinson’s disease was unknown, I began looking at the published research for myself. I soon discovered that many researchers strongly believed that oxidative stress (the presence of too many oxidising molecules) in neurons was a strong candidate and was backed up by considerable experimental evidence. Furthermore, there was also good reason to believe that a possible therapy to halt or moderate oxidative stress in neurons had also been known for more than 10 years. Various methods had been tested in laboratory experiments and on animals and had been shown to work.
So if all this was known, why was there still no approved therapy to counteract the progression of Parkinson’s disease?
The answer to that is simple. The known techniques involved using very inexpensive natural molecules that cannot be patented. In consequence, no company or health institution has been prepared to bear the huge cost of clinical trials for a therapy that could not be patented, even if it would reduce the suffering of millions of Parkinson’s patients worldwide.
Oxidative stress in all cells including neurons is controlled by a very complex process involving a protein that goes by the acronym Nrf2. This protein activates genes that combat oxidative stress in cells by releasing antioxidant molecules and enzymes that in turn eliminate oxidizing molecules (also called Reactive Oxygen Species or (ROS)). More Nrf2 means less ROS.
It has been demonstrated by many researchers that a molecule called sulforaphane, an isothiocyanate which can easily be made from broccoli seeds increases the amount of Nrf2 in our cells and reduces oxidative stress in neurons.
I began researching the activation of Nrf2 in June 2019 and making and using experimental doses of isothiocyanates in December 2019 to try to slow down the progression of my Parkinson’s disease. Since then, I have made many observations concerning my own symptoms that strongly support the hypothesis that sulforaphane can be very beneficial to Parkinson’s patients. Over the 12 months of testing a range of isothiocyanates and experimenting different processing and delivery methods, I was able to considerably reduce many of my symptoms, both motor and non-motor, but progress was far from linear. My experience and a later study by 8 individual Parkinson patients strongly suggest that many non-motor Parkinson’s symptoms respond rapidly to sulforaphane treatment, whereas motor symptoms were unaffected in the short term.
The dosing regime and delivery method are both critical to getting a good result. The protocol I used was not designed and is not practical for use as a therapy. The useful dosing range appears to be quite low and narrow, estimated at 15 to 25 micro mol of fully bioavailable sulforaphane per day. Exceeding this range appears to reverse the beneficial effects of the treatment in the short term, but once corrected, produces a positive effect in the longer term. Many details still need to be addressed.
The study by 8 individual Parkinson’s Patients that is reported in other posts on this site shows what can be achieved when a small group of People with Parkinson’s coordinate their efforts. To go further will require a much larger number of participants, a more professional approach, a rigorous design and delivery method, institutional support, chemical and clinical analysis of blood and urine and of course, funding to pay for all that.
Hopefully, this will be the next step, but it will require a lot of determination to get it on the road. There is now little doubt in my mind that isothiocyanates (N=C=S) could play a role in attenuating the symptoms of Parkinson’s disease. They may also be effective in slowing disease progression, but we don’t yet know that. For the sake of the millions of Parkinson’s disease sufferers worldwide, this research must continue.
The next step which is already in preparation will be to launch:
A call for “Expressions of Interest” from researchers, medical professionals, research institutions, Parkinson’s patient advocates, funding bodies…
to design, organise and execute what I have provisionally entitled :
N=C=S for Parkinson’s Disease: an Innovative Open Research Project
This project will be designed and formulated by those who respond to the “Call for Expressions of Interest” and participate in its realisation. The initial purpose of the project will be to accumulate further evidence in favour of a “Proof of concept” that isothiocyanates have the potential to be used in a disease-modifying therapy for Parkinson’s disease. This proof of concept is an essential condition to be met before a phase II clinical trial can be considered. If this is successful, the intention is that the project leaders will continue to support the organisation of a phase II trial.
Dr Albert F Wright