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How it started…
I was diagnosed with Parkinson’s disease in 2018, but had many of its invisible but debilitating symptoms for years before that. These included acute and painful fatigue, daytime sleepiness, poor sleep with vivid dreams, confusion, balance problems and severe urinary urgency.
At the time of diagnosis I was told that the causes of Parkinson’s disease were unknown, but as a research scientist, I analysed the published research for myself. I discovered that many researchers were convinced that oxidative stress in neurons, combined with a failure of mitochondrial function, were strong candidates for the basic cause of Parkinson’s disease. This was backed up by considerable experimental evidence.
Oxidative stress in neurons is normally controlled by gene transcription involving a signalling protein called Nrf2. In healthy people, Nrf2 controls the expression of hundreds of genes that combat oxidative stress in cells by releasing antioxidant molecules and enzymes which rapidly neutralise oxidizing molecules (also called Reactive Oxygen Species or ROS). With increasing age, the activity of Nrf2 declines and oxidative stress increases, leaving some neurons particularly susceptible to damage, malfunction and even death.
Many researchers have demonstrated that sulforaphane, a molecule that can be made from broccoli seeds, increases the activity of Nrf2, reduces oxidative stress and improves mitochondrial function in neurons. The choice of seeds, the preparation process, the dosing regime and the delivery method are all critical to getting a good result
I began researching how to increase Nrf2 in June 2019 and six months later I began using experimental doses of Nrf2 activators to stabilise my own Parkinson’s disease. Since then, the severity of my non-motor symptoms has been reduced to the point of remission through experimentation with broccoli seed teas containing sulforaphane.
The contrasting responses of motor and non-motor symptoms to sulforaphane suggests that these 2 symptom groups are caused by different processes or conditions. This developed into my hypothesis that non-motor symptoms might be caused by oxidative stress and mitochondrial dysfunction in the axons of dopaminergic neurons in the striatum, whereas motor symptoms may result from imperfect reorganisation of brain connections to work around the reduced functional capacity of the striatum. By exploiting these ideas, I now consider my Parkinson’s disease to be potentially stabilised in its present state, where sulforaphane controls the cause of non-motor symptoms. On the other hand, I still require dopamine replacement therapy (Levodopa) to control motor symptoms.
Dr Albert F Wright