I was diagnosed with Parkinson’s disease in 2018, but I had been grappling with many of its symptoms for years before that. It all started with the loss of my sense of smell, but it was the symptoms that affected my daily life the most that really played havoc in the 5 years leading up to my diagnosis: fatigue, uncontrollable daytime sleepiness, poor sleep, brain fog, constipation, and catastrophic urinary urgency. At first, everyone brushed off these symptoms – the urinary urgency was attributed to a prostate issue, the constipation to a poor diet, and the fatigue to aging.

The expert opinion shifted once I began to encounter difficulties with movement. I became rigid and slow. My left leg began to drag, and my left hand started trembling. In 2018, my neurologist delivered the diagnosis of Parkinson’s disease, attributing many of the symptoms that I felt over the previous 5 years to this condition. It’s truly striking how convincing opinions from experts can evolve. I found myself asking, “What can be done to manage this illness?“

“So, you’re saying that my dopamine neurons have been dying off for years? And I may have lost up to 70% of them? And this is a neurodegenerative disease, so I’ll keep losing more each year?” “And what leads to the demise of these neurons? “

“The cause remains a mystery, and unfortunately, there is no treatment available to halt or reverse its progression.” “I’ll schedule your next appointment in 6 months. Take care, and have a nice day.”

Could neurons potentially suffer damage long before their demise, leading us to question whether some of the 70% of “lost” neurons could still be hanging on, albeit in a weakened state that impairs their functionality?

As we get older, neurons, unlike many other cells, are not renewed, they are as old as we are. “Neurons carry with them the scars of a lifetime of service.”

A glimpse into the world of neurodegenerative disease research unveils a multitude of potential causes. One particularly influential factor is the relentless assault on neurons by aggressive chemicals, including free radicals and Reactive Oxygen Species (ROS) or Reactive Nitrogen Species (RNS), which are bi-products of the processes used by mitochondria to make energy from glucose and oxygen. These chemicals behave as highly potent oxidants. In individuals with Parkinson’s disease, the Redox Balance System (RBS) within cells fails to eliminate the ROS and RNS that trigger oxidative stress, thereby inducing cellular damage, inflammation, and ultimately, cell demise.

Can anything be done to combat oxidative stress and activate the body’s natural defense system against it? Even though there is currently no approved therapy, dedicated researchers are exploring ways to activate the Redox Balance System to mitigate oxidative stress. They have identified several potentially powerful molecules, including the remarkable compound sulforaphane, an isothiocyanate found in broccoli seeds or sprouts. While it has demonstrated promising results in laboratory and animal models of Parkinson’s disease, its potential for human use remains untested and “not approved.“

In the last quarter of 2020, a small group of Parkinson’s patients embarked on a journey to explore the potential of sulforaphane in easing their symptoms. Taking matters into their own hands, they acquired the necessary seeds and equipment, concocted a homemade infusion containing sulforaphane, and meticulously monitored the changes in their PD symptoms. The outcome of this experiment unequivocally revealed a remarkable reduction in their non-motor symptoms within a mere 6 weeks, igniting a spark of hope, while their motor symptoms remained unchanged.

So what in the world happened here? Could this mean that the once dysfunctional neurons were starting to show signs of getting better? “Could it be that they weren’t actually dead after all?”