Norman Doidge, M.D. is the New York Times bestselling author of ‘The Brain That Changes Itself’ and the new release ‘The Brain’s Way of Healing – Remarkable Discoveries and Recoveries from the Frontiers of Neuroplasticity.’ In his new book, Dr. Doidge discusses in chapter 2 how exercise helps fend off degenerative disorders and can defer dementia. Here are a few excerpts:
My walking companion, John Pepper, was diagnosed with Parkinson’s disease, a movement disorder, over two decades ago. He first started getting symptoms nearly fifty years ago. But unless you are a perceptive and well-trained observer, you would never know it. Pepper moves too quickly for a Parkinson’s patient. He doesn’t appear to have the classic symptoms: no shuffling gait; no visible tremor when he pauses or when he moves; he does not appear especially rigid, and seems able to initiate new movements fairly quickly; he has a good sense of balance. He even swings his arms as he walks. He shows none of the slowed movements that are the hallmark of Parkinson’s. He hasn’t been on anti-Parkinson’s medication for nine years, since he was sixty-eight years old, yet appears to walk perfectly normal.
In fact, when he gets going at his normal walking speed, I can’t keep up with him. He’s now going on seventy-seven and has had this illness, which is defined as incurable, chronic, progressive neurodegenerative disorder, since his thirties. But instead of degenerating, John Pepper has been able to reverse the major symptoms, the ones that Parkinson’s patients dread the most, those that lead to immobility. He’s done so with an exercise program he devised and with a special kind of concentration. pg 33
Parkinson’s can also give rise to cognitive deficits. As in any neurological condition that restricts mobility, the effects of the illness (as opposed to the illness itself) can weaken the brain in a secondary way. The neuroplastic brain evolved in ambulatory beings who ranged around the world, always having to explore unknown territories. In other words, the brain evolved to learn. As people become immobile, they see less, hear less, and process less new information, and their brains atrophy from the lack of stimulation (unless they are fundamentally thinkers, and even then the neuroplastic systems require physical movement to generate new cells and nerve growth factor). Whether the cause of the atrophy is Parkinson’s or the lack of stimulation, Parkinson’s patients develop cognitive deficits at rates higher than does the normal population. The cognitive problems can progress to dementia in advanced cases: Parkinson’s patients have have six-times-normal risk of dementia. pg 38
In 1957 the Swedish Nobel laureate Arvid Carlsson, an extraordinary scientist and physician, discovered that dopamine was one of the brain chemicals used to send signals between neurons. He then discovered that about 80 percent of our brain’s dopamine is concentrated in the part of the brain that contains the substantial nigra, the basal ganglia. Dopamine does many things, including – as we now know, years after Carlsson’s discovery – helping to consolidate neuroplastic change. The researcher Oleh Hornykiewicz showed that low dopamine gives rise to Parkinson’s symptoms, and that giving dopamine boosters like levodopa (a chemical that the body can easily transform into dopamine) relieves symptoms. Levodopa is a substance the body normally produces, and in the brain, the neutrons can convert it to dopamine to replace what is missing. Ultimately studies in humans showed that dopamine levels can fall by 70 percent without appearing to affect a person, but when they fall by 80 percent, Parkinson symptoms develop.
These discoveries led many physicians and scientists to conclude that Parkinson’s is caused by the loss of dopamine. But while dopamine loss may be the immediate cause, it would be more precise to say that loss of dopamine describes a crucial aspect of the disease. But what causes the substantia nigra to lose dopamine in the first place? And how do we account for the fact that other brain areas also stop functioning? Is it because they are not getting the proper signals from the substantial nigra, or is there a deeper process affecting the brain that causes all these symptoms? pg 39
As Werner Poewe, who has studied the natural history of the illness, wrote, “Although Parkinson’s disease…is the only chronic neurodegenerative disorder for which there effective symptomatic therapies no treatment has yet been identified that would significantly slow its natural progression.” Most neurologists know this to be the case. So do the drug companies, which claim, each time a new drug comes along, that it has greater benefits and fewer side effects than the last. This deficiency is why scientists are looking for nondrug ways to treat PD. pg 40
The fact that Pepper also has many signs of Parkinson’s disease outside the usual Parkinsonian symptoms -sensory problems (which make it difficult for him to know where his limbs are in space), intermittent memory loss, and nervous system problems typical of Parkinson’s disease, such as trouble regulating his blood pressure, telling if it is cold or hot, profuse sweating, and urinary difficulties – also suggests that he certainly has a widespread, serious disease. Finally, to argue that the fact that he was able to reverse some of his symptoms proves that he doesn’t have the disease, is a stretch. When medication or brain stimulation reverses symptoms, practitioners don’t say that proves the person never had the illness in the first place. pg 72
“He’s got this unique way he’s approached everything, in terms of the way he’s managed to stay off medication,” she says, conveying a sense of appreciation for what he’s done. “He was very proactive in the way he handled his disease. He didn’t sit back and allow the disease to handle him. And you know, John is quite controversial in terms of the way he has approached things locally with the organizations here. But be that as it may, he certainly has overcome many challenges with regard to his Parkinson’s, and he remains extremely well in certain aspects of his condition.” pg 74