Age has long been considered the primary factor in Parkinson’s development. However, there’s growing evidence that neurodegenerative diseases actually begin early in life, and that the cause may be environmental toxins we are exposed to either in utero or soon after birth. These toxins can destroy vital neurons and suppress their replacement by neural stem cells.

It is generally known that neurological diseases do not present until 70 percent to 80 percent of the neurons in a particular area are either dead or nonfunctional. For example, the site of damage in Parkinson’s appears to be a particular group of cells (nucleus) called the substantia nigra pars compacta. But signs of Parkinson’s disease will not manifest until only a minority of the neurons in that area are functioning.

This is called the “two-hit” hypothesis of Parkinson’s disease. The first hit occurs during childhood, in which a person loses 20 percent to 30 percent of the neurons in a particular brain nucleus. At this stage, there are no symptoms.

The second hit occurs years later. It can either be gradual (from the wear and tear of aging) or sudden, with overexposure to environmental toxins such as pesticides or herbicides.

In many cases, the second hit doesn’t actually kill the brain cells; it just weakens them and makes them nonfunctional. In that case, the condition can be corrected by ending the toxic exposure, thus strengthening these neurons so recovery can occur.

As I have written before, a common problem among our population is consuming too many simple carbohydrates. This leads to a deficiency of vitamin B1 (thiamine). In many cases, the deficiency is caused by a metabolic error in B1 absorption from the gut or in the brain’s cells. Vitamin B1 uses a carrier to enter cells in the gut and a similar one to enter brain cells.

There appear to be two types of symptoms associated with Parkinson’s disease: motor symptoms, which include tremor, slowness of movement (bradykinesia), and weakness; and nonmotor symptoms including insomnia, constipation, pain, autonomic problems (usually low blood pressure), cognitive problems, and psychiatric disorders.

In about 80 percent of advanced Parkinson’s cases, patients will gradually develop dementia symptoms similar to those experienced by Alzheimer’s patients. The pathology is the same, but it affects different parts of the brain.

One group of researchers found that the pathological changes occurred in stages, and seemed to begin in the gut and nose.