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Controlling Parkinson's Disease with Supplements :
Part 1: A Bear of a Disease to Bear
By Richard Passwater, Ph.D.
I try not to write about Parkinson's disease because of my abhorrence for it. Life is wonderful, and there are very few things that I despise with a vengeance-you can count them on half of the fingers of one hand. Parkinson's disease (PD) is one of them. However, I want all Parkinson's patients to know the benefits that dietary supplements have to offer them. This month's column sets the stage for an update from the Cochran Medical Foundation on its progress against PD. I follow the research of the Cochran Medical Foundation very closely, speaking with its director, therapeutic biochemist Tim Cochran, on a weekly basis. The last time we visited this subject in WHOLE FOODS was in May 1999. I thought that you might like to know that the patients treated with Cochran's Parkinson formulation (a mixture of natural substances including vitamins, minerals, amino acids, fatty acids, coenzymes and hormones) continue to improve and that his research continues to make progress.
Perhaps some readers may remember that my first discussion with Cochran regarding PD was in April 1998. That report followed a March 1998 interview that discussed the clinical trials conducted by the Cochran Medical Foundation in the area of heart disease.
The clinical results were astounding, but I chided Tim for merely solving relatively easy problems such as heart disease, rather than tackling really difficult challenges such as PD. He smiled and replied that he had a subset of patients who took his supplement cocktail designed for heart disease but were delighted to discover that they also experienced dramatic improvements in their PD.
In the heart disease clinical trials, the patients using the Cochran heart formulation (a formulation that differs from the Parkinson formulation, but still is a cocktail of vitamins, minerals, amino acids, fatty acids, coenzymes and hormones) rapidly improved from a New York Heart Association level clinical condition of 3.1 (level 4 is near death) to an average of 1.4. This healing, as measured by clinical condition improvement, was accompanied by direct objective improvements in cardiac function and blood chemistries as well. On average, patients' total blood cholesterol levels dropped 39.6 mg/dl, but more importantly, the LDL-cholesterol (the so-called bad cholesterol) levels dropped 48.3 mg/dl and the HDL/LDL-cholesterol (the so-called good cholesterol) increased by 14.5 mg/dl. The net result was that the HDL/LDL ratio improved by a remarkable 216?%. The triglycerides also dropped 29.3 mg/ell. Each of these changes was beneficial.
In addition, on average, patients' blood pressures fell front 153.7 over 113 to 101.5 over 69.11, and pulse rates improved significantly, dropping from an average of 104 to 76 beats per minute. These results are indeed remarkable but to realize that the supplements also dramatically improve brain and neurological chemistry, even for those patients affected by disease, is astounding!
PD is a horrible disease. I do not want PD patients to read this first of a two-part series. PD patients already know about the symptoms and progression of PD, and they don't need to be reminded of its horror. If you are a PD patient, please go directly to Part 2 in January 2001, which will report the good news on putting the bear back into its cage.
I remember when my mother first learned that she had PD. She was devastated. I tried to ease her burden with stupid remarks implying that at least it wasn't a fatal disease or as bad as cancer. Those remarks haunted me for years as I helplessly witnessed her insidious deterioration and resultant misery. Soon after her diagnosis, my community's volunteer fire department, of which I had the privilege of being chief, initiated an ambulance service and I trained to become an emergency medical technician (paramedic). I soon encountered the suffering of many PD patients at various stages of their disease.
It may be technically true, as the National Parkinson Foundation states in bold letters, that "PD is not a fatal illness," but PD can indirectly be the cause of death. If the patient doesn't die of other causes first, PD can lead to great debilitation and emaciation that results in death. When one no longer can swallow food or digest what little can be swallowed, the body becomes mostly thin skin and frail bones and the heart eventually loses the ability to beat. But before that endpoint is reached, there is a slow and long-suffering trip-one that is full of dementia, depression and other devils. To hide behind the technicality that PD is not a fatal disease is almost as bad as saying that breast cancer is not a fatal disease because breasts are not vital organs. The truth is that breast cancer can spread to vital organs.
Although I have participated in 13 successful cardiac resuscitations (reviving clinically dead persons), most of which I initiated through CPR, I had mixed emotions when called to try to revive elderly PD patients who obviously had suffered enough. The result of a long battle with PD in elderly patients usually is readily apparent, and the family seldom has to be asked if the patient has PD. Maryland law and ethics dictate that we must do all in our power to revive someone unless the patient has signed a "do mot resuscitate" order or the person is deemed beyond resuscitation by qualified responders. However, the frailty of the patient, which is caused by a loss of the ability to swallow or digest foods properly, frequently weakens the xiphoid process at the bottom of the sternum (breastbone) to the point where it fractures under even the gentlest fractures under even the gentlest pressure needed to accomplish heart compression in CPR
What causes PD and what can be done about it? PD is named after Dr. James Parkinson, a London physician who is credited with being the first to describe this disease in 1817. According to the National Parkinson Foundation (www.parkinson.org), PD is a slowly progressing disease of the nervous system. It affects a region in the mid-brain called the substantia nigra. A gradual degeneration or reduction in nigral cells results in the reduction of nigral dopamine. Dopamine is called a neurotransmitter, as it is a chemical messenger between brain or nerve cells.
Dr. Arvid Carlsson of the University of Goteborg in Sweden is one of three scientists awarded the Nobel Prize in Medicine this year. At the age of 77, he still is working at the University. He was honored for work in the late 1950s that showed that a substance called dopamine is a key messenger between brain cells. He realized the implication for Parkinson's disease, which was later shown to result from a dopamine deficiency in part of the brain. Dr. Paul Greengard of Rockefeller University in New York and Dr. Eric Kandel of Columbia University in New York shared this year's Nobel Prize in Medicine with Dr. Carlsson for related research with neurotransmitters.
The cells of the substantia nigra use dopamine to communicate with the cells in another region of the brain called the striatum. Thus, the reduction in nigral dopamine also results in a decrease in striatal dopamine.
Nigral cell deterioration is caused by copious amounts of free radicals produced in the substantia nigra. Certain injuries, illnesses such as encephalitis, medicines, illicit drugs and possibly other chemicals that increase free radical production have been shown to cause nigral damage and result in Parkinson-like symptoms. The most important free radical scavenger in these cells is glutathione. Glutathione levels in PI) patients are low. As we will discuss in Part 2, dietary, glutathione and antioxidants that increase cellular glutathione, such as lipoic acid, NAC, Pycnogenol and others, are effective in restoring normal function There is no known gene associated with PD and the question of possible familial predisposition still is being researched and debated.
PD symptoms are the result of inadequate striatal dopamine. The four classic symptoms of PD are a resting tremor on one side of the body, a generalized slowness of movement (bradykinesia), stiffness or rigidity of limbs, and walking and/or balance problems. However, not all PD patients experience all of these symptoms.
It is estimated that in the U.S. and Canada there are about 3.5 patients per thousand population, which translates into about 1.2 million PD patients. New cases are diagnosed at the rate of about 480 per million population. In the United Kingdom, the incidence is estimated at about two per thousand population. PD progresses from diagnosis to major disability over 10-20 years. Eventually, it leads to death as a secondary consequence of its debilitating actions.
Most people tend to think of PD as "tremors" that affect old people. Actually, 10% of PD patients are under 40 years of age, and 15% are under 50. The peak onset age is 60. PD affects 1% of the citizens of the United States and Canada over 60 years of age, and 2% of those over 70. PD affects men more than women (55% vs. 45%) and more Caucasians than people of color.
It's Not Always PD
Before discussing further the bad news associated with PD, here is good news for those whose hands are unsteady or shaking. Fortunately, everything that trembles is not necessarily PD. The most common cause of tremor is "Essential Tremor" (ET). Sometimes ET is called Benign Essential Tremor or Familial Tremor because it usually doesn't result in disability. There are many sub-classifications of ET, and together they affect about 10 million Americans, about 10 times as many people as PD. Among people over 60 years of age, the incidence of ET may be as high as 5% of the population over 60 years of age.
According to Dr. Abraham Lieberman, professor of neurology at the University of Miami, ET is characterized by involuntary rhythmical trembling or oscillation of a body part, usually the hands. With ET, the trembling usually begins essentially simultaneously on both sides. This is opposed to PD, in which the trembling usually begins on one side. Also, ET usually begins in a finger, whereas PD usually begins in a thumb. ET tremors are amplified when exercising or moving the hands such as in drinking from a glass (action tremor) or when trying to hold ones' arm fixed at length (postural tremor). PD tremors occur at rest or when muscles are relaxed, and usually affect only one hand or an arm or leg.
Earlier, I described the four classic symptoms of PD. There are other signs and symptoms as well. It is very common for PD patients to become stuck in place. They become frozen and can't get their feet moving to walk. After they can start walking, they often have a foot drag on one side and a lack of an arm swing on that same side. They often have trouble turning or going through narrow passages and doorways.
PD patients often become depressed or anxious. Mental slowing, intellectual decline, cognitive impairment, mood disorders and memory loss are common in PD patients. In long-term PD patients, the debilitation and mental confusion/dementia often means that the patient is confined to bed and is not aware of persons or events around him or her. PD patients often have sleep disorders and sudden drops in blood pressure (orthostatic hypotension) that can cause fainting. They can develop a "Parkinson's mask" or a decrease in facial expression (hypomimia). Not being able to smile is a curse that is worse than it sounds. PD patients have increasing difficulty in swallowing and swallow less often. They blink their eyes less frequently. Their voice becomes lowered (dysarthria). Their handwriting becomes small and cramped (micrographia). Intestinal motility, digestion and constipation become serious problems.
Since striatal dopamine is believed to cause the PD symptoms, most drugs used to treat PD are aimed at temporarily replenishing or mimicking dopamine. Such drugs are called dopaminergic drugs. They improve some symptoms, but do not restore normal brain function nor halt brain cell deteriation. Dopaminergic drugs can overstimulate nerve cells elsewhere in the body and cause confusion, hallucinations, nausea and fluctuations in the movement of limbs.
Dopaminergic drugs are generally effective at first in reducing many PD symptoms, but lose their effect over time and cause severe side effects. Common dopaminergic drugs include carbidopa/ levodopa (Sinemet, Atamet), pergolide, bromocriptine, ropinirole and pramipexole. In addition, there is a slew of adjunctive drugs that help relieve other symptoms and the side effects of the dopaminergic drugs. The net result, however, is that there is no single drug or combination of drugs that cures PD or alleviates the symptoms of PD over the long haul.
You can imagine the amazement and disbelief when PD experts are told that the Cochran Parkinson formulation achieves results that drugs cannot. In some patients, the Cochran regimen relieves all symptoms, including all but occasional tremors. When occasional tremors return, all that is required is putting additional glutathione under the tongue or adjusting the lipoic acid, glutathione or amino acid levels in the regimen.
Typically, patients experience a dramatic increase in energy and the diminution of stiffness in the first 24 to 72 hours and increased reduction and/or absence of stiffness within two to 10 weeks. AntiPD medication may be reduced within the first seven to 60 days depending on the rate of improvement. The degree of reduction in anti-PD medication ranges from 30% to 70% over several months, depending on the recovery rate. Depression and sleeping medication can be reduced or eliminated within the first one to three weeks. Mental acuity, as well as outlook and snood, greatly improve in this same short time.
Normally, signs of improvement are dramatic within three to 15 days from starting the formulation. This is especially important as it prevents and/or reverses dementia that often is associated with antiPD medication and is a common companion of the disease. Tremors lessen within four to 12 weeks in moderate-stage patients. In some patients in very early stages of PD (first year of diagnosis), tremors disappear within 48-72 hours. The success rate is as follows:
70% of patients have excellent to moderate rates of improvement.
15% have a lesser rate of improvement.
Approximately 10% show little or no improvement.
An additional benefit of the Cochran treatment is that heart and blood chemistry indicators also improve as discussed in early paragraphs of this article. Cardiovascular, liver, intestinal and kidney function also improve.
Since it is so difficult for experts in the field to believe that supplements can do the job that drugs have not, in Part 2 I not only will interview Tim Cochran, but I will interview a representative number of the patients receiving the Cochran Parkinson formulation and their personal physicians. I hope that Part 2 will give great encouragement to PD patients and encourage more physicians to use the Cochran regimen in their practices. Unfortunately, there are many uninformed "experts" who counsel their patients not to even consider trying nutritional regimens. WF
© 2000 Whole Foods Magazine and Richard A. Passwater, Ph.D.
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