Program Update

Strategies for Parkinson’s Disease Therapy

Editor’s note: Annetta Freeman is a 60-year-old housewife from Beverly Hills, California. We first interviewed her two years ago about her novel program for treating her own Parkinson’s disease, which is based on high-dose, broad-spectrum antioxidants with high-purity liquid deprenyl citrate [see “an Improved Parkinson’s Therapy” in SDN v4n6p1]. One core aspect of her approach involves the role of mitochondria in the Parkinson’s disease process. Mitochondria are tiny organelles within the cells that generate the vast majority of the energy that is needed to power healthy metabolism. A year ago, we published a full-length feature article about the role that mitochondrial impairment plays in Parkinson’s disease [see “Mitochondrial Nutrition, Aging and Cognition” in SDN v5n2p1]. Anne Fowkes serves the dual role of Office Manager and Assistant Editor here at CERI. She is interested in Parkinson’s disease because it runs in her family (mother, uncle, and several other relatives) and she is showing early signs of mitochondrial problems.

Click on the golden diamond to see Annetta’s updated personal treatment regimen.

Finding a viable treatment for Parkinson’s disease has been a real detective process for me. In many ways, my search was very different from what happens in standard medical practice. The standard medical approach is to treat the disease rather than the patient. I am much more interested in my well-being and ability to function than I am in Parkinson’s itself. Therefore, my investigation went beyond superficial dealings with dopamine levels and shaking symptoms (although these are definitely a large part of my treatment program). My purpose was to support my general health and well-being, and, to whatever degree I could, to address the root causes of my disease and alleviate its resulting degenerative effects.

Standard medical practice is often forwarded by drug companies, which, as money-making ventures, naturally tend to see diseases as economic opportunities. Of course, they would necessarily have to have an impact on the disease to make their product, a drug, viable in the marketplace, but a total cure or an inexpensive treatment would not necessarily be compatible with making money. This is not to say that all the people who work for drug companies are insensitive creeps or mercenary profiteers, just that their purpose within such an institutional structure would not tend to lead them to certain solutions that might be in the best interest of the sufferer.

Much of my investigation has been detailed in a previous interview [see SDN v3n6], so I will not reiterate that part of it here. This article, written in collaboration with Anne Fowkes [Assistant Editor] will cover 1) some practical tips for someone wishing to follow the program I developed for myself, 2) an update on what changes I have made in my regimen since the interview, and 3) some speculations about Parkinson’s disease that are based on my personal circumstances and corroborated in conversations with other people.

Parkinson’s runs in Anne’s family and she has begun to show some signs of tremor and mitochondrial insufficiency, both symptoms of which are associated with Parkinsonian pathology [see SDN v5n2 for further details]. So Anne’s experiences in dealing with the beginning of the disease will be quite different from mine in dealing with the advanced stages.

It would be simple if everyone could just follow my program and alleviate their symptoms as I have. Although it is almost that simple, I have spoken to many people who thought they were not making progress on the program when they really were. When I took the time to talk to them at length, I would find out what they were not doing or were doing wrong that they were not telling me.

But even under the ideal circumstances of perfect compliance with my lengthy regimen, everyone’s body is different. The degree of damage is different. The location of damage may be different. The way each person’s body uses or responds to drugs and nutrients is likely to be different. And the time it takes to recover and which aspects of function are recovered first varies dramatically from person to person. For this basic reason, anyone who wishes to get the best benefits from following my program will have to track their progress as I have done.

Keeping a journal is a very important aspect of tracking a personal program (or any investigation for that matter). If you don’t want to do a written journal, use a tape recorder. The most important things to track are your symptoms, both the ones that are constant and the ones that occur sporadically, and what nutrients and drugs you take. It is also important to track when the symptoms occur (what time of day, during what activities) and what time of day you take the nutrients/pharmaceuticals.

Keeping track of the symptoms allows you to see the progress you are actually making. The mind is designed to forget that which is unpleasant or painful (isn’t there a song about that?). For instance, I had a problem where saliva would run down my throat and into my lungs. It was because a muscle was paralyzed and it would not adequately close off the airway to stop it. I had gone an entire month without this happening and had not noticed. It was only after reading over my notes that I realized that the symptom had stopped. I had forgotten all about it, and if it hadn’t been for the notes, I would never have realized that aspect of my improvement. This kind of thing is more common than most people realize.

Anne is not yet very good at keeping a journal. She had an incident where keeping track of the nutrients she took on a day-to-day basis might have assisted her. When she raised the dosage of her deprenyl to raise her dopamine levels, she started craving sugar. When I told her she could take chromium to mitigate the cravings, she remembered that she hadn’t taken her chromium at the time she was upping her deprenyl. She went back to taking the chromium and the cravings disappeared. If she had been tracking her nutritional supplementation with a journal, she could have seen that for herself.

One of the trickiest parts of the program is finding your dopamine window. This task requires tracking your symptoms and nutrients throughout the day on an hour-by-hour basis. If your dopamine levels are too high, you will shake just as much as if they are too low. Since many of the drugs and nutrients in my regimen influence dopamine levels either strongly or subtly, dopamine levels can be too high or too low at different times of the day depending upon the timing of your supplementation.

To better illustrate this point, I’d like to discuss an important example. I take two things for raising my dopamine levels: NADH and deprenyl. I take 10 mg of deprenyl in the form of 10 drops of Discovery-brand liquid deprenyl (1 mg per drop) and 10 mg of NADH in the form of two 5 mg Enada tablets. I have tried a number of combinations over the years and found that inevitably, if I took the Enada at the same time as the deprenyl, I would shake. In my current regimen, I take the two Enada tablets right when I wake up, following the directions on the bottle and not eating anything for at least 30 minutes. I don’t start the deprenyl until after breakfast, and then I take it in four separate doses (3 mg first, then 2 mg after lunch, 3 mg in the late afternoon and finally 2 mg in the evening).

Anne takes 2 mg of the liquid deprenyl and 1-3 2.5 mg tablets of NADH a day. She takes the deprenyl before or right after breakfast. Then she takes her NADH tablets sublingually when she feels her energy or drive begin to lag later in the day. The quantity she takes depends upon the workload and stress levels of her day and if she gets unreasonably cold in the evening. Coldness is a sign of mitochondrial insufficiency, which NADH corrects [see SDN v5n2, v5n3]. Mitochondria are the energy powerplants of the cell which produce the energy which stokes the brain’s antioxidant defenses and produces warmth for the body.

The recommended dosage of deprenyl for Parkinson’s is 10 mg a day. However, that’s not the correct dosage for everyone. If Anne takes 5 mg for two days in a row, her tremor will return. Her standard dose is 2 mg a day. It was after taking 2 mg a day for two weeks that the tremor she initially noticed disappeared. So the amount you take is dependent upon the progression of the condition and the state of your body.

Following my program is relatively straightforward if you are just being diagnosed with Parkinson’s or have recognized the signs in yourself prior to diagnosis, as Anne has. The whole process gets more complicated if you are on any of the standard drugs which are routinely applied to Parkinson’s disease — especially if you have been taking them for a long time.

When I was first diagnosed with Parkinson’s, I was put on Sinemet by my neurologist. Sinemet is a combination of levodopa (a dopamine precursor, also called L-dopa) and carbidopa (a drug which inhibits levodopa metabolism outside the brain so that more levodopa gets into the brain). Because vitamin B-6 enhances the process that carbidopa is supposed to suppress, people who take Sinemet should not take vitamin B-6. Since vitamin B-6 is used in a host of biological (and mental) processes, your overall bodily function can be inhibited just for the privilege of using carbidopa. This is, of course, not something your standard neurologist will tell you up front when they prescribe Sinemet.

The effects of Sinemet, especially at the outset of its use, are good enough that many people would probably make the choice to use Sinemet even at that particular cost. However, I think that Sinemet can cause tremor in and of itself. In my case, I was also on Inderal (propranolol) to offset the tremor caused by (or not alleviated by) the Sinemet. Adding deprenyl to this program increased my dopamine levels beyond the desired window and I had to adjust my Sinemet downward. It was difficult to weather the process, but I eventually got myself off of Sinemet and Inderal and am very pleased with my program now.

A number of other people on the program have lowered but not given up these other drugs. One person made some incredible strides, recovering a great deal of mental function (going from a state of dementia to a state where he could deal with difficult mathematical theories) and was actually writing a novel, but he still had some dyskinesia (shaking) because of the Sinemet.

These drugs are addictive. This addiction leads to withdrawal symptoms when you try to go off them. Many people are absolutely terrified of going through that withdrawal. Instead of riding through it and letting the body get over the addiction, they panic and run back to the drug that is causing it in the first place.

Tracking my own reactions to the substances I was taking is what led me to my current program. For myself, I think it was well worth the effort, both of keeping the journal and in withdrawing from standard Parkinson’s medications.

I have searched in many places for information on Parkinson’s disease: the medical literature, product papers, lectures, whatever source I could find. The advantage of reading the studies in the medical literature for oneself is that one does not have to wait for the medical community to catch up on new research developments — which usually takes about 10 to 20 years.

One of the things that I have learned is that some Parkinson’s disease is a result of a defect in mitochondrial DNA in the area of the antioxidant defense system. Losing the antioxidant defense system for a highly energized system such as the dopaminergic nervous system might be likened to losing the grillwork and bricks that surround your fireplace, leaving the sparks and flames to set fire to your house. In that situation, when you do things to feed the flames, you are stoking the fire which is burning down the house.

I think it makes perfect sense that taking antioxidants would help to offset the damage caused by the insufficiency in the antioxidant defense system, and my personal experience attests to that. The research which has been done on antioxidants suggests that different ones work on different systems. Every time I added a new antioxidant to my regimen, I seemed to get better.

It scares me that the current medical approaches to Parkinson’s don’t seem to make any attempt address these issues. No one, to my knowledge, has tested large-dose, broad-spectrum antioxidants in the treatment of Parkinson’s either with or without other standard treatments. I have not had either the fetal cell transplant operation or a brain surgical procedure, but I have known others that have. The results were great at first, but several months later, they had not only lost the ground they had gained, they were actually in worse shape than they were before the operations. A failure to address the underlying problems in the antioxidant defense system would predict such an outcome. Until the antioxidant studies are done, I think the medical community is fighting half a battle, and maybe even the wrong half.

For a complete listing of what is currently in my program, you can refer to the sidebar in this newsletter. Good luck and remember, keep a journal, drink lots of water, take your nutrients, use liquid deprenyl, and lower your stress.