PARKINSON’S: AN ALTERNATIVE APPROACH

Dr. Sharon Rabb

Parkinson’s disease (PD) is a chronic neurological disorder caused by a progressive degeneration of the nigrostriatal dopamenergic neurons in the pars compacta of the basal ganglia. Other neuronal fields and neurotransmitter systems are involved including non-adrenergic, serotonergic and cholingeric neurons. As the neurons in the ganglia degenerate there is a loss of the neurotransmitter dopamine. When the individual initiates an action such as walking, the basal ganglia help smooth the movements and coordinate the posture by signaling the thalamus in the brain which then communicates with the cerebral cortex. All of these signals are coordinated by neurotransmitters and the neurotransmitter used by the basal ganglia is dopamine. As the neurons degenerate in PD the amount of dopamine is decreased and the number of nerve connections with other nerve and muscle cells also decreases. Levo-dopa (L-dopa) is the precursor of dopamine and is widely used in the treatment of PD. However, it loses effectiveness as the disease progresses and has negative side effects. Pd is characterized by slowness of movement, muscular stiffness, rigidity, tremor, poor posture and balance and sensory motor integration deficits. It is the second most common neurodegenerative disease, as Alzheimer’s is the first (Kasture 2009; Abde-Salam, 2008). Apparently, the neurons in the ganglia degenerate due to oxidative stress which causes among other things an energy crisis in the mitochondria in the neurons. The key question is what factors cause the degeneration because genetics is not the total answer, although PD does run in families.  Some of the known precursors for the disease are listed below.

  • Constipation
  • Adiposity
  • Exposure to pesticides
  • High consumption of polyunsaturated fatty acids

Sixty to eighty percent of Pd patients have constipation which seems to appear between ten and twenty years prior to the onset of symptoms (Abbott 2003). Constipation is defined in this study as less than one bowel movement in three days. It is my belief that you need to have at least one movement a day. In fact, Abbott found that lower frequency of bowel movements could actually predict the disease. Now, why is this so important? One reason is because, constipation results in a build-up of toxins which can cause degeneration of the neurons. Lewy neuritis and Lewy bodies, the hallmark of PD pathology, appear in the dorsal nucleus of the vagus nerve in the earliest stages of the disease and then extend upward toward the brain to reach the substantia nigra in the third stage. This results in impaired bowel motility and the build-up of toxic substances (Ueki 2004). Toxins from the bowel break through the mucosal barrier of the intestines and are incorporated into the axon terminal of the vagus and transported in a retrograde manner to the vagus nucleus. This results in toxic overload of the neurons and early degeneration. It is estimated that between seventy to eighty per cent of the neurons in the ganglia are destroyed by the time symptoms appear. I believe these toxins not only decrease bowel motility but also hasten degeneration of the neurons in the ganglia. These toxins are in part from protein metabolism and include guanidine one of the most toxic substances in the breakdown of protein. Dr. Harrower (1957) in his classic book Practical Endocrinology states that the parathyroid controls the elimination of acid waste via calcium and other nutrients. “The parathyroid hormone has been called “a calcium mordant” and exerts destructive influence on certain wastes –especially guanidine” (p. 557). He goes on to say that the complete removal of the parathyroid glands result in tetany (neuromuscular hyper-excitability manifested by tonic spasms and eventually death). Harrower and a few early doctors that practiced endocrinology used parathyroid extracts to treat PD and other neuromuscular diseases. Some patients responded remarkably well to this glandular while others did not. The knowledge of this therapy seems to have almost been lost as I could not find it mentioned in the current literature. As far back as 1907 W.N. Berkeley was treating PD with parathyroid. He published a paper in the New York Medical Journal which Harrower summarizes below. At that time PD was more often referred to as paralysis agitans. Dr. Berkeley in his article gave 3 good reasons to treat Pd with parathyroid extract:

1. The blood calcium is often unusually low. Parathyroid raises this figure, thus increasing calcium reserves.  Lime (calcium) of course is one of Nature’s neutralizers.

2.  Certain protein split products, such as guanidine, are often in excess in hypoparathyroidism. Parathyroid therapy lessons this excess, and at the same time gives symptomatic benefit. A condition sometimes called ‘hyper-guanidinemia’ is not infrequently found in paralysis agitans (PD), and it is known that these guanidine congeners have a special predilection for the nervous system.

3.  There are on record, a number of autopsy reports of patients dying with PD, showing parathyroid atrophy or pathology. “The effects of parathyroid in favorable cases are in every way beneficent. The rigidity and tremors are controlled, salivation is diminished, and restlessness and insomnia are relieved. Occasionally a miracle is worked (Berkeley, 1907)”.

Harrower goes on to say that the best proof of the essential correctness of these conclusions about the connection between the parathyroids and PD is just this: the empirical use of parathyroid extract has been of symptomatic benefit in many cases of paralysis agitans. In 1926 Berkeley reported a 60 to 70 per cent success rate using parathyroid extracts. Giving parathyroid extracts also make it possible to retain calcium in a suitable form for the body. Calcium is very important in fighting infections. Researcher in the early 20th century found that in certain ulcerative conditions that there was not enough calcium in the ionized form in the serum to aid healing. Giving calcium alone was not enough to heal the ulcer, but giving both calcium and parathyroid extract induced healing.

 

We can now trace the problems of constipation

Toxins such as guanidine leak out of the gut impairing the GI motility and causing constipation as well as degeneration of the neurons, whether this causes hypoparathyroidism or the hypo condition already existed and was responsible for the build-up of toxic guanidine is as far as I know not known. The body uses calcium reserves to neutralize the toxins and this puts a further stress on the parathyroid system. Dr. Harrower also advocated using adrenal cortical extracts in treating PD. This makes sense because the adrenals are involved in muscular toxemias. Also, many Pd individuals are excessively depleted and fatigued and need adrenal support for that reason. Adrenal extracts facilitate the intramuscular chemistry by catalysis---hastening or completing the destruction of large amounts of fatigue poisons.

Adrenal cortical extracts have shown great benefit  in treating PD, in 1931 doctor DH Plank of San Francisco wrote to doctor Harrower, “The more I use adreno-cortin, the more I am impressed with its value in various dysfunctions. My patient with Parkinson’s continues to improve in every way; the pain is all gone, he sleeps well, appetite is good, and he can assist himself in every way. He is using his left arm, which has been helpless for more than 2 years, and can now raise it above his head. This patient is now using a Whitley exerciser, with his back to it to develop the arm and shoulder muscles and to bring the head erect. I consider this to be quite remarkable for less than three months.”

Adreno-cortin was an extract of the cortical adrenal developed by Harrower, and is no longer in existence. However, we can probably get very similar results from various standard process adrenal products. The point is that it might be very beneficial to PD individuals to give them both parathyroid and adrenal extracts along with diet modifications, whole food vitamins and minerals plus certain potent herbs.

 

D I E T

Diet modifications are critical in the PD individual. Research substantiates the adoption of a relatively high fat low protein diet, with plenty of fresh fruits and vegetables for vitamins, minerals and anti-oxidants. There are several reasons for a low protein diet. One of these is that as explained earlier, the protein breakdown products cause toxicities to the neurons and thus destroy them, especially in a hypothyroid state. Also, L-dopa is transported through the blood brain barrier on transport molecules that also transport other amino acids (protein building blocks). In high concentrations of amino acids, in other words a high protein diet, L-dopa has to compete with other amino acids and may get “left behind” (Tyrrell ,1998). Protein foods may also interfere with PD meds for this very reason. I have found that all chronic illnesses do better on a moderate to low protein diet and replacing animal sources with vegetable ones with the exception of eggs, cheese, and yogurt. Vegetable fats seem to be good because the PD brain reportedly does better on a ketogenic diet (Tai, 2008). Also, every nerve cell is encased in a fatty sheath which protects and facilitates function. I understand that certain oils such as coconut, flax, sesame, and others to be very beneficial. Diet for any disease needs to be personalized for every individual based on needs and other conditions in the body, but a general diet for PD would include low protein, moderate fat intake with calorie restriction (CR) if possible and weight loss is not an issue.

CR can have beneficial effects on health and it is beyond the scope of this article to delve thoroughly into the concept and explore exactly how it benefits chronic illnesses, but I will give a general outline as refers to PD. CR can have profound effects on brain function and vulnerability to injury and disease. CR is defined as the lowering of caloric intake to a range of from 900 Kcal to 1400Kcal per day depending on the individual. There is an organization of people called the Caloric Restricted Society and they have been extensively studied because of the surprising effects that CR has in animal models on health and aging. Benefits appear to be the result of a cellular stress response that stimulates the production of proteins that enhances neuronal plasticity and resistance to oxidative and metabolic stress. These include neuronal factors such as brain derived neurotrophic factor (BDNF), mitochondrial proteins and other proteins known as chaperone or heat shock proteins. These metabolic changes in CR protect neurons from degeneration in animal models and can also stimulate the production of new neurons from stem cells.

Clearly, CR would be of great benefit in treating Pd if the patient is not already debilitated.  In researching caloric restriction I found that the most important types of food to restrict are proteins.  Again, I would like to emphasize the importance of a high fruit and vegetable diet. These foods provide the necessary phytochemicals needed by the body to heal from chronic illness, especially important are the whole food vitamins such as vitamin C and the B complex (Martin, 2002).

 

I found several supplements listed in the research literature that report to benefit PD).

 

Protomorphogens (PMG) by Dr. Royal Lee:

I will not take the space here to give a lengthy description of PMGs as I have two articles on my web-site devoted to the theory and how it works. Briefly, PMGs are the blue prints used by the body to create a particular cell type, such as muscle or nerve. Two types exist. The first type is called endogenous PMG and is created in the body and used for either growth or repair of body tissues. The second type is exogenous and is usually taken in when protein is consumed. Exogenous PMGs in food can in a very small way influence cell repair. The reason its action is small is because there is not very much PMG in say an ounce of fish. Dr. Royal Lee and a team of other researchers developed the PMG theory but Lee was the only one to figure out a way to process it into concentrated supplement form. He has developed a PMG for almost every cell type including nerve, muscle, parathyroid, adrenal, and others. He also developed a few extracts from glandulars including adrenal and hypothalamus, a part of the brain that controls the endocrine system. By using the PMGs plus the glandular extracts or cytosols and the desiccated glandular products when available, one can have a full range of glandular products to facilitate healing. The PMGs taken orally upregulate the formation of new neurons and other cells depending on the type of PMG taken. They also diminish any inflammatory response. Wow! What a supplement, and to think they have been available to health care professionals for over 50 years. The PMGs are only blue prints, so you also have to add the building blocks in order to build a new “bodily House”. The buildings blocks include the raw materials found in fresh whole non processed foods such as proteins, fats, carbohydrates, vitamins, mineral, and other phytochemicals. Phytochemicals are part of vitamin complexes and are not found in the vast majority of supplements sold over the counter in stores. Again, Lee came to the rescue and developed processing equipment to formulate REAL vitamins, with their co-factors intact, and organic minerals from organically grown produce (see articles on web-site for discussion on real vs. artificial vitamins).  Synthetic vitamins are harmful and are not to be used if healing is your goal. Ascorbic acid is NOT vitamin C but only the synthetically manufactured artificial copy that does NOT function as a real vitamin in the human body (Lee, 1998). I have used PMGs and other glandular for healing chronic diseases with spectacular results.

 

Real Vitamins:

I have discussed vitamins in the previous discussion, but would like to add a few comments here. Since PD is considered a disease in which free radicals damage the nerve cells it is important to supplement with real whole food anti-oxidant vitamins such as vitamins C and E (Martin, 2002). Selenium is actually a part of the E complex and I will discuss it further later. The research literature is contradictory in reports on these two vitamins and their benefits for chronic illnesses. This is partly due to the fact that some studies use whole foods containing the nutrients they are testing and others use artificial supplements. Of course, the artificial supplements show either little or no value. The vast majority of people do not understand that vitamins are living systems and contain many co-factors not found in the artificial supplements. Therefore, synthetic supplements are not FUNCTIONAL as they do not contain the co-factors needed. There are very few companies that sell whole food vitamins, Lee’s company is by far the best. There is substantial evidence that poor nutrition is causative in the pathogenesis of neurodegenerative diseases such as PD (Martin, 2002).

 

Folate and Vitamin B12:

A deficiency of dietary folate can modify the vulnerability of dopaminergic neurons leading to dysfunction and early death. Also, lack of folate exacerbates dopamine depletion, neuronal degeneration and motor dysfunction. It also exacerbates oxidative stress, and to mitochondrial dysfunction of human dopaminergic cells exposed to the pesticide rotenone or the pro-oxidant Fe(2+)(iron) (Duan, 2002). In fact excess iron seems to be very detrimental to PD, but in the presence of vitamin C this is ameliorated (Logroscino, 2008). Both folate and B12 seem to influence the effects of homocysteine (Hcy). Hcy is a metabolite that builds up in the body when folate, B12 and or B6 is deficient. The metabolite is harmful to the neurons and other cells in the body. L-dopa drug therapy increases the need for these B vitamins as it increases the levels of Hcy (Lamberti, 2005). The B vitamins are very important in nerve tissue, in fact, their primary function in the body is to ensure proper nerve health. I have seen individuals with undifferentiated tremors heal themselves with diet and whole food B vitamins. B vitamin deficiency is a major issues because these vitamins have been removed from our food supply and been replaced with artificial and or synthetic substitutes that do not function as the real ones do. Dr Lee called heart disease white flour disease because of the absence of real vitamins B and E and essential fatty acids in processed flour. In a future article I will enumerate the various B vitamins and their functions, although to some extent this has been done in the article on diabetes. Suffice it to say that all PD patients need to take whole food B supplements, but I generally put different individuals on different ones.

 

The minerals, copper, selenium, and zinc:

Selenium is part of the vitamin E complex and is itself an anti-oxidant.  Imbalances between oxidants and ant-oxidants in the body can lead to PD. Selenium supplementation has been shown to successfully up-regulate the anti-oxidant status and to decrease dopamine loss and the time it takes to reach functional recovery. Pd induced rats were tested for neurobehavioral activity, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glutathione status and all were shown to decrease dopamine loss after selenium supplementation (Zafar, 2003). Copper is part of the vitamin C complex and is an important supplement for PD patients. Zinc and copper are in a delicate balance in the body and sometimes need to be given together.

 

 

 

 

L-tyrosine:

L-Dopa (L-3,4-dihydroxyphenylalanine) is produced from the amino acid L-tyrosine. This reaction is catalyzed by tyrosinase. L-Tyrosine is also the precursor for other catecholamines which are produced in the chromaffin cells of the adrenals, sympathetic nerve cells, and the neurons of various parts of the brain. Tyrosine uptake occurs via a transport carrier located in the blood brain barrier in the brain and it is in competition with other large neutral amino acids (LNAA) such as tryptophan, phenylalanine, leucine, isoleucine, and valine. PD Patients who received an oral administration of L-tyrosine of 50 to 100mg/kg per day for 4 to 7 days improved as much on L-tyrosine as L-dopa. L-tyrosine was more effective when administered to mild and early onset patients as some did not respond as well as others. Of course L- tyrosine did not cause the complications and side-effects that L-dopa did (Tyrrell, 1998). L-tyrosine has also been used to treat depression and individuals with high stress levels although I do not recommend L-tyrosine for these problems unless other supplements are also given.

 

Bacopa monnieri:

Bacopa has been used for cognitive issues for many years in the herb world. It has been shown to enhance mental clarity and support cognitive function, support normal memory function, support physical endurance, ease the effects of temporary and occasional stress, and to nourish the nervous system.  In a study using fruit flies, bacopa significantly decreased the levels of oxidative stress, inhibited dopamine depletion and decreased mortality (Hosamain, 2009).

 

Valerian:

I have used valerian with great success in supporting various types of hyper- irritability states. It is a calmative to the central nervous system and probably also to the autonomic nervous system.

 

Ginkgo biloba:

Ginkgo is one of the most widely studied herbs on the market and it supports a variety of issues. It provides ant-oxidant protection so needed in PD as it is oxidation that causes the neurons to degenerate. It supports mental function and mental clarity as well as increases blood flow to the brain. It is widely used in cardiovascular health and it has anti-aging properties. Oxidative chemicals such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) are able to damage cellular structures like DNA, proteins and lipids in the body. The concentration of these harmful chemicals increases as we age and they also increase in disease states. Improper diet and stress also effects the concentration and the amount of damage these substances can do. The accumulation of oxidatively damaged proteins is a hallmark of PD and other neurodegenerative diseases. Also, the process of aging is connected to their accumulation because cellular function is disturbed. These reactive chemicals damage ferritin (iron) which then significantly increases oxidative damage to proteins in the body. Ginkgo has been shown not only to counteract this oxidative damage to the brain, but also to increase the number of dopaminergic neurons. Ginkgo was shown to be able to chelate transitional metals, such as excess iron, thus slowing oxidation. There is a great need to develop protocols that include neuroprotective agents that can stop and prevent oxidative damage (Rojas, 2008; Voss, 2006).

 

Blueberry extract (BBE):

Several studies exist on substances that improve the life of transplanted neuronal cells in vitro, but few studies concentrate on changing the internal environment of the host.  This is probably because the research community is controlled by the drug companies and many of these phytochemicals that protect our internal environment are natural and not drugs. Flavonoids and other beneficial nutrients found in produce and herbs have strong anti-oxidant and anti-inflammatory properties. In one study BBE was shown to significantly prevent oxidative stress associated with impairment of striatal motor function during aging and RESTORED lost motor function in aged rats. BBE improved survival of embryonic dopaminergic neurons. It increased the survival of DA neurons and ameliorated rotational behavioral asymmetries (McGuire, 2006). I have found BBE very effective for both nerve health and eye repair from macular degeneration. BBE apparently reduces inflammation and improves blood flow. Two other supplements also help with this and they are turmeric and phosphatidyl serine. I will not expound here on these two supplements, but will address these in a later article.

 

Mucuna puriens (MP):

Mucuna seems to the miracle herb for PD. In several studies it was shown to be more effective than L-dopa in terms of neuromuscular behavior. MP has been used in traditional Indian medicine for centuries. It contains L-dopa and other synergistic ingredients which act together to “out perform” L-dopa. MP at 16mg/kg showed improved turning behavior and a reduction in abnormal involuntary movements (AIM) in rats, significantly out performing L-dopa (Kasture, 2009). In a small clinical study in 2004, Katzenschlager observed a more rapid onset of action and longer “on-time” without concomitant increase in dyskinesia when MP seed was administered as compared to L-dopa, suggesting that MP possesses advantages over conventional L-dopa in long-term management; 48 mg of MP contains 6 mg of L-dopa. In another study, MP restored specific motor deficits such as akinesia and gait impairment. MP decreased time required to initiate movement and also tremor (Hussain, 1997). Apparently, MP contains 5-hydroxytryptophan as well as L-dopa which plays a role in ganglia physiology and decreases long term complications with L-dopa treatment (Kasture 2009).

 

Portulaca  grandiflora:

I would like to mention this plant as I found one reference that is noteworthy. According to Rani portulaca produced more L-dopa from L-tyrosine that mucuna puriens in cell cultures. I have not as yet located a source for this as it appears to be a moss rose (Rani, 2007).

 

In summary, the main goals of supporting PD are to cease adding toxins via the diet and to detoxify the existing toxins in the body, to include the needed herbs that supply L-dopa, to protect the remaining dopaminergic neurons and to rebuild new ones. This can only be achieved with a multi-deminsional program to include diet modification, stress reduction techniques, whole food supplementation with certain glandulars and protomorphogens (PMG), and high potency herbs. Each program needs to be tailored to the specific needs of the patient based on medical, genetic and dietary histories. Each “prong” of the protocol works synergistically with the others to bring about a more affective outcome. A good source of herbs is critical to success as most of the herbs sold in this country have minimal concentrations of phytochemicals. That is why I use herbs produced In Australia because I can be assured of their quality and potency. Both the herbs and the concentrated whole food supplements can only be purchased through a health care professional and are more expensive than the synthetic artificial ones sold over the counter, but they are well worth the money. I also sometimes add various energy medicine techniques which act synergistically with the other modalities to further improve the outcome of the program. I believe that every illness can be cured by the body itself if given the correct raw materials and the person abstains from toxic chemicals.

 

References

 

1.  Abbott, RD., et. al.(2003). Environmental, life-style, and physical precursors of clinical Parkinson’s                  disease: recent findings from the Honolulu-Asian aging study.  J Neurol, 250(3), 30-9.

2.  Abdel-Salem, OM.,et. al. 2008). Drugs used to treat Parkinson’s disease, present status and future direction.  CNS Neurol Discord Drug Targets, 7(4) 321-42.

3.   Duan, W., et.al. (2002). Dietary  folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson’s disease. J Neurochem 80(1) 101-10.

4.   Harrower,H.R. (1932) Practical Endocrinology.( Rev. Ed.)Glendale, Ca: Pioneer.

5.   Hosamani, R., et. al. (2009). Neuroprotective efficacy of Bacopa monnieri against rotenone induced oxidative stress and neurotoxicity in Drosophilia melanogaster.  Neurotoxicology, 30(6) 977-85.                                 

6.   Kasture,S. , et. al. (2009). Assessmentof sumptomatic and neuroprotective efficacy of mucuna pruriens seed extract in rodent model of Parkinson’s disease. Neurotox Res, 15(2) 111-22.

7.   Lambert, P., et.al. (2005). Hyperhomocysteinemia in L-dopa treated Parkinson’s disease: effect of cobalamine and folate administration. Eur J Neurol,  12(5) 365-8.

8.   Lee, R. (1998) Lectures of Dr. Royal Lee. Fort Collins: Selene River Press.

9.   Logroscino,G., et. al. (2008). Dietary iron intake and risk of Parkinson’s disease.  Am J Epidemiol, 168(12) 1381-8.

10.  Martin, A., et.al. (2002). Roles of vitamins E and C on neurodegenerative diseases and cognitive performance.  Nutritional Reviews, 60(10) 308.

11.  McGuire,SO., et.al. (2006). Dietary supplementation with blueberry extract improves survival of transplanted dopamine neurons.  Nutr Neurosci, 9(5-60) 251-8.

12.  Rani, N., et. al. (2007), Cell Suspension cultures of Portulaca grandiflora as potent catalysts for biotransformation of L-tyrosine into L-dopa, an anti-aging Parkinson’s drug.  Pharm Biol, 168(12) 1381-8.

13.  Rojas, P., et. al.(2008). G6761 protects against nigrostriatal domaminergic neurotoxicity in 1-methyl-4-phen-1,2,3,6- tetrahydropyridine-induced Parkinsonism in mice; role of oxidative stress.  Eur J Neurosci, 28(1) 41-50.

14.  Tai, KK., et.al. (1996). Ketogenic diet prevents cardiac arrest-induced cerebral ischemic neurodegeneration.  J neurol Transm, 115(7) 1011-7…

15.  Tyrell, H., et. al. (1998). Tyrosine: food supplements or therapeutic agent?  J Nutr and Envir. Med., 4(8) 349-59.

16.  Ueki, A., et. al. (2004). Life style risks of Parkinson’s disease: association between water intake and constipation.  J Neuro, 251(70) 18-23.

17.  Voss, P., et. al. (2006). Ferritin oxidation and proteasomal degradation: protection by antioxidants.  Free Radic Res, 40(7) 573-83.

18.  Zafar, KS., et.al. (2003). Dose-dependent protective effect of selenium in rat model of parkinson’s disease: neurobehavioral and neurochenical evidences.  J Neuro chem., 84(3), 438-46.