Understanding Parkinson’s Disease

by John G. Connor, M.Ac., L.Ac., edited by Barbara Connor, M.Ac., L.Ac.

Table of Contents        

Introduction        

Biomarkers Elevated in Parkinson’s Disease         
Recommendations for Preventing or Reducing the Rate of Progression of Parkinson’s Disease
Diet and Parkinson’s Disease
Acupuncture and Parkinson’s Disease
         
Herbal Medicine and Parkinson’s Disease         
The Beneficial Effects of Adaptogens on Reducing Parkinson’s Disease         
Botanicals for Symptomatic Relief of Parkinson’s-Related Tremor       
Iron Imbalance Linked to Parkinson’s Disease         
Exercise and Parkinson’s Disease        
Other Studies Highlighting the Importance of Various Natural Compounds for Preventing or Reducing the Rate of Progression of Parkinson’s Disease·        
References

Introduction
Aged men have a greater incidence of Parkinson’s disease (PD) than women. PD is a neurodegenerative condition associated with the loss of dopamine neurons in the nigrostriatal pathway. The primary pathological feature of PD is the loss of dopamine neurons within the substantia nigra pars compacta of the midbrain. Oxidative stress is involved in mediating this loss of dopamine neurons in PD. Furthermore, animal models of PD have shown that oxidative stress leads to initiation of the apoptotic pathway. (Cunningham et al 2009)

What is the relationship of Parkinson’s disease to free radicals?  Free radicals are involved in the pathology of Parkinson’s disease. (Gassen 1999)  Therefore supplementation with antioxidants may prevent or reduce the rate of progression of this disease.  Supplementation with multiple antioxidants at appropriate doses is essential because various types of free radicals are produced.  Antioxidants vary in their ability to quench different free radicals and cellular environments vary with respect to their lipid and aqueous phases.  (Prasad 1999)

Inflammation and TNF-alphaThe overproduction of inflammatory byproducts has been linked to the onset and progression of Parkinson’s Disease, as well as other neurodegenerative diseases. Inflammatory pathways, such as COX-2, NF-kB, and tumor necrosis factor (TNF)-alpha, are often up-regulated in Parkinson’s Disease.  Blockage of the pro-inflammatory cytokine TNF alpha will attenuate the loss of dopaminergic neurons typical of Parkinson’s Disease.      There are a number of herbal and nutritional therapies that effectively target inflammation and mitochondrial dysfunction, and have been shown to reduce the progression of the disease.

Elevated Homocysteine
Elevated homocysteine is associated with levodopa and is proportional to peripheral neuronal dysfunction in Parkinson’s Disease. Levodopa metabolism via catechol O-methyltransferase (COMT) increases levels of homocysteine, a neurotoxin which induces an axonal-accentuated degeneration in sensory peripheral nerves. Elevated homocysteine can be avoided with inexpensive and well-tolerated therapies such as vitamin B supplementation.  An elevated level of homocysteine in Parkinson’s Disease is also associated with an increased risk of bone fractures.

Discovery of the enzyme catechol-O-methyltransferase (COMT) in the 1950s resulted in an explosion of research activity surrounding the enzyme and Parkinson’s Disease. In the presence of magnesium, COMT catalyzes the transfer of a methyl group from S-adenosyl-L-methionine (SAM) to one of the hydroxy groups of a catechol substrate. Generally, COMT functions to eliminate biologically active or toxic catechols and their hydroxylated metabolites. This is one of the many important magnesium dependent enzymes in Parkinson’s Disease and why creatine magnesium chelate is an important nutrient for the treatment of Parkinson’s Disease.

New research shows that people who have used amphetamines such as Benzedrine and Dexedrine appear to be at an increased risk of developing Parkinson’s disease, according to a study released Feb. 22, 2011 that was presented at the American Academy of Neurology’s 63rd Annual Meeting.

Biomarkers Elevated in Parkinson’s Disease
Copper – 
In Parkinson’s disease, we found significantly increased levels of especially Cu and Zn in particular (p<0.01) and Mn (p<0.05) in CSF. A multiple comparison test suggested that the increased level of Mg in ALS and that of Mn in PD were the pathognomonic features. (Hozumi et al 2011)

C-reactive Protein (CRP)
 It was found that hs-CRP levels in the early Parkinson’s disease (PD) group were higher than those of healthy controls. Furthermore, when compared with normal controls, the odds ratio for PD based on hs-CRP level cut-off of 0.5 was 2.094 (95% CI = 1.017-4.311, P = 0.045). In this study, our findings support the hypothesis that neuroinflammatory reactions play an important role in the pathogenesis of PD. (Song et al 2011)  Oxidative damage markers are systemically elevated in PD, which may give clues about the relation of oxidative damage to the onset and progression of PD.(Seet et al 2010)

Ferritin – 
As compared to controls, serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), urate and PON1 activity were significantly reduced, and serum ferritinlevels were significantly increased in male and female Parkinson’s Disease patients. Serum urate levels and PON1 activities were inversely related, and serum ferritin levels were correlated with Yahr stage and PD duration in men and women. (Ikeda et al 2011)

Homocysteine
 – Our findings might imply that Hcy (homocysteine) and MMA (methylmalonate) are released as a consequence of neurodegeneration regardless of the underlying cause and serve as surrogate markers of neurodegeneration. Alternatively they might be directly implicated in the pathogenesis of these diseases. Since elevated levels of both Hcy and MMA are neurotoxic, further studies might investigate the effect of vitamin therapy on disease progression. Levels of Hcy and MMA did not differ significantly between the neurodegenerative diseases: progressive supranuclear palsy (PSP), amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD). (Levin et al 2010)

Iron – 
High iron concentrations in the brain have been consistently observed in Alzheimer’s (AD) and 

Parkinson’s (PD) diseases. A loss or an abnormal metal homeostasis might cause cellular death or severe dysfunction, and it has been recognized as a triggering factor for different neurodegenerative disorders such as Alzheimer’s (AD), Parkinson’s (PD), and Huntington’s (HD) diseases as well as amyotrophic lateral sclerosis (ALS) (Salvador et al 2010)

Recommendations for Preventing or Reducing the Rate of Progression of Parkinson’s Disease
Diet and Parkinson’s Disease
The diet should be rich in organically grown fruits, vegetables, whole grains, legumes (fava beans, rich in L- dopa, are particularly good), and omega-3 fatty acid-rich fish, and low in other animal foods. A diet of this type is associated with both a reduced risk of Parkinson’s Disease and a slowing down of the disease’s progression.

The intake of animal protein foods, particularly meat, refined sugars and starches, and refined fats should be minimized. Refined sugars, starches, and fats increase inflammation and oxidative damage.
Increasing numbers of studies have demonstrated the efficacy of polyphenolic antioxidants from fruits and vegetables in reducing or blocking neuronal death occurring in the pathophysiology of these disorders. These studies revealed that mechanisms other than the antioxidant activities could also be involved in the neuroprotective effect of these phenolic compounds.

One study found that a protein-restricted diet during the daytime offers a fascinating technique for the control of motor response fluctuations in patients with Parkinson’s Disease undergoing long-term levodopa treatment. The consumption of meat is possibly associated with Parkinson’s Disease due to the fact that meat contains high levels of iron.

Iron and Parkinson’s Disease
Iron, which can easily oxidize in the body and accelerate free radical damage, has been found, at elevated levels, to increase the risk developing Parkinson’s Disease.

A recent study found that people with high levels of iron are nearly two times more likely to develop Parkinson’s Disease than those with the lowest levels of this mineral in their diets. The study compared 250 people who were newly diagnosed with the disease to 388 people without it. Interviews were conducted to determine how often participants ate certain foods during their adult life. Those who were shown to have the highest levels of iron in their diets – those in the top 25% – were 1.7 times more likely to be Parkinson’s patients than those in the lowest 25% of iron intake.

Mitochondrial Optimization
The optimization of mitochondrial function to improve the production of energy may depend on uti- lizing both carbohydrate- and fat-burning pathways. Adaptogens improve the ability of the body to utilize both carbohydrates and fats, and proteins as well. These processes can be further enhanced with the addition of critical nutrients that support mitochondrial function. Some of these include: 1) carnitine for fatty acid trans- port into mitochondria; 2) coenzyme Q10 in the electron transport chain; 3) lipoic acid in the citric acid cycle; 4) creatine magnesium chelate to enhance ATP uptake; 5) NADH, in coupling the citric acid cycle to the electron transport chain; and 6) B-complex vitamins which function as co-enzymes in many of these processes.

One of the main effects of taking adaptogens is to provide protection against the harmful systemic effects of stress. Adaptogens help by providing a quicker, more efficient response to stress, as well as a faster recovery. Efficient recuperation from an overly stimulated sympathetic nervous system can conserve dopamine by inhibiting the overproduction of norepinephrine and epinephrine, produced from dopamine.

Another element of particular detriment to the brain is oxidative damage. Neuronal cells are largely post-mitotic, that is, damaged neurons cannot be re- placed readily via mitosis. During normal aging, the brain undergoes morphological and functional modifications resulting in observed behavioral declines such as decrements in motor and cognitive performance. The addition of phenolic-rich companion adaptogens offers protection from Parkinson’s Disease by reducing inflammation, through redox cycling, and through the scavenging of free radicals.

Anabolic Restoration
Parkinson’s Disease is a disease associated with increased catabolic activity. The rate of body weight and lean mass loss in a catabolic state is 5- to-10-fold faster than the rate of restoration due to the marked increase in catabolism relative to anabolism associated with any significant insult. During recovery, endogenous anabolic activity only returns to normal, and in Parkinson’s Disease, it is already low. The aging process alone causes a shift away from anabolic metabolism towards more catabolic activity. However, by taking anabolic/anticatabolic adaptogenic botanicals and other nutritional agents, one can markedly increase the rate of cellular and muscular restoration and minimize the protein degradation that occurs during both the catabolic and recovery phase. This is a critical area in successful recovery and health promotion in Parkinson’s Disease, but there is a lack of any real focus or attention by either the conventional medical or holistic health communities.

Holistically-minded herbal practitioners often just focus on herbs that merely reduce the symptoms of Parkinson’s Disease and do not address the underlying causes. It is my intention to expose both the causes and solutions to Parkinson’s Disease in order that we may offer our patients the most complete and thoughtful assistance with their health.

Parkinson’s Disease is associated with distinct endocrine alterations involving reduced secretion of anterior pituitary hormones, leading to “wasting syndrome.” The impaired pulsatile secretion of growth hormone, thyrotropin, and gonadotropin can be re-amplified by relevant combinations of releasing factors, which also substantially increase circulating levels of insulin-like growth factor (IGF)-1, IGFBPs (binding protein), thyroxin, tri-iodothyronine, and testosterone. When anabolism is clearly overtaken by catabolism, a lethal outcome of Parkinson’s Disease can be predicted by a high serum concentration of IGFBP-1, which points to an impaired insulin effect.

Survival was recently shown to be dramatically improved by strict normalization of glucose and insulin. Endocrine function testing in Parkinson’s Disease patients represents a major challenge due to the complexity and the multiple altered hormones.

Stress is a risk factor for a variety of illnesses that involve the same hormones that ensure survival during a period of stress. Although there is a considerable ambiguity in the definition of stress, a useful operational definition is “anything that induces increased secretion of glucocorticoids.” The brain is a major target for glucocorticoids. Whereas the precise mechanism of glucocorticoid-induced brain damage is not yet under- stood, adaptogens aimed at regulating abnormal levels of glucocorticoids are important agents in controlling age-related, stress-induced, neurological decline.

Acupuncture and Parkinson’s Disease
Acupuncture, as an alternative therapy for Parkinson’s Disease (PD), has beneficial effects in both PD patients and PD animal models, although the underlying mechanisms therein remain uncertain. The present study in a mouse model of PD found that acupuncture treatment at acupoint GB34 improved motor function with accompanying dopaminergic neuron protection against MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) but did not restore striatal dopamine depletion. Instead, acupuncture treatment increased dopamine release that in turn, may lead to the enhancement of dopamine availability in the synaptic cleft. Moreover, acupuncture treatment mitigated MPTP-induced abnormal postsynaptic changes, suggesting that acupuncture treatment may increase postsynaptic dopamine neurotransmission and facilitate the normalization of basal ganglia activity. (Kim et al 2011)

Herbal Medicine and Parkinson’s Disease
The use of adaptogens, which enhance mitochondrial energy transfer, and companion adaptogens, which reduce inflammation and oxidative stress, are the foundation of my protocols for Parkinson’s Disease. They are aimed directly at the causative factors. Research confirms that many plant-based phenolic extracts (companion adaptogens) increase the redox/antioxidative abilities of the body and can effectively slow the progression of Parkinson’s Disease. The basic ac- tion of adaptogens, companion adaptogens, and natural compounds, such as resveratrol, green tea extract, and grape seed extract, is to provide protection from the neurological damage induced by mitochondrial inefficiency, oxidative stress, and inflammation.

Many adaptogens and companion adaptogens reduce the abnormal production of COX-2, NF-kB, and TNF-alpha. The overproduction of inflammatory pathways such as these has been linked to the onset and progression of Parkinson’s Disease, as well as other neurodegenerative diseases. These adaptogens are not anti-inflammatory herbs per se, or blocking agents in the way a pharmaceutical drug would be. Rather, they mediate gene behavior, single transduction, and cytokine activity, as well as assisting in the normalization of inflammation. Examination of the neuroprotective actions of Panax ginseng and other adaptogens may provide a potential means of slowing the progression of Parkinson’s Disease.

Adaptogenic agents are also able to improve cellular-mitochondria energy in the citric acid cycle, the beta oxidation spiral, and the electron transport chain by enhancing energy efficiency, protecting mitochondria from oxidative stress (free radical damage), and through the removal of harmful agents (free radicals). Recently, the traditional adaptogen Schisandra chinensis demonstrated an ability to fortify mitochondrial antioxidant status. The compound schisanhenol, from Schisandra, has shown particular protection with cerebral cells.
 
Herbs such as Panax ginseng, he shou wu (Polygonum multiflorum), mumie, ashwagandha (Withania somnifera), Mucuna pruriens, or gotu kola (Centella asiatica), used for thousands of years by traditional people, have been written into traditional medical textbooks and now have a massive amount of modern scientific data to support their use for neurological health. That said, few people reach for these safe, proven, effective remedies as age-retardant tonics. Rather than take a multivitamin and extra vitamin C and E as most Americans do for their health, greater benefit would be received by taking multi-botanical adaptogenic tonics.

Improving anabolic metabolism is also important for treating any age-related disease, and Parkinson’s Disease is no exception. An overall restoration of anabolic metabolism can result in significant up-regulation of cognitive ability, demonstrated by the deceleration of brain de- generation, as well as increased immunity evidenced by greater monocyte, NK cell, and T-cell numbers and activity. Adaptogens, with their enhanced anabolic actions, combined with specific nutritional agents, can enhance anabolic metabolism, increasing protein synthesis (essential for neuron development and repair) and enhancing mitochondrial function. Since mitochondrial energy production accounts for the vast majority of total energy production, mitochondrial function is a necessary and essential aspect of the regulation of neuron cells

Primary adaptogens, such as Rhaponticum carthamoides, rich in ecdisterones, increase anabolic metabolism and antioxidant defenses, both critical for neuroprotection. Not to be overlooked, adaptogens are primarily protective against neuronal stress-induced injury, another vitally important target in the fight against Parkinson’s Disease.
The use of adaptogenic remedies also produces the general effects of neurological enhancement, immune enhancement, physical strength and endurance enhancement, as well as improving mood and vitality, and inhibiting cancer, heart disease, diabetes, and aging. It is these remedies that lay an essential foundation for the treatment of neurological disorders.

The Beneficial Effects of Adaptogens on Reducing Parkinson’s Disease
1.HPAA enhancement/regulation: reduces brain cortisol, anti-stress (reduces the neurotoxin glutamate), enhances neuronal stress response.

2.Anabolic/anti-catabolic effect: enhances optimal mitochondrial energy transfer and ATP production and optimizes the utilization of fats, proteins, and sugars.

3.Modulates inflammation: reduces COX-2 and other inflammatory pathways including TNF-alpha.

4.Protects against oxidative damage: quenches free radicals, such as reactive oxygen species.

5.Inhibits chemically induced brain damage, chelates and removes heavy metal toxins and other neurotoxins.

6.Improves oxygen and blood circulation; anti- thrombotic – normalizes blood flow and oxygen uptake into the brain, preventing ischemia.

7.Enhances cholinergic function in the central nervous system (CNS).

8.Insulintrophic – reduces the neurologically damaging effects of glucose and insulin, inhibits AGEs; improves insulin signaling and cellular glucose utilization.

Mucuna pruriens
Herbal preparations containing Mucuna pruriens have been used in the treatment of Parkinson’s Disease both in India and the Amazon basin. In Brazil, the seed has been used internally for Parkinson’s Disease and is considered a diuretic and kidney protectant, a nerve tonic, and an aphrodisiac.

Mucuna is the most researched and most effective herb for Parkinson’s Disease. Several studies have confirmed its ability to raise dopamine levels in Parkinson’s Disease patients. It has been found to be the richest natural source of L-dopa, and concentrations of serotonin have also been found in the pod, leaf, and fruit. The extract we use is standardized to 40% L-dopa (the crude herb itself is between 3-5%).

Mucuna pruriens also possesses compounds that are redox-enhancing, free radical scavenging, inhibiting of cataract formation, anti-diabetic, cholesterol lowering, anti-parasitic, and protective against snake venom, all important contributing actions for slowing down the progression of neurological diseases such as Parkinson’s Disease. It has also been shown to enhance growth hormone and testosterone, which are important contributions to its overall anti-aging effects.

Testosterone deficiency
 is common in the older male population and has an increased prevalence in pa- tients with Parkinson’s Disease. Depletion of plasma testosterone is caused by inhibition of mitochondrial complex I, a commonly seen abnormality in Parkinson’s Disease. Testosterone therapy has been shown to improve the non-motor symptoms of Parkinson’s Disease and was recently revealed to affect the motor symptoms as well.

We routinely check testosterone levels in the aging population and often finds them low. However, rather than administer testosterone therapy alone, we recommendss the use of anabolic botanical extracts that will not just increase testosterone but enhance the endocrine system as a whole. These would include such herbs as Rhaponticum carthamoides, summa, Mucuna, and some non-herbal anabolic compounds, including pantocrine (deer antler extract), royal jelly, and mumie.

Panax ginseng
Panax ginseng (ginseng) is classified as a primary adaptogen, tonic, and central nervous system enhancer. It improves overall mental performance, particularly during prolonged stress, helps with poor concentration due to fatigue or old age, and is also considered a general anti-aging tonic for the elderly. Panax ginseng has recently been shown to possess neurotrophic (improves neurological health) and neuroprotective properties, which may be useful in preventing various forms of neuronal cell loss, including the degeneration observed in Parkinson’s Disease.

Ginseng has the effect of blocking morphine-induced thymic apoptosis by lowering plasma corticoste- rone levels, thus reducing the damage caused by excess cortisol. Like other adaptogens, ginseng potentiates and spares cortisol and ACTH, reducing the breakdown of cortisol and delaying the exhaustive state. Ginseng has also demonstrated the properties of affecting a marked increase in learning capacity.   

Ginseng and Schisandra extracts taken together, and administered orally as a tonic, improved learning and memory performance (anti-senescence) in an animal study, suggesting that combining ginseng and Schisandra might be useful for treating physiological aging and age-related memory deficits in humans.

The potential neuroprotective actions of ginseng extract were examined in two animal models of Parkinson’s Disease. Treatment by oral administration significantly and dramatically blocked tyrosine hydroxylase-positive cell loss and reduced the appearance of loco-motor dysfunction. Thus, ginseng appears to provide protection against neurotoxicity in Parkinson’s Disease. Further examination of the neuroprotective actions of ginseng and its various elements may provide a potential means of slowing the progress of Parkinson’s Disease.

One of the main constituents in Panax ginseng, a pharmacologically active component labeled ginsen- oside Rg1, caused a significant increase in the number of dividing cells in the hippocampus of animals. These findings suggest that the ginsenoside Rg1 is involved in the regulation of proliferation of hippocampal progenitor cells and this effect may serve as one of the elementary mechanisms underlying its neurological-enhancing and anti-aging actions.       
Ginsenoside-Rg1 also demonstrated neuroprotective effects on nigral neurons against rotenone toxicity in an animal model.

In the present study, the mechanism underlying the neuroprotection provided by ginsenoside Rg1 was studied against apoptosis induced by exogenous dopamine in PC12 cells. Pretreatment with ginsenoside Rg1 markedly reduced the generation of dopamine-induced reactive oxygen species, reduced the release of mitochondrial cytochrome c into the cytosol, and subsequently inhibited the activation of caspase-3. In addition, Rg1 pretreatment also reduced inducible nitric oxide (NO) synthase protein level and NO production. These results suggested that ginsenoside Rg1 may attenuate dopamine-induced apoptotic cell death through suppression of intracellular oxidative stress and that it may rescue or protect dopamine neurons in Parkinson’s Disease.

In another recent animal study, an additional active component labeled ginsenoside Rg3, was shown to induce neuroprotection against homocysteine toxicity in the hippocampus.

Withania somnifera
, known as ashwagandha, is classified in Ayurveda, the traditional medical system of India, as a Rasayana: a group of elite herbal medicines reputed to promote physical and mental health, augment the body’s resistance to disease and adverse environmental factors, revitalize the body in debilitated conditions, and increase longevity. It is considered a premiere herb for all negative conditions associated with aging, such as for the prevention and inhibition of senile dementia and Alzheimer’s disease (AD).
 
Ashwagandha and mumie together revealed a GABA-like effect, as well as an enhancing effect on acetylcholine receptors, and ashwagandha alone also evidenced inhibition of heavy metal (copper) induced neurotoxicity. These effects explain how ashwagandha may enhance memory and inhibit age-related neurological diseases. Withania somnifera root extract (WSRE) administered to an animal was found to be helpful for symp- toms of tardive dyskinesia (repetitive, involuntary, and purposeless movements). Although, L-dopa-induced dyskinesia is different from neuroleptic-induced tardive dyskinesia, they do share a commonality in the presence of oxidative damage to neurons. In a separate experiment; WSRE also mediated oxidative stress and inhibited haloperidol (HP)-induced orofacial dyskinesia.

The combining of multiple adaptogens with secondary adaptogens such as licorice, an importantsecondary adaptogen with harmonizing action, and the nervine mood harmonizer Hypericum (St. John’s wort), is well worth considering in the treatment of Parkinson’s Disease, particularly when depression is a factor (Hypericum extract has been shown to improve resistance to stress and prevent the exhausting of the hypothalamic-pituitary-adrenal system).    

Green Tea Polyphenols
Drinking 2 or more cups of green tea per day is associated with a reduced risk of all neurodegenerative diseases by more than one half.108 Green tea polyphenols (GTP) are potent chemopreventive agents that curb neurodegeneration by inhibiting NK-kappa beta (a pro-flammatory protein), reducing oxidative neuron damage, reducing heavy metals, and by enhancing oxygen uptake.

GTP revealed protective mechanisms against apoptosis induced by the pro-Parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA). It was shown to rescue the changes in condensed nuclear and apoptotic bodies, attenuate 6-OHDA-induced early apoptosis, prevent the decrease in mitochondrial membrane potential, and suppress accumulation of reactive oxygen species (ROS) and intracellular free Ca(2+). GTP also counteracted increases in 6-OHDA-induced nitric oxide, over-ex- pression of nNOS and iNOS, and decreased the level of protein-bound 3-nitrotyrosine (3-NT). In addition, GTP inhibited the auto-oxidation of 6-OHDA and scavenged oxygen free radicals in a dose- and time-dependent manner. Our results show that the protective effects of GTP on SH-SY5Y cells are mediated, at least in part, by controlling the ROS-NO pathway.

Curcuminoids from Turmeric
In Parkinson’s Disease, as well as all neurological diseases, “a number of biochemical and physiologic stimuli, such as perturbation in redox status, expression of misfolded proteins, altered glyc(osyl)ation and glucose deprivation, overloading of the products of polyunsaturated fatty acid peroxidation (hydroxynonenals, HNE), or cholesterol oxidation and decomposition, can disrupt redox homeostasis, impose stress, and subsequently lead to accumulation of unfolded or misfolded proteins in brain cells.” Curcuminoids, from turmeric are compounds that can inhibit, retard, or reverse the multi-stage patho- physiology changes that progressively occur and cause neurological diseases, including Parkinson’s Disease.

Protein conformational diseases, such as, Parkinson’s Disease, AD, and Huntington’s disease, share a common “pathogenic dysfunctional aggregation” involving “proteins in non- native conformations which are associated with metabolic derangements and excessive production of reactive oxygen species.” A decrease in cellular expression and activity of antioxidant proteins results in increased stress from oxidation. Free-radicals from mitochondrial dysfunction and from cyclooxygenase (COX)-2 enzyme activities instigate the production of pro-inflammatory prostaglandins that can contribute to neuro-inflammation and subsequent brain injury. COX-2 has been demonstrated to play a pathogenic role in both Parkinson’s Disease and AD.

“The brain responses to detect and control diverse forms of stress are accomplished by a complex network of ‘longevity assurance processes’ integrated to the expression of genes termed vitagenes. Heat shock proteins are a highly conserved system responsible for the preservation and repair of correct protein conformation.” Curcumin and other phenolic compounds up-regulate repair mechanisms within the brain, mediating oxidative damage that could otherwise induce brain damage associated with Parkinson’s Disease and AD.

Animals pretreated with curcumin showed clear signs of neuroprotection against Parkinson’s Disease. The ability of curcumin to exhibit neuroprotection against Parkinson’s Disease is related to its antioxidant capabilities and its capability to penetrate into the brain.

Protection of Mitochondrial Complex I
Selective damage of mitochondrial complex I within the dopaminergic neurons of the substantia nigra is the central event during Parkinson’s Disease. Peroxynitrite is one of the important free radicals most suspected of mediating complex I damage. Peroxynitrite inhibits brain complex I mainly by encouraging formation of 3-nitrotyrosine and nitrosothiol. Pretreatment with curcumin protected brain mitochondria against peroxynitrite by direct detoxifica- tion and prevention of 3-nitrotyrosine formation and by elevation of total cellular glutathione levels.

The beneficial effects of both curcuminoids and green tea extract can further be enhanced by combining them with companion adaptogens, such as grape seed extract (95% OPCs) and resveratrol.118 In one recent study, animals that drank 10% grape juice from age 19 to 21 months evidenced improvements in the release of dopamine and in cognitive performance, and a group that drank 50% grape juice showed improvements in motor function as well. Both improvements correlate with signs of neuron protection.

Botanicals for Symptomatic Relief of Parkinson’s-Related Tremor


Corydalis (Corydalis yanhusuo)
 is an herb native to the Chinese province of Zhejiang. The portion of the plant used medicinally is the tuber. In TCM, corydalis is said to invigorate the blood, move Qi, and alleviate all types of pain, including menstrual, abdominal, hernia, and pain associated with cancer. It is used extensively by practitioners of Chinese herbal medicine both for pain and as a muscle relaxant. Corydalis is also anti-convulsant and one of the most effective anti-spasmodic herbs.

Peony
 also possesses potent free radical scavenging ability and its active constituents, paeonol and paeoniflo- rin, effectively cross into the brain to specifically inhibit neuron damage, a contributor to the cause of Parkinson’s Disease. It also exhibits anti-epileptic activity and can aid in the relief of Parkinson’s Disease related tremors.

Bacopa (Bacopa monniera) Bacopa,
 rich in steroidal saponins called bacosineA and B, has been shown to modulate stress hormones released from the brain. Bacopa appears to affect the CNS by stimulation of the gaba-aminobutyric acid (GABA) and cholinergic systems. This has a calming effect on the brain while increasing its ability to concentrate and retain information. In India, yogis would often drink Bacopa tea while meditating in order to relax the mind and enter into a deeper, more relaxed state of consciousness. Bacopa has been clinically proven to inhibit neurodegeneration and to improve memory and mood; it exhibits antidepressant behavior, antioxidative actions, and displays adaptogenic and anti-stress qualities as well. Bacopa also possesses potent free radical scav- enging effects to aid the body in ridding itself of various toxins and heavy metals.

Avena sativa (Oat Seed Extract)
The fresh extract made from the milky seed of Avena sativa (oats) strengthens and nourishes the nervous system. Avena is a classic nervine tonic which both builds energy and reduces stress. It raises the mood, helps re- store vital energy, aids in recovering from illness and/or prolonged stress, and is the best remedy for feeding the nervous system

Hypericum perforatum (St. John’s Wort)
 is another nervine tonic useful for muscular twitching and tremors. Like skullcap and Avena, Hypericum is nutritive and restorative to the nervous system. It has also been found to be extremely effective for mild to moderate depression. The results of several recent studies indicate that Hypericum extract is in no way inferior to anti-depressants and is easier to tolerate for the treatment of moderate depression.

Scutellaria lateriflora (Skullcap)
 is a classic relaxing/nervine tonic. It is specifically indicated for conditions of nervous agitation and exhaustion (and often combined with Avena), with associated muscular twitching and tremors. If tremors tend to be worse at the end of the day, or following a lot of activity, skullcap is a good herb to consider.

Lobelia (Lobelia inflata)
 is a general systemic relaxant with diffusivestimulation – best suited for people with a strong pulse. Use low doses: 10-20 drops tid or 5-10% in a formula.

Mitochondrial Enhancing Agents
Several agents are available that can both modulate cellular energy metabolism and exert coinciding antioxidative effects. There is substantial evidence that the mitochondria are a major source of free radicals within the cell. These appear to be produced at both the iron-sulfur clusters of complex I and the ubiquinone site. Agents shown to be beneficial in animal models of Parkinson’s Disease include creatine, coenzyme Q (10), Mucuna pruriens, NADH, and carnitine (the best form for Parkinson’s Disease is acetyl- L-carnitine). Creatine has been shown to be effective in several animal models of neurodegenerative diseases and currently is being evaluated in early stage trials in Parkinson’s Disease.

Similarly, coenzyme Q10 has also proven effective in animal models and has shown promising effects in clinical trials of Parkinson’s Disease, as well as in clinical trials for Huntington’s disease and Friedreich’s ataxia. These agents therefore are promising candidates for further study as neuroprotec- tive agents in Parkinson’s Disease.

Co-enzyme Q10 (CoQ10)
CoQ10 is thought to prevent the deterioration of mitochondrial function. Previous research found that CoQ10 levels in the body were reduced in patients with neurological damage. This led to the theory that CoQ10 supplementation might help protect nerve cells, slow the progression of the disease, and improve quality of life.

A recent study involved 80 early-stage Parkinson’s patients. For up to 16 months, half the patients con- sumed varying amounts of CoQ10: 300, 600, or 1,200 milligrams respectively, and half took placebos. Symptom progression was monitored for the duration of the study. Results showed that by the eighth month, the 23 patients on the highest dose (1,200 mg) showed significantly less impairment than the others. In fact, these 23 patients showed 44 percent less of a decline in mental function, movement, and ability to perform daily living tasks than the placebo group.

Creatine Magnesium Chelate
Creatine is a nonessential dietary component that, when supplemented in the diet, has shown physi- ological benefits in athletes, and recently in patients with various muscle, neurological, and neuromuscular diseases, including heart disease, dementia, chronic fatigue, cachexia, and sarcopenia. Creatine plays a very powerful role in energy metabolism as a muscle fuel in regenerating ATP. It exerts its influence by increasing muscle creatine and phosphocreatine concentrations, creating a higher rate of ATP re-synthesis. This results in a delay in the onset of muscle fatigue and facilitates more rapid recovery during repeated rounds of high-intensity exercise – a true anabolic nutrient.

Creatine supplementation displays neuroprotective effects in several animal models of neurological diseases, such as Huntington’s disease (HD), Parkinson’s Disease, and amyotrophic lateral sclerosis. All these findings point to a close correlation between the functional capacity of the creatine kinase/phosphorylcreatine/creatine system and proper brain function. They also offer a starting point for a novel means of delaying neurodegenerative disease, and/or for strengthening memory function and intellec- tual capabilities. Creatine supplementation normalizes mutagenesis of mitochondrial DNA and inhibits the functional abnormalities that may otherwise occur that can lead to neurological disease.

Creatine biosynthesis has been postulated as a major effector of homocysteine concentration in the plasma, which has been identified as an independent, graded risk factor for atherosclerotic disease, and neurological diseases including Parkinson’s Disease. Homocysteine metabolism is sensitive to methylation demand imposed by physiological substrates such as creatine. Creatine supplementation has also been shown to decrease the production of homocysteine, another mechanism by which it may suppress Parkinson’s Disease.
Creatine was shown to specifically improve energy-dependent conversions commonly impaired in HD and Parkinson’s Disease.

Creatine Magnesium Chelate is a patented form of creatine-magnesium-glycine chelate with enhanced bioavailability of both creatine and magnesium. It provides the body with a readily available source of magnesium (also a very important nutrient for Parkinson’s Disease) while making the creatine more active by protecting it from cyclization. This mineral amino acid chelate contributes to an overall positive impact on many body functions, including, but not limited to, a non-steroidal anabolic enhancing effect. Creatine also provides rehydration, replenishes magnesium, and increases endurance (creatine monohydrate provides no magnesium, may contribute to dehydration, and does not increase endurance).

Magnesium
Magnesium (Mg) is essential to numerous metabolic reactions, including lipid metabolism, amino acid activation, the glycolytic cycle, and the citric acid cycle. Its primary function is as an enzyme cofactor, producing energy, synthesizing lipids and proteins, regulating calcium flow, parathyroid hormone (PTH) secretion, forming urea, and relaxing muscles. Magnesium affects mitochondria, enzymes, membrane receptors, and protein, lipid, and carbohydrate synthesis. Low levels of magnesium result in muscle weakness, nerve spasms, cramps, muscle spasms, and damage to mitochondria. Magnesium supplementation has also recently been shown to reduce systemic inflammation.

Aging constitutes a risk factor for magnesium deficit, and magnesium is important for protection from Parkinsonism-dementia complex (Parkinson’s Disease) and amyotrophic lateral sclerosis (ALS). A recent experiment was performed in rats that were exposed to low Ca and/or Mg intake over two generations, thus simulating the conditions of human life on Guam, where several generations live continuously in the same environment. Significant loss of dopaminergic neurons was identified exclusively in the 1-year-old rats that had been exposed continuously to low Mg intake (one-fifth the normal level) over generations. The present study demonstrated that low Mg intake over generations may be involved in the pathogenesis of Parkinsonism-dementia complex (Parkinson’s DiseaseC) and amyotrophic lateral sclerosis (ALS) instigated degeneration in humans.

L-Carnitine
Carnitine tautrate, a high-quality form of carni- tine, frees fatty acids for ATP production (this process is called beta oxidation). Carnitine is essential in the transport of long-chain fatty acids into the mitochondrial matrix and plays a key role in the oxidation of lipids. This means that carnitine improves fatty acid utilization and energy production.

Carnitine also significantly reverses age-associ- ated mitochondrial decay. It increases cellular respira- tion, membrane potential, cardiolipin levels, and has been shown to improve energy production within brain cells. Carnitine is considered a neuroprotective agent due to its antioxidant action and membrane stabiliz- ing effects.

B Vitamins
In clinical studies, individuals with Parkinson’s Disease indicated higher concentrations of plasma homocysteine than did controls. Experimental evidence suggests that folate defi- ciency, or focal administration of homocysteine, sensitizes dopaminergic neurons to the neurotoxicity of 1-methyl- 4-phenyl-1, 2, 3, 6-tetrahydropyridine. The recently conducted Rotterdam Study looked into reports that increased levels of homocysteine might promote Parkinson’s Disease. Numerous studies have reported that higher intakes of folic acid, vitamin B12, and vitamin B6 decrease plasma homocysteine levels and therefore might offer protection and lower the risk of Parkinson’s Disease.

Vitamin B-6
Vitamin B-6 is involved in the regulation of mental function and mood, in neuron communication, and is an essential homocysteine re-methylation cofactor. Vitamin B-6 deficiency is associated with an increase in blood homocysteine levels, which is associated with both AD and Parkinson’s Disease.

From October 1990 to July 2003, researchers from the Erasmus Medical Center in Rotterdam recruited 5,289 people over the age of 55. Individual dietary intakes were assessed at the onset of the study using semi-quantitative food frequency questionnaires (SFFQ), and physical examinations, including neurological exams, were conducted at baseline and at three yearly intervals. After an average of ten years of follow-up, 72 new cases of Parkinson’s Disease had been diagnosed. The average vitamin B-6 intake was found to be 1.63 milligrams per day, average B-12 intake was 5.3 micrograms per day, and average folate intake was 218.7 micrograms per day. The researchers found that individuals who achieved the highest total daily intake of vitamin B-6, 230.9 micrograms or more, were 54 percent less likely to develop Parkinson’s Disease than those who had average daily intakes lower than 185.1 micrograms.

Pyrodoxal alpha-ketoglutarate (PAK)
 is a unique form of vitamin B-6 bound to alpha-ketoglutarate, a member of the citric acid (Kreb) cycle. PAK transports pyridoxine and AK into the mitochondria, resulting in higher muscle ATP levels during heavy exercise. It has also been shown in human trials to significantly increase V0 max and anaerobic metabolism. Although few people are familiar with PAK, it is the form I most frequently use in my practice. I combine it with creatine MP, L-carnitine, lipoic acid, and magnesium glycyl glutamine, all of which are important mitochondrial enhancing agents.

Vitamin B-1
High doses of fat-soluble vitamin B-1 (thiamin) and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s Disease patients. Benfothiamine is a highly efficient, fat-soluble form of vitamin B-1 shown to be highly effective against various forms of neuropathy and neurological conditions.Benfothiamine, like lipoic acid and carnosine, reduces glycation, especially inside endothelial, retinal, kidney, and nerve cells.

Nicotinamide adenine dinucleotide (NADH
) is an activated form of the B vitamin niacin. Through a series of reactions with acetyl and oxygen, NADH is able to produce energy in the form of ATP. Therefore, a good supply of NADH optimizes energy production in the body. Another function of NADH is its ability to help transform the amino acid tyrosine into dopamine. NADH has been shown to improve memory, athletic performance, and generally appears to slow the aging process. An important nutrient for ATP production, it is helpful in treating Parkinson’s Disease, chronic fatigue syndrome, depression, and to counter overall lack of energy.

Alpha lipoic acid (lipoic acid) 
helps break down sugars so that energy can be produced through cellular respiration. In addition, recent research has discovered that alpha lipoic acid plays a truly central role in anti- oxidant defense. It is an extraordinarily broad-spectrum antioxidant able to quench a diverse array of free radicals in both aqueous (water) and lipid (fat) domains. It has been called the ‘universal antioxidant’ for its remarkable ability to recycle several other important antioxidants, including vitamins C and E, glutathione, coenzyme Q10, and even itself! Lipoic acid can also effectively boost glutathione levels and chelate metals such as mercury, iron, and copper.

Lipoic acid has been shown to control the forma- tion of glycation end products (AGE) and reduce protein damage from glycation in both humans and animals. Glycation is the name of the process in which glucose reacts with protein in an undesired way, resulting in sugar-damaged proteins (similar to browning food in the oven) called advanced AGE. The formation of AGE happens in everyone and is a major factor in the aging process itself. These damaged proteins may lead to pre- mature signs of aging (wrinkles and brown spots) and in the long run, exhibit damaging effects on most organ systems within the body. Glycation has been shown to cause damage to neurons; and glycation reactions appear accelerated in patients with diabetes and contribute to the development of diabetic complications.194-197EPA and DHA Fatty Acids from Fish Oil Concentrate

The omega-3 fatty acid, docosahexaenoic acid (DHA), has been shown to limit amyloid and oxidative damage, as well as synaptic and cognitive deficits in animals tested. Boosting levels of DHA in the blood, either by eating about three fish-meals each week and/or supplementing the diet with a DHA/EPA-rich fish oil, can reduce the risk of AD by one-half in elderly men and women.198, 199 A decreased level of plasma DHA did not appear solely limited to patients with AD but may be common in cognitive impairment with aging as well.

A study was conducted to investigate the effect of DHA on levodopa-induced dyskinesias (LIDs) in Parkinsonian 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-treated animals. The results illustrated that “DHA was able to either reduce the severity or delay the development of LIDs” in these animals. This leads to the theory that DHA supplementation may be able to improve the quality of life of patients with Parkinson’s Disease.

Iron Imbalance Linked to Parkinson’s Disease
Too much or too little iron intake may have a sig nificant impact on the brain, increasing the risk of Parkinson’s Disease. A new animal study was the first to demonstrate that both iron deficiency and toxicity are linked to the specific genes and neuronal suicide that can lead to dopamine shortages responsible for the development of Parkinson’s Disease.

It has been reported that high intake of iron, especially in combination with high manganese intake, may be related to risk of Parkinson’s Disease. High levels of iron can cause Parkinson’s-like symptoms in healthy mice without apparent risk factors for the illness. It can also accelerate the decline and death of those already diagnosed with the disease. In contrast, low levels of iron delayed the onset of Parkinson’s Disease in mice with risk factors and slowed the progress of the disease in those already affected. This low iron news, however, is mixed. It appears that iron excess or deficiency can lead to decreasing levels of dopamine. People who had higher-than-average dietary intake of iron, and who also took, on average, one or more multivitamins or iron supplements per day, were 2.1 times more likely to be Parkinson’s Disease patients than those who had lower-than-average dietary iron intake, and/or who took fewer than one multivitamin or iron supplement per day.

It is worth repeating the idea that a possible contributing factor in the association between a high intake of red meat and Parkinson’s Disease is the rich iron content of red meat.I don’t ever recommend taking iron supplements unless you are iron anemic. In order to know for sure if you might need iron, it is important to have your ferritin level checked. I prefer the level to be between 20 and Lactoferrin, present in colostrum and un-denatured whey protein, is an iron-binding protein that assists cellular iron utilization, reducing the risk of iron-induced free radical damage. Adaptogens are also very important here for their blood building/normalizing effects. They can improve iron uptake in iron-deficient states, decrease iron-induced free radicals, and/or bind to iron and assist in the elimination of excess iron if there is too much present in our bodies.

Eat Organic Foods and Avoid Foods Treated with Pesticides
Exposure to pesticides is one cause of mitochon- drial dysfunction that can lead to Parkinson’s Disease. “The pesticide ro- tenone (ROT) inhibits complex I and reproduces features of Parkinson’s Disease in animal models, suggesting that environmental agents that inhibit complex I may contribute to Parkinson’s Disease.” In a recent study, exposure to not only ROT but several other commercially used pesticides evidenced direct inhibition of complex I, causing oxidative damage, and appeared to play a potential role in the development of Parkinson’s Disease. The oxidative damage could be attenuated by the redox/antioxidants alpha-tocopherol and coenzyme Q10.

Sulforaphane and Other Isothiocyanates
Isothiocyanates (ITCs), dietary compounds avail- able through consumption of cruciferous vegetables, have demonstrated strong anti-cancer activity in animal mod- els. Many isothiocyanates (ITCs) such as sulforaphane (SFN), phenethyl isothiocyanate (PEITC), and allyl isothiocyanate (AITC), are highly effective in chemo- prevention, or reduction of the risk of cancer, and other chronic diseases including neurological diseases.

ITCs function as indirect antioxidants. As such, these compounds do not directly neutralize free radicals, as direct antioxidants do, but rather, they induce (or boost) the activity of the Phase 2 detoxification enzymes which act as a defense mechanism, triggering broad spectrum antioxidant activity, neutralizing various free radicals before they can cause cell damage that may instigate mutations leading to cancer. The effect of indirect antioxidants remains even after they have left the body – unlike direct antioxidants which neutralize only one free-radical molecule at a time and are destroyed in the process. The indirect antioxidant effects are long-lasting, triggering an ongoing process that remains in action for several days.ITCs are crucial for the maintenance of glutathi- one homeostasis.204 They have recently been shown to inhibit neurological diseases by controlling inflammation, and through the enhancement of levels of glutathione in the brain, which reduces oxidative stress.

SFN inhibits Parkinson’s Disease by inducing quinone reductase, the enzyme that catalyzes the reduction of quinone, effectively protecting dopaminergic neurons.206 SFN prevents cancer in animals by triggering the induction of carcinogen-detoxification enzymes and by aiding in cellular gene stability. It is an excellent preventative agent against many forms of cancer, including prostate, breast, colon, and brain cancer. Organic broccoli sprouts are an exceptionally rich source of SFN.

Exercise and Parkinson’s Disease
Higher levels of physical activity can lower the risk of Parkinson’s Disease in men, even though men predisposed to Parkinson’s Disease tend to avoid strenuous physical activity in their early adult years. Home physiotherapy programs based on rhythmical cueing of gait, and gait-related activities, demonstrated improvements in patients with Parkinson’s Disease. Also, patients with Parkinson’s Disease who took part in regular home exercise evidenced a reduction of fall events, a decrease in injurious falls, and established a positive effect from exercises on near-falls, and on quality of life overall.

Moderate exercise has also been shown to increase the clinical efficacy of Levodopa. Tests with mice revealed that exercise is effective for reducing symptoms of Parkinson’s Disease. The study showed that sustained exercise for a time span of at least three months prevented cell death in the substantia nigra of adult mice. Researchers used MPTP, a toxin known to cause the same results in mice that “designer drugs” do in humans, to reproduce symptoms of Parkinson’s in the mice. Inside the mice, MPTP is converted into MPP+, a reactive molecule that triggers formation of free radicals that cause damage in the brain. Increased production of the protein known as glial-derived neurotrophic factor (GDNF) was the key to the protective effect of exercise. GDNF not only helps to preserve nerve health but may also protect against stroke, seizures, and other brain disorders caused by free radical damage. The idea that exercise can protect people against MPP+ damage leads researchers to believe that exercise could also protect people from environmental toxins.

An addition, the study was designed to find out whether or not a so-called “enriched environment” would aid in protecting mice injected with MPTP. Components of this environment included exercise wheels, companion- ship, and a tunnel with a configuration that was changed weekly. In three months time, the amount of GDNF in the substantia nigra of mice in the first group increased 350% over the level of mice in the control group.

Other Studies Highlighting the Importance of Various Natural Compounds for Preventing or Reducing the Rate of Progression of Parkinson’s Disease
1.      Decrease consumption of animal fats because fats are one of the major sources of oxygen radicals.  Diets with high fat content have shown toxic effects on tissue formation in the brain. (Logroscino 1996)

2.      The prevalence of vitamin D insufficiency in patients with early Parkinson’s disease was similar to or higher than those reported in previous studies. (Evatt et al 2011)

3.     Supplementation with CoenzymeQ10 may play a role in cellular dysfunction in Parkinson’s disease and may be a potential protective agent for Parkinsonian patients.  (Shults 1999) and (Beal 1999) In a recent study the benefit of CoQ10 was greatest in subjects receiving 1200 mg per day. (Shults 2002)

4.      Taking anti-inflammatory prostaglandins appear to be helpful.  The omega-3 fatty acids, especially DHA and EPA found in fish oils, tend to reduce pro-inflammatory cytokine production in vivo. (Kidd 2000) Thus taking an omega-3 fatty acids supplement would be helpful.

5.      Supplementation with oral GSH (glutathione) and GSH precursors such as N-acetylcysteine and alpha-lipoic acid are appropriate.  GSH exhibits several functions in the brain chiefly acting as an antioxidant and a redox regulator.  GSH is also a systemic antioxidant, and its ongoing supplementation may help ameliorate Parkinson’s related damage in the heart, liver, muscles and other organs.  (Kidd 2000)

6.      Supplementation with vitamin C will also provide antioxidant reducing equivalents known to conserve GSH.  (Kidd 2000)

7.      Vitamin E supplementation may be important for Parkinson’s disease patients.  (Kidd 2000)

8.      Vitamin B supplementation may be helpful because a number of B vitamins may be deficient in Parkinson’s disease patients.  (Kidd 2000)

9.    Lowering one’s caloric intake appears to be helpful. (Logroscino 1996)

REFERENCES

Anderson. C et al “Dietary factors in Parkinson’s disease: the role of food groups and specific foods.”  Mov Disord 1999 Jan;14(1):21-7
Balch, James F, M.D. and Phyllis A. Balch, C.N.C., Prescription for Nutritional Healing, Garden City Park, NY: Avery Publishing Group, 1997
Beal, M.F., “Coenzyme Q10 administration and its potential for treatment of neurodegenerative diseases.” Biofactors 1999;9(2-4):261-6
Bharath, S., et al, “Glutathione, iron and Parkinson’s disease, Biochem Pharmacol 2002;64:1037-1048
Gassen, M, and Youdim, M. B., “Free radical scavengers: chemical concepts and clinical relevance.” J Neural Transm Supple 1999; 56:193-210
Guthrie, Catherine, “Coenzyme Q10: What Doesn’t’ it Do?” Alternative Medicine, March 2003, Issue 55, pp. 43-48
Kidd, Parris M., PhD, “Parkinson’s Disease as Multifactorial Oxidative Neurodegeneration: Implications for Integrative Management.” Alternative Medicine Review, Vol. 5, No. 6 Dec. 2000, pp. 502-529
Logroscino, G., et al, “Dietary lipids and antioxidants in Parkinson’s disease: a population-based, case control study.” Ann Neurol 1996 Jan; 39(1)”89-94
Martinez, Marcos, et al, “Hypothesis: Can N-Acetylcystine be beneficial in Parkinson’s disease?” Life Sciences, Vol 64, No. 15, pp. 1253-1257, 1999
Prasad, K.N. et al, “Multiple antioxidants in the prevention and treatment of Parkinson’s disease.” J Am Coll Nutr 1999 Oct;18(5):413-23
Shults, CW et al, “A possible role of coenzyme Q10 in the etiology and treatment of Parkinson’s disease.” Biofactors 1999; 9(2-4):267-72
Shults, C. W., et al, “Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline, Arch Neurol 2002: 59:1541-1550
Yance, Donald, “Parkinson’s Disease – And the Use of Botanical and Nutritional Compounds”, Monograph, 2010

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Compassionate Acupuncture and Healing Arts, providing craniosacral acupuncture, herbal and nutritional medicine in Durham, North Carolina. Phone number 919-309-7753.

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One Response to Understanding Parkinson’s Disease

  1. Hi, this blog is really amazing and provide me answers to all my questions. This is really informative and I will for sure refer my friends the same.
    Thanks
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