Neurodegenerative Disorders and
the Expanding Role of Complementary Medicine in Treatment and Prevention

Paul Reller, L.Ac.

Parkinson's, Parkinson-like disorders, Alzheimer's, Primary Progressive Aphasia, and Other Neurodegenerative Disorders

Whether the patient has early signs of a neurodegenerative disorder, mild and manageable symptoms, or has progressed to severe manifestations such as Parkinsonism and Alzheimer's disease, the key to both prevention and treatment in any stage is understanding and adopting a health regimen that restores healthy function and tissue to the brain. Health problems with the nervous system are no different than health problems with the digestive or cardiovascular system, and you should not be put off by stigma or fear of acknowledging these problems. A wealth of research is now available concerning these now common conditions, and this scientific evidence is what guides Complementary Medicine to provide individualized care that is centered on the health of the central nervous system. Of course, like any common health problem, the best time to treat is early in the pathology. The central problem to this type of health care is the complexity of factors that combine to create the pathology. Effective treatment with holistic medicine involves attention to all of the contributing health problems that combine to create the neurodegenerative condition.

In 2011, the National Insitutes of Health (NIH), National Institute on Aging and the Alzheimer’s Association announced that diagnostic guidelines had been widely accepted that divided the disease into three stages, Preclinical, Mild Cognitive Impairment, and Alzheimer’s Dementia. It is recommended that patients suspected of developing preclinical (no obvious symptoms) or mild cognitive impairment take measures to prevent or slow the development of the neurodegeneration to Alzheimer’s Dementia. Appropriate testing guidelines are still being developed, but will include a PET scan and analysis of cerebral spinal fluid (CSF). PET scans (positron emission tomography) may reveal reduced glucose uptake in areas of the brain, perhaps associated with insulin resistance, and altered levels of amyloid beta and tau proteins in the CSF will be detected with study of the cerebral spinal fluid, perhaps associated with advanced glycation endproducts (AGEs). These findings indicate key pathological mechanisms of Alzheimer’s and Parkinson’s diseases. MRI studies may confirm physical atrophy of areas of the brain as well. In addition, changes in cognitive function, as well as signs of underlying diseases linked to the pathology should be considered when determining risk of a preclinical stage or early cognitive impairment. Learning about these subjects helps the individual patient understand how to best approach preventive measures. Patients diagnosed with preclinical disease or mild cognitive impairment may choose to integrate effective treatments in Complementary Medicine to prevent the progression of the disease without side effects or fear of adverse outcomes with harsher therapies. If drug therapies are necessary, these side effects and adverse consequences of long-term drug therapy may be alleviated with Complementary Medicine. The National Institute on Aging and the Alzheimer’s Association admit that effective drug regimens have yet to be developed, and do recommend some treatment protocols of Complementary Medicine.

Recent research is now uncovering a variety of tests that reveal when these neurodegenerative conditions are developing, allowing patients to start reversing this complex pathophysiology at an early stage. The NIH states that Alzheimer's and other neurodegenerative diseases, such as Parkinson's, start developing 10-20 years before any health problems are evident. The New York Times, in an article on July 14, 2010, outlines the new diagnostic criteria, and the problems inherent in this new set of definitions of Alzheimer's and cognitive impairment disease: http://www.nytimes.com/2010/07/14/health/policy/14alzheimer.html. A simpler explanation is found in an article on the same day in the Los Angeles Times: http://www.latimes.com/news/health/la-heb-alzheimersdiagnosis-20100714,0,1811001.story. We see from these articles that the two main problems with early diagnosis is 1) there is currently no treatment for early neurodegenerative disease in standard medicine, and 2) there is an expected reluctance to be diagnosed with an early stage of neurodegenerative disease. The first problem can be overcome by utilizing Complementary Medicine and the wealth of research and treatment protocols, which are explained on this web article. The second problem has been helped by the upcoming elimination of the pre-existing clauses in health insurance by the Obama health care reform. The most important problem, though, may be the way the public views neurodegenerative conditions, and the fear of being diagnosed with such a problem. This article is intended to educate the patient population on the fact that neurodegeneration is a fact of life that most of us will encounter with aging to some degree. The positive way to handle such health problems is to understand them and do the right things to maintain one's optimum health, rather than to wait in the dark for the problem to become severe enough to make it very difficult to treat. The fact that it is now estimated that a high percentage of the aging population will be affected by Alzheimer's, Parkinson's, or one of the other neurodegenerative diseases that are potentially debilitating should be a wake up call to the general population that we should all work to understand and prevent these health problems.

The array of neurodegenerative diseases includes a number of disorders that come with aging, and an array of accompanying health problems. Primary Progressive Aphasia (PPA) is one of these neurodegenerative disorders that often affect the patient soon after menopause, often affecting just the speech and memory centers in the left hemisphere first, but usually progressing to a more complex disorder, such as Alzheimer's later in life. Nonspecific degeneration is associated with PPA in 60 percent of advanced cases, affecting the superfical cortex of the brain, while Alzheimer's degeneration is seen in about 20 percent of advanced cases (plaque accumulation and tangles). Pick's Disease is also seen in about 20 percent of advanced PPA (specific types of cell inclusions called Pick's bodies). The various types of advanced neurodegeneration seen in autopsy studies of advanced PPA suggest that there is a variety of paths that the neurodegeneration may take. These paths imply that individuals have different health imbalances that contribute in various ways to progressive neurodegeneration. We also see classic Parkinsonian degeneration with Lewy bodies in the substantia nigra and other related areas, as well as diffuse Lewy Body Disease. Corticobasoganglionic Degeneration is another type of neurodegenerative disease, and these various classifications are diagnosed with the use of EEG, PET scans, and CT scans, as well as the signs and symptoms. The variety of presentations imply that the patient should try to understand the various health problems associated with neurodegeneration in the many scientific studies devoted to this complex health problem.

Reducing the risk of neurodegenerative progression

With the realization that there is no single therapeutic measure found to be effective for the treatment of Alzheimer's, Parkinson's, and other debilitating neurodegenerative disease syndromes yet in 2010, and that these serious neurodegenerative disease are almost always diagnosed too late, the public is growing very concerned about reducing their individual risk as they age. In 2010, the National Institutes of Health sponsored a jury of 15 medical scientists with no vested interest in Alzheimer's research to explore all of the current evidence. This jury of experts found that strong evidence of risk was associated with two factors: 1) the use of synthetic estrogens and progestins in hormonal replacement therapies and birth control, which doubled the risk for Alzheimer's, and 2) the presence of an E4 variant of the ApoE gene, which tripled the risk (see the link to a New York Times article on this NIH panel below). The ApoE gene is a gene that expresses apolipoprotein, or proteins that bind to fats, and is expressed in the now familiar LDL, HDL, VLDL, and IDL, which are often mistakenly referred to as cholesterol. These chylomicrons contain cholesterol as 1-3% of their makeup, but are mainly composed of triglycerides and phospholipids. Apolipoprotein E binds to specific receptors on liver cells, and peripheral receptors. There is a strong link via these liporoteins between cardiovascular disease, metabolic syndrome, and Alzheimer's, as well as diseases of immune dysfunction, such as autoimmune disease. Genes consist of alleles, or base pairs, and the E4 allele of ApoE is implicated in both atherosclerosis and Alzheimer's disease. In addition, some respected research organizations (e.g. Northwestern University) have indicated that Alzheimer’s might be realistically called “Type 3” diabetes, or a new type of Metabolic Syndrome.

Research has shown that there is a strong connection between neuron failure in Alzheimer's disease and depleted myelin cholesterol (via ApoE deficiency) that has been linked to cholesterol depletion and poor expression of cholesterol as a result of chronic use of statin cholesterol blocking drugs, or as an adverse reaction to statins. Since synthetic hormone therapies and statin drugs are prescribed to a large percentage of the population, this has become an issue of concern, even to standard medicine. In addition, there is strong evidence linking accumulation of heavy metal toxins to neurodegenerative diseases, and most of these toxins exist as airborn lead and mercury molecules allowed into our air from coal fired power plants, smelters, chloralkili and concrete production. The instituting of clean coal technology has been woefully slow in the United States, and the highest levels of this type of pollution in the world has existed in the United States for a number of decades. In addition, the now widespread use of high fructose corn syrup, which purportedly introduces more mercury into the body, has also alarmed many experts. Adoption of clean coal technologies, elimination of high fructose corn syrup from processed foods, and a decrease in consumption of advanced glycation endproducts (AGEs) are ways to reduce risk of these neurodegenerative conditions. Use of safe chelation therapies may also be an effective preventive measure.

There are a number of healthy protocols that have been shown to reduce risk for neurodegenerative disease, and supported by the NIH panel in 2010. Increased regular exercise, a diet rich in fresh vegetables and whole grains, with less meat consumption, less sugar consumption, and healthy cognitive activities (exercising the brain and getting away from the television and idle internet browsing) have all shown to reduce risk. Reducing chronic inflammation, improving sleep quality, treating depressive disorders, and treating myofascial syndromes that may inhibit healthy blood flow to the brain, are also ways that are proven to reduce risk. Research done by the Scripps Research Institute in California, and supported by research across the world, has shown that mild use of marijuana in a patient's history is also associated with significant reduction of risk for Alzheimer's and Parkinson's diseases, and the THC actually prevents formation of lipoprotein plaque in Alzheimer's disease by preventing excess acetylcholinesterase activity. Stress reduction is highly recommended as well (refer to the article on this website to better understand stress). In other words, the treatment protocols and advice given by your Licensed Acupuncturist (minus marijuana use) for the last twenty years, especially one that incorporated the Tui Na physiotherapies into the treatment with acupuncture, herbal and nutrient medicines, provides an excellent overall protocol for reducing risk of neurodegenerative diseases. While no single herb or nutrient medicine has been found to be significantly effective on its own, and no large acupuncture clinical trials have been adequately designed as of yet, the information in this web article will show the potential for a broad protocol of a variety of treatments that have all been proven to show mild positive effect, and probably need to be taken together, as a thorough and holistic protocol, to show significant benefits.

Research presented at the 2011 Alzheimer’s Association International Conference in Paris, France, by UCSF researchers led by Deborah Barnes PhD, noted that over half of Alzheimer’s disease cases could potentially be prevented by treatment or prevention of chronic medical conditions along with diet and lifestyle changese. This worldwide study found that the biggest modifiable risk factors appeared to be smoking, lack of physical activity, depression, mid-life hypertension, diabetes or metabolic syndrome, and mid-life obesity. A lack of cognitive activity represented by low education and lack of cognitive challenges was also found to be a modifiable risk factor. Adopting a healthier lifestyle and utilizing Complementary and Integrative Medicine to help resolve chronic health issues is highly recommended to achieve these simple goals. While standard medicine has little to offer in real preventive medicine, much can be accomplished with a holistic regimen that utilizes acupuncture, herbal and nutrient medicine, and even soft tissue physiotherapies, to resolve metabolic problems, decrease stress and hypertension, and solve the problems associated with obesity, such as insulin resistance. The senior investigator with this large UCSF study, Dr. Kristine Yaffe MD, chief of geriatric psychiatry at SFVAMC, noted that the number of people afflicted with Alzheimer’s disease is expected to triple over the next 40 years, and that the public should get serious about preventive measures.

The lack of an effective treatment protocol for Alzheimer’s, Parkinson’s, and other neurodegnerative diseases points to the need to integrate Complementary Medicine into the treatment strategy

How does standard allopathic medicine treat these neurological syndromes? If you go the website of the National Institute of Neurological Disorders (see link below in additional information), you will see that modern medicine does not have a cure, or even a dependable effective treatment yet. The allopathic approach still involves finding a chemical that blocks one symptom-causing mechanism. The complexity of these neurodegenerative disorders demands a more involved therapeutic protocol. In Parkinson's Disease, L-Dopa has long been the key drug used in treatment. L-Dopa synthetics supply increased dopamine to the brain, but we now know that the problem is not a simple deficiency of dopamine to the specific brain centers involved, but a complex dysfunction at a number of dopamine receptor types. Scientists exploring the physiology of these dysfunctions have found a variety of factors that work synergistically in the brain to create these dyfunctions. Obviously, a variety of treatment strategies are necessary to bring this codependant physiology back into line. Allopathic medicine still wants to find one chemical to affect one piece of the puzzle rather than correcting the whole puzzle. This will result in nothing more than temporary relief of few of the many symptoms. Integrating this approach with restoration of healthy brain function utilizing a comprehensive package of care is the sensible approach, and involves no risk or side effects. Many patients now realize that just blocking a symptom is not a cure, and just such a comprehensive approach to restoration of health of the central nervous system is absolutely necessary, whether you are taking drugs to decrease symptoms or not.

The growing awareness of the Alzheimer’s disease and prevalence in the United States has led to a huge investment into new drugs. The most popularly prescribed drug, Aricept (donepezil), though, was approved by the FDA in 2010 against the advice of the FDA review committee, due to the lack of alternative cures or treatments. This drug is a cholinesterase inhibitor, designed to increase the amount of acytlcholine in the brain by blocking its rate of breakdown, or catabolism. The FDA and the NIH (National Insitutes of Health) state that Aricept only helps control the symptoms of Alzheimer’s disease, but does not cure it. At a low dose, the common side effects include nausea, diarrhea, loss of appetite, frequent urination, muscle cramps, nervousness, depression, confusion, changes in behavior, insomnia, and excess tiredness. These side effects have generated much criticism, as most of the patients are elderly and their quality of life is already impacted by such health problems. In fact, due to the frequency of these health problems in the Alzheimer’s population, the drug is rarely blamed. In 2012, the patent protection is set to expire for Aricept, and so the FDA approved a new patent protection of the same drug at a much higher dosage (an increase from 5 to 23 milligrams, called Aricept 23). A single drug trial was used to justify this new higher dosage, with just 1400 patients involved, conducted by the maker Pfizer/Eisai. This clinical trial noted that the higher dosage led to substantially more nausea and vomiting, alarming many physicians, as many of the patients prescribed the drug would be in poor health and struggling in nursing facilities (see and article on these issues in the March 23, 2012 New York Times entitled Drug Dosage Was Approved Despite Warning). Dr. Steven Woloshin, professor of medicine at Dartmouth Institute for Health Policy and Clinical Practice, stated: “It doesn’t really have much benefit, but does substantially more harm.” Dr. Woloshin noted that Pfizer had made false claims in advertising to doctors and on the label, claiming that drug had improved clinical and overall functioning when that was not the case. The clinical trial showed only a slight improvement in cognitive measures, and no improvement in global measures. Dr. Woloshin and his colleague Lisa M. Schwartz alerted the FDA to these false claims, and only then was the request for a correction made. Dr. Sidney Wolfe, director of the Public Citizen’s Health Research Group, alarmed at the risks of the drug Aricept 23, and lack of efficacy in the single clinical trial, asked the FDA to remove the drug from the market. Both clinical and statistical reveiwers for the FDA recommended against approving the higher dosage of Aricept, but the FDA approved this drug against the reviewer’s opinions. Patients, as well as a small number of medical doctors, are becoming aware, though, that herbal cholinesterase inhibitors, such as the FDA approved Huperzine A, an extract from the Chinese herb Huperzia serrata, a species of clubmoss, and galantamine, a chemical from a Chinese herb Lycoris radiata (Shi suan), licensed as an effective anticholinesterase inhibitor, as well as Salvia miltiorrhiza (Dan shen), and Anemarrhena asphodeloides (Zhi mu), Gentiana rhodantha, Swertia punica (Zi Hong Chang Ya Cai), Mangiferrin indica, all of which contain mangiferin (see clinical link below), may be as effective as Aricept, as shown in clinical trials at the University of California (cited below). Neither Aricept or Huperzine A by itself is proven to have a statistically significant effect on cognitive scores in the short term, although their effects are statistically about equal (S.L. Rogers et al, Donezepil Study Group, Neurology 1998;50:136-145). With a more comprehensive treatment strategy in Complementary Medicine, though, these cholinesterase inhibiting effects may be enhanced, and constitute a small part of the sensible holistic treatment strategy.

In 2010, with the proof of efficacy of early diagnostic tests for Alzheimer’s disease, there was a rush to market new drugs. The problem with the pharmaceutical drug rush, though, is that the complexity of neurodegenerative disease is high, and we still haven't defined the array of causes. Biologic medicines are focusing on blocking enzymes that prevent the formation of beta amyloid protein plaques in the brain, but the latest drug trial by Eli Lilly (semagacestat) found that the new drugs do reach the brain in sufficient dosage, and do block the correct enzyme metabolism, but actually worsen the condition rather than improve it (see the link below to an article on this subject). Dr. Lon Schneider, a leading researcher from the University of Southern California, states: “We don't know what the drug targets for Alzheimer's disease are. We don't know because we don't know the causes of Alzheimer's.” Dr. P. Murali Doraiswamy, an Alzheimer's researcher at Duke University believes that: “our current views may be too simplistic.” A common belief in the rich field of neurodegenerative research is that the causes are many, the mechanisms are complex, and reversal of neurodegeneration will require a complex treatment protocol. Complementary and Integrative Medicine supplies a rich diversity of treatment protocols supported by current research, and treatment should start with prevention and early intervention. The good thing about Complementary and Integrative Medicine is that this therapeutic approach is actually good for the patient and without significant risks or side effects. General health will improve when the patient utilizes the skills and knowledge of the Licensed Acupuncturist and herbalist to prevent or treat these neurodegenerative diseases.

There is an underlying link to many of the common health problems now affecting up to a fifth of the population, and this concerns gradual focal degeneration of the central nervous system. Whether your child is affected by attention deficit and hyperactivity disorder, you are bothered by problems with attention span, or your parents are diagnosed with Alzheimer's or a Parkinson's disorder, or even Glaucoma, the health concern is a complex and multifaceted problem that concerns the health maintenance of the tissues and function of our brain.

The most well known of these neurodegenerative diseases is Parkinson's Disease, which is actually not a specific disease, but a group of neurodegenerative disorders technically called Parkinsonism. Parkinsonism is still not understood despite extensive research and theory that has been conducted since the first extensive treatise on the subject by the British physician James Parkinson in 1817. A number of attempts to define the disorder by basing medical theory on a particular pharmaceutical drug have failed miserably, and stifled research into the multifaceted aspects of neurodegenerative disease. Parkinsonism is defined by the Stedman’s medical dictionary as: “A neurological syndrome usually resulting from deficiency of the neurotransmitter dopamine as the consequence of neurodegenerative, vascular, or inflammatory changes in the basal ganglia, or a syndrome similar to parkinsonism appearing as a side effect of certain antipsychotic drugs.” The key to this definition is the multifaceted origin of the disease in neurodegeneration, vascular problems, and inflammatory dysfunction.

A key issue in the complex subject of causes of Parkinsonism is the potential for this disease to be caused by chemicals. The medical dictionaries point out the fact that antipsychotic drugs, which are now frequently prescribed for conditions other than psychosis, may cause parkinsonism as a side effect. This class of drugs, antipsychotics, are given attractive names and now prescribed to a majority of our elderly in nursing homes and assisted living facilities. Often, the excess use of antipsychotic drugs is deemed necessary to control the erratic behavior of our elderly in nursing facilities when a well-staffed and efficient care program is not available. In other words, when profiteering health companies cut costs by reducing staff and cheapening the environment, they then increase costs by overprescribing expensive antipsychotic drug regimens. An alternative to this miserable outcome would be to promote non-profit nursing facilities for our elderly that utilize increased trained staffing, and healthy environments that reduce behavioral problems, and offset the costs by reducing the drug consumption and eliminating the profit motive. The relatives of these excessively drugged elderly wonder why their loved ones mental states are deteriorating, and the chronic excessive prescribing of antipsychotic drugs with cute names may be the reason.

Various environmental neurotoxins have also been widely studied as contributors to these common neurodegenerative diseases. Paraquat, the most widely used herbicide in the world for some time, has an analog chemical called cyperquat, which is a chloride of MPP+ (1-methyl-4-phenylpyridinum) that has been shown to be neurotoxic, interfering with oxidative phosphorylation in mitochondria of brain cells, and causing Parkinson's neurodegeneration, depleting ATP, the primary fuel for these cells, and leading to neuron apoptosis, or cell death. Cyperquat is still used as an herbicide. Another widely used herbicide and pesticide, Rotenone, is also implicated in causing Parkinsonism neurodegeneration, but is considered safe since it breaks down quickly and easily and is poorly absorbed by the human gastrointestinal tract. This safety assessment is questioned by many experts, though. Since Rotenone is derived from a plant source it is marketed as an organic herbicide for the garden, giving many customers a false impression of safety. Rotenone is also widely used in commercial food production to reduce mite infestations on chickens, and by the fish farming industry to kill various species of invasive fish. Contact with the chemical before it is broken down, or complex compounds that may be created by the chemical in its use, have potential to cause neurodegeneration. While these chemical scenarios have not yet been studied enough to create legal banning of the pesticide, the risk is real. The list of potential chemical causes or contributors to neurodegeneration is now long, and our ability to decidedly link these chemicals to a particular case is problematic in a legal sense, inhibiting effective regulation or the disincentive for use via lawsuits. The ubiquitous pollution of our foods, soils, and water with such agents may be integral to the onset of Parkinson's disease in a great number of people, though.

Of course, our immune and detox systems protect us from these environmental and food chemicals and the cellular damage they may cause to a great extent. In many patients, imbalance of these systems itself is shown to potentially create a neurotoxic mechanism that leads to a degenerative condition. Poor health of the immune and detox systems is thus a double threat. Utilizing Complementary Medicine to enhance the health of the immune and detox systems int the body is a sensible approach to prevention. Many herbal and nutrient aids may also prevent or alleviate the specific pathological mechanisms associated with these chemicals. For instance, since MPP+ depletes ATP, interferes with oxidative metabolism, reduces levels of dopamine and norepinephrine (adrenalin), inhibits catecholamine synthesis (cortisol), and inactivates tyrosine hydroxylase, a number of nutrient and herbal medicines may work to decrease these harmful effects. ATP cofactors (specific forms of vitamins B1 and B2), antioxidants, dopaminergic herbs, the amino acid L-tyrosine, vitamin B12 and P5P, and aids to adrenal health and function may correct these pathological metabolic processes. While debating the origin of the individual's disease is not going to achieve a cure, patients with these disorders, their families and friends, and all of us, need to understand that such chemicals should be taken out of our environment. In the meantime, cleaning up the mess internally is a healthy option as well.

The continuing debate over causes of Neurodegenerative Disorders and the approach to treatment

To date we still have strong debate about the very nature of Parkinson's, with researchers arguing over the location of the origin of the disease in the central or peripheral nervous system. There is also strong debate continuing over the location of the metabolic and neural oscillations that trigger the tremors and disrupt the cognitive processes, with some arguing that the origins lie within the cells, and others arguing that the neuronal network is responsible. Standard therapeutic approaches with pharmaceutical agents continue to be disappointing, and remain focused on increasing dopamine purely for lack of a better strategy, and despite the fact that we now know that even the dopamine deficiency is related to an imbalance of dopamine stimulation at various receptors, rather than a simple matter of poor dopamine availability. One thing is for certain. This disease is a neurodegenerative disorder that demands a multifaceted and holistic approach in treatment. Research into Parkinsonism has also provided us with a wealth of knowledge and treatment strategy for all of the other neurodegenerative disorders. There is no single pill that will reverse neurodegeneration, which is a complicated multifactored disease mechanism.

At the same time, much research has supported a variety of key strategies for both relieving symptoms and reversing the neurodegenerative aspects of Parkinson's, as well as Alzheimer's, Attention Deficit Disorder, and other neurodegenerative diseases. We now know that even glaucoma is a neurodegenerative disease. Complementary Medicine must play a key role in these treatment strategies. These include stimulation and bioavailability of dopamine in the central nervous system, coupled with replenishment of endocannabinoids and cholines, which are needed to restore a balance in the regulating cells of the substantia nigra, caudate and putamen striatum of the basal ganglia, to help control the tremors and loss of motor control. Restoration of healthy cellular function is also a key, especially health of the mitochondria, or oxidative energy-producing parts of the cells, which contain the key protein enzymes of the fatty acid oxidation and citric acid cycle. Antioxidant therapy and balance of essential fatty acids, with increase in Omega-3 DHA and EPA are also keys to neuroprotective strategies. Recent research has focused on adrenal stress and chronic overstimulation of neuroreceptors as a key aspect of the overall pathophysiology. Here too, acupuncture and herbal medicine can play a key role in improving the treatment outcome. Acupuncture, or TCM, utilizes a combination of therapeutic protocols based on sound scientific evidence. The licensed Acupuncturist may be skilled and knowledgeable with nutrient therapy, herbal medicine, needle stimulation, and lifestyle advice. This combination is very important when treating or preventing neurodegeneration. Neurodegenerative disease, because of its complex nature, requires a thorough, comprehensive, and persistent treatment approach. Anything less is doomed to failure.

Neurodegeneration usually occurs over time, and the causes are usually multifaceted. Chemical causes are the chief concern, but hormonal imbalance, effects of aging, physiological stress, and a genetic or epigenetic inherited propensity to neurodegeneration are also important concerns. In recent years, theories of a systemic bacterial endotoxicity (see the article on this subject on this website) creating an inflammatory response, has been added to the factors that may cause neurodegeneration and Parkinsonism. Overuse of antibiotics and creation of many antibiotic-resistant strains of bacteria may have contributed to endotoxicity. These disorders present both a public health threat that should be addressed by our government, as well as an individual threat, that should be addressed by the physician most important in the treatment team, you. The individual must take a more proactive approach to prevent or treat neurodegenerative disorders. The complexity of the problem should not deter the individual from taking decisive action, and the Complementary Medicine physician is ideal to integrate into this treatment and prevention strategy at any level. Food additives, preservatives, unhealthy diets, environmental toxins, especially heavy metal toxins, adrenal stress, oxidant stress, fatty acid imbalance, endocrine disorder, especially melatonin dysregulation (e.g. workers on the night shift, or airline attendants), chronic inflammatory states, and advanced glycation endproducts (e.g. patients with obesity, metabolic syndrome, or atherosclerosis) are all significant factors implicated in the pathology of neurodegeneration. This array of causes and contributors is now supported by sound research. Some other important causes are still less well known.

Neurodegeneration and mitochondrial dysfunction may also be a result of iron overload toxicity. Iron is an important metal ion in our body and the levels of iron are usually tightly controlled. Since iron is highly reactive as an oxidative agent, normally up to 70% of our iron is bound to the ferritin or transferrin proteins, or other transport and storage proteins, where it cannot participate in oxidative reactions. The fact that it is able to oxidize quickly (as in rusting outside of the body) makes it an ideal carrier of oxygen in our red blood cells. When the neutralizing capacity of these storage and carrier proteins is exceeded, excess iron binds weakly to other proteins in the blood and cells, where it participates in oxidative reactions and peroxidation of cellular components, or organelles, such as mitochondria, lysosomes, and sarcoplastic membranes (integral to nerve conduction). Iron overload toxicity is not uncommon, but is only looked for in diagnosis when it becomes very serious, resulting in heart disease, dysfunctions of the pancreas or liver, or gonadal dysfunction and infertility. Patients with thalassemia, sickle cell anemia, hepatitis, cirrhosis, chronic inflammatory conditions (e.g. autoimmune disorders with rheumatic disease and positive rheumatoid factor), infections, alcoholism, repeated transfusions, or even in patients that take too many iron supplements, or eat an unusual excess of red meat, may have a history of iron overload toxicity. If the iron in our bodies is not handled by the appropriate metabolism of transport and storage, gradual accumulation in tissues may lead to a neurodegenerative condition, and iron chelation may have a positive effect.

An array of food additives called excitotoxins, such as hydrolyzed vegetable protein, aspartame, and MSG, are also the subject of much research into neurodegenerative pathology and central nervous system (CNS) dysfunctions that may lead to neurodegenerative states. A growing body of sound research has linked these food additives to a wide array of neurological problems, including Parkinson‘s disease, Alzheimer‘s disease, Huntington‘s disease, ALS, learning disorders (ADD), developmental disorders, neuropsychiatric disorders, dementia, and even obesity, migraines, seizure disorders, certain endocrine disorders, and CNS problems in chronic aftereffects of Lyme‘s Disease. These food additives are now present in almost all processed foods. Since scientists discovered health risks associated with MSG additives in the 1970s (MSG is a natural glutamate compound that enhances neurochemical systems related to attraction and enjoyment of food), the food industry did not heed public health warnings, but instead developed a vast array of glutamate compounds, called excitotoxins, that increase our desire to buy their products.

Today, MSG-like excitotoxins are disguised as “natural flavorings”, soy protein extract, textured protein, yeast extract, hydrolyzed vegetable protein, and artificial sweeteners such as aspartame (read below to gain a better understanding of aspartame). These altered glutamate molecules accumulate in the brain and cause neural dysfunction over time, as the amino acid glutamate is a key basic building block of many important regulatory chemicals in our brain, as well as itself being a neurotransmitter. Since glutamate is tightly controlled in the brain, and is normally kept at very small concentrations in extracellular fluid, these altered glutamate compounds begin to overload neural firing as they accumulate. The main drug used to treat Parkinson‘s disorders is L-Dopa, or synthetic dopamine, which itself is a weak excitotoxin that has now been proven to actually accelerate Parkinson‘s neurodegeneration with chronic use. At first, L-Dopa may relieve symptoms, but in time these symptoms will worsen in an accelerated fashion. The public needs to start expressing outrage that our food industry treats food chemistry with such a cavalier attitude, and demand that the commercial food industry hire public health experts to guide what they put into our food. Surely, we could have processed foods that improve our health rather than destroy it.

Studies investigating the role of bacterial endotoxins in neurodegenerative pathology have turned up some surprising evidence of a multifactorial component to Parkinson’s disease. Researchers at Texas Christian University, in 2007 (cited below), found that a combination of inflammatory bacterial endotoxin lipopolysaccharide (LPS) promoted significant dopamine depletion and neurological impairment only when combined with a neurotoxin (MPTP). Such research shows that the various environmental toxicities linked to neurodegeration may only cause significant disease symptoms when combined. To date, research into studying these multifactorial causes has constituted only a small portion of the research. This is because research today is dominated by a need to produce a single allopathic pharmaceutical, and is not centered on purely finding the true array of causes of disease. The neurotoxin studied, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), has been proven to cause permanent symptoms of Parkinsonism, and so has been utilized as a study model. MPTP may be produced during the manufacture of street narcotics that include MPPP, a synthetic opioid, and the investigation into these drugs led to the discovery of the neurotoxicity of MPTP. MPTP by itself, though, cannot cause neurotoxicity, and the subjects affected by this chemical apparently had other symbiotic factors that caused the neurotoxicity. The search for these symbiotic factors has led to many interesting findings in the etiopathology of Parkinson’s. Such research confirms that an array of factors must work together to cause severe disease. Chronic inflammatory pathways, reactive oxygen species, and chemical neurotoxins in the environment are the most likely trio of causes that work synergistically to cause neurodegeneration in most subjects.

Metabolic dysfunctions and their relationship to Alzheimer’s

Researchers have uncovered a variety of metabolic imbalances contributing to the progression of Alzheimer’s neurodegeneration. In 2007, researchers at Northwestern University published findings that showed that insulin resistance was a key component of neurological dysfunction. The protein called amyloid beta-derived diffusable ligand (ADDL) appeared responsible for the progression of Alzheimer’s dysfunction from synapse to synapse, spreading across the brain, and one effect of this neurotoxicity was the depletion of insulin receptors from neurons. Key research widely accepted by health organizations involved with Alzheimer’s disease indicates that levels of brain insulin and insulin receptors on affected cells are lower in Alzheimer’s patients, and the level of this insulin and insulin receptor deficiency is a marker of the progression of the disease. Insulin is a hormone in the body with complex effects at a wide array of receptor types. In the brain, insulin does not regulate sugar and energy usage so much, but is integral to development, tissue growth and maintenance, memory and learning (see my article on this website entitled Insulin Use and Support Therapies to gain a better understanding). The binding of ADDLs to brain synapses prevents the accumulation of insulin receptors at these synapses, contributing to poor cellular maintenance and repair. Increased insulin receptors express inside the cell, not on the membrane, decreasing the usage and need for insulin. These researchers at Northwestern University, William L. Klein, professor of neurobiology in the Weinberg College of Arts and Sciences, and Fernanda G. DeFelice, from the Federal University of Rio de Janeiro, found that neurons affected by ADDL showed a virtual abscence of insulin receptors on the dendrites of the neuron, or the branched projections of nerve cells that conduct the electrochemical signals. Dendrites with an abundance of insulin receptors showed no ADDL binding. Clearly, both dysfunction with insulin metabolism and the accumulation of advanced glycation endproducts, such as beta-amyloid, are integral to this aspect of the disease.

These findings of the ADDL accumulation and effects on neuron maintenance, with decrease in insulin receptors on the membranes of affected cells and the subsequent decrease in insulin effects, explains why there is an unclear association with overall beta-amyloid plaque burden and cognitive defects in all cases. It is probably not just the accumulation of the advanced glycation endproduct plaques that is important, but the accumulation of specific variations on these problematic protein, fat and sugar molecules. These ADDLs, or amyloid beta-derived diffusable ligands, are oligomers of amyloid beta molecules. A number of oligomers, or molecules that consist of just a few atoms or small molecules (monomers) that bind easily to form larger polymers, of beta-amyloid protein complexes, are found to be integral to the Alzheimer’s pathology. The most common natural monomer is glucose. A ligand is a small molecule that easily forms a complex with a biomolecule, and serves to increase the signal, or trigger, increased binding to a site on a target protein. Metabolic dysfunction is seen as the origin of these ligands of beta-amyloid protein, fat and sugar complexes.

Metabolic Syndrome, typically still called diabetes type 2, and Alzheimer’s disease have signs of increased oxidative stress and accumulation of advanced glycation endproducts (AGEs) in common. Patients with Metabolic Syndrome, or diabetes type 2, appear to have an increased risk for Alzheimer’s disease, primarily because these AGEs accumulate in neurofibrillary tangles and amyloid plaques. A sequence of studies have demonstrated the importance of this pathological mechanism. The Rotterdam study followed over 6000 elderly patients for a number of years and determined that insulin resitance and Metabolic Syndrome, called type 2 diabetes, doubled the risk of the patient acquiring a neurodegenerative disease. Patients taking synthetic insulin showed 4 times the risk. A high incidence of diabetes and Metabolic Syndrome now exists in our aging community, and just the maintenance of blood sugar and total cholesterol with drugs such as synthetic insulin has not decreased the potential for these health dysfunctions to result in neurodegenerative states. In fact, these studies show that the risk is perhaps increased with the use of the synthetic insulin, statin drugs, etc. The term diabetes type 3 was coined in 2005 to define Alzheimer’s disease by Dr. Suzanne de la Monte, a neuropathologist at Brown University, when her research on postmortem brain tissue of Alzheimer’s patients found that Alzheimer’s disease may be defined as a neuroendocrine disease associated with insulin signaling defects. Her research showed that a reduced insulin, insulin-like growth factor, and insulin receptors on the outer parts of neurons, reduced the regulatory tau protein, and ultimately led to cell death. While introduction of synthetic insulin produces immediate improvement in glucose utilization in the brain, memory, and cognitive abilities, long-term use may be problematic, as the Rotterdam study indicated. The restoration of the insulin metabolism, correction of Metabolic Syndrome, inhibition of advanced glycation endproducts (AGEs), and improved neuroendocrine balance, all of which can be accomplished with Complementary Medicine, provides a safe and effective therapeutic protocol to patients.

The various treatment strategies and concerns in Complementary Medicine

Complementary Medicine, and especially the array of therapies available from Licensed Acupuncturists and herbalists that are familiar with these neurodegenerative diseases, present the patient with an array of therapeutic approaches that will make the standard pharmacological therapy more successful. Immune modulation, decrease of chronic inflammatory problems driving immune dysfunction, hormonal balancing, resolution of nutritrional deficiencies, antioxidant therapies, enhanced cellular detoxification by boosting the glutathione metabolism, clearing of excess misshapen proteins from the cells and glial tissues, clearing of accumulations of toxins and heavy metal molecules from the brain tissues, clearing advanced glycation endproducts (AGEs) associated with plaque accumulations in brain tissue, aiding vascular health, and increasing metabolic supply for brain cells, are all strategies that have been scientifically studied and are being utilized in the Complementary Medicine strategy. Coupled with manual therapies, such as needle stimulation, which is well proven in its ability to stimulate brain function and modulate immune inflammatory mechanisms, as well as the soft tissue therapies (Tui na) that may help by reducing cervical chronic inflammatory problems that push excess inflammatory mediators (see the article entitled Deep Tissue Massage and it‘s many benefits), this presents a comprehensive strategy for a very difficult array of problems to treat. All of this therapy may be daunting to the patient at first, and all of it may not be needed in the treatment protocol, but for patients with progressive severe neurodegenerative diseases, this intensive approach, coupled with the latest pharmacological medicines, may produce the successful outcome that is so elusive.

The evidence for effective treatment with Complementary Medicine for both prevention and treatment of neurodegenerative diseases is mounting. The National Institute on Aging (NIA), a part of the U.S. National Institutes of Health (NIH), and the leading governmental research group on Alzheimer's and Parkinsons's diseases, has completed clinical human trials of Huperzine A (NCT00083590), an herbal constituent derived from a species of fir clubmoss called Huperzia serrata, which is a traditional Chinese herbal medicine and has been heavily researched in China for decades to prevent and treat neurodegenerative diseases. Huperzine A is an effective acetylcholinesterase inhibitor similar in scope to the pharmaceutical drugs galantamine (Reminyl, Razadyne, Nivalin), donepezil (Aricept), and rivastigmine (Exelon), although the herbal chemical is found to be reversible and selective, or what we term an evolved biomodulator. This herb Huperzia serrata, an arctic species, was used for centuries in China for the treatment of blood disorders, swelling, and fever, as well as senile dementia. The herbal constituent Huperzine A, a sesquiterpene alkaoid, was isolated from the herb and synthesized as well, by the Chinese, and has been prescribed heavily in China with very good results. Besides its modest effects on cognition, similar to the pharmaceuticals prescribed today, huperzine A has also been found to have neuroprotective effects that go beyond the inhibition of acetylcholinesterase. Study at the Chinese Academy of Sciences in Shanghai, China (cited below), states that “potentially beneficial actions include modification of beta-amyloid peptide processing, reduction of oxidative stress, neuronal protection against apoptosis (programmed cell death), and regulation of expression and secretion of nerve growth factor (NGF) and NGF signaling.” (PMID: 17056129).

Studies have revealed that Huperzine A can penetrate the brain blood barrier easily, is potentially a more potent acetylcholinesterase inhibitor than its pharmaceutical counterparts, can increase the endplate potential at the neuromuscular junction to control tremor, can increase the levels of dopamine, norepinephrine and acetylcholine in the brain tissues significantly without affecting the 5HT neurotransmitter, and is proven to enhance cognitive function and memory in humans, without the side effects of the comparable pharmaceutical drugs. The only reason this phytochemical is not prescribed in the United States is that it is a natural herbal chemical that cannot be patented, and thus will not make billions of dollars for the pharmaceutical industry. This phyotchemical is available in formula as Vinpurazine, combined with Vinpocetine (Vinca minor extract) and rosemary extracts, other proven cognitive enhancers, from Health Concerns. It is recommended that the formula be taken with phosphatydilcholine, an active lecithin metabolite, to enhance the availability of choline and accelerate acetylcholine syntheis in the brain, as well as Inositol hexacotinate, a vitamin in the B3 family, that is a non-flushing version of niacin. Perhaps a more potent form of phosphatidylcholine is L-alpha-glyceryl-phosphorylcholine (Alpha GPC), also offered as CogniSpark by Health Concerns. To increase effectiveness, the nutrient medicines R-Lipoic acid and Acetyl-L-carnitine are also recommended in combination. The nutrient formula Neuron Growth Factors from Vitamin Research contains two forms of acetyl L-carnitine, combined with Gingko biloba, Gotu kola, and uridine (an essential growth factor for neuron axonal and dendrite growth). Uridine has been studied and proven to be effective for treatment of depression in combination with the omega3 fatty acids EPA and DHA by the Harvard Medical School, as well. These nutrient chemicals have been tested and proven to be independently effective for mild cognitive impairment, and studies to prove efficacy for their use in combination with current Alzheimer's drugs are being designed. The NIA has still not released its results from the phase II human clinical trial of Huperzine A, although we can surmise that the phytochemical is proven to be effective, or else it would not have been advanced to a phase 2 human trial.

Resveratrol is also a chemical constituent of a Chinese medicinal herb that has undergone many clinical trials and is widely prescribed in China, and is now undergoing advanced human clinical trials in the United States, and is prescribed by many neurologists for treatment of Parkinson's. This phytochemical is most effective in a concentrated high dosage of a particular isomer of the chemical, all of which were developed in China. The effectiveness of the herbal chemical is dose dependant and a low dose is generally prescribed for many disorders as an antioxidant in the United States. A high quality product at a high dose is recommended for more advanced neurodegenerative states. Curucumin is another promising herbal chemical derived from Chinese herbal medicines, and has been researched in the U.S. and found effective. Currently, human clinical trials to prove efficacy in the treatment of Alzheimer's are being designed, and researchers at the Mayo Clinic Department of Neurology have stated that: “Several mechanisms of action have been proposed which may be relevant to Alzheimer's Disease based upon preliminary in vitro and in vivo data. Curcumin has been well tolerated in clinical trials investigating its use in other diseases. It is generally accepted as safe.” Curcumin is found in its most concentrated form in the Chinese herb Curcumin longa (turmeric, or Jiang huang), but is also found in significant concentration in the roots of Curcuma zedoaria (E zhu), Curcuma aromatica (Yu jin), and Curcuma kwangsiensis (Zhong cao yao).

Gingko biloba is also an effective herbal medicine that has been heavily studied for the treatment of cognitive impairment and neurodegenerative disease. The Mayo Clinic researchers have stated: “Overall, there is weak evidence that Gingko biloba extract may provide modest cognitive benefit in some patients with Alzheimer's disease. Although pooling several small (and less rigorous) clinical trials of Gingko extract suggested a modest benefit, the recently published large, well-designed, clinical trial that employed current diagnostic criteria and outcome measures showed no overall benefit (used by itself at low dosage). No long-term data exists comparing Gingk with cholinesterase inhibitors or memantine, or evaluating Gingko biloba extract use in combination with those agents. Although case reports of bleeding problems exist (with no proof), as well as theoretical interaction with platelet inhibiting medications (the term theoretical is emphasized), it is currently widely used and seems to have a good safety profile.” These M.D. neurologists make no effort to disguise their disdain for Complementary Medicine (see the NIH article link below), but yet do acknowledge the preliminary proof of modest efficacy and overall safety.

While the benefits from the isolated and concentrated high dosage of these active ingredients from Chinese herbal medicinals are easier to design clear clinical trials for, the bottom line is that in nature, a combination of herbal and nutrient chemicals is generally more effective in many ways. This is because nature has evolved complex chemical interactions that have proven to be effective in the survival and progress of animal species. These complex chemical groupings, and the effects of the chemical transformations that occur within the organism present enormous challenges to our scientific study. More importantly, the system of clinical trials in medicine we have designed and chosen are geared to clearly differentiate the effects of one particular pharmaceutical chemical molecule at a time. This does not actually negate the effectiveness of complex combinations of chemicals that are found in herbal medicines, and we do realize that sufficient dosage of these various herbal medicines in their natural form may have very significant positive outcomes.

The real problem is not the effectiveness of these herbal and nutrient medicines, but the ability to convince the patient population that they should take them at sufficient effective dosage for a long enough period of time to be effective, and to integrate into a comprehensive treatment protocol with acupuncture and tuina. Billions of dollars per year are spent by the U.S. population on nutrient supplements that are poorly regulated and generally of poor quality and show little effect. If a small portion of this money was instead directed to professional care in Complementary Medicine, the public health benefits would be dramatic. The intelligent patient will work with a knowledgeable TCM physician and take a research proven combination of herbal and nutrient medicines at a sufficient effective dosage for a prolonged period of time. Unfortunately, this rarely happens. When it does, we generally see a very significant improvement in clinical practice. In addition, much research utilizing functional MRI studies of the brain responses during acupuncture stimulation in the last 15 years has proven that acupuncture does indeed stimulate the key centers of the brain, and helps coordinate and modulate brain activity in ways that are proven to be effective in neurodegenerative states (see the research links to Harvard studies below). These studies now also prove that the type of stimulation is very important to the effect, and the choice of an acupuncturist that provides clear stimulation with correct control of this stimulation is very important. Acupuncture is not a completely mechanical treatment technique, and the ability and expertise of the acupuncturist is indeed very important. The patient must also realize that combining effective acupuncture stimulation while taking sufficient dosages of proven herbal and nutrient medicines can only help these medicines achieve greater overall effects on the brain.

One can see the potential in a therapeutic protocol that includes a variety of benefits for brain function and restoration when treating neurodegenerative disease, especially Alzheimer’s. A prolonged protocol with Vinpurazine, Cognispark, Neuron Growth Factors, R-Lipoic acid, Resveratrol, EPAq omega 3 essential fatty acids, Turmeric, and acupuncture, along with Tui Na physiotherapy, and potentially hormone balancing with bioidentical hormone stimulating topical creams, offers hope as an effective integrated adjunct therapy for these diseases. Of course, the disease progression is slow, and the progress with therapy in reversing this neurodegeneration may be slow as well. Starting treatment as early in the course of degeneration is most important, and early diagnosis is thus a great benefit to the patients. Waiting until the symptoms are so severe that behavior prevents effective use of a complex therapeutic routine is not reasonable.

Of course, the most intelligent use of Complementary Medicine in the arena of neurodegeneration is with the prevention of these disease mechanisms. Complementary Medicine offers the patient the ability to utilize very safe and effective therapeutic agents and treatments to prevent neurodegenerative disease, and the only side effect is all of the other health benefits that will be derived from this therapy. With more than one fifth of the U.S. population expected to experience some form of neurodegenerative problem in life, especially with aging, early utilization of Complementary Medicine would seen to be the best available approach to decrease risk of falling into this one in five category.

How Complementary Medicine may even help caregivers in the treatment of advanced Alzheimer's disease

A January 1, 2011 article in the New York Times demonstrates the current effective approaches in the treatment of advanced Alzheimer's disease, and findings that providing a better environment for the patient is much more effective than giving them pharmaceutical drugs to control behavior, which have been proven ineffective to a large extent, and often even worsen the patient's condition. This article details how progressive and effective care facilities adapt to patients by increasing individualized activities and improved environments that create positive emotional experiences for the individual patient. Catering more to the individual needs and desires of the patient was found to be much more effective than a rigid one-size-fits-all routine and increased control of the patient. Giving patients more independence and providing stimulation of emotionally soothing activities and routines proved very beneficial to both patients and caregivers, who themselves experience much stress. Programs of providing training and counseling in this regard for family members that provide home care also was proven able to delay the time that the patient had to be transferred to a specialized care center. The article is available by clicking here: http://www.nytimes.com/2011/01/01/health/01care.html.

Incorporating the care of Complementary Medicine physicians into the care of a relative with advancing Alzheimer's and Parkinson's diseases can be problematic. Combative and confused patients may be difficult to convince to go to a clinic to be treated. By learning how to handle these patients better at home, though, relatives may be able to more easily soothe apprehensions and convince the patient to attend treatments. Often, after the patient experiences the relaxation and calming effects of acupuncture, and even some physiotherapies, there is an emotional memory, though, that provides an incentive to go back to the clinic and be treated. This may not happen after the first few treatments, but an emotional memory and appreciation may develop. Patience and persistence may be the key. Addressing not only stress in treatment, but pain as well, may address some of the reasons why the patient is unhappy and responding with negative emotional outbursts and bad behavior. New research suggests that emotional memory and emotion-driven behavior persists after cognition deteriorates, and therapy that provides an emotional relief may stick with the patient even when cognitive memory fails.

With the aging of the U.S. population, an explosive growth in the area of geriatric nursing care is presenting us with significant alarm concerning the way the elderly patients in nursing care facilities are treated. A New York Times article on May 10, 2011, reports that the U.S. Health and Human Services (HHS) has revealed in an audit that about 1 in 7 patients in nursing homes were routinely prescribed an anti-pychotic medication that was charged to Medicare. The actual number of prescriptions may be much higher, as Medicare supplement insurance policies also cover the prescription of drugs, and patients with a high expenditure on pharmaceuticals have been denied payment for drugs that fell within the “doughnut-hole” of drug expenditures. This audit revealed that about 50% of these anti-psychotic prescriptions charged to Medicare in 2007 did not meet FDA guidelines for usage, and did not meet the standards set by Medicare for prescription and payment, and have been deemed erroneous claims. In fact, this HHS audit found that 83% of these prescriptions were for off-label uses, meaning for conditions not approved by the FDA, and that 88% of these antipsychotic medications were prescribed to patients with dementia, despited FDA warnings of a higher risk of death and serious side effects in this population. The government has investigated drug companies for illegally marketing these drugs, resulting in many billions of dollars in settlements in lieu of fines, and fines for illegal kickbacks by pharmaceutical companies paid to nursing care companies have also occurred. For example, in 2009, a pharmacy chain tied to nursing homes, Omnicare Inc., paid a settlement of $98 million to avoid fines and settle accusations that major drug companies paid hundreds of millions of dollars in kickbacks to get Omnicare to overprescribe antipsychotic medications. Often medical doctors are paid very little to prescribe care at these facilities, spending only minutes with patients, and prescribing a large number of drugs. Senator Charles Grassley, head of a commerce committee oversight panel on abuses in the health care industry, called for this audit, and stated: “These results are alarming. Medicare officials need to pay attention.“ Patients and their families need to address the issue of proper care of the elderly with dementias, and to do more to prevent these diseases from progressing at early stages.

The study of acupuncture as an adjunct therapy for Parkinson‘s disease

In recent years, the study of specific acupuncture stimulations in relation to the treatment of Parkinson‘s disease has increased due to improved means of testing brain function and specific effects on brain chemistry in various parts of the brain. This is largely due to the progress with use of fMRI studies combined with improved use of chemical analysis. Much of this research, of course, must be performed on laboratory animals (unfortunately), but has proven that acupuncture does exert specific beneficial effets that will benefit the patient with Parkinsonism. These studies will advance in the next few years to human clinical trials. In 2010, at the Capital Medical University in Beijing, China, Key Laboratory for Neurodegenerative Disorders, researchers found that electroacupuncture stimulation at 100 Hz on specific points significantly improved moter coordination in Parkinsonism subjects by normalizing the GABA content in the midbrain nuclei responsible for the typical tremors and motor dysfunction. This stimulation was shown to have no effect on GABA content in neurons of other parts of the brain, such as the globus pallidus. This type of electroacupuncture effect was shown to improve motor impairment by increasing GABAergic inhibition in the output nuclei of the basal ganglia (see study cited below). This type of electroacupuncture stimulation has been used for some years in China, but these recent research studies now confirm its efficacy.

This study in Beijing had also previously found that specific electroacupuncture stimulation showed neuroprotective effects on dopaminergic neurons in the substantia nigra, and beneficial modulation of substance P and glutamate decarboxylase in the midbrain, which would explain the positive effects on improved motor function in Parkinsonism seen in studies. These findings showed that restoration of homeostatic mechanisms of dopaminergic transmission were achievable with electroacupuncture stimulation. The benefits to the Parkinsons patient with this therapy may be significant, and exert restorative rather than chemical blocking mechanisms. Combining this electroacupuncture with various other restorative protocols in Complementary Medicine shows great promise in the slowing of, or reversing of, neurodegeneration in Parkinson‘s Disease.

Neurohormonal imbalance in Neurodegenerative disease

One intriguing theory as to the origins of the pathophysiological mechanisms that create the Parkinson's syndrome, that has resulted from the more holistic research in recent years, examining the various interrelated problems in the central nervous system, has been the theory that Parkinson's is the result of a neurohormonal imbalance related to melatonin and dopamine interactions. It has been discovered that dopamine supplementation may work to some extent because it has an effect on the circadian production of melatonin, and that deficient circadian melatonin production leads to hyperplasia in key areas of the brain through a variety of mechanisms, including the lack of antioxidant acitivity that melatonin provides. Since the neurotransmitters in the brain are constantly being produced and converted in a balancing manner, restoration of neurohormonal health may be a more productive strategy in the long term therapy than simple supplementation or inhbition of specific neurotransmitters. A 2008 summary of this scientific study from the Brownoski Institute of Behavioral Neuroscience in Victoria, Australia, states: “For the first time, abundant evidence is presented describing Parkinson's Disease (PD) as an endocrine disorder of melatonin hyperplasia. The role of circadian interventive therapies and internal desynchrony in the aetiology and progression of PD provides a new direction for understanding the underlying physiology of a disease which is currently in a state of impasse and provides new hope for those who suffer from its debilitating effects.” Melatonin hyperplasia refers to a condition where melatonin producing cells are abnormal in number. This condition would occur when there is a deficiency of melatonin and increased need, or when the hormonal feedback system is stimulating a need for increased melatonin production.

Melatonin is both a hormone and neurotransmitter, and increases in melatonin production and secretion occur naturally in the circadian cycle of wake and sleep at night. In 2010, studies found that more than 10 percent of Americans suffer from insomnia, implying that circadian melatonin imbalance is perhaps a problem for a large number of people (35 million). Secretion of hormones and neurotransmitters in the brain, as well as metabolic conversion and creation of these molecules, is fundamental to healthy brain function. Both the nervous system and the endocrine system must be involved and coordinated in this process, making restoration of health a complicated problems. Research in recent years has explored this link between insomnia and neurodegenerative disease, as there is a very high rate of insomnia and sleep disturbances, such as sleep apnea and anxiety disorder, in the population identified with neurodegeneration. Simply taking melatonin has not been effective, as the much regulated neurohormonal system quickly adapts to supplementation and renders this ineffective after a short period of time. Combinations of herbs and supplements that aid the various balancing mechanisms have been researched because of this, and a combination of cofactor Vitamin B6, 5HTP, St. John's Wort, and melatonin, is one intriguing combination created by the company Vitamin Research. A comprehensive therapeutic protocol is recommended to achieve better sleep and melatonin metabolism, though, and utilization of acupuncture, herbs, nutrient medicine, and hormonal balancing may be needed for an eventual return of healthy neurohormonal function and balance.

Melatonin is produced in abundance by the pineal gland in the cycle of day and night, and this rhythm of secretion is controlled by various suprachiasmatic nuclei in the hypothalamus, the command center of the endocrine, or hormonal system. There is evidence of much occurence of deficient hypothalamic function in the aging population, often related to subclinical hypothyroid disorders and adrenal stress syndromes, and this could cause decreased melatonin bioavailability and stimulate melatonin hyperplasia. Melatonin has a variety of functions in the brain besides stimulating deeper sleep, and has remarkable antioxidant effects. These antioxidant effects are extremely important to maintaining healthy brain cells, as melatonin both stimulates free radical oxidant clearing, and creates melatonyl radicals in this process that combine with superoxide anions (charged mineral molecules) and detoxifies them. Melatonin also stimulates other antioxidant and detoxifying activities, stimulating increases in superoxide dismutase, glutathione enzymes, and glutathione, which is the fundamental detoxifying chemical in our body (read about glutathione metabolism in another article on this website). Researchers at the Hospital Neuro-Cardiologique in Lyon, France, in 2005, explain the complex role of melatonin in our bodies: “The circadian organisation of other physiological functions could depend on the melatonin signal, for instance immune, antioxidative defences, hemostasis, and glucose regulation. Since the regulating system of melatonin secretion is complex, following central and autonomic (nervous system) pathways, there are many pathophysiological situations where the melatonin secretion can be disturbed.” (PMID: 15649735). This certainly implies that a thorough holistic treatment protocol is needed in melatonin imbalance, and with careful analysis and a multifactorial treatment tailored to the individual, melatonin production in the circadian cycle can be restored. While increasing melatonin bioavailability may not immediately relieve symptoms of Parkinson's disorder and other neurodegenerative disease, it is a key aspect of the long-term holistic therapy.

The most important neurohormone involved in circadian rhythms (variations during the 24 hour cycle) is cortisol, a glucocorticoid constantly secreted by the adrenal (tip of the kidney) gland. In hormonal analysis diurnal cortisol levels are very important, and often clearly relate to symptoms. With adrenal insufficiency, or adrenal stress syndrome, cortisol production may be sluggish, resulting in low cortisol during the day and excess production at night, which accounts for daytime sluggishness and insomnia, as well as a cycle of depressed affect during the day and anxiety in the evening and night. Cortisol is also intimately involved in maintaining blood pressure, glucose and fat metablism, muscle weakness due to impaired glucose uptake, protein catabolism, fat redistribution, limited immune responses, and variability in immune suppression and excess immune responses. TNf-alpha, a key immune mediator involved in cellular degeneration and neurodegenerative conditions, may be significantly inhibited by diurnal cortisol imbalance. Recovery of this systemic and chronic condition will not happen overnight. The patient needs to patiently work to restore diurnal melatonin and cortisol homeostasis, address adrenal insufficiency, correct subclinical hypothyroid conditions, and hypothalamic insufficiency. Of course, for those of us that fear neurodegenerative conditions, we need to address these subjects earlier in life, before the neurodegenerative condition becomes symptomatically severe. As we age and are challenged by menopausal and andropausal hormonal deficiencies we should have an analysis of hormonal balance and work to achieve better hormonal homeostasis. The utilization of relatively inexpensive tests to give a hormonal profile with analysis of active hormonal metabolites in saliva and veinous blood stick samples provide the patient and physician a clear objective basis for this rebalancing and restoration.

Recent research has uncovered a number of ways to help restore cortisol balance. A 2010 research study sponsored by the NIH at UCLA proved that deep tissue massage (called TuiNa in Traditional Chinese Medicine) dramatically improved cortisol levels and regulatory modulation (see the article entitled Deep Tissue Massage and it‘s many benefits on this website. Since cortisol is an adrenal hormone that operates in a feedback mechanism within the neuroendocrine system, therapy to balance hormonal homeostasis, with acupuncture, topical bioidentical hormone creams, and herbal and nutrient medicines, as well as stress reduction therapies, are all important aspects of a comprehensive protocol that may be individually tailored to each patient. Inexpensive tests utilizing saliva samples to measure active hormone metabolites may be utilized to guide this type of therapy. The only way to find out how well this approach works is to try it.

Hypothalamic hypofunction or dysfunction has also been implicated in neurodegenerative disease in other ways than melatonin imbalance. The hypothalamus, coupled with the pituitary, is the chief gland of the brain involved in neurohormonal balance, and the command center of the endocrine system. The glutamate and NMDA metabolism is integral to both hypothalamic function and is implicated in neurodegenerative disease. Excess glutamate metabolism was found to be involved in acute strokes and brain cell destruction in the past, and research showed that the long term effects produced cell death, or apoptosis. This spurred much research into the possibility that excess glutamate could be responsible for neurodegenerative cell damage and death. Today, NMDA glutamate receptor antagonists are used to treat various neurodegenerative diseases. These same drugs were found to affect the hypothalamic functions, and hypothalamic dopamine and corticosteroid metabolism, as well as pathologies related to hypothalamic dysfunction and hormonal imbalances of prolactin. Excess glutamate metabolism was found to hyperstimulate the hypothalamus and result in stress-induced high circulating prolactin and corticosterone. Today, much research has revealed that many patients may suffer form a subclinical hypothalamic deficiency, or hypofunction, that is related to various hormonal imbalances seen clinically. More physicians are treating the hypothalamic dysfunction in a system of hormonal restoration with bioidentical hormones, herbs, nutrient medicine, and acupuncture. Further research may show the potential for benefits in such hormonal restoration as it effects the dysfunction of glutamate metabolism in regards to neurodegenerative disease.

Another aspect of neurodegenerative pathology related to hormonal deficiency and imbalance is the subject of estrogen deficiency and its role in mitochondrial dysfunction. The mitochondria are small parts of the cell that produce much energy from glucose. It has been well established that the mitochondrial dysfunctions are responsible for much of the oxidative stress that leads to neuron degeneration. In 2008, researchers at the University of Southern California Program of Neuroscience found that estrogens signal a number of pathways of cell protection and enhance mitochondrial function (see the link in additional information at the end of this article). Estrogens were found to maintain calcium homeostasis, enhance glycolysis (glucose usage), sustain and enhance mitochondrial functions, protect against free radical oxidative damage, and aid cholesterol metabolism and clear beta-amyloid stick protein accumulation. All of these mechanisms enhanced natural neural defense and maintenance, and explains why many women suffer from neurodegenerative disorders post-menopausally. Some neurodegenerative disorders are seen at a relatively early age postmenopausally, such as primary aphasia, and could be highly related to the estrogen deficiency. Synthetic estrogens in hormone replacement are problematic, with much research revealing the array of risks and side effects, but natural bio-identical hormone therapy is becoming very common now. Achieving physiological normal production of estrogens and an estrogen progesterone balance could both prevent neurodegenerative conditions and treat them effectively. Of course, once neurodegeneration occurs, the treatment protocol should be more thorough, in order to address the many aspects of the cascade of problems seen in study. The research at USC also reveals that there is a danger of metabolic exacerbation with advanced neurodegenerative disease with the use of higher dose synthetic estradiol, since the same mechanisms that would drive improvement in healthy neurons may stimulate exacerbation in unhealthy ones. This is why the use of very low dose bioidentical estriol cream with careful monitoring and hormonal balance is believed to be a potential successful strategy.

Hormonal balancing, especially with restoration of the melatonin and estrogen metabolism, is thus the linchpin of a more thorough holistic protocol when trying to reverse neurodegeneration. No patient wants to hear that their disorder is highly complex and requires a complex treatment protocol, but with neurodegenerative disorders, there is usually limited success unless the patient accepts a complex holistic treatment strategy, and proceeds in a step-by-step manner, hopefully guided by a knowledgeable physician. When utilizing acupuncture combined with herbal and nutrient medicine, an initial course of 12 weeks is seen in most of the scientific studies. Of course, if the results are excellent before this period of 3 months, the treatment may be pared down. Each individual will have a different presentation and need.

So-called sticky protein accumulation and immune disorder

A significant contributor to neurodegeneration in Alzheimer's disease is the misshapen proteins in the brain support tissues, or glial tissues. These are sometimes referred to as ‘sticky proteins’. Brain tissue is apparently destroyed by ‘sticky proteins’, where misshapen beta-amyloid proteins cause adjacent proteins to become misshapen with cross-beta links. Breakdown of APP (amyloid precursor protein), with certain enzymes interfering, coupled with problems with the tau protein found in tangles, a microtubule-assisted protein abundant in neurons in the CNS, are believed to be the results of whatever pathological process lies at the root of the disorder, probably an inflammatory dysfunction and excess accumulation of oxidant free radicals. A similar finding has revealed that altered or defective proteins, and the inability of the body to break down and remove these proteins, may be a core problem in early stages of Parkinsonism. One protein, called alpha-synuclein, reacts with dopamine and is linked to ‘sticky proteins’ and accumulation of protein fragments that are not efficiently cleared from the CNS, resulting in cell death. 5-10 percent of patients studied revealed mutations of the alpha-synuclein protein, which may cause a more severe problem with cell death. A majority of patients studied in the general population, with normal alpha-synuclein proteins, were able to adapt to this negative effect of alpha-synuclein and dopamine interaction and clear protein fragments, until excess oxidative stress or other health problems decreased the body's ability to handle the problem. Certain antioxidants and proteolytic enzymes have been discovered that are very helpful to clean up this mess. Examples include resveratrol (from the Chinese herb Hu zhang), and serratiopeptidase (from the silkworm), as well as milk thistle, and other herbal chemicals, including curcumin, an anti-inflammatory immunomodulating chemical found in 3 Chinese herbs, E zhu, Yu jin, and Jiang huang (turmeric).

Resveratrol, a chemical constituent of a number of Chinese herbs, especially Hu zhang, or Polygonum cuspidatum (also called Japanese knotweed), is now considered the most promising therapeutic biologic to treat Alzheimer's, due to its proven effect to activate protein enzymes called sirtuins, which are linked to cell protection and neuroprotection in aging. Hu zhang (Polygonum cuspidatum) is the primary source for resveratrol in medicines today, although a miniscule amount of resveratrol is also found in grape skins, and red wine has been touted as a source of resveratrol. Studies have found, though, that almost 2 gallons of red wine per day would be needed to provide a minimal dosage. Small amounts of resveratrol are also found in bilberry, cranberry, blueberry, mulberry, and certain species of pine. The Chinese have been researching resveratrol for many years, and have found that specific extraction methods produce a concentrated dosage of a particular type of resveratrol. Dosage and the correct isomer of the chemical resveratrol are very important therapeutically. The actual chemical name of this herbal and food nutrient is (E)-5-(4-hydroxystyryl)benzene-1,3-diol, or 3,5,4'-trihydroxystilbene. The sirtuin enzymes regulate apoptosis (programmed cell death) and metabolism, and have been found to be the link between metabolism and longetivity in studies. Currently, the U.S. NIH is sponsoring a second stage human clinical trial with resveratrol, and pharmaceutical companies are experimenting with biologic versions that deliver more of the chemical to the brain. In its natural herbal form, resveratrol has a number of bioactivities that are beneficial, including immunomodulation, modulation of the lipid metabolism, antiproliferation (anticancer), and an antifungal effect, as well as a potent antioxidant mechanism. Resveratrol has been proven to reduce excess triglycerides, and stimulate free fatty acid release in adipose tissues, so that a use of resveratrol in weight reduction as well as normalization of insulin resistance is also being explored. The antifungal aspect of this phyotchemical is also being researched, as the fungal form of candida, and candidiasis is linked to neurodegeneration as well. In addition, resveratrol is also being researched as a novel agent to inhibit the carcinogenic effects of estrogen metabolites, along with N-acetyl-cysteine, R-lipoic acid, and melatonin. As stated above, estrogen metabolites, such as estradiol-3,4-quinone, and 4-hydroxyestradiol, are known to play a significant part in the etiology of breast cancer, but also are implicated in neurodegenerative mechanisms. All of this research points to the use of this Chinese herbal extract as an important part of the holistic therapy in Alzheimer's, Parkinson's, and other neurodegenerative diseases.

In 2004, the Eve Topf and USA National Parkinson Foundation Centers for Neurodegenerative Diseases Research released a report on findings of the complex pathology of Parkinsonism and other neurodegenerative diseases, and the finding of free iron, or iron accumulation, in the central nervous system, was central to the cascade of events that lead to Parkinson’s disease (see study link cited below). These researchers found that the abnormal accumulation of iron in the brain, especially the substantia nigra pars compacta and melanin-containing dopamine neurons. Lewy body, a hallmark of Parkinson’s disease, is composed of redox-active iron, altered lipids, and aggregated alpha-synuclein, and it was found that this iron accumulation induces the aggregation, or clumping of alpha-synuclein protein into toxic aggregates in Lewy body. Iron accumulation and cytotoxicity also increases oxidative stress and the generation of reactive oxygen radicals, another hallmark of the disease. The accumulation of iron and reactive oxygen species (ROS) in these cells also degrades iron regulatory proteins via ubiquitination, where the protein ubuquitin (not to be confused with ubiquitol, or CoQ10 enzyme), inactivates regulatory proteins within the cells. These researchers noted: “Radical scavengers such as R-apomorphine and green tea catechin polyphinol (-)epigallocatechin-3-gallate, as well as recently developed brain-permeable VK-28 series derivative iron chelators, which are neuroprotective against these neurotoxins in mice and rats, prevent the the accumulation of iron and alpha-synuclein in substantia nigra pars compacta. This study supports the notion that a combination of iron chelation and antioxidant therapy, as emphasized on several occasions, might be a significant approach to neuroprotection in Parkinson’s disease and other neurodegenerative diseases.” Chelation formulas with EDTA, and a growing number of Chinese medicinal herbs, are proving effective in reversing iron cytotoxicity. Scutellari baicalensis, or Huang qin, a commonly used Chinese herb, is shown to be a strong chelator of iron accumulation (see study link below). Quercetin, a component of many Chinese herbs, is also shown to effectively modulate iron biochemistry and aid iron chelation, and is found in the herbs Lou bu ma (Apocynum venetum), Sang ji sheng (Loranthus parasiticus), Fan shi liu (Psidium guajava, or Apple guava), Di er cao (Hypericum, or Saint Johns Wort), and Man shan hong (Rhododendron dahuricum). Milk thistle has also been found effective to aid the liver in detoxification of heavy metals.

Inflammatory mediators, or cytokines, are also found to drive the creation of unwanted and misshapen proteins in the neural cell nucleus. TNF-alpha is a cytokine that is much studied in this regard, and is the target of recent therapy to reduce the pathological cellular mechanisms that drive neurodegenerative disesases. The TNF-alpha drug Enbrel (etanerocept) is being used to inhibit TNF-alpha with modest success via injection of the drug around the spinal cord in the neck. Unfortunately, this procedure is still in early phases of clinical trials, and will by costly (estimates of $10-40,000 per year). The effects may give the patient much benefit in the future, though. The current strategies of acetyl-cholinestase and NMDA glutamate receptor inhibitors provide very modest benefits, as do an array of past pharmaceuticals. While TNF-alpha inhibition may be beneficial in the future, the overall damage to the brain in neurodegneration is not addressed by this approach alone. Coupled with this is the research that has shown potent TNF-alpha inhibition with specific herbal chemicals for some time. Complementary Medicine would thus both provide more avenues of TNF-alpha inhibition, as well as modulatory effects, and could provide an array of other studied effects that would be necessary to fully rehabilitate and correct hypometabolic dysfunction, stimulate repair and regeneration, and correct underlying causes that may continue to bring back the disease even if it is improved with pharmacological therapy. TNF-alpha, or tumor necrosis factor, may be just one of the cytokines involved in driving specific neuron and glial cell death. This cytokine is called tumor necrosis factor because it was found to be integral to cancer cell necrosis, or cell death, and while it exerts a beneficial inflammatory response in a balanced system, may exert unwanted necrosis, or cell death (apoptosis), in neurodegenerative disorders. TNF-alpha is not only expressed from immune cells, such as mast cell in acute inflammatory responses, but is also expressed in brain cells. Various mechanisms may drive the unwanted high expressio of this cytokine in neurodegenerative disorders, especially primary progressive aphasia. An integrative medical approach would utilize both the pharmaceutical and an array of holistic therapies to counter this complex disease.

Research now links Advanced Glycation Endproducts (AGEs) with this pathological process related to ‘sticky proteins’. These molecules accumulate due to dietary intake as well as metabolic disorder in our bodies, and a complete article on this subject is found on this website under Practitioners and Treatment Protocols. AGEs are unregulated sugar and protein complexes related to modern food production, with use of unnatural sugars such as high-fructose corn syrup, as well as processed and fast foods that cook meat proteins by charring, especially with sweet sauces, or by heating protein foods with carbohydrates in the abscence of water, such as potato chips. Inside our bodies, these unnatural sugar protein complexes may form due to a combination of oxidative stress, dietary regimes, even supposedly healthy dietary habits, liver dysfunction, and metabolic disorder. When diagnosed with neurodegenerative disease, it is very important that you take a serious look into improving your diet and reversing harm that has been caused in the past by a poor diet. We have been tricked into overconsumption of unhealthy processed foods, many of which are advertised as natural and organic, and the time to finally pay attention to the sins of the food industry is now. Utilizing a knowledgeable TCM physician, or Licensed Acupuncturist, to help sort out this information and guide both dietary changes and integrative or complementary treatment is a practical choice. A number of Chinese herbs, as well as the nutrients P5P (active Vitamin B6), thiamin (B1), L-Carnosine, N-acetyl cysteine, and R-Lipoic acid, all have been shown to help clear excess AGEs.

The most intriguing breakthrough in understanding of the problem of ‘sticky proteins’ has occurred at Harvard Medical College in 2010, where genetic research led by Rudolph E. Tanzi found that expression of the protein beta-amyloid was produced by the same genes that produce protein immune molecules for the innate immune system, the primary immune defense in the brain. An immune modulator, LL-37, was almost identical to the beta-amyloid protein. LL-37 is produced in the body in response to brain infections, and is associated with atherosclerosis. In laboratory studies, A-beta, or amyloid beta, like LL-37, was found to destroy various pathogens, including a variety of bacteria associated with low level deep tissue infections, and Candida albicans, which is also a known cause of brain infections (meningitis). Samples of tissues from Alzheimer's patient brains (obtained from people who had died from Alzheimer's) were 24 percent more active in killing these bacteria and other pathogens. This implies that, for a large percentage of Alzheimer's patients, clearing of chronic infections and overgrowths in the body, and stimulating a better response by the innate immune system, could be a key to resolving the neurodegenerative process. Once again, we see the importance of recognizing the complexity and holistic nature of these diseases, and the need for a comprehensive holistic treatment strategy that is persistent. The patient that keeps looking for the simple ‘silver bullet’ and does not stick with a sensible comprehensive treatment strategy based on research, will probably not find success. Even if allopathic pharmaceuticals are tried in these disorders, they will not address all of the potential aspects of the disease, and Complementary and Integrative Medicine should play a key role in the overall treatment strategy.

Innate immunity is a type of immune response that utilizes immune modulators that recognize and respond to pathogens in a generic way, as opposed to the adaptive (learned), and autoimmunity (automatically attacking any foreign cell). Innate immunity utilizes the complement cascade of mediators that work together, as well as physical barriers and phagocytic cells (cells that literally eat other cells). Innate immunity may be the oldest form, and the most complicated. It does not rely on antibodies and memory T-cells, which have a difficult time passing the immune barrier into the brain. Most of the chemical mediators in the innate system are called cytokines, and each type of cytokine has a specialty. This cascade of proteins that usually complement the antibody responses is synthesized by the liver. Cytokines identify and tag pathogens, trigger the recruitment of inflammatory mediators, disrupt the membranes of infected cells, causing cellular death, and remove the debris from these immune processes. Foreign substances, such as toxins, may be identified and marked for dissolution by white blood cells, and the adaptive immune response may be activated by presenting the antigen to the B and T cells. This complex cascade of mechanisms is how the innate immune system works. Apparently, when it doesn't work optimally, neurodegeneration may occur. The key cells of the innate immune system are Natural killer (NK) cells, mast cells, eosinophils, basophils, macrophages, neutrophils, and dendritic cells. Some of these cells are highly activated in allergic responses, such as mast cell, macrophages and neutrophils. These processes of killing infected cells and toxins create free radical oxidants, or oxygen molecules that are free from larger molecules. Antioxidants help clean up the mess. Neutrophils attack pathogens by creating reactive oxygen species (ROS). Neutrophils and basophils release histamine as well as free radical oxidants, and also create accumulations of toxic proteins and protein fragments. The excess reaction of the innate immune system creates the oxidant and protein fragment accumulation in the brain tissues that many eventually cause dysfunction and degeneration. As stated, various powerful antioxidants and proteolytic enzymes may help clean up the mess, and various powerful immune stimulating herbs may improve the function of the innate immune system.

The brain has a relatively high level of fat, yet a relatively low level of antioxidant activity compared to other organs in the body. Oxidized fatty acids thus accumulate with physiological stress in the brain, and contribute to the various cellular dysunctions described above. Most scientists agree that increased antioxidant activity is needed in these neurodegenerative diseases, especially lipid oxidant clearing from high levels of lipid peroxidation. The chief antioxidant mechanism in the body is the glutathione metabolism. Glutathione is a molecule that practically defines cellular detoxification and antioxidant activity in physiology. It is produced in our cells and kept in balance via a variety of homeostatic mechanisms. As our brain cells are repaired and maintained, oxidant free radicals are produced and the available glutathione accepts the oxidants and then is reduced to transform harmful oxidants into oxygen molecules that can be utilized, such as water, or eliminated, such as carbon dioxide. Glutathione balance and bioavailability is thus extremely important in cellular maintenance in the brain. Since glutathione cannot be simply eaten and utilized well, indirect methods must be employed to aid glutathione metabolism. A separate article on this website helps explain this glutathione metabolism, and suggests the variety of ways one can help improve this most important metabolism in the body. Science continues to search for more direct ways to improve glutathione bioavailability in neurodegenerative disease, and the current hope is that supplementation with liposomal glutathione will have some effect in this protocol. Encapsulating glutathione in liposomes, or fatty encapsulation, will delay the breakdown of glutathione and perhaps allow some of this supplemental glutathione to aid the cellular processes in the brain. Further research will tell whether this approach is effective.

Liver dysfunction has been proven to be a key factor in the systemic cycle of events contributing to amyloid beta (Abeta) accumulation (sticky protein) in the brain in Alzheimer’s pathology. Amyloid beta peptide excess coupled with deficiency of low-density lipoprotein receptor protein (LRP) is a hallmark of the disease, and liver clearance of amyloid beta peptide from the blood is a major concern. This amyloid clearance is mediated by low-density lipoprotein receptor-related protein (LRP-1). Research has found that a high incidence of cerebral amyloid beta deposition occurs with insulin resistance and Metabolic Syndrome, typically called Diabetes Type 2. Studies have shown that insulin in the blood circulation facilitates LRP-1 translocation to the liver plasma membrane from the intracellular pool, contributing to LRP deficiency and poor amyloid beta clearance. Correcting metabolic dysfunction and aiding liver health and function are thus key components of a holistic protocol to prevent or reverse Alzheimer’s disease. We have also seen that the inability of the liver to remove toxins from the blood may result in hepatic encephalopathy and worsening of brain functions. While standard medicine focuses on this pathology only when it is severe, this points to a need to address liver function before brain function deteriorates. There are a number of known triggers to hepatic encephalopathy, including electrolyte imbalance, potassium deficiency, low grade infections such and bacterial endotoxicity, aldehyde toxicity, excess protein consumption with ammonia toxicity, and use of medications that suppress the CNS, such as benzodiazepines. Holistic medicine offers the patient the professional assessment and treatment of these potential problems.

No matter what type of neurodegenerative disease you have been diagnosed with, or whether you are experiencing early signs, or just wanting to have more insurance that you won't end up with these serious health problems in the future, Complementary Medicine provides you with a wealth of evidence-based treatment approaches. While none of these approaches is a ‘magic pill’, they all improve aspects of neurological and immune health to maintain and improve the health and function of your central nervous system. The benefits to this approach exceed the cure, because we all live a healthier, happier and more productive life when our brain is healthier and well maintained. The key to patients seeking effective treatment protocol in neurodegenerative disease is to combine the key strategies to form a more comprehensive overall treatment. This approach, of course, is not popular, as it entails taking a variety of pills, and getting fairly frequent treatment. The lure of a simple single magic pill still is strong. Yet, more and more patients are educating themselves and deciding that the sensible course involves this approach, and a knowledgable Complementary Medicine physician is needed to guide therapy.

The history of the causes of increases in incidence of Parkinson's, Alzheimer's and other neurodegenerative diseases and syndromes

In the 1950s the food industry stripped vegetable oils of Omega-3 fatty acids to extend the shelf life on products and allow for more success in corporate food production. Transfats were used instead, such as margarine and shortening, and a dramatic increase in incidence of Parkinson's and other neurodegenerative disorders occurred, as scientists link an imbalance of essential fatty acids to neurodegenerative pathology. Essential fatty acid balance is a key aspect to immune function and physiological ability to clear excess oxidative free radicals and repair unhealthy tissues. This isn't the complete answer to the cause of neurodegeneration, but it is a piece of the puzzle. As mentioned above, commercial food production also produced advanced glycation endproducts (AGEs), which produced dysfunction in a different way. At the same time, our country expanded energy production dramatically, mostly with coal fired power plants that spew tons of organic lead and mercury molecules into the air, which enters our lungs, and becomes part of the food and water supply. These heavy metal contaminants accumulate in our brain tissues and eventually cause many problems with neural firing and oxidative clearing (a complete article on lead, mercury and heavy metal pollution is also available on this website). The widely used herbicide paraquat and other pesticides and herbicides have also been implicated in neurotoxicity and Parkinson's disease. These combinations of unhealthy and poorly regulated environmental toxicities and harmful products of industrial food production are at the root of the explosion of neurodegenerative diseases in the modern population.

In 2012, a study at Columbia University in New York, headed by Dr. Nikolaos Scarmeas MD, and published in the online medical journal Neurology, confirmed that sufficient levels of omega-3 fatty acids in the diet, such as EPA and DHA, was the most significant nutrient dietary factor associated with lower levels of beta-amyloid proteins AB40 and AB42 in blood plasma, which is linked to plaque accumulation in the brain and Alzheimer’s neurodegeneration. Previous study of diet and neurodegeneration by this research team had indicated that populations that ate a so-called Mediterranean-type diet, with an array and balance of healthy fats, showed a decreased risk of neurodegenerative disease and cognitive impairment (dementia). This further study showed that the decrease in omega-3 fatty acids in the modern diet, a consequence of the modern processing of common vegetable oils to achieve longer shelf-life of processed foods, was directly responsible for increased levels of beta-amyloid, the so-called “sticky protein”, which is the key component of neurodegenerative “tangles” associated with Alzheimer’s disease. The study group also reviewed levels of saturated fats, monounsaturated fats, omega-6 fatty acids, folate, beta-carotene, and the vitamins C, D, E and B12, to see if these affected the levels of circulating beta-amyloid. None of these nutrients showed a significant relationship to the problematic types of beta-amyloid proteins in blood plasma. This analysis (a study review is available below in additional information) confirms that the change in the content of fatty acids in processed vegetable oils and transfats is responsible for a key factor of neurodegenerative disease, the increase in problematic types of beta-amyloid “sticky proteins” in circulation contributing to the gradual formation of beta-amyloid plaques in the brain, the hallmark of Alzheimer”s disease. This analysis does not rule out the other contributing factors to the disease, but does confirm what many experts have surmised is a key public health factor that has led to the extreme rise in neurodegenerative disease in the United States.

Today, more than 5% of people over 75 are diagnosed with some type of serious neurodegenerative disorder, and as far back as 1989 studies by Brigham and Women's Hospital in Boston, published in the Journal of the American Medical Society, stated that an estimated 10.3% of the population over 65 years of age had probable Alzheimer's disease (JAMA 1989 Nov 10;262(18):2551-6). Less serious neurodegenerative disorders, such as attention deficit and hyperactivity disorder, affect an even greater percentage of the population, even our children. These numbers are growing and do not even reflect the undiagnosed population who are just thought to be suffering from the effects of aging, called mild cognitive dysfunction clinically, and cynically called senility in the past. Incidence of neurodegeneration are not just limited to the elderly population, as new research uncovers the pathophysiology of Attention Deficit and Hyperactivity Disorder, and this disease too shows that measurable neurodegeneration is occurring, even in children. Early stages of serious neurodegenerative disorder may be without symptoms for many years, and treatment at the endstage may only accomplish a slowing or stopping of the neurodegeneration that causes symptoms at this stage. The aging baby boomer population, and indeed all of us, need to understand that there is a need to act now, both to prevent and reverse one's own neurodegeneration, but also to act now to get our government to address the causes of neurodegenerative diseases in our country.

To counter the awareness of environmental causes of neurodegenerative disorders and subsequent alarm by the public, many articles and research studies were engendered by industry funding espousing a genetic link to these disorders, rather than an environmental cause. So far, scientific study has found only rare links to potentially inherited Parkinson's and Alzheimer's. A mutation of the LRRK2 gene called PARK8 was found in only 5% of the Parkinson's population, showing little causative genetic link in reality. The public needs to be diligent to get our government to clean up heavy metal toxicities and to regulate the food industry to prevent these types of neurodegenerative health problems for future generations. The real causes of these neurodegenerative pathologies are not genetic, but a combination of public health issues, industrial food production, environmental toxins, overuse of antibiotics, immunodeficiency, and lifestyle stress. Unless we become educated to this complex problem and act now, the population of the United States is going to face ever increasing problems with these neurodegenerative diseases. Since the cost of care of these patients, and the loss of productivity, is enormous, this health problem affects not only the patients, but all of us, especially when the cost of health care and social spending has already spiraled out of control.

What are the causes or contributors to attention deficit and hyperactivity at an early age? ADHD has also proven to be a neurodegenerative condition, even at an early age. We all know by now of the growing problem of hyperactivity in children and the treatment with the dopamine reuptake inhibitor Ritalin that is also used to treat adult ADHD. Clinical blinded placebo trials have shown that such chemicals as artificial food coloring and sulfite and benzoate preservatives have increased hyperactivity in children diagnosed with the disorder. See: http://courses.washington.edu/envh111/Student%20Articles%202008/Week%202/26_Do%20food%20dyes%20affect%20kids'%20behavior_Itaya.pdf. How do benzoate preservatives and artificial food dyes contribute to neurodegenerative pathology? Once again, the answer is complicated, but a few key points elucidate the basic process. Read on.

Benzoic acid, a common food preservative, has been demonstrated to cause oxidative stress. These preservative acids also have a negative consequence on cellular membranes, that both act to insure effective metabolism at dopamine receptors, and to protect the cell from environmental cytotoxins that enter the bloodstream. Cell membranes protect the mitochondria in our brain cells, the small oxygen factories that supply energy to our cells, and which are the subject of much study of the root of neurodegeneration. While organic food preservative acids, such as benzoic and sorbic acid, are stable, or cytostatic, under conditions used for food preservation, they may cause a disruption of the cellular plasma membrane and cause a cytocidal effect when they reach our brain, especially under acidic conditions in the body. Acidity in the body is increased when there is too much intake of simple carbohydrates like sugar, refined grain, beer, granola, etc. Periods of high body acidity may also occur with poor stomach function, or poor hormonal regulation of key antacids, such as calcium. High body acidity may make benzoic acid food presersetives toxic and damaging to our brain cells.

High intake of benzoic acid preservative, coupled with a lack of healthy fats, or lipids, that make up the phospholipid membranes, and with a deficiency of oxidative potential to clear the damage, results in neurodegenerative cell death and functional cell membrane disruption that may occur at an early age. As mentioned, advanced glycation endproducts (AGEs) are also a dietary and metabolic problem that affects healthy cell membranes. When children eat too much processed food with these ingredients, it is easy to understand how the health of their brain cells are damaged. The problem in children is probably easily reversed by sticking to a healthy diet that avoids preservatives and food dyes, transfats, and simple carbohydrates, and includes sufficient antioxidant foods and omega-3 fatty acids. Even parents that believe that they are keeping their children's diet healthy are sometimes mistaken, as large intake of fructose, in the form of fruit juices and supposedly healthy carbonate beverages, can create an excess of AGEs. Over time, without ingredients for cellular repair, such as antioxidants, essential fatty acids, attention deficit and hyperacitivity disorder may become chronic. All scientific studies of neurodegeneration now demonstrate a measurable decrease in tissue quantity in key areas of the brain that are the result of this type of cellular damage, utilizing newer functional MRI imaging. This objective data is irrefutable.

All of the above causes of neurodegeneration leave our bodies more susceptible to inflammatory degeneration. Most studies of neurodegenerative disorders now focus on excess inflammatory processes and lack of oxidative clearance as the prime problem in neurodegeneration. Studies show that increased exposure to viral illnesses, and the penetration of some strains of these viruses deep into the organ tissues, generates excessive lipopolysaccharides that are released from antigen cell walls, and increase pro-inflammatory cytokines such as interleukin-1 (IL-1) and TNF-alpha. The chronic increases in expression of IL-1 has been shown to have both direct and indirect mechanisms that exacerbate neurodegeneration of dopaminergic neurons as well. IL-1 directly triggers 6-OHDA-triggered dopaminergic toxicity, and increases oxidative stress. Lipopolysaccharides were found to directly accelerate and increase motor signs in study animals, showing a positive link to direct hyperactivity cause. Some of the new pharmaceutical utilized (e.g. Enbrel) inhibit the cytokine TNF-alpha to reduce symptoms. These same effects, inhibition or modulation of inflammatory ctyokines, are proven to be achieved efficiently with herbal medicine. We can't completely eliminate viral illness from our world, but we can work to create a healthier response to viral illnesses in our bodies. Complementary Medicine has many therapeutic tools to enhance the immune system as well as directly help in inhibiting the harmful imbalances of inflammatory mediators. Scientific study allows the TCM physician to better utilize these herbal chemicals and specific acupuncture stimulations to achieve these goals.

In summary, the known history of causes of increased incidence of neurodegenerative disorders in the United States population include unhealthy ingredients in commercial processed foods that go unregulated, increasing amounts of lead, mercury and other heavy metal organic compounds, primarily from dirty coal fired power plants that go unregulated, and the increased oxidative stress and decreased immune health generated by our modern lifestyle, diet, and environment. Hormonal imbalance has also proven to play a significant role in mitochondrial dysfunction and neurodegeneration. As individuals, and as a population, we can change these harmful aspects of our world now, and clean up both our own bodies, and the environment. By utilizing Complementary Medicine, understanding and improving our habits, and urging our politicians to act now, future generations as well as our own will benefit immensely.

Basic physiology of Parkinson's, Alzheimer's and neurodegenerative disorders

While a complete explanation of all the theories of the pathophysiology of these disordes is too extensive for this article, a number of key points are helpful for the patient to understand the pathology. Basic physiological study has confirmed that dysfunction of Dopamine and other neurotransmitters in regulation and inhibition of excess neural transmission in the basal ganglia and putamen is responsible for tremors and a number of symptoms in Parkinson's. An imbalance between cholinergic (autonomic nervous) and dopaminergic influences on striatal tissues in these parts of the brain leads to dysfunction. The striatal tissues contain two types of cells that activate and restrain physical motion, and cellular degeneration leads to the inability to produce sufficient levels of the dopamines and acetylcholines to control this mechanism synergistically and prevent intention tremors. Simply increasing dopamine in circulation has limited effect, as a changing balance and pulsatile release of dopamine at various receptors is needed to maintain a normal physiological effect. Endogenous cannabinoids are produced to control the cholinergic overstimulation when insufficient dopamine occurs. Dopamine depletion may be due to excess metabolic needs, insufficient bioavailability, insufficient production, or excess need in relation to dysfunction of the degenerated neural cells that require dopamine inhibition. Neural degeneration may cause hyperactive states in the surviving cells. Metabolic disorders may contribute to altered rates of neurotransmitter production as well as disorder in the complex control of rates of firing a various receptors. Even the simplest of explanations uncovered about these neurodegenerative disorders poses more questions than answers, but does point us in productive directions.

The key areas of the brain that produce the unwanted tremors in Parkinson's are located in the basal ganglia, which are the large masses of gray matter at the base of the cerebral hemisphere. Modern anatomy defines the basal ganglia as the striatal tissues of the caudate and lentiform nuclei, and the cell groups associated with the striatal tissues, the substantia nigrum and subthalamic nuclei. In neurodegenerative disorders, many of the cells that control body movements may be damaged, and the remaining cells, regulated by dopamine and other neurotransmitters, become hyperactive in the corpus striatum. Study has proven that as Parkinson's worsens past the early stages, that degeneration of neurons and dopamine receptor decline, spreads to the anterior cingulate cortex, the dorsolateral prefrontal cortex, and the thalamus. This is why treatment at later stages may only slow the neurodegeneration, and also why simple drug therapies have limited effect.

Besides the problems of deficiency of bioavailability of dopamine and the endogenous cannabinoids, or metabolic problems with dopamine related protein enzyme regulation, there are a number of dopamine receptors that are implicated in the dopamine metabolic dysfunction. Different receptors respond differently to the same neurotransmitter chemical, and various metabolic deficiencies or other neural pathologies may contribute to neuroreceptor dysfunction. D2 receptors are abundant in the motor regions, such as the striatum, and D3 receptors are in relative abundance in areas of the brain that affect cognitive function and emotional stability, such as the limbic system and globus pallidus. The limbic system is linked to emotional well being as well as the hormonal regulation of the body. The globus pallidus is linked to pre-filtering of external stimuli, and dysfunction leads to an overactive mind and anxious states. A part of the globus pallidus, the ventral pallidum is also involved in the control and regulation of the signals from the striatum, which controls inhibition of movements, or tremors. D3 dopamine receptors are postsynaptic receptors that may be inhibitory to motor locomotion, resulting in the slow movements seen in advanced neurodegenerative disease. Dopamine metabolic dysfunction, whether it involves actual dopamine dificiency or problems with dopamine enzymes and protein regulation, may affect a number of key centers in the brain in different ways. A number of problems with dopamine metabolism and neural metabolism may act together to cause the various symptom presentations to these neurodegenerative disorders, and various approaches in therapy must thus be combined to be effective.

Dopamine receptors D2 and D3 are found within the same cells, and the differences have been studied thoroughly. Scientists find that a number of metabolic factors alter the rates of firing and the affinity for dopamine and dopamine metabolites at these two key receptor sites, explaining why the brain dysfunction changes over time and between patients. In animal studies, when there is less stress or demand upon the receptors, the D3 receptors have a much higher affinity for dopamine agonists than D2 receptors. As the stress on the cells is increased, and they are activated by G-proteins, the affinities for the dopamine molecules is equalized. Dopamine activation of the D3 receptors, though, always results in 2-5 fold less outgoing activity than D2 receptors, even within the same cell. Levels of G-proteins affect the activation states of both of these dopamine receptors. G-proteins are important signaling molecules throughout the body, and a number of pathologies, including diabetes, allergies, depression, cardiovascular defects and certain forms of cancer are thought to arise from derangement of G-protein signalling. Both D2 and D3 receptors can activate more than one pathway in the brain, and the differences in function between these types of receptors is affected not so much by the dopamine agonists and dopamine, but by a number of metabolic factors that act together in a quantum field. These findings present less and less hope for an allopathic solution to the disease.

The subject of G-protein derangement may be another important key to understanding the dysfunctions at dopamine receptors. This protein was discovered by scientists as they sought to understand how adrenaline stimulated cells. They found that when a hormone like adrenaline bound to a receptor, that the receptor did not stimulate enzymes directly, but instead, the receptor stimulated an enzyme to produce a second messenger. This discovery won them the Nobel prize in 1994. In the brain, stress levels induce increased adrenaline and other hormonal responses, that in turn stimulate greater levels of G-protein. The G-protein can be stimulated by either hormones or neurotransmitters like dopamine. Adrenal stress syndromes, and other hormonal imbalances may thus have a large impact on neurodegenerative dysfunction processess. When levels of G-proteins are maintained at a high level, this puts extra oxidative stress on the dopamine receptors. Recent research has focused on Adrenal stress syndromes and the link to neurological disorders. Chronically elevated adrenal hormones, or glucocorticoids, have been shown to desensitize serotonergic 5-HT receptors within the hypothalamus, which may explain suppression of the endocrine system following long periods of adrenal stress. Similar mechanisms could play a significant role on desensitization of dopamine receptors.

There is considerable concern over imbalance of dopamine and serotonin in the brain due to a variety of affectors over time, and the potential effects this would have on dopamine receptor function. Drugs that affect serotonin, especially selective serotonin reuptake inhibitors, or SSRIs, are frequently prescribed in recent years as rates of neurodegenerative diseases increased. Serotonin is balanced with dopamine in the body, and many of the side effects of SSRI medications, such as loss of libido and sexual function, are explained by a relative suppression of dopamine that accompanies increased concentrations of serotonin. In addition, early stages of neurodegenerative diseases usually involve some anxiety and depression which is often treated with SSRI medication. Studies have found that Fluoxetine (Prozac) may increase Parkinson symptoms more than other available SSRIs, and guidelines have recommended other SSRI medications due to this effect. Each patient may react to, or metabolize, SSRI medication differently, and guidelines suggest that each patient be started on a small dose and observed for toleration before increasing the dosage to effective levels. Serotonin syndrome is also seen, usually with concurrent prescription of MAO inhbitors for depression or anxiety, or with a host of other medications, but sometimes because an individual does not metabolize the SSRI at the same rate as another, and the accumulation of the SSRI over time produces a syndrome of serotonin excess. Often, the type of SSRI medication is changed due to side effects and guidelines state that a pause in prescription, or clearing phase, be utilized to avoid Serotonin syndrome. These precaution are often not followed, though, as the patient is anxious about returning to periods of higher anxiety or depression. The array of psych drugs commonly prescribed in recent years has also increased, with off label prescription of anti-seizure and anti-psychotic medications becoming more prevalent, which alter an array of neurotransmitters, incuding serotonin and dopamine. Combinations of these drugs may be problematic in the gradual onset of dopamine receptor dysfunctions.

Complementary Medicine utilizes a number of treatment strategies to affect these disease mechanisms in neurodegenerative disorders. Antioxidant herbs and supplements are utilized, 5HTP from the griffonia seed may be prescribed, and acupuncture may reduce stress levels and benefit adrenal function. Hormonal balance can be analyzed inexpensively in labs that test saliva or bloodstick samples, and topical creams that adjust hormonal levels with very safe low dosage herbal extracts can be utilized. Evidence-based herbal medicine allows the acupuncturist/herbalist to utilize dopaminergic herbs in treatment. Nutritional knowledge helps the Licensed Acupuncturist to effectively guide changes in dietary habits that specifically work for the individual. A number of herbal chemicals have been proven effective as a part of the therapy for various neurodegnerative disorders, such as Huperzine, and these may be incorporated into the overall treatment protocol. Since the disease mechanism is complicated, logic dictates that the treatment protocol will also be complicated. The Licensed Acupuncturist, utilizing Complementary Medicine, can integrate effectively with the M.D. specialists and help make the right choices to narrow this complicated treatment strategy and find the most efficient treatment for each individual. Quality of herbal and nutrient products is also important, and FDA regulation is almost nonexistent. The Licensed Acupuncturist has access to professional products that insure quality and reliable effectiveness.

ADD and ADHD, Attention Deficit and Attention Deficit Hyperactivity Disorder, may also be neurodegenerative conditions with a similar pathological concern, although different in manifestation of symptoms

Attention deficit and hyperactivity disorder has been linked to dysfunction with the D3 dopamine receptors, but the pathology is still poorly understood. Neural degeneration, or metabolic dysfunction related to dopamine enzymes, both could be causative of ADHD disorder, and this is demonstrated by the neuroimaging studies demonstrating atrophy or size decrease in key areas of the brain in ADHD patient populations, as well as the metabolic studies, such as those that demonstrate that excess benzoic acid (food preservative) may induce protein kinase A (PKA) pathways that are autophagic (self-destructive) in a nitrogen starved cellular metabolism. Certain areas of the brain associated with ADHD have been found to consistently smaller than normal in patients both young and old that have been afflicted with ADHD. Hyperactivity in these areas of the brain, which leads to short attention span, is a result of overstimulation of dopamine D3 receptors due to a decrease in the number of these D3 receptors overall.

The reasons for loss of the dopamine D3 receptors and neurodegenerative atrophy of these areas of the brain associated with functions of attention span, memory, control of muscle spasticity etc. are the subject of current study, and may reveal more and more novel ways to utilize Complementary Medicine in a long-term treatment protocol. G-proteins are immunoglobulin (Ig)-binding proteins produced in chronic low grade infections and allergic immune responses. G-protein coupled receptors are stimulated by a variety of chemicals in the brain, including neurotransmitters such as dopamine, hormones, light-sensitive compounds, odors and pheromones. Neurohormonal imbalance as well as hypersensitivity disorder may stimulate G-protein receptors that are overexpressed due to chronic deep subclinical infections. Since parts of these G-protein receptors can be glycosylated, excess accumulation of advanced glycosylation endproducts (AGEs) are also a known cause of dysfunction (see my article on AGEs under For Practitioners - Treatment Protocols). Overexpression of G-protein coupled receptors then produces excess accumulation of G-proteins and may cause deficiency of dopamine. Activation of dopamine D3 receptors by excess G-proteins inhibits the enzyme adenylyl cyclase, a second messenger, causing dysfunction and desensitization of a percentage of dopamine D3 receptors. In ADHD, as in Parkinson's, loss of a percentage of these neurons or receptors could have led to overactive stimulation of the surviving healthy neurons, causing hyperactivity of the mind as well as attention deficit. The goals of therapy must not be to just block specific functions in the brain with drugs, but to actually work in a comprehensive manner to stop the disease mechanisms and restore healthy cells and function to the parts of the brain that have suffered neurodegeneration.

Ritalin, or methylphenidate, is a norepinephrine and dopamine reuptake inhibitor, which means that it works by increasing the level of dopamine stimulation. Ritalin only works in the ADHD patient when levels of an important neurotransmitter, Phenylethylamine (PEA), is increased. It has been established that Ritalin acts by stimulation of parts of the brain that have become underactive, possibly due to neural degeneration. Phenylethylamine is a trace neurotransmitter that is biosynthesized in the neural cells from the amino acid phenylalanine by enzymatic decarboxylation. Dietary sources of phenylethylamine do not reach the brain because they are quickly broken down by the enzyme MAO-B. Increase in cell production of PEA is probably best aided by healthier protein metabolism, or liver function. Stories about how chocolate contains PEA and is beneficial are thus misleading. Chemicals that are similar to phenylethylamines and are substituted may cause dysfunction in cellular metabolism of the real phenylethylamine in the brain. These chemicals include the drug ecstasy (MDMA), mescaline, ephedrine, amphetamines, Phen-fen, various anti-depressants, and some bronchodilators. We see that the potential for environmental and drug causes of ADHD are widespread and common. Even the taking of Ritalin, or the other drugs that treat ADHD, requires that healthy neural function, and increase in PEA, is achieved. This gives new meaning to the term 'PEA-brain'. Complementary Medicine can even help the patient taking these pharmaceuticals achieve better results.

Deficient decarboxylation via protein enzymes may be an important part of the pathophysiology of these various neurodegenerative disorders. Decarboxylation refers to the removal of carbon dioxide waste from the cell. Deficiency of enzymatic decarboxylation will not only result in low levels of the essential neurotransmitter phenylethylamine, but results in deficient metabolism of a number of key transformations of amino acids to amines in the brain. Tryptophan to tryptamine, tyrosine to tyramine, glutamic acid to GABA, 5-HTP to serotonin, and L-DOPA to dopamine are are regulated by decarboxylation. Deficiency of copper may decrease the rate of decarboxylation, as copper, and various ketones, are natural catalysts of decarboxylation. Chronic kidney deficiency could play a role in reduced ketone catalysts as well. Relative states of acidity could also play a key role in decarboxylase enzyme rates. A number of factors could influence this key metabolic function, and only a holistic approach can bring the whole organism back to proper function, or homeostasis.

Oxidative decarboxylation is a vital part of the metabolism of the citric acid cycle within the mitochondria of neurons that are subject to oxidative damage and neurodegeneration. Both antioxidant metabolism and supply of sufficient oxygen via adequate microcirculation are important to mitochondrial function in brain cells. One molecule produced by decarboxylation is histamine. Histamine dilates capillaries and increases capillary permeability to supply sufficient oxygen to brain cells. Histamine has different effects on different receptors in the body. In the stomach, histamine stimulates gastric secretions, while in the sinuses it stimulates swelling and congestion in allergic response. Chronic use of antihistamine medications, with allergy meds, asthma meds, or medications to control stomach acids, are well known causes of side effects in the central nervous system. Overuse of antihistamines may contribute heavily to the pathology of neurodegenerative disease.

Another subject of research concerning neurodegeneration and ADHD, Parkinson's and Alzheimer's diseases is the subject of cannabinoids. Cannibinoids are not only found in marijuana, but are endogenously produced in everyone's brain to control mood swings, pain perception, etc. One large long-term study at six universities across the world showed that a patient population that had a history of marijuana smoking exhibited a 15% decrease in risk of developing Parkinson's disease. Not everyone smokes pot, but everyone does produce cannibinoids in their brain. Endocannabinoids are important molecules produced in the brain that moderate symptoms of Parkinson's, and are also activated by decarboxylation. By enhancing decarboxylation metabolism in the ways mentioned above, and by other natural means, we may be able to prevent or reverse neurodegnerative disease in many patients. Although this is only one of the metabolic factors being researched at present, it may hold the key to reversal of neurodegenerative changes.

Can herbal medicine affect these metabolic pathways, such as rates of decarboxylation? Although study is still underfunded in the West, and studies of herbal chemistry are still underpublished here, much research in China shows the potential for such herbal chemical benefits. Astragalus was studied in 2002 and shown to promote cell differentiation by means of inducing ornithine decarboxylase in animal studies. To see this study, click here: http://www.ncbi.nlm.nih.gov/pubmed/12585191. Myrrh is used in Chinese herbalism to speed tissue healing, and British research has revealed that it is able to increase dopamine-beta-decarboxylation.

Lack of protection from oxidative stress seems a key to most of theories concerned with the gradual worsening of these parts of the brain. Oxidative stress may increase due to accumulations of toxic heavy metals in the tissues, misshapen proteins, or sticky plaque, accumulation, or excess stimulation of G-protein second messengers by adrenal hormones or other hormonal imbalances. These are just some of the metabolic stresses that result in excess metabolic oxidant free radicals and require increased antioxidant metabolism to clear. For instance, transient ischemic attacks, or TIAs, often go unnoticed in the population, and studies reveal that the amount of neural cell death that results may occur over a number of days, and is related to the lack of antioxidant protection in different areas of the brain. Lead and mercury toxicity has been proven to cause neurodegeneration, and is an ubiquitous environmental toxin due to the tons of organic small particle lead and mercury pollutants that enter the air from coal fired power plants. Levels of glutathione and SOD are key to neuroprotection in these cases. Restoration of antioxidant metabolism is the first step in a long course of therapy necessary to finally achieve a potential reversal of neuron cell death and return of function. In utilizing Complementary Medicine for these neurodegenerative problems, much patience is required. Some symptom relief can potentially be achieved quickly, but most improvement will be noted over a long period of time.

Lifestyle, Diet and therapeutic regimens may be a key to successful prevention and therapy for neurodegenerative disorders

Healthy diet and exercise routines are very important in the prevention of Alzheimer's and Parkinsonian neurodegeneration, and possibly for other neurodegenerative diseases as well. As we age, or acquire health problems that could lead to a more serious neurodegenerative condition, we should increase our focus on an effective and efficient daily exercise routine and improve our diet. A Harvard study showed that the most physically active men cut their risk of acquiring a Parkinson's syndrome by 50%. Women showed a more modest beneficial effect from a lifestyle that included daily exercise. A University of Pittsburg study showed how exercise prevented degeneration of nerve cells that are normally destroyed by disease. Researchers concluded that increased oxidative metabolism was probably responsible for the mitochondrial preservation within the nerve cells. A diet rich in antioxidants along with a routine of simple exercise is thus a key in neurodegenerative medicine.

A 2010 study by Columbia University in New York followed 2,148 older adults in Manhattan with an average age of 77 years, for four years. None of these subjects had dementia, or signs of neurodegeneration, at the beginning of the study, but 4 years later 253 had been diagnosed with Alzheimer's disease, which is an amazingly alarming percentage (over 10%). Of course, these people did not just suddenly acquire neurodegeneration, as this is a very slow process, and we can also assume that a much greater percentage of the subjects had a level of neurodegeneration that did not result in a full Alzheimer's diagnosis. The study followed the diets of this diverse cross section of the population. It found that those persons that ate a diet with sufficient dietary folates, essential fatty acid balance, and Vitamin E metabolites fared well, while those who ate more red meat, organ meat (lunch meats), and fatty dairy products fared poorly. The study concluded that a diet rich in dark, leafy green vegetables, oil and vinegar dressings on salads with hearty greens, fresh nuts, fish, poultry, and fresh fruit lowered the risk of Alzheimer's by over 30 percent.

A University of Toronto study of carbohydrates and cognitive function found a 37% increase in memory and cognitive function occurred in a group of subjects that ate a porridge of barley each morning. Simpler carbohydrates resulted in short lived memory and cognitive benefit. Complex carbohydrates may thus be very important to supplying your brain with the necessary chemicals for neuronal health. While barley may be difficult for many to incorporate into their breakfast diet, steel cut oats, amaranth and various whole grains can be made into delicious warm cereal porridge. Barley sprout powder can be used as a morning supplement, slowly pouring a tablespoon of the powder into warm liquid in a blender. Research concerning the effects of Ritalin on increased memory, cognition and control of hyperactivity in the brain showed that this drug increased glucose metabolism in the brain by 50%. It is suggested that an increased level of glucose bioavailability from a complex carbohydrate diet could achieve similar results.

Omega 3 fatty acids are also important to incorporate into the diet. Studies of Parkinson's patients found a consistent imbalance between Omega-6 and Omega-3 fatty acids in key areas of the brain. Deficiency of the Omega-3 DHA and EPA were common, and linked to various theories of metabolic dysfunction concerning inflammatory regulation and lipid peroxidation. DHA and EPA mutually support each other in the function of vascualar renewal, and deficiency could result in a poor vascularization that contributes to neural cell death or poor neural receptor function. DHA is essential to brain development and growth, and deficiencies have been linked to poor fetal development of brain function. These essential fatty acids are obtained from both foods and supplements. Various fatty ocean fish, as well as some fresh water fish are high in these EFAs, and this preformed DHA increases level more quickly than the foods and herbs rich in alpha-linolenic acid, but this latter class of foods is more commonly eaten and dietary changes incorporating these foods is recommended. The DHA levels rise more slowly from foods and herbs containing the Omega-3 alpha-linolenic acid, but the eventual change may be more dramatic.

Scientists long invested in treatment of populations with malnutrition of Omega-3 and Omega-6 fatty acids highly recommend using a combination of fatty fish with spirulina, blue-green algae and chlorella, which are rich and balanced with these nutrients. Salmon, mackeral and sardine are the fish highest in Omega-3 fatty acids. Trout, herring, anchovy, butterfish and tuna are also high in content. Various cooking, baking and salad oils are high in content, including pumpkin seed oil, and toasted walnut oil. Tempeh and dark, leafy green vegetables, such as collard greens, spinach, kale, chard, some endives, etc. are also rich in alpha-linolenic acid, the precursor to the DHA and EPA. Herbs such as digupi, and xuanshen that clear deficiency heat, and chaihu and cheqianzi, which benefit the liver and kidney, as well as duhuo, sangshen, gouqizi and nuzhenzi are all commonly used in TCM formulas and are rich in linolenic and linoleic acids. Nutritional benefits are one of the side effects of Chinese herbal formulas, a beneficial side effect.

Studies have also shown that excess alcohol consumption is proven to have a detrimental effect on the mitochondrial function of neurons. It is strongly advised that alcohol consumption be kept to a minimum in these disorders. Often, the habitual alcohol consumption increases with the neurodegenerative disorders, since depression and anxiety often result. The informed patient will find healthier means of calming anxiety and dealing with depression. Here, too, herbs, acupuncture, and nutrient medicine can help the patient deal with these problems and ease the elimination or reduction of alcohol consumption. This does not mean that all bits of alcohol must be eliminated, though. Many herbal chemicals need to be extracted into an alcohol medium, or tincture, to be effective, and small amounts of alcohol pose no risk of ill effects.

Key herbal and nutrient medicines in the treatment of neurodegenerative disorders

Unlike synthetic pharmaceutical medicines, herbs usually contain a long list of synergistic chemicals that help your condition in a variety of ways. In this section, key herbs will be explained, but many of the beneficial actions of the numerous chemicals in the herbs will not be explained due to the need for brevity. Of course, in this complicated subject, brevity is a relative term. If you want, you may do further research on the herbs and chemicals contained within the herbs yourself. Often, a small group of herbs and nutrients will be listed in the description of the herb or nutrient, so that you may see how to increase the potential of treatment with a small formula of substances. Of course, therapy guided by a knowledgable professional will achieve the best results, tailoring the treatment to the individual, and proceeding step-by-step in a logical manner to achieve medical goals. Despite the large number of products needed in neurodegenerative therapy, which is a drawback that discourages most patients, those patients that proceed with herbal and nutrient therapy patiently and persistently are thrilled with the results over time.

Is there evidence that herbal medicine really works in the treatment of Parkinson's and neurodegenerative diseases? A growing body of evidence is proving that herbal medicine can work in a variety of ways to reverse neurodegenertion. There are currently 158 scientific citations on the NIH website PubMed concerning herbal medicine and Alzheimer's disease. See some of this great body of evidence by clicking here: http://www.ncbi.nlm.nih.gov/pubmed/18719316 and here: http://www.ncbi.nlm.nih.gov/pubmed/18324353?

Chinese medical schools and research institutes have been studying the pharmacology and efficacy of Chinese herbal treatments. A review of the promising integrative therapies in 2007 from the Institute of Neurosciences at the Fourth Military Medical University in Xi'an, China stated: (click to link to the U.S. PubMed database PMID: 17691984) http://www.ncbi.nlm.nih.gov/pubmed/17691984 Each year the science of herbal pharmacology progesses exponentially, although economic interests in the United States continue to promote an idea that the science of herbal medicine is still undeveloped. Below is some explanation for the various strategies that have been found useful in the therapeutic protocol.

• Essential nutrients for cognitive function and nervous system health: patients with neurodegenerative disorders should start with a period of replenishment of key nutrients that may be deficient and thus necessary to reverse the disease. You do not need to take these nutrients constantly or forever, but replenishing the body's store and metabolism may be essential to the success of therapy. Vitamin B6 has been found to be deficient in 50% of the U.S. population, and is essential for dopamine production. Choline is necessary for proper transmission of nerve impulses and is a key component of the cholinergic system, as well as fatty acid metabolism in the neural mitochondria. Phosphatidylcholine is an active metabolite of lecithin, and has been proven in human trials to decrease neurodegenerative disease. To utilize choline as as supplement, inositol, Vitamin B12 (sublingual high dose), folic acid, and Vitamin B complex are essential. Inositol hexacotinate is a Vitamin B3 (no flushing effect), and is the preferred type of inositol in this type of therapy. Choline as a food source is available in egg yolks (lecithin source as well), legumes, milk, soy and whole grains, and the taking of choline and inositol supplement with these foods is recommended. DMAE, or dimethylaminoethanol, is another supplement that stimulates production of choline by the brain cells, and also may be very useful. Lecithin, a B Vitamin, is also helpful to increase choline bioavailability, and to aid nerve transmission. The Glutamic acid metabolism is a necessary part of the central nervous system function and GABA regulation, and is best enhanced by taking a combination of L-Glutamate, niacinamide and Vitamin B6 with Choline and inositol (or the combination of P5P, L-glutamine, and inositol hexacotinate). A complete essential nutrient formula may include Choline (phosphatidylcholine), inositol (inositol hexactinate), Vitamin B6 (P5P), L-Glutamine, Vitamin B12 (sublingual or intramuscular injection), folic acid (5MTF is the active form), DMAE and lecithin (phosphatidylcholine). Foods that are dopaminergic include steel cut oats, fermented soy (tempeh), lentils, barley, rice, alfalfa, avocado and fenugreek. A quality dried barley sprout supplement is highly recommended for its array of beneficial chemicals, which include three types of anti-inflammatory biologics, chlorophyll, PD41 and mucopolysaccharides, as well as being a rich source of healthy proteins, enzymes and Vitamin A. Barleygrass sprouts also contain SOD, super-oxide dismutase, to help clear heavy metal toxicities and their oxidant free radicals.
• Omega-3 Fatty acids, EPA and DHA: a 2007 study listed below confirms that these essential fatty acids are often deficient in the Parkinson's, Alzheimer's and ADD patients studied. A study published in the medical journal Neurology in 2012, headed by Dr. Nikolaos Scarmeas of Columbia University, showed that a broad population study confirmed that individuals with a dietary deficiency of omega-3 fatty acids had significantly higher levels of the problematic beta-amyloid proteins AB40 and AB42 in circulating blood plasma, despite differing levels of saturated and monounsaturated fats, omega-6 fatty acids, and other key nutrients. An excess of the Omega-6 essential fatty acids in our diet (usually due to a high intake of red meat) contributes to a dysfunction of the cells and inflammatory regulation in key areas of our brains, but the key point in this study is that the stripping of omega-3 fatty acids in commercial oils and transfats may be largely responsible for the increased problematic beta-amyloid proteins that comprise the core of brain plaques in Alzheimer’s patients. The Omega-6 fatty acids should be balanced with Omega-3 for optimal health of the metabolism in neurodegenerative disorders, but the inclusion of fats and oils with omega-3 fatty acids, and a decrease in consumption of processed foods, fast foods and transfats is perhaps the most important factor related to problematic beta-amyloid proteins. A relative deficiency of Omega-3 fatty acids may impede membrane fluidity at the dopamine receptor sites by allowing stiff membranes to form. The best source of Omega-3 fatty acids, DHA and EPA, is krill oil, concentrated and possessing a natural preservative, unlike fish oils and flaxseed oil. EpaQ by Health Concerns is recommended. This oil is so concentrated in the right type of essential fatty acids that just one or two small capsules per day is needed, instead of the tablespoons of fish oil required. If you are a vegetarian, or vegan, you may have a deficiency of omega-6 fatty acids. The balance of omega 3 and 6 is essential to optimum health. A healthy source of omega-6 fatty acids are the algaes, spirulina, chlorella and blue-green algae (chlorella is also effective as a chelating agent to clear heavy metal accumulations).
• Rhodiola rosea or Hong jin tian: imnproves dopamine optimization and serotonin bioavailability. Dopaminergic herbs include Muira puama, Murcuna pruriens, Salvia miltiorrhiziae (Dan shen), Alismatis orientalis (Ze xie), and Uncaria tomentosa (Gou teng or Cat's claw). Dapamine receptor sites will be enhanced through the nutrient Sam-E. Dopamine is a neurotransmitter that accounts for 90% of the catecholamines in the nervous system and is a precursor to norepinephrine and epinephrine, key adrenal neurohormones. Adrenal insufficiency could result in increased demand for dopamine as a precursor. Adrenal health can be enhanced by the use of a small formula called Adrenosen, from Health Concerns, that contains PKA, barley sprouts, wild mountain yam, schizandra berries and the hyacinth bean. In women, copper is in greater demand, and is sometimes deficient. The catecholamine oxidative metabolism of dopamine in the citric acid cycle of mitochondrial health, as well as oxidative conversion to norepinephrine, is dependant on a copper-containing enzyme, dopamine beta-monooxygenase. Copper in the diet is derived from organ meats, some seafood, dried beans, quality nuts and whole grains. Copper supplementation must include cofactors of zinc methionine (Opti-zinc) and folic acid to assimilate, but the 2.5 mg copper supplement (in the form copper amino acid chelate) should be taken about 2 hours after the zinc supplement to avoid competition in absorption. Rhodiola, muira puama, Cat's claw, SamE, Adrenosen formula, Essential Minerals, and zinc monomethionine (OpticZinc) would provide a course that is sure to improve dopamine optimization.
• Uncaria Tomentosa or Cat's Claw: uncarine alkaloids (the Chinese herb Gou teng is analagous) have been studied and found to exert a beneficial effect on memory impairment induced by cholinergic dysfunction. Cat's claw is also dopaminergic and stimulating of the glutamate metabolism. Maca has been studied as a synergetic herb used in combination with Cat's claw to achieve enhanced effect (maca also contains uridine, an essential cofactor for mitochondrial neural glucose usage). Alpha-glyceryl-phosphoryl-choline, or Alpha-GPC, also aids the cholinergic system, acting as a precursor to acetylcholine, or ACh, and has been proven in studies to enhance memory and cognitive function. Inositol and Choline are often useful to enhance the treatment of cholinergic dysfunction, allowing for greater bioavailability of choline. To enhance assimilation of Choline, inositol, Vitamin B12 (sublingual large dose), folic acid, Vitamin C, and Vitamin B complex are helpful cofactors. Alpha-GPC is available in the Health Concerns product called Cogni-Spark.
• Resveratrol, an active chemical found in the Chinese herb Polygonum cuspidatum, or Bushy knotweed, Hu zhang: this antioxidant is now well known and utilized, even by M.D.s, to protect dopamine neurons from degeneration. Patients report significant benefit soon after starting the herbal supplement. Perhaps due to this success there is now a plethora of misinformation about this chemical. Many doctors tell their patients that the chemical is extracted from red wine or grapes, when all studies show that the amount of this chemical in red wine is very small, and the companies marketing this herbal supplement obtain the chemical from the Chinese herb Polygonum cuspidatum. Newer studies cite the poor absorption of reservatrol from red wine and grapes to counter it's success. The truth is that a concentrated supplement from the herb prepared properly, or an extract in an alcohol tincture is effectively absorbed and utilized by the human body. http://www.herbalextractok.com/Herbal-Extract/Resveratrol-extract.html
• Huperzine and Vinpurazine, from Clubmoss and Vinca Periwinkle: studies in Shanghai confirm that huperzine works better than tacrine or E2020 (the analogous drug used in the U.S. is Aricept), chemical anticholinesterases, to enhance memory and reverse neurodegeneration. The first group of drugs approved by the FDA to treat mild to moderate Alzheimer's are the acetylcholinesterase inhibitors, and huperzine is one of six herbal chemicals in Chinese herbs found to have significant anticholinesterase effects in scientific studies, and is also approved by the FDA now. http://www.find-health-articles.com/rec_pub_18573242 The Health Concerns product Vinpurazine combines these two herbal chemicals with rosemary extract to form a potent combination, which also clears excesses of chronic inflammation in the CNS cells. A companion formula to aid function and maintenance of brain cells is called CogniSpark, consisting of L-alpha-glyceryl-phosphyl-choline (Alpha-GPC), which should be taken with L-carnitine and R-lipoic acid before 6 pm. The benefits of Huperzine A have been found to be broad, with significant acetylcholinesterase inhibition, antioxidant effect, modification of the amyloid beta pathway to decrease tangles, and enhancement of the beta-catenin pathway of neurovascular regrowth and cell adhesion.
• Trypterygium wilfordii or Lei gong teng, and Scutellaria baicalensis, or Huang qin: studies have confirmed that these herbs will protect dopaminergic neurons from inflammatory processes and inflammation mediated damage by inhibiting microglial activation of inflammatory mediators. Many citations of research published by the NIH on the PubMed research database show significant benefit from Trypterygium wilfordii. PMID 12504865 shows that the herb is found to benefit dopaminergic degenerative neurons. PMID 16989518 shows that there is some mild toxicity to the herb and should be used only with professional guidance, but that it contains alkaloids useful in chronic inflammatory states. PMID 16989518 shows that safety and efficacy has been confirmed in human clinical trials in the United States and abroad. PMID 17240858 shows that the herb inhibits key inflammatory cytokines that are linked to chronic inflammatory states. There are many beneficial chemical effects of Trypterygium, including immunomodulation and the inhibition of TNF-alpha, and IL-12, cytokines suspected in the cause of many cases of neurodegeneration.
• Alpha Lipoic Acid plus L-Carnitine: this combination will aid mitochondrial efficiency and clear buildup of sticky proteins that have been linked to Parkinson's and Alzheimer's pathologies. Sticky proteins are misshapen beta-amyloid extracellular plaque deposits, sometimes called tangles. Causes of the misshapen lipoproteins may be linked to toxic heavy metal accumulation, such as alumninum from cookware, along with accumulations of oxidant free radicals as the body tries to clear this accumulation. ALA helps to neutralize the effects of free radicals by enhancing the antioxidant benefits of Vitamins C, E, and glutathione. Carnitine is a B vitamin with a chemical structure similar to amino acids, whose main function is to help transport long-chain fatty acids, and also enhances the antioxidant effects of Vitamines C and E. Carnitine is produced in the body if sufficient amounts of B1, B6, lysine and methionine are available, and Vitamin B6 deficiency is common in the population. Vegetarians are more susceptible to deficiency, and a chief symptom of deficiency is confusion. The combination of these two nutrients helps antioxidant maintenance of neuron mitochondria as well as prevention of unwanted lipid proteins called sticky proteins, which are the subject of much research into the pathophysiology of Alzheimer's. Research has revealed that R-Lipoic Acid may be more effective, and Carnitine is included in the product Neuron Growth Factors (Vitamin Research).
• SAMe, or S-adenosylmethionine, converts to methionine at D4 dopamine receptors sites, which becomes part of the healthy beta-amyloid protein structure at dopamine receptors. Dopamine receptor sites also need 5MeTHF, a folate and methyl donor for homocysteine, to methylate phospholipid membranes, and allow for healthier fluidity, or transport of molecules, across the membranes of dopamine receptors. 5MeTHF is deficient in the livers of patients with riboflavin, or Vitamin B2 deficiency, which is another common deficiency in the population, especially for patients who have used oral contraceptives, consumed excess alcohol, taken prolonged courses of antibiotics, or engaged in strenuous exercise. One of the signs of B2 deficiency is slowed mental response. 5MeTHF may also be deficient if the body has a folate deficiency, and dietary folic acid does not satisfy the demand for natural folate metabolism. A Vitamin B12 deficiency, also common in the elderly, contributes to this metabolic neurodegeneration. A combination of SAMe, Vitamin B2, B12 methylcobalamin, and 5MTHF folate is recommended to reduce sticky proteins and stiff membranes at dopamine receptor sites to insure healthier metabolism. To reduce beta-amyloid (Abeta) accumulation, or sticky protein plaques, the chemical S-allyl-L-cysteine from water extract aged garlic has also been proven effective. Astra Garlic is a formula from Health Concerns that is a synergistic blend of herbs for this effect. The Chinese herbs Yu jin and E zhu (curcuma zedoaria), which contain curcuma, have also been proven to break up and prevent beta-amyloid plaque accumulation. Regeneration is a formula from Health Concerns is a formula that contains curcuma and has a blend of herbs that could greatly benefit the Alzheimer's patient. Since the effects of curcuma are dose dependant, the herbalist sometimes prescribes a decoction of curcuma for a period of time, and this decoction has the added benefit of aiding digestion by increasing stomach and pancreatic secretions and bile flow, as well as being a proven anti-cancer agent. Short courses of these supplements and herbs may have a significant effect on neurodegeneration.
• Bioflavonoids, such as are found in Gingko biloba and many Chinese herbs: there are many bioflavonoid chemicals in the body, including quercetin, rutin, hesperidin, and eriodictyol, and bioflavonoids cannot be produced by the body, and are thus called essential nutrients. Depletion of our soil chemistry by modern farming methods has resulted in widespread deficiencies of bioflavonoids, which are linked to neurodegenerative disorders. These nutrient chemicals are important in microcurculation, antioxidant clearing, and cellular metabolism. A number of herbs are rich in bioflavanoids, which account for much of their success in therapy, the most well known being Gingko biloba. It is recommended that you ingest a variety of bioflavonoids to insure success. I recommend the herbal formula Flavonex, from Health Concerns, along with a tincture of fresh Gingko biloba leaf, and a diet that includes organic oranges, lemons, grapes, dried apricots, dried cherries, black currants, bell peppers, and dried buckwheat sprout powder. Vitamin C is an excellent cofactor to bioflavonoids, and the supplement formula Astra C, from Health Concerns, is highly recommended a part of the flavonoid regimen.
• Antioxidants, especially CoQ10: Coenzyme Q10 is a vitaminlike substance that is also called ubiquinone, because it is needed by most cells in the body, hence ubiquitous. This chemical is essential to mitochondrial function and oxidative processes, and has long been an important part of standard medical therapy in Asia for treatment of Parkinson's, Alzheimer's and other neurodegenerative diseases. CoQ10 also aids circulation and microcirculation, stimulation of the immune system, prevention of cell aging or cell death, and tissue oxygenation. Deficiencies of CoQ10 are common, and are linked to such diseases as muscular dystrophy. Deficiencies may be caused by a number of common pharmaceutical medicines, including the cholesterol lowering statins, beta-adrenergic inhibitors prescribed for hypertension, tricyclic antidepressants, and anti-diabetic sulfonylurea drugs. More than 12 million patients are prescribed CoQ10 in Japan by their medical doctors. CoQ10 supplements vary considerably in quality and bioavailability, and enhanced forms, as well as sublingual powders are available. CoQ10-H2 is a form that is much better absorbed and significantly more active as a metabolite. CoQ10 is oil soluble and best taken with fatty or oily foods, especially sardines, mackerel and salmon, which contain the highest amounts of CoQ10 in foods. Peanuts, beef and spinach also contain CoQ10. Taking CoQ10 supplement with Krill oil, a potent source of essential fatty acids, especially EPA and DHA, or omega 3 and 6, is recommended as well.
• Other antioxidants proven to protect dopamine neurons: epigallocatechin gallate in tea (camellia sinensis), especially quality green tea, is effective. Super oxide dismutase, or SOD, is a potent antioxidant the clear superoxides, which are a more harmful type of reactive oxygen species. A short course of copper/zinc SOD may be helpful, if you can find this supplement, but SOD is found in abundance in dried barleygrass powder, and this may be an easier supplement to find. Numerous large studies also point to the positive effects on memory from intake of barley, and properly prepared dried barleygrass contains an array of nutrients that make it a superfood. Gingko biloba standardized extract EGb761 was shown to be significantly neuroprotecive of dopamine depletion. Go to my article on antioxidants to learn more.
• Glutathione metabolism and the nutrients needed to insure health: a deficiency of glutathione function is linked to many types of oxidative stress, and oxidative stress in the mitochondria of key nerve cells is a major part of the neurodegenerative process. To insure a strong glutathione metabolism it is recommended that liver function is optimal, and that a number of nutrients that are precursors to cellular glutathione metabolism are available in the body. These include, L-glutamate, N-acetyl-L-cysteine, and L-glycine. B12, active folate (5MTHF), and methylselenocysteine are also some of the essential aids to restoration of glutathione metabolism. Milk thistle and Schizandra berry are also beneficial to the glutathione metabolism of the liver. Studies of stroke patients revealed that those with deficient glutathione metabolism had a marked increase in oxidative damage in the hippocampus and corpus striatum. Excess glutamate metabolism may be responsible for some cellular damage in acute ischemic stroke, as the chemical floods the cells. In chronic pathology, it is believed that poor conversion of glutamate to glutathione may be responsible for excess glutamate metabolism. Simple taking of glutamate is a problem, and promoting of an improved glutamate metabolism is often needed, which is more complicated. Glutamates such as MSG, or monosodium glutamate, are now common in the food industry, and have resulted in the human organism acquiring specialized glutamate receptors in the brain and brainstem, often which interfere with normal brain function. To understand the key ways to restore glutathione function in your cells, and to understand how the glutamate metabolism may be made healthier and functional, you may refer to my articles entitle Glutatione Metabolism: restoration and function, as well as the article entitled Brain Health and Function. Unfortunately, helping your cells to detoxify and reverse excess oxidant stress is not a simple process, but it may be an essential task with neurodegenerative disorders.
• L-Tyrosine: this amino acid is a precursor to dopamine and norepinephrine, which regulate mood and muscle firing, and are the key neurotransmitters deficient in function in Parkinson's and other neureodegenerative disorders. Tyrosine is used extensively by the thyroid gland and attaches to iodine to form thryroid hormones. Hypothyroid states, as well as deficient iodine states, could be related to deficient tyrosine, and this supplement could be a key part of therapy in both neurodegenerative disorders and hypothyroid dysfunction. Food sources include almonds, avocadoes, bananas, dairy, lima beans, pumpkin seed, and sesame seed. L-Tyrosine supplements should be taken with high carbohydrate meals, such as breakfast porridge, or with a small snack at bedtime so that the intake does not compete with other amino acids in the diet. Studies have demonstrated that increased tyrosine bioavailability can enhance dopamine synthesis in and release from nigrostriatal neurons if the firing rates of these neurons are accelerated, as in more advanced cases of Parkinson's degeneration, where the surviving cells are found to fire at increased rates to compensate. (Proc Natl Acad Sci USA 1980 Jul;77(7):4305-9 6254020 (PSGEB) E Melamed, F Hefti, R J Wurtman). As with all amino acids, concurrant use of active Vitamin B6, or P5P, will also enhance absorption and utilization.
• R-Lipoic Acid: R-Lipoic Acid is rightly called the ‘mitochondrial antioxidant’, and many scientific studies (cited below) demonstrate its role in preventing or decreasing depletion of glutathione antioxidant compound (GSH). Lipoic acid is one of the most thoroughly investigated dietary supplements and most healthcare practitioners agree it is a preventive supplement of choice. R-Lipoic Acid is a more potent form – the more biologically active form – of alpha lipoic acid. As such, it offers more benefit with a lower dose. Lipoic acid serves to regenerate vitamins C and E, and helps maintain glutathione levels, a vital cellular antioxidant and liver protectant. It is a vascular and neuroprotective agent. The effects of R-Lipoic acid may occur after weeks of taking this supplement due to the positive indirect effects it produces.
• 5HTP: there is some link between the serotonergic fibers in the striatal tissues of the basal ganglia and dopamine conversion and production in these 5HT (5-hydroxytryptophan) fibers in scientific study. Taking the 5HTP supplement (from Griffonia seed) may aid the dopamine metabolism. Study on animals found that the drug L-Dopa may be converted to dopamine within the 5HT fibers, and 5HTP possibly has some effect that may enhance the effectiveness for patients taking L-Dopa. 5HTP is also a precursor to melatonin, which is proven to be a potent neuroprotector for dopamine neurons. Both the amino acid L-Tryptophan, and 5-HTP, are precursors to serotonin and melatonin, and 5-HTP is able to pass the brain blood barrier to provide increased bioavailability of these important neurotransmitters. To enhance this metabolic bioavailability further, a blend of low dose 5-HTP, melatonin, P5P and St. Johnswort extract is recommended (re: Positrol from Vitamin Research).
• St. John's Wort, Hypericum perforatum: this much maligned but effective herb has been both proven safe for use and effective in the treatment of Alzheimer's and neurodegenerative disease. Prior reports that chemicals in St. John's Wort could alter levels of other pharmaceutical medications through competition in liver catabolism of the P450 enzyme pathway were shown to be overblown. Studies revealed that the effects of chemicals in St. John's Wort were modulatory of liver function, and that effects on the P450 enzyme pathway were modulated and normalized within two weeks of use to achieve a homeostatic effect despite catabolic competition from harsh pharmaceuticals. This was accomplished because a variety of chemicals in hypericum act to improve liver function. Of course, this also implies that the whole herb extract, and not pharmaceutical products with just the active ingredient enhanced, should be used. To see the current research on St. John's Wort, click here: http://www.ncbi.nlm.nih.gov/pubmed/16880827
• Topical progesterone and pregnenelone creams: studies show that progesterone modulates dopamine release in the corpus striatum and the pregnenelone could modulate the dopamine transmission in the corpus striatum by causing changes in the activity of tyrosine hydroxylase and/or in the pre- and post-synaptic dopaminergic terminals. This neurosteroid mechanism could be a new kind of neurotransmitter systems modulation affecting dopamine metabolism significantly. (Neurol Res 2007 Jan 16; 17535560 (PGSEB)). Since estrogens also are integral to neuron mitochondrial health, estriol cream may also be useful. Use of these simple bioidentical hormone therapies could have significant effect, especially if there is a progesterone and estradiol deficiency. Testing and administration should be overseen by a professional, as we want to utilize low doses of bio-identical hormone creams, and do so in a balance manner. These same hormones may have negative impact if too high of stimulation is suddenly introduced in a neurodegenerative patient. Studies reveal that hormonal deficiencies are the key to the beginning of the neurodegenerative process, so patients should try to maintain healthy hormonal homeostasis as they go through menopause and andropause. These simple herbal products could be the key to prevention.
• Vitamin D3 cholecalciferol: recent studies of Parkinson's patients found a significantly increased incidence of Vitamin D3 hormone deficiency over the general population, which also shows a high rate of deficiency in this important hormonal chemical (85% in some studies). While these results are not highly significant at this stage of investigation, supplementation with cholecalciferol might help the neurodegenerative patient. Cholecalciferol Vitamin D3 is the prohormone, and is generated each day in our skin with exposure to midday sunlight for 5-10 minutes. Take the pills or liquid D3 in the morning with breakfast, and also go for a walk in the midday sunlight with the face and arms exposed each day. D3 supplements are still of relatively low dosage, and both supplements and sun exposure without sunscreen is recommended. Even these methods, though, may not be enough, as the endproduct hormone D3 is dependant on healthy kidney and adrenal function. A complete regimen, with both supplementation, sun exposure, and a combination of acupouncture and herbal medicine to insure improved kidney and adrenal function is recommended.
• Herbal formula to enhance brain circulation: circulatory aids are helpful both for brain circulation, as well as peripheral circulation in Parkinson's. Circulatory aid is beneficial to improve cognitive function, repair of the nervous tissues, increased benefits from the other herbal and nutrient medicines, and peripheral circulation. I recommend Cir-Q from Health Concerns. A number of professional herbal formulas address the stimulation of increased circulation in the brain, as well as cognitive and mood benefits, though, and the Licensed Acupuncturist and herbalist is able to provide an individually tailored herbal formula for each patient.
• Red Mold Rice extract: a number of polylipids from specific fermented grains have been proven to affect lipid metabolism in a healthy way and now show promise in the treatment of Alzheimer's. A combination of effects, including reduction of amyloid beta-peptide plaque, called neurofibrillary tangles, as well as various antioxidant and antiinflammatory mechanisms were found in this herbal supplement. I prescribe the Health Concerns supplement Polylipid, as well as Red Mold Rice extract. This common nutrient food and natural food color in China was the source for the statin drugs created to lower cholesterol. To review the research, click here: http://www.ncbi.nlm.nih.gov/pubmed/18438657
• Endocannabinoids: research around the world has confirmed that cannabinoids are not just chemicals found in marijuana, but actually are important chemicals used by the brain to regulate excessive activity of dopamine neurons in the corpus striatum. Studies at numerous universities found that patients that had used marijuana for some time in their life had a 30% decrease risk of acquiring Parkinson's. Stimulation of endocannabinoid cellular production, as well as the bioavailability of endocannabinoids from hemp seed in the diet, are being explored by scientists today. It could be that a topical cannabinoid cream that is oil based is the answer to immediate effect. Such a cream has been developed in England and is used to decrease neuralgia. Unfortunately, U.S. pharmaceutical lobbying has prompted the FDA to delay approval on the U.S. market of this benign topical medicine. There is no connection between the drug effects of THC in marijuana and this valuable herbal medicine.
• Anticholinergic herbs: sometimes cholinergic dysfunction in Parkinson's can be calmed with anticholinergic chemicals, which have been used successfully at times by modern medicine. This treatment protocol runs counter to the anticholinesterase protocol, but in some cases has reduced acute symptoms related to cholinergic nerve stimulation. Some herbs have both anticholinergic chemicals and anti-cholinesterase chemicals, implying a modulatory effect on the cholinergic system. These effects will be milder than those produced by synthetic anticholinergic chemicals, but will have no side effect. The herbs that contain anticholinergic chemicals include the mulberry parts, leaf, bark, stem, and fruit, called Sang ye, Sang bai pi, and Sang shen, as well as Corydalis, or Yan hu suo, and Artemesia abrotanum, or Southernwood. Horse chestnut bark also contains an anticholinergic, and is beneficial for the health of the veins and veinous circulation. This herb is found in the Health Concerns formula, Formula V, along with butcher's broome and stoneroot. Some antichonlinergic herbs contain scopolamines, and are a little toxic, thus are rarely used, and monitored professionally. These include Jimsonweed and Anisodus tanguticus, or Zang qie. This type of therapy may be indicated for more advanced cases to control symptoms.
• Immunomodulating herbs: recent research in neurodegenerative disease has led us to discover how the immune system is directly involved in a complex process leading to the persistence of degenerative failure of the process that protects our brain cells and glial support. While genetic research has failed to find specific genes that may be affected to reverse this disorder, the genetic research has delivered a lot of information important to therapy. For instance, the neurodegenerative condition called amyotrophic (muscle atrophy) lateral sclerosis (scarring of nerve tissue), or ALS, has revealed that mutations in the gene that produced cellular superoxide dismutase (SOD) results in a deficiency of this important antioxidant mechanism in about 20% of inherited cases of ALS. While no single genetic mutation has been found, 135 different mutations in the gene have been discovered that are associated with the ALS disease process. There is no single pharmaceutical agent that will correct this. The mutations discovered reveal that the SOD enzyme, which normally functions to clear free radical oxidants from the brain cells, now may be causing misshapen proteins in the cell nucleus of the neuron. The cause of the numerous genetic mutations is exceedingly complex, and the immune complement system has been heavily researched to find an imbalance in inflammatory mediators that could be driving these mutations. TNF-alpha is the immune mediator usually involved in driving excess mutations that lead to cancerous cells, and is the target of both much research, and now a novel approach to treatment of neurodegenerative conditions. Herbal research has also revealed how nature has created potent chemicals to modulate the activity of TNF-alpha, both by inhibiting its expression and by modulating the balance of immune chemicals that keep it in check. This highly evolved system of immunomodulation produces effective chemicals that are evolved to be free of the harsh side effects that the man-made chemicals create. A number of herbs are proven effective in this regard, and are now being tried and tested to determine the efficacy.
• Carnosine and AGE block formula: Carnosine is an amino acid that is useful in the treatment for reduction of AGEs, or advanced glycation endproducts, which are implicated both in arterial plaques (atherosclerosis) and in neural plaques in neurodegenerative disease. Research in recent years has found the carnosine exerts potent inhibitory effects of excess glutamate and NMDA neurotoxicity (see link to the research below). NMDA glutamate receptor blockers or antagonists, as well as non-NMDA glutamate antagonists are now a widely used pharmaceutical for the treatment of various neurodegenerative conditions (re: Amantadine and other drugs). Carnosine and AGE block presents a safe and effective form or this treatment to use in the overall strategy.
• Uridine: uridine is a nucleoside (RNA component) that is formed when uracil is attached to a ribose ring in health sugar metabolism. Uridine is an essential component for sugar utilization by neuron mitochondria, and has been touted as an effective aid in neurodegenerative states. Uridine is found in the Chinese Siberian ginseng, as well as the Peruvian herb Maca, and is now widely used as a supplement. Neuron Growth Factors (Vitamin Research) combines uridine with other essential aids to neuron health in a formula. Foods high in uridine content include natural brewer's yeast, sugar beets, unprocessed sugar cane or sugarcane extract, and organ meats (e.g. liver).

Information Resources

1. A review of theories and approaches to Parkinson's treatment from the National Institute of Neurological Disorders and Stroke: http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease_backgrounder.htm
2. An August 18, 2010 article in the New York Times outlines the current failures and reasons for failure in new drugs developed to treat Alzheimer's: http://www.nytimes.com/2010/08/19/health/19alzheimers.html
3. An August 29, 2010 article in the New York Times outlines the findings of the recent NIH panel on risks, prevention and treatment of Alzheimer's, finding that there is no pharmaceutical treatment that is effective in prevention or treatment, and no single health measure that is proven to prevent neurodegenerative disease on its own: http://www.nytimes.com/2010/08/29/health/research/29prevent.html
4. A study in 2007 at Texas Christian University found that a combination of factors was responsible for the dopamine depletion and neurological impairment of Parkinsonism, and that research was lacking that explored multiple factors of causation acting synergistically. Here, systemic bacterial endotoxicity producing low-grade inflammatory responses, when combined with a neurotoxin (MPTP), reproduced the dopamine depletion and neurological impairments of Parkinsons, while each individual factor did not: http://gradworks.umi.com/32/75/3275084.html
5. A study in 2007 at Tohoku University in Japan explored the role of liver dysfunction and Metabolic Syndrome in the pathology of Alzheimer's disease. Poor clearance of amyloid beta peptide may contribute to excess amyloid beta accumulation in the brain and deficient LRP (low density lipoprotein receptor protein), which is induced by excess insulin that occurs with insulin resistance and Metabolic Syndrome: http://www.ncbi.nlm.nih.gov/pubmed/17609417
6. A 2009 article by Zina Kroner, DO, medical director of Advanced Medicine of New York, outlines the findings of a succession of research studies demonstrating how insulin metabolism dysfunction and advanced glycation endproducts lead to the progression of Alzheimer’s disease and other neurodegnerative states: http://acam.typepad.com/blog/2010/04/the-relationship-between-alzheimers-disease-and-diabetes-type-3-diabetes-.html
7. A 2010 review of the scientific study of acupuncture and its effects on the brain by Harvard Medical School reveals that correct stimulation and sensation from needle stimulation is proven to significantly effect the brain with an integrated response at multiple levels, especially with evoking deactivation of a hyperreactive limbic to cortical response, as well as activation of key somatosensory areas in the brain. The researchers found that acupuncture mobilizes the functionally anti-correlated networks of the brain to correct such disease states as Alzheimer's, depression, schizophrenia, autism, and chronic pain syndromes: http://www.ncbi.nlm.nih.gov/pubmed/20494627
8. A 2005 study of acupuncture with functional MRI imaging proved that different acupuncture points activated specific areas of the brain. The intelligent choice of acupuncture points, individualized to the patient, as well as the correct stimulation techniques, also individualized and performed with proper patient feedback during therapy, is proven to be very important to treatment outcomes: http://www.ncbi.nlm.nih.gov/pubmed/15876491
9. A 2010 study at the Capital Medical University of Beijing, China, of specific electroacupuncture effects on laboratory animals with Parkinsons disease found that 100 Hz stimulation at specific points normalized the GABA content in specific parts of the brain associated with poor motor control, while not affecting other parts of the brain, exerting GABAergic inhibition in the output nuclei of the basal ganglia: http://www.ncbi.nlm.nih.gov/pubmed/20364891
10. A 2009 study at the Capital Medical University of Beijing, China, of specific electroacupuncture effects on laboratory animals with Parkinsons disease found that 100 Hz stimulation at specific points protected dopaminergic neurons from degeneration in the substantia nigra, and reversed excess substance P and deficient glutamate decarboxylase in the midbrain, showing modulatory affects to restore motor function in Parkinsons disease: http://www.ncbi.nlm.nih.gov/pubmed/19549545
11. The National Institute on Aging (NIA), part of the National Institutes of Health (NIH) maintains an Alzheimer's Disease Education & Referral Center that provides a conservative source of research news and data, as well as referrals to caregivers in your area: http://www.nia.nih.gov/Alzheimers/
12. An excellent overview of the subject of excitotoxins as food additives in a majority of processed foods, and the research links to neurodegenerative conditions, is available at the website of Dr. Russel Blaylock: http://docs.google.com/viewer?a=v&q=cache:Jg9An6V9RJ4J:landofpuregold.com/
13. Published research into the neurodegenerative effects of excitotoxins and altered glutamate molecules in food additives has been paltry, given the evidence of its neurotoxicity. This research article from 1996, at Humbolt University in Germany, confirms the seriousness of this problem, though: http://www.ncbi.nlm.nih.gov/pubmed/8971131
14. The initial research in 1995 at Humbolt University in Germany, shows that strong and specific explanations existed for the link between ecxitotoxins and gradual neurodegeneration, although the only suggestion for remedy by such research is the development of new drugs that act as glutamate antagonists, which were developed due to the soundness of this research, but proved to be problematic in therapy: http://www.ncbi.nlm.nih.gov/pubmed/8845937
15. A 2001 review of the class of drugs called glutamate antagonists, by the Neurological Clinic of RWTH Aachen, in Germany, reveals that this class of drugs are widely prescribed in serious neurological disease, but not found to be effective as a neuroprotective agent in chronic neurodegenerative disease, and come with serious side effects, that include agitation, disorientation, and psychosis: http://www.ncbi.nlm.nih.gov/pubmed/11433698
16. A 2009 mega-analysis of the drug class called glutamate antagonists, found that use of these drugs has fallen with findings of failure to work in clinical studies due to nonselective or competitive antagonism, and serious side effects, such as loss of cognitive function, sedation, and psychomimetic effect. Nevertheless, the subject of glutamate metabolites, and glutamate accumulation in brain tissues, was still taken seriously, and a class of new drugs called NMDA receptor antagonists, and other drugs, were developed and marketed for central nervous system pathology: http://www.ncbi.nlm.nih.gov/pubmed/19538098
17. A 2008 review of Parkinson's research from Australia reveals how a more holistic approach to understanding the pathophysiology leads us to interrealated neurohormonal imbalance and eventual stimulation of hyperplasia due to improper circadian melatonin levels may be responsible: http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=20083925
18. An excellent report on CoQ10 deficiencies is found on the LifeExtension magazine website: http://www.lef.org/magazine/mag2000/july2000_review.html
19. Research publication on progesterone and pregnenelone therapy in relation to dopamine metabolism in the corpus striatum in Parkinson's: http://lib.bioinfo.pl/pmid:17535560
20. Research in 2008 at USC Program in Neuroscience revealed the many ways that normal estrogen levels signal CNS pathways to prevent neurodegeneration, suggesting that restoration of estrogen homeostasis may be a key part to restoring mitochondrial function and neurological health; since estrogen mechanisms may have a negative impact on unhealthy degenerated neurons, a cautious approach is recommended with estrogen therapies: http://lib.bioinfo.pl/pmid:17535560
21. A study by Thomas Jefferson University Medical College in Pennsylvania concerning the efficacy of herbal chemicals as neuroprotective antioxidants, especially reservatrol in Hu Zhang: http://www.ncbi.nlm.nih.gov/pubmed/11897104
22. A 2009 review of the research on common herbal and nutrient medicines widely used to treat Alzheimer's disease, from researchers at the Mayo Clinic Department of Neurology, shows much bias against these medicines, but a grudgingly genuine acknowledgement of their modest proven efficacy and overall safety. We must also realize that no pharmaceutical medicine to date has been proven to have more than mild effectiveness in the treatment of Alzheimer's disease: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731997/
23. Research in 2007 concludes that deficiency in DHA and EPA, or Omega-3 essential fatty acid, is linked to Parkinson's, and that a balance between Omega-6 and Omega-3 fatty acids is essential to Neuronal health.: http://www.medicalnewstoday.com/articles/89928.php
24. A double-blind placebo study of Alzheimer's patients and patients with diagnosis of mild cognitive impairment in 2008 showed that the Omega-3 fatty acid EPA, used alone, produced significant improvement in cognitive function in the patients with mild cognitive impairment and overall improvement in the severe Alzheimer's patients as noted by the clinical physician. EPA and DHA, in krill oil, is thus an effective part of the holistic protocol in treatment of Alzheimer's and neurodegenerative disease: http://www.ncbi.nlm.nih.gov/pubmed/18573585
25. A 2008 study at UCLA Institute for Neurological Research found that the TNF-alpha inhibitor Enbrel (etanercept) exerted potent benefits in reducing neurodegenerative effects with injection around the cervical spine. While this drug is the subject of a number of lawsuits over injury from long term use, a number of Chinese herbs have been proven to have potent TNF-alpha inhibiting effects: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2491668/
26. 2010 research at Harvard Medical School revealed that a genetic link exists between immune disorder and Alzheimer's pathology, with so-called sticky protein (beta-amyloid) generated in response to a variety of pathogens infecting the brain. The problem with such genetic causes are the findings of numerous mutations of the genes involved, and as stated, the effects of various pathogens, environmental chemicals, and epigenetic triggers involved. The research does point to the potential for reduction of pathogens, as well as immunomodulatory effects with Chinese herbs: http://www.nytimes.com/2010/03/09/health/09alzh.html
27. A 2004 study by the Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research found that iron overload, or iron cytotoxicity, was integral to the etiopathology of Parkinson’s disease and other neurodegenerative diseases, both by inducing “sticky protein” accumulation and promoting oxidative stress that may degenerate neurons and inhibit protein regulation in the brain cells: http://www.ncbi.nlm.nih.gov/pubmed/15655262
28. A 2010 article in the New York Times outlines how new imaging techniques are proven to accurately diagnose Alzheimer's disease now, but using a radioactive dye that reveals the amyloid plaques. Misdiagnosis, revealed in autopsy studies, was a huge problem up to now, and resulted in a high percentage of case being given the wrong therapy. This improved diagnosis also helps the provider of integrated Complementary Medicine improve the treatment strategy, and perhaps provide preventative treatment for patients with early asymptomatic stages of Alzheimer's: http://www.nytimes.com/2010/06/24/health/research/24scans.html?pagewanted=2&ref=health
29. The U.S. NIH website provides an outline of the disease mechanism called Alzheimer's and reveals that we are certain that the disease process starts 10-20 years before its manifestation as symptoms. The time to start reversing this neurodegeneration is at an early stage, and the preventative medicine provided by Complementary Medicine physicians such as Licensed Acupunturists and herbalists not only helps prevent neurodegeneration, but is a very healthy form of medical care with many positive benefits and not side effects: http://www.nia.nih.gov/Alzheimers/Publications/adfact.htm
30. In vitro studies in 2007 proved that S-allyl-L-cysteine, found in water extract of aged garlic, inhibited beta-amyloid (Abeta) accumulation, or sticky protein plaques, that are linked to Alzheimer's: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=18023978
31. A 2012 study at Columbia University, headed by Dr. Nikolaos Scarmeas, showed that a dietary deficiency of omega-3 fatty acids was highly correlated with excess levels of problematic beta-amyloid proteins in circulation: http://www.medpagetoday.com/Neurology/AlzheimersDisease/32466
32. A 2009 joint study at Arizona State University and the University of Colorado Departments of Chemistry found that the chemical curcumin, found in the Chinese herbs E zhu, Yu jin and Jiang huang, reduces alpha-synuclein induced cytotoxicty, which is related to the “sticky protein” accumulation of beta-amyloid plaque in Parkinson’s and Alzheimer’s diseases: http:/http://
33. Studies in 2008 revealed that the amino acid Carnosine was effective to reduce glutamate neurotoxicity as well as the reduction of plaques accumulating in brain tissue. Drugs to antogonize glutamate receptors, or NMDA glutamate receptor blockers, are widely used in therapy for various neurodegenerative conditions today: http://www.ncbi.nlm.nih.gov/pubmed/18027086
34. Research in 2010 at the Rensslaer Polytechnic Institute in the United States found that resveratrol, a chemical extracted from the Chinese herbs Hu zhang, was effective in remodeling of 3 types of misshapen proteins found in the brain cells of Alzheimer's patients, and did so in a modulatory fashion: http://www.ncbi.nlm.nih.gov/pubmed/20511235
35. Research in 2001 showed that standardized extract of Gingko biloba, or AGb761 was significantly effective in partial prevention of dopamine depletion of corpus striatum cells subjected to neurotoxicity.: http://www.springerlink.com/content/l18dtptbnlvb6g4e/
36. Research in 2002 at the University of California at Berkeley, The Children's Hospital in Oakland, and the Buck Institute of Aging in Novato, California revealed that R-Lipoic Acid is a potent preventative supplement for neurodegnerative conditions: http://www.sciencedirect.com/science
37. Research at the University of Massaschusetts Center for Cellular Neurobiology and Neurodegenerative Research in 2009 found that a formula comprised of alpha-lipoic acide (R-lipoic acid is the more active metabolite), acetyl-L-carnitine, phosphatidylcholine, phosphatidylyserine, and DHA (an omega 3 fatty acid found concentrated in krill oil) reduced ROS (reactive oxygen species) in the mouse brain with induced neurodegneration by 57% and markedly prevented cognitive decline; another study at the University of Toronto found that phosphatidylserine, Gingko biloba, Vit E, and P5P (B6) markedly increased cognitive function in dog brains: http://www.naturalnews.com/025616_brain_nutrients_supplement.html
38. Research in 2000 showed that neurodegeneration spread from the corpus striatum to the cortex and thalamus over time with the progression of the disease.: http://www.neurology.org/cgi/content/abstract/54/7/1482
39. Research in 2009 at the University of Columbia in Vancouver found that chronic adrenal stress could desensitize serotonergic 5HT receptors in the hypothalamus and cause endocrine suppression. Such findings may implicate adrenal stress in the suppression of dopamine receptors as well.: http://www.sciencedirect.com/science
40. Research in 2005 at the Neuroendocrine Research Laboratory in Budapest, Hungary, revealed that hypothalamic response to stress includes increased prolactin and corticosterone, and that inhbition of the NMDA glutamate receptor decreased these circulating neurohormones, linking the pathology of neurodegenerative diseases, as well as some of the symptoms, to the pathology of deficient hypothalamic function and adrenal stress syndrome: http://www.springerlink.com/content/6653053k623937r1/
41. Research in 2005 at the State University of New York Department of Neurology and Sleep Medicine, coordinated with studies at universities around the world, found that melatonin exerts a potent antioxidant and detoxifying effect in the brain, and deficiency of melatonin in the circadian cycle and sleep disorders may be a primary cause of neurodegeneration.: http://www.springerlink.com/content/m25357432233607m/
42. Research review in Parkinson's treatment approaches in 2007 is outlined in this article and shows that adrenal stress is now a primary focus in study of the pathology, and the the neuroprotective and adaptive approaches of herbal medicine are now being explored by modern pharmacology: http://vml.med.uoc.gr/molmedgp-guide-2007/molmedgp_guide_2007_page_076-080.pdf
43. In vivo studies in 2005 found that curcumin, from the Chinese herbs Yu jin and E zhu (curcuma zedoaria), both broke up and inhibited beta-amyloid (Abeta) accumulation, or sticky protein plaques, that are linked to Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/15590663
44. For a complete research review of Attention Deficit and Hyperactivity Disorder and the complex science of potential causes: http://www.acnp.org/asset.axd?id=26c3b427-a7b2-4e3b-9c5f-8245305786bb
45. A small human clinical trial of Huperzine A, an herbal cholinesterase inhibitor that has shown great benefit in neurodegeneration in clinical trials in China, as well as potent acetylcholinesterase activity in vitro, was conducted at the University of California San Diego School of Medicine, in La Jolla, California. The trial showed modest benefits compared to placebo, with a 2.27 point improvement in the ADAS-Cog scale at 11 weeks versus a 0.29 point decline with use of placebo. This shows that, while Huperzine A does not by itself show a statistically significant benefit, that it compares in statistical benefit to the widely prescribed cholinesterase inhibitor Aricept, which scored a 2.49 difference from placebo. This herbal extract has no side effects, and is combined with a variety of herbs and supplements to increase effectiveness in Chinese Medicine. The mean score at baseline for Alzheimer’s patients on the ADAS-cognitive scale is about 27.: http://www.ncbi.nlm.nih.gov/pubmed/21502597
46. In 2006, the Academy of Sciences in Shanghai, China, released a meta-review of studies of Huperzine A, a constituent of a Chinese herb standardized from a type of Club moss, Huperzia serrata. The findings stres that Huperzine A is an effective cholinesterase inhibitor, but this effect alone will not cure Alzheimer’s disease, and have a limited effect on cognitive function. The alkaloid Huperzine A was also found to exert neuroprotective effects, modify beta-amyloid processing, reduce oxidative stress, protect against early programmed cell death (apoptosis), and regulate expression and secretion of nerve growth factor and NGF signaling. These benefits make Huperzine A an ideal part of a comprehensive long-term treatment protocol, as well as an effective preventive medicine: http://www.ncbi.nlm.nih.gov/pubmed/17056129
47. In 2011, research at China Medical University showed that Huperzine A decreases the amyloid plague tangles and supports the nonamyloidogenic pathway, as well as enhancing the beta-catenin signaling that is important for neural and vascular epithelium, regulating cell growth and adhesion. Huperzine A is shown in animal studies to enhance the Wnt pathway of beta-catenin, which is deficient, or depleted in Alzheimer’s: http://www.ncbi.nlm.nih.gov/pubmed/21289607
48. In 2003, the chemical galantamine, from a Chinese herb Lycoris radiata (Shi suan), was licensed to treat Alzheimer's Disease, exerting significant anticholesterinase activity. This review of scientific study from the Royal Botanic Gardens, Jodrell Laboratory, in Surrey, England, reveals that a number of Chinese herbs have shown pharmacological activities relevant to the treatment of cognitive disorders: http://www.ncbi.nlm.nih.gov/pubmed/12895669
49. In 2011, chemicals in the common Chinese herb Salvia miltiorrhiza (Dan shen), tanshinones and polyphenols, demonstrated remarkable acetylcholinesterase activity in vitro, compared to the drug galanthamine hdrobromide, as well as reducing amyloid beta plaques. This research was conducted at the New Medicine Research and Develpment Center for the Disha Pharmaceutical Group in Weihai, Chinaz: http://www.ncbi.nlm.nih.gov/pubmed/21787715
50. In 2011, chemicals in the Chinese herb Gentiana rhodantha (mangiferrin and rhodanthenone), were found to be effective acetylcholinesterase inhibitors as well, by the Chinese Academy of Sciences, in Kunming, China. The chemcial mangiferrin exhibited a 13.4 percent ACHE inhibitory effect, and is also found in the herbs Anemarrhena asphodeloides (Zhi mu), Gentiana rhodantha, Swertia punica (Zi Hong Chang Ya Cai), and Mangiferrin indica. : http://www.ncbi.nlm.nih.gov/pubmed/22006717
51. In 2003, research at the Shanghai Second Medical University in China found that the Chinese herb Anisodamine (aniso), from the Chinese herb Anisodus tanguticus, ameliorated the side effects of the cholinomimetic drug pilocarpine, a muscarinic agonist used to treat Alzheimer’s, but discouraged due to side effects. : http://www.ncbi.nlm.nih.gov/pubmed/12812833
52. A 2010 study of aging individuals in New York, conducted by Columbia University, found that a diet rich in folates, essential fatty acids and Vitamin E, or rich in dark, leafy greens, hearty salads with oil and vinegar dressing, fresh fruit, fresh nuts, fish and poultry had over a 30% decreased risk of developing Alzheimer's: http://www.nytimes.com/2010/04/20/health/research/20aging.html
53. A type of shitake mushroom, the Yamabushitake (Hericium erinaceus) was proven in a double-blind placebo study in Japan to significantly increase cognitive function in 50-80 year old patients diagnosed with neurodegenerative cognitive impairment, such as in Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/18844328
54. A study in 2010 at the Medical School of Xian Jiatong University in China revealed that a chemical in the herb Polygonum cuspidatum (Hu zhang, the common source of resveratrol) called Emodin, protected brain cells against beta-amyloid neurotxicity seen in Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/20573598
55. Food preservatives, such as benzoic acid, produce oxidative stress and disruption of cellular membranes, and the science is available to utilize healthier alternatives in the food industry to decrease incidence of neurodegeneration: http://aem.asm.org/cgi/reprint/70/8/4449.pdf
56. Scientific study in 2007 uncovered the role of chronic inflammatory cytokines and the link to viral lipopolysaccharides as both a direct stimulation of symptoms of hyperactivity and a major cause of dopaminergic neurotoxicity. Of course, the recommendation was to increase use of corticosteroids that have harsh side effects, but Complementary Medicine offers safe effective alternative to this approach: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2442423

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