Alzheimer's, ADHD, Parkinson’s and other Neurodegenerative disorders

Paul L. Reller L.Ac. / Last Updated: August 03, 2017

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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, and standard medicine has no treatment for early stages of neurodegenerative disease. Integration of Complementary Medicine is sorely needed. The central problem to this type of integrative health care is the complexity of factors that combine to create the pathology in neurodegenerative disorders. Effective treatment with holistic medicine involves attention to all of the contributing health problems that combine to create the neurodegenerative condition. Patient understanding and a proactive approach is vitally important.

In 2013, two large studies of neurodegenerative dementia were published in the esteemed British medical journal The Lancet, clearly showing that rates of dementia have dramatically dropped in the last 2 decades in subsets of the population studied in Great Britain and Denmark. This was attributed to a variety of health factors, or improvements in the general health, diet and lifestyles of this group of aging participants. No specific reasons for this improvement were found in the studies. Experts in the United States, such as Dr. Dallas Anderson of the National Institute on Aging, and Dr. P. Murali Doraiswarmy of Duke University Medical School, hope that these same trends will be shown in the United States, as well. In 2015, research at Duke University Medical School showed that the progression from mild cognitive impairment to dementia appears to progress much faster in women than men, and studies in the UK in 2014 indicated that diagnosis of neurodegenerative conditions in patients between the age of 40 and 60 may be missed in 50 percent of case. There is now widespread agreement that neurodegenerative dementia appear to affect many more women than men, and that both metabolic and neurohormonal factors are key in this phenomenon.

In 2016, researchers at the Harvard University School of Medicine released new findings that low-grade bacterial infections may lie at the heart of the pathology of Alzheimer's disease, with bacterial endotoxins and Pleomorphic bacteria evading the blood brain barrier to enter the brain, especially as this membrane barrier ages, and stimulating a reaction of rapid growth of amyloid beta to inhibit the spread and growth of the microbial infection. Prior studies have shown that amyloid beta protein complexes are used throughout that body as part of the immune response, and that a slow 10-15 year accumulation of amyloid beta plaque leads to the neurodegeneration in the disease. The areas of the brain most affected, such as the hippocampus, are least protected from bacterial endotoxins and Pleomorphic bacteria. Dr. Robert D. Moir began this study to finally explain the formation of amyloid beta plaque, which had been assumed to be due to an unknown genetic defect. Dr. Moir noted that many studies have found that amyloid beta is used by the immune system to trap and contain the growth of many microbial infections, especially from the bloodstream, that are low-grade, and then the white blood cells are able to clear the infection. Dr. Rudolph Tanzi became involved and they found that in laboratory animals that these bacterial toxins stimulated a rapid growth of amyloid beta, especially in the hippocampus. Each plaque had a bacteria in the center. Pleomorphic bacteria are adapted to become smaller and simpler to penetrate membrane immune protections, and bacterial endotoxins are part of the bacterial membrane and survive even when the bacteria itself is destroyed. To clear and prevent these microbial infections we need to take a more holistic approach, both helping the immune system to clear low-grade microbial infections of many types, and to help clear the plaque after it is formed. Simply prescribing more antibiotics will do more harm than good.

There is hope for success for those who adopt a healthier and more holistic approach to prevention and treatment of neurodegenerative disease. The rates of dementia in these studied subset populations in Europe mentioned above were still 6.5 percent of the total aging population, though, and are expected to be higher in the United States. The number of serious cases of neurodegenerative dementia worldwide is expected to more than double by 2050, reaching an expected 227 million clinically diagnosed cases, and the number of cases of mild cognitive impairment (MCI) have been underdiagnosed by half. Since no pharmaceutical medications have been shown to be effective, these experts in Alzheimer's and Parkinsonism that published the above study surmise that a variety of factors concerning improved patient understanding and improvements in holistic health in the last two decades are the reason for this improvement in specific geographic areas in Europe. In 2014, a meta-analysis of health records headed by the University of Cambridge, in the United Kingdom, and built upon data from a prior meta-analysis at the University of California in San Francisco, showed that half of all future cases of Neurodegenerative diseases such as Alzheimer's and Parkinsonism could be prevented by a holistic program of preventive medicine, including treatment of sleep disorders, obesity, Metabolic Syndrome, Mood Disorders and Cardiovascular disease. This clearly points out that a holistic health approach, and utilization of holistic medicine and physician advice, is the key to this prevention of neurological degeneration, or dementia. Gaining understanding and utilizing Complementary and Integrative Medicine (CIM) is the key to this approach. Over 100 million citizens of the European Union utilized Complementary Medicine in 2012, with over 80,000 physicians practicing acupuncture, and over 50 million patients utilizing herbal medicine, according to a study by the group CAMbrella. Obviously, this had an enormous part to play in the improvements seen in subsets of the European population.

In 2011, the National Institutes 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. In 2015, experts from the Center for Cognitive Neuroscience at Duke-National University of Singapore, published a study that showed that tests for cognitive decline in executive functioning and processing speed, combined with fMRI studies of atrophy to specific areas of the brain, and tests of the cerebral spinal fluid amyloid beta 1-42 level, could effectively screen patients for mild cognitive impairment (MCI) and lead to tests to determine the APOE4 carriers to more distinctly analyze the individual risk and progression (PMID: 25524955). Such screening and testing should help patients to develop better preventive protocols in these slowly progressing diseases at an earlier stage. 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 as well. 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 and Integrative 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 and Integrative Medicine (CIM) and the wealth of research and treatment protocols, which are explained on this web article. The second problem has been helped by the elimination of the pre-existing clauses in health insurance by the Obama health care reform called the ACA. 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.

More and more sound scientific research validates the positive effects of acupuncture, herbal and nutrient chemicals on the central nervous system. For many years, experts have touted the importance of neuroprotective and antioxidant therapy to both prevent and treat neurodegenerative disorders. As research continues to reveal the pathophysiology of these complex neurodegenerative diseases, and the very slow progression that is now evident, Complementary Medicine is able to utilize these findings to improve the specific treatment protocols for each individual, whether they have been diagnosed with an early stage of disease, wish to prevent these diseases, or have clinical symptoms. Patient understanding of these neurodegenerative disorders is all-important, as well as an early pro-active approach. Health problems are the responsibility of the individual, not just the doctor, and choosing to integrate the knowledgeable Licensed Acupuncturist and herbalist is an intelligent choice in the realm of neurodegenerative disease and prevention.

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 and Integrative 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 percent 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 neurodegeneration may only cause significant disease symptoms when combined, but when low-grade infection and inflammation, and biotic imbalance, are present, that common environmental toxins may significantly contribute to the pathogenesis of Parkinsonism. Further research has confirmed the role of immune dysfunction and inflammatory stress in the disease. To date, research into studying these multifactorial causes has constituted only a small portion of the research, though. 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. Only a more holistic and integrated treatment protocol is likely to address this whole cycle of causes.

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. In Alzheimer's neurodegeneration, beta-amyloid proteins accumulate to form plaques, and an imbalance between types of beta-amyloid proteins leads to aggregation and fibrils in support tissues of the brain. Tau proteins that are hyperphosphorylated accumulate in the hippocampus, temporal lobe, and lateral parietaltemporal regions of the brain, and the frontal cortex, forming neurofibrillary tangles. The subsequent neurodegeneration leads to a deficit in acetylcholine, affecting memory and creating a lack of inhibition of many excesses in the brain. This cholinergic deficit is the target for most therapies at present, as well as the deficits in serotonin and adrenergic activity in brainstem neurons. Abnormal cerebral and seretonergic and adrenergic activity is thought responsible for the symptoms of dysphoria and insomnia in Alzheimer's disease.

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.

A study in 2014, at the University of Cambridge in the United Kingdom, measured the effects of SSRI antidepressants in patients with advanced Parkinson disease and found that the responses to the drug therapy varied considerably. They concluded: "the behavioral effect of citalopram (SSRI) on response inhibition depends on individual differences in prefrontal cortical activation and frontostriatal connectivity. The correlation between disease severity and the effect of citalopram on response inhibition may be due to the progressive loss of forebrain serotonergic projections" (PMID: 24578545). While studies have focused on the potential of these drugs and negative immediate interactions in causing an acute serotonin syndrome, they may be missing the point. The salient points seem to be the potential for serotonin-dopamine imbalance over long periods of time contributing to the disease state, and the potential that integrative care with stimulation of critical areas of the brain and increased connectivity, as well as neuroprotective and antioxidant therapy, could greatly improve outcomes.

Much research is revealing the potential for acupuncture, electroacupuncture, and herbal and nutrient medicine to supply these effects. For instance, in 2014, researchers at Kyung Hee University, in Seoul, South Korea, and the World Health Organization (WHO) Collaborating Centre, noted that "acupuncture is increasingly used as an additional treatment for patients with Parkinson's disease." These researchers used neuroimaging to see which points would aid connectivity in the prefrontal cortex and precentral gyrus. One acupuncture point, GB34, in a randomized controlled human clinical trial, showed significant benefit to achieve these integrative goals. The stimulation of GB34 "evoked different brain activation in patients with Parkinson's disease than in healthy participants." Such study is presenting more and more proof that will lead to the best choices in acupuncture care in the future. To see this study summary, click here: http://www.ncbi.nlm.nih.gov/pubmed/25220656 . Of course, a simple insertion of a needle at GB34 alone is not the best treatment protocol, but professional stimulation of the point within the context of a more elaborate and individualized holistic treatment protocol could have enormous benefits that would even make standard therapy work better for more patients.

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 an actual relative dopamine deficiency, 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 effectors 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 neurodegenerative 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. Cordyceps is shown to exert significant inhibition of histidine decarboxylase. As part of a broader set of herbal formulas, these integrative herbal treatment strategies could have great benefit.

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.