Herbs and Nutrients for Neurologic Disorders

Treatment Strategies for Alzheimer's, Parkinson's, Stroke, Multiple Sclerosis, Migraine, and Seizures

Sidney J. Kurn, Sheryl Shook

• Publisher: Healing Arts Press
• Year: 2016
• Print ISBN: 9781620555538
• eBook ISBN: 9781620555545
• Edition: 2
• Topic: Medicine
• Subtopic: Alternative & Complementary Medicine

A guide to herbal and holistic medicine for brain health and neurologic disorders• Provides detailed herbal, antioxidant, and nutritional strategies for Alzheimer's, Parkinson's, multiple sclerosis, stroke, migraine, and seizures• Supported by scientific studies and years of successful clinical practice• Discusses potential side effects, counter-indications, and the proper dosages to reduce symptoms, slow disease progression, and lessen the chances of recurrenceNumerous medical journals have published studies supporting the use of herbs and nutrients in the treatment of neurodegenerative disorders. Yet in practice most neurologists rarely include them as part of their protocols. In this practical guide, Sidney Kurn, M.D., and Sheryl Shook, Ph.D., explain how to safely and easily incorporate herbs, antioxidants, and nutritional supplements into the standard conventional treatments for 6 common neurologic disorders: Alzheimer's, Parkinson's, multiple sclerosis, stroke, migraine, and seizures.For each condition, the authors provide detailed strategies supported by scientific evidence and years of successful clinical practice. They examine the biochemical role of each recommended herb, nutrient, or antioxidant and discuss potential side effects, counter-indications, and proper dosages to reduce symptoms, slow disease progression, and--in the case of stroke, migraine, and seizures--lessen the chances of recurrence. The authors explore the nutrient deficiencies and physiological mechanisms, including inflammation, heavy metal toxicity, and mitochondrial dysfunction, that can cause oxidative injuries and initiate neurologic disorders. They reveal which common substances, such as aspartame and glutamate, can trigger these mechanisms at the cellular level and recommend specific herbs and antioxidants, such as turmeric, cannabinoids, resveratrol, and N-acetyl cysteine, to counteract their effects. They discuss the importance of sleep to overall well-being, especially for those suffering from neurologic disorders, and offer tips to help ensure a good night's sleep.Integrating neuroscience, biochemistry, herbalism, and decades of clinical experience, the authors lay the scientific foundation for a holistic, naturopathic approach to neurologic disorders and a way to enhance the quality of life for those suffering from these conditions.

1

Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS). In America there currently are over four hundred thousand diagnosed cases. Myelin, a fatty tissue that surrounds nerve fibers and is essential for their function, is lost in different regions of the brain, spinal cord, or optic nerves as a result of the disease. This causes dysfunction in the signals being transmitted throughout the nervous system and can result in a wide range of symptoms such as fatigue, depression, difficulty walking, dizziness, numbness, memory problems, bowel/bladder disturbances, sexual-function changes, vision problems, or pain. Symptoms vary significantly between individuals and can change over time. MS generally occurs as episodic relapses or a slowly progressive course. Although the ultimate cause is unknown, it has definite autoimmune features including a reduction in suppressor lymphocytes during attacks and an increase in the proinflammatory cytokines, interferon (IFN)-gamma and tumor necrosis factor-alpha (TNF-α).

CURRENT PHARMACOLOGIC TREATMENTS

Two injectable agents, IFN-beta-Ib (Betaseron, 0.25 mg subcutaneously every other day) and IFN-beta-Ia (Avonex, 30 mcg intramuscular once/week), appear to inhibit release of IFN-gamma and tumor necrosis factor (TNF), partially restore suppressor cell function, and attenuate disease activity. There is approximately a 30 percent reduction in relapse rate with these agents and a reduction in new lesions, as shown on patient magnetic resonance imaging (MRI) films. Unfortunately, after twenty-four months of treatment, 40 percent and 16 percent of patients treated with IFN-beta Ib and IFN-beta Ia respectively, develop neutralizing antibodies. Neutralizing antibodies are proteins produced by the body to block the effect of the drug. A newer agent, Copaxone (glatiramer acetate), is the acetate salt of synthetic polypeptides containing four naturally occurring amino acids, L-glutamic acid, L-alanine, L-tyrosine and L-lysine. It reduces the incidence of experimental allergic encephalomyelitis (EAE), the animal model of MS. It appears to reduce the immune reaction to myelin, stimulate lymphocytes to release anti-inflammatory signaling molecules, and stimulate the release of a trophic, or nurturing, substance for brain cells called brain-derived neurotrophic factor (BDNF). Patients treated with Copaxone have approximately 30 percent fewer relapses.¹ Additionally, there are significantly fewer side effects as compared with the interferons mentioned above. Antibodies do develop that react with Copaxone but do not appear to diminish its efficacy. Copaxone dosage is 20 mg/day subcutaneously.

Two newer injectable drugs for MS are available including Rebif, a more potent form of Avonex, and Tysabri. Tysabri is a monoclonal antibody against an adhesion molecule alpha4-integrin. This blockade prevents immune cells from attaching to cells lining the blood-brain barrier and thereby preventing entry into the central nervous system.

Three newer oral drugs for treatment of MS are on the market, Gilenya, Aubagio, and Lemtrada. Gilenya is a metabolite of the fungus Isaria sinclairii. It sequesters lymphocytes in lymph nodes thereby inhibiting their movement into the central nervous system. It also has multiple other mechanisms of action including stimulation of glial cell repair. Aubagio is an active metabolite of leflunomide used in rheumatoid and psoriatic arthritis. Its mechanism of action appears to be related to the inhibition of an enzyme necessary for the rapid division of T cells, cells essential for the MS disease process. Lemtrada is a monoclonal antibody that binds to CD52, a protein present on the surface of mature lymphocytes. This may be its mechanism in MS. Its use may be limited due to significant side effects.

MS AS A NEURODEGENERATIVE DISORDER

Several studies also bring MS into the neurodegenerative framework. Although traditionally viewed as a primary demyelinating disorder, new research calls this view into question.² Axonal loss, now viewed as the major factor in irreversible disability, may begin at disease onset and may be the principal factor in the progressive phase of the disease.³ Questions remain whether axonal loss is secondary to the inflammation involving myelin or occurs secondarily to different, albeit overlapping, mechanisms. Axonal involvement may explain the relative lack of correlation between MRI images and clinical symptoms and signs. Of particular interest is the potential role of mitochondria in axonal degeneration, perhaps similar in some respects to its rather central role in Parkinson’s disease (PD). One interesting hypothesis involves the exhaustion of mitochondrial function in the long chronic phase of the disease.⁴ Conduction along a demyelinated axon is difficult, with redistribution of sodium channels, essential elements in the transmission of the electric current along the fiber. More energy is required in this setting, supplied by mitochondria, the energy-producing organelles in all cells. As discussed throughout the book, free radical production is unavoidable in mitochondrial energy production. Increased mitochondrial function yields increased free radicals and a consequent increase in oxidative damage to mitochondrial components. Loss of mitochondria ultimately leads to nerve cell death (apoptosis). The final common pathway of MS may be the same as that which occurs in the more commonly designated neurodegenerative disorders.⁵

Research reveals that the white matter, or myelin, in otherwise normal appearing areas of the brain in an MS patient is biochemically altered. Myelin basic protein (MBP), an important protein in myelin, has a significant increase in the amino acid citrulline compared to the white matter of individuals without MS. The increased citrulline occurs at the expense of arginine via an enzyme peptidyl arginine deiminase 2 (PAD 2). This change in amino acids apparently reduces the magnitude of positive charge of MBP and interferes with the protein’s ability to interact with the lipid bilayer that composes myelin.⁶ The same research group at the Hospital for Sick Children in Toronto, Canada, then discovered that the gene responsible for the enzyme PAD 2 is significantly more active. This increased activity is traced to a demethylation of the promoter portion of the gene, the portion of the gene that interacts with transcription factors (molecules that tell the gene to turn on production of its protein product). Methylation of a gene, the addition of a methyl group (a carbon attached to four hydrogens), turns off a gene. Demethylation, or loss of the methyl group, turns on the gene. This in turn appears related to an increase in an enzyme DNA demethylase, to twice normal levels.⁷ The demethylation of the PAD 2 gene, resulting ultimately in changes in MBP, may respond to resveratrol. This polyphenol, found in the skin of grapes, is discussed in detail in the chapter on PD. Of its many salutary properties, it appears to favorably affect the epigenetics of the organism, discussed further in the “What These Six Disorders Have in Common” chapter of this book.

The research just discussed has a significant potential to impact MS theory. For many years, plaques, or volumes of demyelination, in the brain has been the pathologic hallmark of MS. Axonal injury, mitochondrial dysfunction, and in particular, biochemical abnormalities in seemingly normal brain areas, moves our understanding of MS into a much wider, potentially more fruitful area of investigation. It also suggests the possible application of various neuroprotective nutrients discussed in the chapters on PD and AD, particularly in the progressive phase of the disease. Coenzyme Q10 (CoQ10) and acetylcarnitine provide mitochondrial support and Ginkgo biloba is protective of the energy-producing enzymatic reactions in the mitochondria. Antioxidant protection is supported by alpha-lipoic acid (ALA), N-acetylcarnitine, and vitamins C and E. Excitotoxicity can be mitigated by magnesium, taurine, gammaaminobutyric acid (GABA), and huperzine A. None of these nutrients is particularly immune-stimulating and should prove safe in MS.

HEALTH ISSUES RELEVANT TO MS AND THE POPULATION AS A WHOLE

Health issues in MS are part of a larger set of problems facing the population as a whole.⁸ All of the problems mentioned below have been shown to be particularly salient in the development or progression of MS.

Pervasive Deficiency of Essential Nutrients in the Diet

Nonsustainable agriculture and the loss of nutrients in our food has resulted in widespread deficiency of essential nutrients in the diet. According to Paul Bergner’s book, The Healing Power of Minerals (Prima Publishing, 1997), charts from the U.S. Department of Agriculture document a greater than 80 percent drop in the mineral content of vegetables from 1914 compared with 1997. We have lost a significant percentage of our topsoil as well as the humus layer, the portion of the soil that contains the minerals and other nutrients essential to human health. Often, fruits and vegetables are picked before they ripen, and before flavonoids and other important nutrients have a chance to reach the concentrations present in vine-ripened fruit and vegetables. Readers interested in studying these issues in more depth are referred to Mr. Bergner’s excellent book. Up to 50 percent of the population fails to ingest the recommended daily allowance (RDA) of essential vitamins and minerals. One solution is to buy organic foods, which contain higher levels of vitamins and minerals and are farmed using sustainable methods that support the environment.

Diets Deficient in Essential Fatty Acids

Due to the use of processed foods, margarine, and refined grains, a dietary deficiency in essential fatty acids is common. Many processed foods transform the normal cis form of fatty acids to the toxic trans form. These are called trans fats and hydrogenated or partially hydrogenated oils, and they have been proven to cause disease even in very small amounts.⁹ It is essential to check food labels and avoid all products containing trans fats or hydrogenated oils. In 2013, the FDA made a preliminary determination ...

Table of contents

• Cover Image
• Title Page
• Dedication
• Epigraph
• Acknowledgments
• Table of Contents
• How to Use This Book
• What These Six Disorders Have in Common
• The Importance of Sleep
• Chapter 1: Multiple Sclerosis
• Chapter 2: Parkinson’s Disease
• Chapter 3: Alzheimer’s Disease
• Chapter 4: Atherosclerosis and Stroke
• Chapter 5: Migraine Headaches
• Chapter 6: Seizure Disorders
• Conclusion
• Postscript. New Supplement: Pyrroloquinoline Quinone
• References
• Recommended Reading
• About the Authors
• About Inner Traditions • Bear & Company
• Books of Related Interest
• Copyright & Permissions
• Index