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Applied Phytotherapeutics I Dwelling in the Heart: Cardiovascular By Terry Willard ClH PhD, Todd Caldecott ClH Lesson 5

©2011 Wild Rose College of Natural Healing All Rights Reserved.

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Dwelling in the Heart: Cardiovascular Function and Botanical Medicine

Introduction

DWELLING IN THE HEART: CARDIOVASCULAR FUNCTION AND BOTANICAL MEDICINE ......................................................................................................................................................................... 1!INTRODUCTION ......................................................................................................................................... 1!PART ONE: ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM ............... 4!

I. THE BLOOD .............................................................................................................................................. 5!II. THE HEART ............................................................................................................................................. 8!

Anatomy ................................................................................................................................................. 8!Pericardium ........................................................................................................................................... 9!

III. BLOOD VESSELS ................................................................................................................................... 11!PART TWO: WESTERN HERBAL CONCEPTS IN CARDIOVASCULAR FUNCTION ............... 14!

CARDIOVASCULAR DEFICIENCY ................................................................................................................. 17!CARDIOVASCULAR EXCESS ........................................................................................................................ 17!MIXED SYMPTOMS ..................................................................................................................................... 18!CARDIAC TROPHORESTORATION ................................................................................................................ 18!



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PART THREE: TRADITIONAL CHINESE CONCEPTS OF BLOOD ............................................... 19!PART FOUR: NUTRITIONAL FACTORS AND CARDIOVASCULAR DISEASE .......................... 21!

Niacin (vitamin B3) .............................................................................................................................. 24!Pyridoxine(vitamin B6) ........................................................................................................................ 25!Cobalamin (vitamin B12) ..................................................................................................................... 25!Folic acid ............................................................................................................................................. 26!Ascorbic acid (vitamin C) .................................................................................................................... 26!Tocopherol (vitamin E) ........................................................................................................................ 27!Calcium ................................................................................................................................................ 27!Chromium ............................................................................................................................................. 28!Copper .................................................................................................................................................. 28!Iron ....................................................................................................................................................... 28!Magnesium ........................................................................................................................................... 29!Selenium ............................................................................................................................................... 29!Flavonoids ............................................................................................................................................ 29!Ubiquinone (coenzyme Q10) ................................................................................................................ 30!Essential fatty acids ............................................................................................................................. 31!Fiber ..................................................................................................................................................... 31!

A NOTE ABOUT CHOLESTEROL ................................................................................................................... 32!PART FIVE: ETIOLOGY, PATHOLOGY AND TREATMENT OF CARDIOVASCULAR DISEASE ...................................................................................................................................................... 33!

ARTERIAL DISEASE, ATHEROSCLEROSIS AND HYPERTENSION .................................................................... 33!PATHOGENESIS OF ATHEROSCLEROSIS ....................................................................................................... 37!

Medical treatment ................................................................................................................................ 38!Holistic treatment ................................................................................................................................. 40!

HEART FAILURE ......................................................................................................................................... 43!Medical treatment ................................................................................................................................ 45!Holistic treatment ................................................................................................................................. 46!

VARICOSE VEINS ........................................................................................................................................ 49!Holistic treatment ................................................................................................................................. 50!

ANEMIA ..................................................................................................................................................... 51!Deficient erythropoiesis ....................................................................................................................... 52!Excessive hemolysis ............................................................................................................................. 53!Holistic treatment ................................................................................................................................. 54!

REFERENCES ............................................................................................................................................ 56!

We sit at a unique time in history when heart issues, both emotionally and physically, play one of the most prominent roles in people lives. This can’t be just coincidence! There are many risk factors that contribute to cardiovascular issue and we will look into several of them; but I would have to say that the lack of emotional contentment and spending too much time in the head, thinking about things has to be the largest contributing factor. Unfortunately this is not even on the radar of most health care practitioners that deal with cardiovascular issues. This is something that I hope changes in upcoming times



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The concepts used by the modern Clinical Herbalist benefits from blending together some of the older understanding of circulation and heart issues, with present medical information of the cardiovascular system (CVS). Modern medicine has a pre-occupation with disease states of CVS such as: hypertension, high cholesterol, athero-sclerosis, clotting disorders and coronary diseases. Traditional medicine focuses on the vital flow of fluids to the tissue and the elimination of waste out of the tissue. To this we can add the feelings associated with lifestyle, as related to ones social-psycho-spiritual interactions. By incorporating these concepts together, we can do a great benefit to our clients. Botanicals and life style issues can greatly improvement cardiovascular (CV) health. For several decades cardiovascular conditions were the number one killer in North America and Europe. In early 2005 cardiovascular conditions were replaced by cancer as the number one killer. Many authorities suggest that the much publicized advice on the benefits of making lifestyle changes has finally hit home and the result has been a decrease in CV disease. Even so, lifestyle issues are still considered the major cause of CV disease. Modern cardiology, as practices in large urban center, has had almost miraculous effect when it comes to acute emergencies. For this we can be thankful for all of the lives they have saved. Where they fail is in the prevention of acute events and maintaining of good health after events. This is an area that a Clinical Herbalist can play a very significant role. Modern Medicine has developed great wonder drugs for use in these emergency issues and even some drugs to lower risks for times of recovery. The area they have overlooked is the potential of gentle toning therapy as seen in regular use of botanicals. Botanicals can clearly play a role in the decrease of cardiovascular disease, as Ginkgo, Garlic, Capsicum and Crataegus (Hawthorn) are four of the biggest sellers in Europe and North America. When looking at these botanicals we can see that they work as much, if not more, on circulation at the tissue level, an area often overlooked by modern medicine. Even though the heart and the tubes (arteries, veins, arterioles, venules) have a lot to do with the CVS, most of the blood is found between the capillaries and cellar tissue. The blood plasma filters through the



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capillary wall to bathe the various tissues, which are embedded in a gelatinous matrix formed by complexes of hyaluronic acid. As the matrix is mostly impermeable to aqueous fluids, the plasma is forced through clefts and cleavages in the matrix. In this way the interstitial matrix, both creates tissue integrity and restricts the free flow of circulation. Edema is a major symptom indicating the breakdown of this system. Regular exercise and especially stretching as found in Tai Chi, Yoga or Qi Cong, contributes to the integrity of the gelatinous matrix. From a vibrational medicine point of view, many have theorized that this interstitial matrix is a ‘living crystal’ that aids in the communication of vibration and electromagnetic frequencies throughout the body. Many forms of bodywork credit this communication network as the bases for their success. The effect the interstitial matrix has on circulation and overall health is quite dynamic and profound. From a tissue point of view, circulation is more of a diffusive process marked by local and wide oceanic currants, rather then one of vascular circulation. Most herbals working on the CVS (like the ones mentioned above) act more on the local circulation. This is particularly true of many flavonoid containing plants. The heart is as much a resonator as a muscle. It sets the ‘drum beat’ for the rest of the body to follow. This is true on an energetic, vibrational level as well as on a physiological level. Herbalists know that issues of the fourth chakra can have an overwhelming impact on the CVS. They also know that the old adage ‘love is the best medicine of all,’ can have profound positive effects on the CVS. For this reason it is wise to consider Flower essence when dealing with issues of the CVS. Clinical Herbalist can provide help for anemia, hypertension, angina, palpitation atheromatous CV conditions, recuperation after CV attacks, venous insufficiency and congestive heart failure.

Part One: Anatomy and Physiology of the Cardiovascular System



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In order for the different cells in the body to maintain their various activities, they are dependent upon a medium that not only transports nutrients and wastes, but also facilitates communication between a group of cells, tissues or organs. This function is performed to a large degree by the blood, which is pumped by the heart and carried by the vascular system. More information can be found in previous courses you have taken, or in your mandatory text: Principles of Anatomy & Physiology by Tortora and Grabowski.

I. The Blood Blood is a liquid connective tissue, and has three primary functions: 1. Transportation: transporting oxygen, carbon dioxide, nutrients, heat, waste, hormones, and other ligands. 2. Regulation: pH with buffers (HCO3

- and H2OC3-);

temperature; water content of the cells, dissolved ions and proteins. 3. Protection: clotting mechanisms prevent blood loss; phagocytic cells; specialized plasma proteins such as interferon, antibodies and complement proteins.

Blood is heavier and more viscous than water, and has an adhesive like quality. Its temperature is slightly higher than the body temperature, about 38 degrees Celsius, and maintains a pH ranging between 7.35 and 7.45. Overall, blood makes up about 8% of the total body weight, and on average, the blood volume is about 5 to 6 litres in men, and 4-5 litres in women. Blood Components: blood plasma (55%) and formed elements (45%, such as cells and cell fragments).



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Blood plasma: straw-colored liquid, 95% water and 8.5% solutes (mostly plasma proteins (7%)). All plasma proteins are synthesized in the liver, including albumins (54% of the plasma proteins), globulins (38%) and fibrinogen (7%). The remaining percentage of solutes (1.5%) includes various waste products (urea, uric acid, creatinine, ammonia, bilirubin), nutrients, vitamins, enzymes, hormones, gases and electrolytes. Formed elements of the blood are erythrocytes (red blood cells), leukocytes (white blood cells) and thrombocytes (platelets). Leukocytes are of two basic types: agranular (e.g. lymphocytes, T cells, B cells and monocytes) and granular (neutrophils, eosinophils and basophils). Erythrocytes (red blood cells, or RBCs): a special pigment called hemoglobin, red colour, transport oxygen, average 4.8 million RBCs per cubic millimeter (mm3) of blood in women, and 5.4

million/mm3 in men; certain proteins called antigens on the plasma membrane, responsible for ABO and Rh blood typing. Leukocytes (white blood cells or WBCs): contain a nucleus; they lack hemoglobin; (5000-10,000/mm3); and typically live for only a few hours to a few days (the exception being T and B memory cells which can last for years). Neutrophils: majority of WBCs (60-70% of total), phagocytosis, respond the most quickly to tissue destruction by bacterium, release several chemicals to destroy the bacteria, including lysozymes and strong oxidants such as superoxide anion (O2

-), hydrogen peroxide (H2O2) or hyperchlorite anion (OCl-), contain defensins



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(broad range of activity against bacteria, fungi and viruses). Monocytes: make up 3-8% of the total WBCs, slower than neutrophils, but arrive in larger numbers and destroy more microbes; wandering macrophages that clean up cellular debris and engulf microbes. Fixed macrophages are fully-developed monocytes that remain in a particular tissue, and are common to the liver and spleen to recycle dead RBCs, WBCs and thrombocytes. Eosinophils: smaller volumes (only 2-4% of total), secrete histaminase, active against certain parasitic worms. Basophils: 0.5 to 1% of the total volume of WBCs release histamine, heparin and serotonin, initiate and enhance the inflammatory response. Lymphocytes are B cells and T cells, both of which form the major combatants in the immune response. Thrombocytes (also called platelets): are generated in the red bone marrow and then enter blood circulation, tiny disc-shaped non-nucleated cells, may or may not contain granules, help to repair damaged vascular tissue, and release granules to promote blood clotting, short life span (5 to 9 days). Hemostasis: stoppage of bleeding via vascular spasm, platelet formation and blood coagulation; blood vessel’s smooth muscles almost immediately spasm to reduce blood flow through the damaged vessel, last from several minutes to several hours. Thrombocyte contain: alpha granules and dense granules. Alpha granules contain clotting factors and platelet-derived growth factor (PDGF), hormone that initiates the proliferation of vascular endothelial cells, smooth muscle cells, and fibroblasts to help repair damaged blood vessels. Dense granules contain ADP, Ca2+ and serotonin, promotes vasoconstriction; produce thromboxane A2 and fibrin-stabilizing factor, which help to strengthen a blood clot; if ruptured, or roughened, thrombocytes gather around the site and stick to the portions of the damaged blood vessel, called platelet adhesion, platelet aggregation, platelet plug, fibrin threads.



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Blood coagulation depends upon vitamin K, required in the synthesis of several of the clotting factors, such as prothrombin (II), VII, IX and X. Vitamin K is a fat-soluble chemical that is produced by bacteria in the colon, and is absorbed into the blood through the intestinal wall. Patients suffering from poor fat absorption, such as the case of insufficient bile release, have a tendency to experience uncontrolled bleeding. Clotting is enhanced with the application of heat or applying a rough surface to a wound, such as a piece of gauze.

II. The Heart The heart is the pumping mechanism of the cardiovascular system. It is a singular organ, pumping 30 times its own weight each minute, and 7000 liters of blood each year, through an estimated 100,000 km of blood vessels, unfailingly throughout a lifetime without a moments rest. In traditional Chinese medicine, and Ayurvedic medicine, the heart is considered to be the seat of the emotions and the intellect.

Anatomy The heart is about the size of a closed fist, weighing about 300g in an adult and is located just superior to the diaphragm in the mediastinum, between the two lungs.



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Two-thirds of the heart lies left of the body’s midline. The apex, or pointed end of the heart is comprised of the left ventricle, and tilts obliquely to the left hip, opposite the flat-like base that is comprised of the right atrium.

Pericardium The pericardium is a triple-layered sac that surrounds and protects the heart from injury, containing it within the mediastinum, but allowing for a degree of movement during vigorous and rapid contraction. Fibrous pericardium: tough inelastic fibrous connective tissue, prevents over-stretching, protects the heart from injury, and contains the heart within the mediastinum. Serous pericardium: thinner, more fragile membrane that forms a double layer around the heart; outer parietal layer is fused to the fibrous pericardium, the inner, visceral layer is fused to the muscle of the heart; between them is the pericardial cavity, contains a thin, viscous secretion called pericardial fluid, reduces friction between the two membranes. Blood flow through the heart: contraction of the myocardium is called a systole, whereas the relaxation of the myocardium is called a diastole; right atrium receives deoxygenated blood, the coronary sinus draining the blood vessels of the heart, pumped into the right ventricle through the tricuspid valve, made up of three flaps of endocardium reinforced with connective tissue, atrial systole the tricuspid valve opens up and allows blood to be forced into the empty right ventricle. Just prior to the ventricular systole, the tricuspid valve again closes, preventing blood from regurgitating back into the right atria, pumped into the pulmonary trunk through the pulmonary semilunar valve; in the lungs, carbon dioxide is released and replaced with oxygen, oxygenated blood, returns to the heart via four pulmonary veins that empty into the left atrium during atrial diastole, then passed into the left ventricle during atrial systole through the mitral valve, bicuspid valve, the ascending aorta, blood flows into the coronary arteries that supply the heart, and into the arch of the aorta, from which arises the brachiocephalic trunk (supplying the right upper extremity and the right side of the head and neck), the left common carotid (supplying the left head and neck) and the left subclavian artery (supplying the



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left upper extremity), past the arch of the aorta the aorta travels downwards to the trunk of the body as the thoracic aorta. Blood supply to the heart: coronary arteries arise from the ascending aorta; supply the myocardium with the nutrients and oxygen needed for muscular contraction. The larger left ventricle receives the majority of the blood. Reduction in blood flow to the myocardium (ischemia), usually results in hypoxia (lack of oxygen), can be the result of problem coronary circulation due to blood clots, atherosclerotic plaques or spasm of the smooth muscle of the coronary arteries, weakening of the muscle fibers in the myocardium. This is experienced as angina pectoris, a severe squeezing pain felt in the chest, labored breathing, weakness, anxiety, dizziness, perspiration and referred pain felt in the neck, chin and left upper arm. Sometimes ischemia will produce no symptoms at all, called a silent myocardial ischemic episode, can be more dangerous because there are no symptoms to warn of an impending heart attack. If the heart receives to little oxygen for too long, the result is a myocardial infarction (MI), or heart attack. Death of an area of the myocardium, called an infarct, most frequently the result of a thrombus (stationary blood clot) or an embolism (a blood clot transported by the blood) lodging in a coronary artery or arteriole. Tissue distal to the obstruction becomes hypoxic, dies, eventually replaced by fibrous connective tissue. Repeated MIs result in a loss of functional myocardial tissue, and a weakening of the heart. An infarction may disrupt the conduction system of the heart, causing ventricular fibrillation (rapid, ineffective ventricular systole) that can lead to sudden death. Conduction system and cardiac pacemaker: the heart muscle is composed of specialized fibers called autorhythmic cells. Signals from the endocrine and nervous systems can modify the heartbeat, but do not establish the fundamental rhythm of the heart. A pacemaker called sinoatrial (SA) node sets the rhythm for the heart, and is located on the right atrial wall below opening of superior vena cava. Impulse travels through the heart via conduction system and gap junctions contained within the intercalated disks. One impulse travels through the heart the atria contract first, followed by the ventricles, atrioventricular (AV) node, located in septum between the two atria. Impulses enter AV bundle (Bundle of His),



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the only electrical connection between the atria and ventricles, enters both the right and left bundle branches that course through interventricular septum toward apex of heart. Conduction myofibers (Purkinje fibers) rapidly conduct the impulse into the ventricular myocardium, an ectopic pacemaker, stimulating extra contractions (other than SA). Sympathomimetic drugs will do this, such as caffeine and nicotine, as can stress and nervous irritability. Pulse: normally same as the heart rate, and at rest the pulse is between 70 and 80 beats per minute, Tachycardia is more than 100 beats per minute, bradycardia less than 60 beats per minute. Blood pressure (BP) is measured by sphygmomanometer, the systolic BP, measure of ventricular contraction, diastolic BP, or ventricular relaxation; BP in young men is 120 mm Hg systolic, 80 mm Hg diastolic, young women, reading tends to be 8-10 mm Hg less. A healthy systolic pressure can be calculated by taking 110 mm/Hg and adding to it one half the patients age (e.g. a sixty year old, the systolic should be within 10 points of 140 mm/Hg), difference between the systolic and diastolic pressure is called the pulse pressure (PP), should averages about 40 mm Hg.

III. Blood vessels Arteries, arterioles, capillaries, three distinct layers:

1. Tunica externa: outer layer of the artery, made up of elastic and collagen fibers. 2. Tunica media: medial layer, the thickest layer, consisting of elastic fibers and smooth muscle. 3. Tunica interna: internal layer, composed of an endothelial layer that is in contact with the blood, a medial basement membrane and an internal elastic lamina that is continuous with the tunica media. The diameter of an artery decreases and the lumen narrows, usually the result of



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sympathetic stimulation or injury to the blood vessel, vasoconstriction is a decrease in the diameter of the artery; lack of sympathetic response causes vasodilation. Large arteries called elastic or conducting arteries, are thin in comparison to their diameter, and contain more elastic fibers and less smooth muscle to accommodate the surge of blood from the heart. Medium-sized arteries, muscular or distributing arteries, are capable of a greater degree of vasoconstriction, containing more smooth muscle and less elastic fiber. An arteriole is a small, almost microscopic artery that delivers blood to the capillaries; constructed similarly to the artery, but the ends of the arterioles that are closest to the capillaries have a simple arrangement of endothelium surrounded by a few scattered smooth muscle fibers, playing a key role in regulating blood flow into capillaries. Capillaries: microscopic vessels that connect arterioles with venules. Almost every tissue contains them, and relies upon them for oxygen, nutrients and waste disposal. This creates the matrix that is a single layer of endothelium and a connective tissue basement membrane, forming extensive networks throughout the body. Blood capillaries in certain parts of the body such as the liver are called sinusoids. A tortuous network of capillaries that are larger on average than other capillaries, and contain spaces between the endothelial cells, sinusoids often contain specialized lining cells that are adapted to the needs of the tissue or organ, in the liver, special phagocytic cells called stellate reticuloendothelial cells are contained within the lining of the sinusoids, sinusoids are also found in the spleen, anterior pituitary, parathyroid and bone marrow. Venules: collect deoxygenated and waste-containing blood from the capillaries to the veins; close to the capillaries are similar in construction. They are consisting of a simple layer of endothelium and a tunica externa, closer to the veins also display a tunica media, similar to veins. Veins: similar anatomical arrangement to that of arteries, but with variations in thickness, tunica interna, and is much thinner in veins, as blood pressure has dropped dramatically. Vein contain one-way valves that prevent the backward flow of blood, and require muscular contraction to actually “pump” the blood back to the heart, skeletal



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muscle pump, a respiratory pump, which by inhalation, causes an increase in the abdominal pressure to move the blood contained in the compressed abdominal veins into the decompressed thoracic veins. Blood pressure: a measure of the hydrostatic pressure of the blood upon the walls of the arteries, dependent upon the pumping action of the heart ventricles, the volume of the blood, and the resistant pressure of the arterial walls as the blood is forced through the blood vessels. Vascular resistance, is dependent upon: the size of the lumen through which the blood travels; the viscosity of the blood; the length of the blood vessel. The size of blood vessel lumen is largely determined through autonomic and hormonal control. The smaller the lumen (i.e. vasoconstriction) the greater the pressure, whereas the larger the lumen (i.e. vasodilation), the lesser the pressure. Viscosity is a measure of the thickness of the blood, the greater the viscosity the higher the resistance, and the higher the pressure. Blood vessel length also determines pressure to some extent, as the farther a liquid travels in a tube the more cumulative friction it encounters: thus, flow and as a result pressure will decline with distance. Nervous control over blood pressure is mediated by stretch-sensitive baroreceptors located in the aorta, send impulses to the cardiovascular center (CV) in the medulla oblongata, which in turn outputs an appropriate response via the autonomic nervous system to the heart and blood vessels. Chemoreceptors function along with baroreceptors to regulate blood pressure by detecting chemical changes in the blood, measure the bioavailability of oxygen and the presence of carbon dioxide and hydrogen ions, input information into the CV. Decrease in oxygen and/or an increase in carbon dioxide and hydrogen ions upregulate cardiovascular activity, increasing heart rate and contractility as well as promoting vasoconstriction through sympathetic control. The CV is also influenced by the higher regions of brain (i.e. cerebral cortex, limbic system and hypothalamus), and by proprioreceptors that measure movement in muscles and joints. Blood pressure is also regulated by a variety of hormonal mechanisms, influencing heart rate, vascular resistance or blood volume: 1. Renin-angiotensin system: When the blood volume



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drops this change is detected in the juxtaglomerular apparatus (JGA) in the kidneys. In turn, the JGA secretes renin into the bloodstream, which acts upon plasma angiotensinogen to catalyze it into angiotensin I. As angiotensin I is passed into the lungs during circulation it is acted upon by another enzyme called angiotensin converting enzyme (ACE). This enzyme catalyzes angiotensin I into angiotensin II. Angiotensin II then acts upon the afferent arterioles that feed into the nephrons of the kidneys to constrict, thereby decreasing the rate at which the blood is filtered through the kidneys, resulting in an increase in blood pressure. Angiotensin II also promotes the secretion aldosterone from the adrenal cortex, which acts upon the kidneys to reabsorb more Na+ and thus more water, increasing blood volume.

2. Anti-diuretic hormone (ADH): ADH is released by the posterior pituitary gland in response to a reduction in water volume in the blood plasma and interstitium, detected by osmoreceptors that feed into the hypothalamus. ADH is then secreted by the pituitary gland to cause the kidneys to reabsorb more water. When the osmolarity of the plasma and interstitium decreases, i.e. it contains more water; a negative feedback loop promotes a reduction in ADH secretion.

3. Epinepherine (E) and norepinepherine (NE): In response to sympathetic stimulation the adrenal medullae release E and NE to increase heart rate and the contractile force of the heart. These hormones also promote vasoconstriction in the arteries that feed the viscera and skin, but promote vasodilation in skeletal muscles.

4. Atrial natriuretic peptide (ANP): ANP acts to inhibit the reabsorption of Na+ by the kidneys, as well as the secretion of aldosterone and ADH. This in turn promotes the excretion of more Na+, resulting in a greater volume of water being excreted in the urine, and thus a reduction in blood volume.

Part Two: Western Herbal Concepts in Cardiovascular Function

The conceptual framework of cardiovascular function elaborated by physiomedical practitioners such as Samuel



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Thomson and William Cook are based on the notion that blood represents the vitality of the body in a fluid, physical form. When these concepts were formed, practitioners had very little understanding of the physical nature of blood, apart from what were then relatively recent discoveries on the nature of circulation. Physiomedicalist practitioners expanded the idea that blood was vitality in fluid motion with the concept of “equalizing the circulation”. This thinking was in large part due to the work of Wooster Beach, although Samuel Thomson’s usage of vapor baths in an attempt to “raise the heat” is essentially the same practice phrased in a different way. To determine if the circulation is equal, physiomedicalists assessed the balance between the arteries, capillaries and veins. In particular, physiomedical theory states that it is the capillaries which command the greatest volume of blood in the body, and are usually the origin of circulatory disturbances, and must be considered first.a This is really seen as blood stored in the small venules and blood reserves such as the vascular sinus of liver and spleen and small veins of the skin. It should be remembered that a large quantity of fluid is retained in the interstitial matrix. The capillaries can be said to exist in two primary states: contraction and relaxation. Capillary contraction results in an impediment to arterial circulation, promoting symptoms of inflammation in the tissues involved. Typically, there is a decrease in function of the secretory glands, and as a result the tissues become dry, hot, irritated and painful. The primary treatment of this state calls for the use of diffusive stimulants and relaxing diaphoretics that act at the capillary level. In states where capillary contraction becomes chronic the tissues eventually become dry and hypotrophic (weak, thin). In addition to the usual stimulants and diaphoretics, this specific situation calls for the use of herbs that repair capillary damage, many of which contain flavonoids to help prevent and repair oxidative damage and restore membrane integrity.1 Diffusive stimulants: Zanthoxylum, Zingiber, Myrica Relaxing diaphoretics: Nepeta, Sambucus, Asclepius Capillary trophorestoratives: Crataegus, Rosa, Vac-cinium

a In actual fact it is the system veins and venules, which contain upwards of 64% of the total blood volume at rest, followed by the systemic arteries and arterioles (13%) pulmonary vessels (9%), heart (7%) and capillaries (7%).



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Capillary relaxation is a state of relative flaccidity of the tissues, with attendant signs and symptoms such as pallor, coldness, clamminess and weakness. Blood flows easily into the capillary bed but because of a lack of tone (“atony”), the tissues do not absorb the blood. Often the venous system is impaired in this state, and allows a backlog to develop. Such states are often characterized by “over-hydration,” in which there is a “free secretion” of various fluids, such as mucus, urine, sweat, diarrhea or blood.2 In a state of capillary relaxation the therapy must be directed towards promoting capillary tone, increasing the inwards radiation of heat, and astringing the venous system.3 This requires the use of stimulating astringents, tonics, and stimulating diaphoretics: Astringing stimulants: Myrica, Hamamelis, Quercus Tonics: Hydrastis, Gentiania, Populus Capillary stimulants: Capsicum, Zingiber, Zanthoxylum Priest and Priest state that herbs that act on the capillary bed are diaphoretics to one extent or another. Relaxing diaphoretics tend to act upon the periphery of the body (relieving arterial pressure), whereas astringing diaphoretics tend to work towards the middle (relieving venous stasis).

The Heart At the center of the cardiovascular system is of course the Heart. A clinical herbalist has much to offer in these are. In fact we can say that even modern medicine has often relied on botanical or the derivatives to treat heart problems. We have seen very strong cardio-active botanicals such as Digitalis spp. (foxglove) in earlier courses. As mentioned when we covered these, we rarely used these botanicals due to their very small Therapeutic Index. Meaning that the toxicity level and the therapeutic level, were really to close and thus could be dangerous. Some Clinical Herbalist do use Convallaria majalis (lily of the valley) as it is safer. Most herbalists prefer to use cardiotonic herbs that are slower and gentler in action, such as: Crataegus (hawthorn) or Tilia (linden flower).

Cardiovascular Tonics Crataegus spp. – hawthorn Allium sativum – garlic Ganoderma spp. - Reishi Tilia platyphyllos – linden Achillea millefolium – yarrow Leonurus cardiac – motherwort Ginkgo biloba – ginkgo Selenicereus grandiflorus – night-blooming cerus Coleus forskoblii – coleus Commiphora mukul - guggul



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Cardiovascular deficiency Symptoms of cardiovascular deficiency are usually a manifestation of peripheral constriction, with coldness in the extremities, especially in the feet and legs, dry skin and dry mucosa. There may be a numbing or tingling in the periphery, and in extreme cases, tissue necrosis (as in diabetes). Moore states that the pulse is typically thready, shallow, and easily compressed, and that under environmental or emotional stress the skin flushes or blanches.4 In most cases the blood pressure is low, and if one stands up to quickly, there will be a tendency to dizziness.

Herbs to stimulate In general, herbs that promote peripheral vasodilation, i.e. “capillary stimulants” are warranted in cardiovascular deficiency. There is a need to ensure an equalization of circulation, allowing the “inward heat” to radiated outwards to the periphery. Some of these herbs may also directly increase the functional activity of the heart, and enhance renal constriction, increasing the blood volume. In some cases the activity of the venous system is impaired, allowing for an atonic state of the tissues. e.g. circulatory stimulants: Zingiber, Zanthoxylum, Rosmarinus e.g. arterial stimulants: Cytisus, Aristolochia, Apocynum (TOXIC) e.g. heart stimulants: Capsicum, Cytisus, Convallaria (TOXIC), Bryonia (TOXIC) e.g. venous astringents: Aesculus, Cytisus, Hamamelis

Cardiovascular excess

Symptoms of cardiovascular excess are warmth in the periphery, easy perspiration, and a strong, bounding pulse. These may be symptoms that are unrelated to any overt pathology, but can be accompanied by essential hypertension, increased blood viscosity (stickiness), with a



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tendency to elevated triglycerides and hyper-cholesterolemia. The blood pressure is typically high, and if the person stands up too quickly a pulse roar can often be heard in the ears. As Moore points out, the attempt to simply lower the blood pressure without addressing the increase in blood viscosity and dyslipidemia is to neglect the cause of the condition, (which is ultimately the approach taken by blood pressure-lowering drugs).

Herbs to relax In general, botanicals that help to down-regulate the sympathetic activities of the autonomic nervous system will be of the most assistance in cardiovascular excess, while at the same time promoting the relaxation of the heart, and assisting in the removal of water to reduce blood volume via the kidneys.

e.g. parasympathomimetics: Leonorus, Verbena, Passiflora e.g. arterial relaxants: Viburnum, Achillea, Viscum e.g. cardiac sedatives: Leonorus, Lycopus, Veratrum (TOXIC) e.g. hypolipidemics: Ganoderma, Cordyceps, Allium, Commiphora, Medicago e.g. diuretics: Taraxacum, Arctium, Urtica

Mixed symptoms Some of the signs and symptoms of cardiovascular deficiency can be accompanied with some of the common features of cardiovascular excess, in particular, an increase in blood pressure and dyslipidemia. These should be addressed as a metabolic problem with an associated cardiovascular deficiency, and thus treatment is directed to treating the mechanism of insulin resistance, while resolving the deficiency state.

Cardiac trophorestoration Some botanicals are of enormous importance in cardiovascular disease because of the trophorestorative effect they have on the heart and the arteries. They are



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typically reserved for deficiency states, but may also be indicated in chronic states of cardiovascular excess, which eventually leads to a deficiency state or a mixed symptomology. e.g. cardiac trophorestoratives: Ganoderma, Cordyceps, Crataegus, Selenicereus,b Allium e.g. arterial trophorestoratives: Vaccinium, Vitis, Crataegus

Primary Actions for the Cardiovascular System

ACTION BOTANICALS Cardio-tonics Crataegus, Ganoderma, Tilia, Allium Cardio-active Convallaria, Cytisus, Lycopus,

Scophularia Circulatory Stimulants

Capsicum, Zingiber, Zanthoxylum

Peripheral vasodilator

Zanthoxylum, Ginkgo

Hypertensive Cytisus Hypotensive Capsicum, Ganderma, Tilia, Viscum,

Allium Diuretic Taraxacum, Achillea, Cardio-active herbs Vascular tonics

Aesculus, Fagopyrum, Ginkgo, Ganoderma,

Nervine Leonus, Tilia, Valeriana, Ganoderma Antispasmodic Viburnun, Valeriana

Part Three: Traditional Chinese Concepts of Blood

From a traditional Chinese perspective Blood (xue) and Qi are interdependent entities, representing the basic dynamics of yin and yang in the body, respectively. Thus in any discussion of Blood and the activities of the cardiovascular system it is important to understand the role of qi. Qi regulates the flow of Blood in the body, and where the qi is deficient Blood begins to stagnate, and similarly, when the Blood begins to stagnate the flow of qi becomes blocked.

b Selenicereus has unique properties: in high doses (> 40 drops) it is a sympathetic stimulant to the heart, but in small doses (<20 drops) Selenicereus has a trophorestorative, regulatory activity on heart conduction.



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The formation of Blood begins in the Spleen where nutrients from the diet are extracted from the waste components by virtue of the Spleen qi, and directed to the upper burner as the food qi. Within the Lungs the ascending food qi is supplemented by the Lung qi, and then directed to the Heart where the final refinement of Blood takes places. Through the cardiopulmonary functions of the Heart and Lungs, the Blood then enters into circulation through the vessels, functioning as the primary form of yin energy to nourish and protect the body, keeping the warming, yang energies in check. During a state of physical inactivity the Blood rests within the Liver, which receives the vital essence (jing) from the Kidneys and uses this to supplement or invigorate the Blood. During physical activity the Liver directs the Blood through the vessels to the muscles and tendons, giving these tissues the energy needed to perform. Thus the Liver is responsible for storing and supplementing the Blood, as well as directing the flow of Blood in the body. From the above, it can be seen that the formation of Blood is dependent upon the qi of the different organs it is associated with: i.e. the Spleen, Lungs, Heart, Liver and Kidney. Each organ is key in either helping to form, move or supplement the Blood, and when any of these organ systems are weak (i.e. qi deficiency), the status of Blood is impaired. • When the qi of the Spleen is deficient, the net result is a

deficiency of Blood, which in turn promotes dysfunctions in the Heart and Liver. The Spleen is also responsible for maintaining the integrity of the blood vessels, and a Spleen qi deficiency is often an underlying factor in hemorrhagic diseases.

Blood stasis is often the consequence of qi stagnation or qi deficiency, both of which can impede the flow of blood and prompt blood coagulation. Of course local trauma, causing injury can also cause blood stasis, which in turn impede the flow of qi.

• When the Blood is deficient the yang energies of the

Liver normally kept in check by the yin aspect of Blood soon become aggravated. The ascending yang energy



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blazes upwards and promotes hot emotions such as irritation, anger and rage, and physical symptoms such as tinnitus, headache, dizziness, redness of the eyes and face, insomnia, and constipation. In chronic states Liver Blood deficiency is responsible for general weakening of the body, pallor, asthenia, dizziness and infertility, and a subsequent deficiency in the yang (qi) of the body.

• When the prerequisite materials of Blood directed from

the Spleen and Lungs to the Heart are deficient the metabolic machinery used to produce the final refinement of Blood begins to rage out of control, causing symptoms of heat similar to Liver yang described above. The Heart however is also the seat of the mind and emotions and the lack of yin qualities in the Heart promotes the mind to be unsettled, anxious and confused.

Heart qi deficiency results in shen (spirit mind) deficiency and heart qi excess can bring on manic-depression.

In TCM theory, the heart outlet is the tongue and erosion, sores and red tip indicate a flaring-up of heart-fire.

Part Four: Nutritional Factors and Cardiovascular Disease

The medical conception of cardiovascular function can be seen to be highly mechanistic, and thus from a strictly rational perspective, is perhaps the easiest to understand: a simple pumping system and series of interconnecting tubes. The relative ease by which it is understood however is in direct contrast to the anxiety, dismay and concern it causes for the practitioner. In North America, and increasingly all over the world, cardiovascular disease (CVD) is a very serious problem indeed: it is number two cause of death in both men and women. As a result of this, the medical approach to CVD is highly pathologized, with a small group of elite expert cardiologists and acclaimed cardiac surgeons that have technical knowledge of the



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cardiovascular system that may seem akin to rocket science. As a result of this extreme form of specialization, a herbalist practitioner might feel that the prevention and treatment of cardiovascular disorders are out of his or her league. But nothing could be farther from the truth.c In his 1939 book Nutritional and Physical Degeneration, dentist and researcher Dr. Weston Price tells us of his research, an endeavor that took him to the farthest reaches of the earth, examining the effects of the modern, industrialized diet in traditional peoples. In this and other books, Dr. Price presents some staggering evidence of how the modern diet has wrought enormous changes in the health of traditional peoples. Among his observations Price noticed a distinct change in the different physical features in traditional peoples that had made the switch to a modern diet. Such changes were compared against those in the same society, often in the same family, that observed traditional eating patterns. Some of the changes included a smaller dental arch, facial deformities and poor dental health. Here in North America, Price revealed some staggering statistics on the rise of heart disease. Price reports that the incidence of heart disease in the United States during the turn of the last century was relatively low, such that many physicians could practice their entire lives and never come across a case of the disease. But as Paul Bergner writes in his well-researched book The Healing Power of Minerals,5 in a space of less than 60 years the incidence of heart disease rose by some 300%. In light of more recent trends, this has only increased in prevalence with no sign of stopping. When one observes the epidemiological factors that led to this shift, the most striking evidence suggests that it is an increase in refined carbohydrates, refined oils, transfatty acids and grain-fed meat in the diet, as well as the practices of modern agriculture that depletes the soil and renders our food poor in many key nutrients. The most important factor associated with CVD is obesity, which is now at epidemic proportions in North American society. In 2004, found 23% of Canadians 18 and older were obese and 36% more were overweight (as determined by body mass index). In children and adolescents, 8% were

c Nonetheless, in cases of organic diseases of the heart, such as congestive heart failure, or when a variety of cardiovascular drugs are being used, the herbalist should approach the situation with the utmost caution.



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obese and 18% overweight.6 About one-third of U.S. adults (33.8%) are obese. Approximately 17% (or 12.5 million) of children and adolescents aged 2—19 years are obese, with a further 25% classified as “overweight.”d These figures are in stark contrast to the 1960 figure, when 13% of Americans were believed to be obese, or the 1994 figure when 22.5% of the population was obese. The trend does not appear to be getting better, with each year the numbers go up. It appears that obesity and related issues will be the number one cost on the health care system by as early as 2020. It is calculated that, in men, for each 10% increase in body weight there is approximately a 20% increase in the incidence of coronary artery disease. For every 10% increase in relative body weight, systolic blood pressure increases 6.5 mm/Hg, plasma cholesterol 12 mg/dL and fasting blood glucose 2 mg/dL. Acquired obesity tends to localize in the trunk, and is now recognized as an independent risk factor for CVD. The simplest way to measure the degree of abdominal obesity is to record the waist circumference and divide it by the hip circumference. In men, the risk of CVD increases sharply when waist/hip ratio (WHR) is above 1.0, and in women above 0.8. Numerous reports have indicated that a high proportion of truncal/abdominal fat to lower body (gluteal) fat is particularly associated with insulin resistance and hyperinsulinemia. Hyperinsulinemia (Syndrome X) is a condition in which the pancreas produces large amounts of insulin to control high blood sugar levels. On a chronic basis, the cells that normally uptake insulin eventually become resistant, and as a result, the pancreas needs to secrete increasing amounts of the hormone to control high blood sugar levels. Chronically high levels of insulin have been shown to disrupt sodium metabolism, promote oxidative damage in cardiovascular tissue, suppress the secretion of human growth hormone, and exhaust the islets of Langerhans in the pancreas. As a result of the association of truncal-abdominal obesity, hyperinsulinemia and CVD, a large part of the focus in treatment is directed to correcting the underlying metabolic abnormalities that promote hyperinsulinemia and truncal

d Obesity is a Body Mass Index (BMI) of 27 or more. See A Life in Balance: Metabolic Function and Botanical Medicine for a complete discussion of obesity, its causes, and the BMI.



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abdominal obesity. The most important and effective method is to implement a low carbohydrate diet, which focuses on controlling the dynamics of insulin resistance and hyperinsulinemia (see The Fire Within: Digestive Function and Botanical Medicine). The results of this diet are clearly observable after a few months, with a significant decrease in truncal-abdominal obesity, a normalization of blood pressure, a correction of dyslipidemia and a significant risk reduction of CVD as well as other associated diseases including diabetes and cancer. A failure to accommodate these important dietary changes in CVD is a failure to understand the underlying mechanisms of its cause. While herbal treatments can be used to lower blood pressure, inhibit free-radical damage and strengthen the heart, they are at best adjunct therapies to changes in diet and lifestyle. Even though we have emphasized obesity in CVD, it should be noted that a large number of patients with lower body weight, are heavy smoker, drink a lot of caffeinated beverages and low blood pressure also have an increased risk of CVD. Often we will find these people with Type A personalities. Living in their mind more than their heart. Often there is a change in lifestyles from a previous very busy life when younger to a more sedentary lifestyle after ‘retiring’. Sometimes high blood pressure in these individuals and the association of blood sugar issues such as hyperinsulinemia can also be found. While the presence of refined carbohydrates in the diet is the single most important factor in hyperinsulinemia, this problem can also be caused or exacerbated by nutritional deficiencies. Once again, these deficiencies appear to be mostly related to the practice of growing foods in nutrient deficient soils, refining foods and stripping away essential nutrients to enhance taste, texture and shelf-life, and the loss of traditional eating patterns and a subsequent decrease in the diversity of foods consumed. The following is an overview of key vitamins, minerals and accessory nutrients, and their basic functions, that are often found deficient in patients suffering from CVD.

Niacin (vitamin B3) Niacin is a water-soluble, non-cumulative vitamin that forms a part of the coenzymes nicotinamide adenine dinucelotide (NAD) and nictotinamide adenine

Goals for Decreasing CVD Risks

Quit or minimize smoking Lower and control Blood pressure Reduce total Cholesterol Decrease LDL Cholesterol Increase HDL cholesterol Loss weight if over weight Increase aerobic exercise



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dinucleotide phosphate (NADH), involved in more that 50 different key metabolic reactions. These include the processes of glycolysis, fatty acid synthesis, deamination and drug metabolism. Niacin also stimulates circulation, and in the form of nicotinic acid (not niacinamide) which produces a characteristic flushing, has been shown to promote vasodilation, lower LDL cholesterol and serum lipoprotein(a), increase HDL cholesterol and reduce the risk of myocardial infarction. Niacin can be manufactured from the amino acid tryptophan, and while deficiencies are more common in corn-based diets, it is less common in meat eaters. • optimal daily intake in adults: 100 mg – 3 g, slowly

increasing the dose over a 2-3 week period

Pyridoxine(vitamin B6) Pyridoxine and its coenzyme form, pyridoxal-5-phosphate (P5P), have a wide range of activities, particularly in amino acid metabolism, the formation of GABA, serotonin and the catecholamines, and the metabolic conversion of tryptophan to niacin. Pyridoxine is particularly important in regulating the balance of sodium and potassium in the body, the status of intracellular magnesium and thus the electrical function of the nerves, myocardium and muscles. Animal studies have consistently shown that a pyridoxine-deficient diet is atherogenic. Pyridoxine is necessary for the conversion of the atherogenic amino acid homocysteine into the non-toxic cystathione, and may inhibit platelet aggregation, and in conjunction with other B-vitamins, prevent dyslipidemia. In excess doses (upwards of 2-5 grams) pyridoxine may cause peripheral neuropathy due to a failure of the liver to convert it to its metabolically active form (i.e. P5P). • optimal daily intake in adults: 100-500 mg

Cobalamin (vitamin B12) Cobalamin is a complex nutrient comprised of cobalt, carbon, oxygen, phosphorous and nitrogen, and plays an essential role in the metabolism of nerve tissue, and in association with iron, folic acid, copper, iron, pyridoxine, ascorbic acid and adequate protein, is a key nutrient in erythropoiesis. Along with pyridoxine and folic acid, cobalamin plays a role in the metabolism of the artherogenic homocysteine. Cobalamin is only found in



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significant amounts in animal protein, and is manufactured in small amounts by the gut flora. A decline in stomach acid, the use of antacids and laxatives all inhibit cobalamin absorption. High folic acid supplementation can mask cobalamin deficiency, particularly common in vegetarians. • optimal daily intake in adults: 20-1000 mcg

Folic acid Folic acid and its coenzyme form tetrahydrofolic acid (THFA) which maintains a range of functions similar to cobalamin, aiding in RBC production, deamination, transamination and the formation of the nucleic acids. In regard to CVD specifically, folic acid is involved in the conversion of the atherogenic homocysteine to the non-toxic methione, particularly in association with pyridoxine. Folic acid has also been shown to increase lipoprotein lipase activity (preventing lipid infiltration) and improve capillary blood flow. Folic acid or folate is easily absorbed and stored in the liver for up to nine months as methyl folate, which requires cobalamin to convert it the metabolically active THFA. • optimal daily intake in adults: 400-1000 mg

Ascorbic acid (vitamin C) Ascorbic acid is a non-cumulative water soluble vitamin that is required in a variety of metabolic processes: the formation and maintenance of collagen, the conversion of folic acid into THFA, the manufacture of indolamines and catecholamines, thyroid function and cholesterol metabolism. Ascorbic acid is an important antioxidant, preventing the oxidation of water-soluble and fat-soluble nutrients, and supporting detoxification mechanisms in the body. Ascorbic acid also plays an important role in immune function, activating neutrophils, lymphocytes, and interferon against microbial infection, while inhibiting histamine release. In CVD specifically, serum ascorbic acid levels have been shown to be deficient in patients with coronary artery disease, and supplementation may lower serum cholesterol, LDL cholesterol, triglycerides, platelet aggregation, and the risk of angina, while increasing HDL cholesterol. Ascorbic acid also plays an important role in the hydroxylation of proline in collagen formation, promoting blood vessel integrity (in conjunction with retinol and tocopherol).

• optimal daily intake in adults: 500 mg – 6 g (to bowel tolerance)



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Tocopherol (vitamin E) Tocopherol is a fat-soluble vitamin that naturally occurs in nature, with at least seven different forms: alpha, beta, gamma, delta, epsilon and zeta. Currently, the d-alpha tocopherol is considered to be the most potent form, in contrast to the synthetic dl-alpha tocopherol. Tocopherols play an important role as antioxidants, inhibiting the peroxidation of unsaturated fatty acids, and stabilizing cell membranes. This activity is particularly functional in preventing lipid peroxidation of the vascular endothelium by lipid peroxides such as oxidized LDL. Tocopherols enhance the efficiency of oxygen utilization helping prevent hypoxia, and also act to inhibit platelet aggregation. There is an inverse relationship between low serum tocopherol, angina pectoris, and mortality from ischemic heart disease. High doses of tocopherol are thought to cause a transient rise in blood pressure, and thus hypertensive patients should be started on small, graduated doses. Iron and vitamin E impair the absorption of each other and should not be taken together. • optimal daily intake in adults: 400-1200 IU

Calcium Calcium, an important macromineral required in significant quantities, is poorly absorbed in the gut, specifically requiring cholecalciferol (vitamin D3) for absorption. We quite often use chelated Calcium to aid in absorption. In the heart and blood vessels calcium is a key nutrient that regulates contraction, and deficiencies often are observed to cause vasoconstriction. Dietary deficiencies may also promote the mobilization of calcium from bone to soft tissues, from the extracellular to intracellular compartment, increasing serum calcium, which may play a role in atherogenesis. In some studies supplementation with calcium has been shown to decrease serum cholesterol. Absorption of calcium generally decreases with age, excess amounts of fat, protein, fiber intake, phosphorus (e.g. soft drinks), oxalates (e.g. leafy greens), and phytates (e.g. grains and legumes). Magnesium and zinc compete with calcium for absorption, as does iron without concurrent vitamin C administration. • optimal daily intake in adults: 800-1200 mg



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Chromium Chromium is a key trace mineral required in relatively small amounts, and is a component of glucose tolerance factor (GTF), comprised of one chromium molecule in a trivalent state, two niacin molecules, and three amino acids (i.e. glycine, cysteine and glutamic acid). GTF functions to enhance the activities of insulin, improving the uptake of glucose at the cellular level. Chromium has also been shown to lower cholesterol levels and increase HDL. Chromium has been shown to be deficient in as much as 90% of the U.S. population, and tissue levels tend to decline with age and certain diseases such as CVD and diabetes. Strenuous exercise, a diet high in carbohydrates, as well as trauma all increase the excretion and thus the need for adequate chromium supplementation. • optimal daily intake in adults: 200-300 mcg daily

Copper Copper is another key trace mineral required in relatively small amounts, forming part of the cytochrome system for cell respiration. Copper also assists in the transport of iron and the formation of hemoglobin, and is an important component of collagen, the myelin sheath and elastin, the latter of which gives blood vessels their capacity to stretch with increases in pressure. Copper is an important component of super oxide dismutase, but can also act as a free-radical when found free in the plasma and not bound to ceruplasmin. A deficiency of copper is specifically associated with hypercholesterolemia and decreased HDL. • optimal daily intake in adults: 2-4 mg

Iron Iron is an important macronutrient required in significant amounts and most importantly is a component of hemoglobin and myoglobin (the form of hemoglobin stored in the myocardium), used to transport oxygen to the tissues. A deficiency of iron is the most common cause of anemia, and may also play a role in atherogenesis. Vitamin C and stomach acid play an important role in iron absorption, especially from non-heme (i.e. non-animal) sources. Phosphates, oxaltes, phytates, tannins, vitamin E and very high levels of calcium and zinc impair iron absorption. • optimal daily intake in adults: 15-20 mg



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Magnesium Magnesium is a macronutrient required in significant amounts and is involved in close to 300 different enzyme systems in the body. Magnesium is particularly concentrated in the myocardium where it plays a role in regulating the heart beat, acts to decrease coagulation, functions as a calcium-channel blocker, and relaxes smooth muscle in blood vessels. In postmortum studies of MI victims it has been observed that myocardial concentrations of magnesium can be less than 42% of that in normal hearts. A deficiency of magnesium is associated with an increased risk of cardiac arrhythmia, coronary artery disease, and myocardial infarction. Supplementation of magnesium may prevent calcification of blood vessels and inhibit atherogenesis. High intake of calcium, vitamin D, alcohol, phosphates, sugar, and sodium as well as thiazide diuretics all increase the need for magnesium. • optimal daily intake in adults: 300-600 mg

Selenium Selenium is an important trace mineral required in fairly modest amounts, functioning primarily as a key component of glutathione peroxidase, and to convert T4 into the metabolically active T3. Selenium deficiencies are in large part a symptom of modern agricultural methods and environmental pollutants such as sulfur dioxide. Although selenium deficiencies appear to be ubiquitous they often have a geographical distribution that is correlated to local soil-selenium deficiencies, and as a result, a significant increase in the risk of CVD. Selenium deficiency is associated with an increase in LDL cholesterol, platelet aggregation, an increase in the risk of stroke, and a poor prognosis following myocardial infarction. • optimal daily intake in adults: 100-250 mcg daily

Flavonoids Flavonoids are a large group of over 4000 different phenolic glycosides found primarily as pigments in flowers, fruits and leaves, usually in association with sugars such as D-glucose, L-rhamnose, D-galactose, L-arabinose and D-



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xylose.e Up to 80% of flavonoids are flavones and flavonols such as apigenin, luteolin, kaempferol, quercitin, rutin and myricetin. Other important flavonoids include the anthocyanidins (e.g. pelargonidin), catechins, and isoflavonoids (e.g. genistein). A number of minor flavonoids can also be found, in medicinal plants such as Silybum marianum (e.g. silymarin). Flavonoids have a wide range of effects in the body, acting as antioxidant and anti-inflammatory agents. Flavonoids prevent the oxidation of ascorbic acid, prevent platelet adhesion and aggregation, and are key in increasing the strength and integrity of capillaries. • optimal daily intake in adults: 1-5 g

Ubiquinone (coenzyme Q10) Ubiquinone is a vitamin-like lipid-soluble antioxidant that functions as an electron carrier in the mitochondria of animal cells, ensuring the production of ATP. The biosynthesis of ubiquinone from the amino acid tyrosine is a multistage process requiring vitamins B and C and several trace elements. Significantly decreased levels of ubiquinone have been noted in a wide variety of diseases in both animal and human studies, and can be caused by insufficient dietary ubiquinone, impairment in ubiquinone biosynthesis, an excessive utilization of ubiquinone by the body, or any combination of the three. Although dietary sources do exist (primarily in oily fish), most ubiquinone found in the body probably occurs via biosynthesis. Ubiquinone is known to be highly concentrated in the myocardium, and several different forms of CVD are strongly correlated with low blood and tissue levels of ubiquinone, either as a primary etiological factor or a secondary phenomenon. Experimental evidence and clinical trials have demonstrated ubiquinone protects against atherogenesis, reduces angina, improves cardiac function and reduces blood viscosity. HMG-CoA reductase inhibitors (i.e. the “statins”) used to treat elevated blood cholesterol levels by blocking cholesterol biosynthesis also block ubiquinone biosynthesis. • optimal daily intake in adults: 20-50 mg

e Some times the term “bioflavonoids” is used to denote flavonoids, but these should not be confused with bioflavonoids, a type of flavonoid that almost exclusively occurs in gymnosperms (e.g. Ginkgo biloba).



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Essential fatty acids Linolenic acid (omega-3) and linoleic acid (omega-6) are essential fatty acids that the body cannot synthesize and thus must be obtained in the diet. These fats are an important constituent of the plasma membrane, and have a variety of regulatory functions in the body. Currently, the modern diet supplies an overabundance of linoleic acid and a deficiency of linolenic acid, in the neighborhood of 20:1. Anthropological research indicates that the traditional human diet displayed a ratio that was more or less equal. Linoleic acid is the precursor to arachidonic acid that yields many of proinflammatory eicosanoids (e.g. PgE2, TxA2, LtB4, PgI2) that are increasingly identified as a major cause or factor in many diseases. In contrast, the metabolites of linolenic acid appear to oppose those of linoleic acid. Although linolenic acid is found in certain plant oils they are most abundant in fatty animal tissues as eicosapentaenoic and docohexanoic acid. These two forms of linolenic acid are far more biologically active than plant sources, inserting themselves in the biosynthesis of anti-inflammatory eicosanoids much further along the chain, avoiding the need for enzymes such as delta-5 and delta-6 desaturase, which are often deficient. Eicosapentaenoic acid results in the production of anti-inflammatory eicosanoids such as PgE3, TxA3 and PgI3 that balance the proinflammatory eicosanoids, whereas docohexanoic acid directly inhibits the activity of series 2 and 4 eicosanoids. Although omega-3 fatty acids are key in a variety of metabolic processes, they appear to play an important protective role in CVD. In particular, omega-3 fatty acids have been shown to reduce the prevalence and risk of coronary artery disease, prevent atherosclerosis in an atherogenic diet, reduce angina, decrease blood viscosity and platelet aggregation, reduce total serum cholesterol and triglycerides, increase HDL, and enhance cardiac function. • optimal daily intake in adults: 1000 mg each of

eicosapentaenoic and docohexanoic acid

Fiber The term “fiber” refers to both insoluble and soluble fibers, but in regard to CVD prevention and treatment, it is only soluble fibers that have been shown to demonstrate a specific benefit. Soluble fibers inhibit stomach emptying, increase transit time and thus lower the glycemic index of carbohydrates. Soluble fiber has been shown to have a



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significant effect on total serum blood cholesterol. Insoluble fibers have a beneficial activity on the colonic flora, increasing fecal mass, balancing the pH, and promoting the elimination of toxins in the gut. Some fibers however, such as beans, may increase the supersaturation of bile with cholesterol and thus increase the risk of cholelithiasis.

A note about cholesterol Although a diet rich in cholesterol is often fingered as a prominent cause of CVD, the data on this is unclear. As we will see in Part Five: Etiology, Pathology and Treatment of Cardiovascular Disease, there is much debate among those who haven’t taken the association of a cholesterol-rich diet and elevated serum cholesterol for granted. Rather than cholesterol specifically, there are some studies that suggest that saturated fat is a causal factor of CVD, and specifically, the ratio of polyunsaturated fatty acids (PUFAs) and saturated fat. These studies suggest that an increasing ratio of PUFAs to saturated fat is associated with a decrease in the negative impact of dietary cholesterol. One should be forewarned however that not all PUFAs are created equal, and hydrogenated PUFAs such as those found in margarine and transfatty acids are clearly causative factors in CVD. There is also ample epidemiological evidence from the Framingham Heart Study and the Tecumseh study that saturated fat has no bearing at all on serum cholesterol levels. According to Sally Fallon, author of Nourishing Traditions, cholesterol has several important functions in the body: • provides stability to cell membranes; a diet rich in

PUFAs is thought to decrease blood cholesterol by driving serum cholesterol back into the tissues to prevent the cell membranes from becoming too fluid and weak from the excess PUFAs

• acts a precursor to steroid hormones and vitamin D • forms the bile salts • may act as an antioxidant • ensures the proper development and function of the

nervous system • plays a role in maintaining the integrity of the gut wall.



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It is important to note however that oxidized cholesterol acts as a free-radical, found in powdered eggs and milk, and meat subject to high cooking temperatures.

Part Five: Etiology, Pathology and Treatment of Cardiovascular Disease

Hypertension Hypertension is an abnormally elevated blood pressure, currently considered greater 140 mm Hg systolic and/or 90 mm Hg diastolic. These numbers have been altered quite a bit over the last 30 years, with 150 / 100 being the start of concern in the 1970’s. Due to the fact that hypertension is considered to predispose a person to more significant pathologies such as Heart disease, Congestive Heart Failure (CHF), Renal Failure, Cerebrovascular accidents (CVA) aortic dissection and retinal changes; it is the first thing check for in cardiovascular concern. There are three basic types of hypertension: essential, secondary and malignant.

General Recommendation For Healthy Cardiovascular System Have a time of the day, or week that can aid in bringing you to a level of heart felt contentment. Eat foods that you like that are low in cholesterol and saturated fats. Eat adequate amounts of fiber. Minimize salt, avoid to many stimulants and drink no or only small amount of alcohol. Don't Smoke. Drink at least 1.5 liter of water daily. Get adequate amounts of enjoyable aerobic exercise – walking 30 – 45 min three times a weeks has shown significant benefit. Maintain health in general. Relax at least 15 minutes every day. Get adequate sleep. Consider the emotional state of your heart. Open your heart with flower essence of Pink Yarrow, Borage and Wild Rose.



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Table of Blood Pressure Level in Adults CATEGORY BLOOD

PRESSURE MM (Hg)

Systolic Diastolic Normal 120 80 High normal 130 – 139 85 – 89 High BP Stage 1 140 - 159 90 - 99 Stage 2 160 – 179 100 – 109 Stage 3 >180 >110 Essential Hypertension: is the most common, representing nearly 90% of the cases. It is of unknown etiology, with several factor that are believed to contribute to it development such as: genetic, increasing age, obesity, physical inactivity, diabetes, stress, smoking and significant intake of dietary sodium. There can be a significant trend in family lines, with essential hypertension being twice as high for African descendants.

Secondary Hypertension: is cause by some other factor such as: renal disease, endocrine disorder (Conn’s syndrome, acromegaly, Cushing’s syndrome, pheochromocytoma or hyperthyroidism), central nervous system disorder, congenital anomalies, drug side effects, or toxemia in pregnancy. Renal disease is by far the most common form of secondary hypertension. Malignant Hypertension: is an accelerated and severe complication of essential or secondary hypertension. Typically it will be associated with a diastolic pressure higher than 120 mm Hg, instead of a healthy 80. Again we will fine this most common in men of African heritage.

Medical treatment

At this time modern medicine has no specific treatment for hypertension, but is focused on inhibiting or alleviating signs and symptoms, or providing treatments that change or modify the results of pressure on the sphygmomanometer.7



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• diuretics: promoting diuresis, decreasing plasma volume and edema, thereby decreasing cardiac output and blood pressure. Major drugs include thiazides (e.g. hydro-chlorothiazide, depletes potassium), loop diuretics (e.g. furosemide, ethancrynic acid; depletes potassium), and potassium-sparing diuretics (e.g. triamterene, amiloride)

• beta-1 adrenergic antagonists: selectively antagonizes beta-1 receptors, often used in conjunction with thiazides (e.g. atenolol, metoprolol, propranolol)

• calcium channel antagonists: inhibits calcium ions from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium during depol-arization (e.g. diltiazem verapamil nifedipine)

• angiotensin-converting enzyme (ACE) inhibitors: act as competitive inhibitors of ACE, reducing angiotensin II levels, and thus decreasing aldosterone secretion (e.g. captopril, enalapril, lisinopril, ramipril)

• aldosterone antagonists: competes with aldosterone receptor sites, reducing blood pressure and sodium reabsorption (e.g. eplerenone)

• alpha-adrenergic agonists: stimulate presynaptic alpha-2 adrenergic receptors in the brain stem, reducing sympathetic nervous activity (e.g. methyldopa)

Holistic treatment As with any other health issue of course the treatment depends on each individual case, but we need to focus on the core of the health issue. A number of botanicals have a good reputation for being hypotensive. By far the one that we use at Wild Rose the most is Ganoderma. Others that can be employed are: Crataegus, Tilia, Viscum album, olive leaf

ACTION BOTANICAL Hypotensive Ganoderma, Crataegus spp. Tilia,

Achillea, Viburnum, Valeriana Cardiotonic Ganoderma, Crataegus spp. Tilia, Diuretic Crataegus spp. Tilia, Achillea Antispasmodic Tilia, Viburnum, Valeriana Vascular Tonic Ganoderma, Crataegus spp. Tilia,

Achillea Nervine relaxant Ganoderma, Tilia, Viburnum,

Valeriana



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Broader considerations As in any lifestyle disease, there are many factors that need to be considered.

• Maintain a healthy body weight • Avoid tobacco, and large amounts of caffeine or

alcohol • Reduce stress factor in ones life • Exercise regularly in a joyful way • Eat lots of fiber such as complex carbohydrates • Eat garlic, onion and ginger along with an array of

herbs and spices • Reduce animal fats and proteins • Keep salt low • Each fish if it is appropriate for your lifestyle • Vitamin C (500 mg, two to six times daily);

Bioflavonoids (250 mg, two to six times daily); Vitamin E (start with 100 IU gradually increasing to 400 - 800 IU daily); Lecithin (1200 mg, two times daily); Calcium (1500 mg); Magnesium (200-500 mg); Multivitamins and minerals; Essential Fatty Acids (200 mg daily or Krill 1 cap BID).

• Coenzyme Q10 50 mg, BID

Arterial disease, atherosclerosis

Arterial disease accounts for the vast majority of patients that suffer from cardiovascular disease, and may be accompanied by diseases of the veins and heart. The primary arterial disease is atherosclerosis, a progressive disease of large and medium large arteries that is marked by the formation of plaques or atherosclerotic lesions in the endothelium. The term arteriosclerosis is the same pathology, and is used when discussing the atherosclerotic lesions that can occur in the smaller arterioles. The major complications of atherosclerosis include ischemic heart disease, myocardial infarction, and gangrene of the extremities. Atherosclerosis is one of the leading causes of death in North America, a percentage of the population that has been on the rise steadily since that turn of the last century.

Suggested Program Breakfast Reishi extract (3 caps) Cayenne (1 capsule) Garlic (2 capsules) BEVC (2 tablets). Lunch Vitamin E (200 IU). Supper Same as breakfast. Ginger root tea is good to drink for this problem



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Pathogenesis of atherosclerosis

For a more thorough review of the pathology of this section, please refer to lesson 4 of your Pathology course. Atherosclerotic plaques: form in the tunica intima of elastic and muscular arteries, proliferation of intimal smooth muscle cells, accumulation of fat, smooth muscle cells release cytokines that stimulates the accumulation of mononuclear phagocytes, lymphocytes and neutrophils, endothelium ruptures and platelets begin to adhere, small capillaries penetrate the vessel wall and supply blood to the plaque, almost like a kind of malignant tumor.8 Various hypotheses for atherosclerotic plaguing: some theories are complimentary and some are antagonistic, insudation hypothesis, lipid found in plaques is derived from plasma lipoproteins, specifically low density lipoproteins (LDL), lesion begins with a mutation of a smooth muscle cell, from exposure to chemical or viral mutagens, resulting in focal regions of accumulation, macrophages then scavenge LDL in the blood and transport the lipid directly into the tunica intima of the blood vessel, producing additional damage to the lesion, exposing circulating platelets to subendothelial collagen, promotes release of growth factors by the platelets, and local macrophages, stimulate the proliferation of smooth muscle cells and make the lesion larger, continued accumulation of fat into the lesion by macrophages, undergoing degeneration, begins to ulcerate and a thrombus forms on the injured luminal surface. Initial lesions (fatty streaks), flat or slightly elevated, contain lipid, histologically comprised of lipid containing macrophages (foam cells). Another candidate for the initial lesion are intimal cells masses, white thickened areas at branch points in the arterial tree, containing smooth muscle cells but no lipid. Characteristic lesion is a fibro-fatty plaque consisting of a fibrous cap and an atheroma, fibrous cap, a layer of thickened connective tissue containing fat-filled macrophages and smooth muscle cells. The atheroma is a necrotic mass of lipid that forms the middle portion of the lesion. Other components include other blood-borne cells including lymphocytes.

Pathogenesis of Atherosclerosis A. Injury to vascular endothelium by

lipids B. Lipids and platelets adhere to the

damaged endothelial surface in aggregates and gain access to the intima (subepithelium)

C. Leukocytes and platelets start to release platelet-derived growth factors and other mitogens, which will cause smooth muscle cells to migrate into the intima from media and proliferate throughout the atherosclerotic process

D. Occupation od the intima by macrophages (monocytes) and lipids leads to phagocytosis of lipids by macrophages, which become “foam cells”

E. Fatty streak with foam cells, platelets, and myocytes (smooth muscle cells) start to grow up by proliferation of smooth muscle cells, as well as increased numbers of foam cells and platelets, forming an atherosclerotic plaque



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The complicated plaque is the clinically significant end-point for the formation of a plaque, characterized by: 1. Thrombosis: the aggregation of platelets, fibrin,

clotting factors and blood-borne elements on and within the plaque

2. Neovascularization: of the cap and edges of lesion 3. Thinning: of the underlying tunica media 4. Calcification: within the atheroma and fibrous cap 5. Ulceration: of the fibrous cap. Net result: may cause occlusion of the blood vessel and the formation of emboli, producing ischemia in the tissues. Characteristic lesion of atherosclerosis requires as long as 20-30 years to form, thus atherosclerosis is primarily a disease of older adults.

Most prevention and treatment of heart disease is based upon the Framingham Heart study, a cohort study of over 5000 adult men and women from the town of Framingham, Massachusetts, started in 1948, second generation cohort study started in 1971, third generation cohort study is now being implemented. Identify risk factors for CVD, including high blood pressure, high blood cholesterol, smoking, obesity, diabetes, physical inactivity, blood triglyceride, LDL/HDL, age, gender, and psychosocial issues. Areas to consider: hypertension, elevated blood cholesterol and triglycerides (including chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL)); hyper-glycemia.

Medical treatment At this time modern medicine has no specific treatment for atherosclerosis, but is focused on inhibiting or alleviating signs and symptoms, or providing treatments that change or modify the results of laboratory investigations. Hypertension is perceived as being a risk factor for atherosclerosis, and is managed symptomatically through the use of antihypertensive agents including above in that section.

Hyperlipidemia is generally perceived as a risk factor for



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atherosclerosis largely based upon the use of hypolipidemic agents that lower serum cholesterol, and an observed reduction in the risk of coronary heart disease events and overall mortality. The primary hypolipidemic therapy consists of HMG-CoA reductase inhibitors or “statins” which inhibit the rate-limiting step of cholesterol synthesis in the liver, thereby lowering serum cholesterol, LDL-cholesterol, and triglyceride levels. Adverse effects include CoQ10 depletion,f hepatotoxicity and myopathy. Example HMG-CoA reductase inhibitors include pravastatin, simvastatin, lovastatin, atorvastatin, and rosuvastatin.

On the preventative side, modern medicine typically recommends a series of general changes to diet and lifestyle to decrease the risk of CVD, based on the prevailing hypotheses, many of which continue to revolve around the insudation hypothesis. The American Heart Association has recently developed an “Eating Plan for Healthy Americans,” and is comprised of the following: • Emphasis upon a variety of fruits and vegetables, eating

five or more servings per day. • Emphasis upon a variety of grain products, including

whole grains, eating six or more servings per day. • Emphasis upon fat-free and low-fat milk products, fish,

legumes (beans), skinless poultry and lean meats. • Emphasis upon fats and oils with 2 grams or less

saturated fat per tablespoon, such as liquid and tub margarines, canola oil and olive oil.

• Limiting consumption of foods high in calories or low in nutrition, e.g. soft drinks and candy

• Limiting consumption of foods high in saturated fat, trans-fats and cholesterol, such as full-fat milk products, fatty meats, tropical oils, partially hydrogenated vegetable oils and egg yolks.

• Limiting consumption of sodium to less than 2,400 milligrams per day.

• Limiting consumption of alcohol to no more than one alcoholic drink per day for women, and no more than two for men. "One drink" means it has no more than 1/2 ounce of pure alcohol, e.g. 12 oz. of beer, 4 oz. of wine, 1-1/2 oz. of 80-proof spirits or 1 oz. of 100-proof

fA trend that has raised alarm bells in many independent researchers, given the importance of CoQ10 in myocardial function. See: Langsjoen PH, Langsjoen AM. 2003. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 18(1-4):101-11.



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Lifestyle recommendations include 20-30 minutes of aerobic-type exercise at least three days a week, and quitting smoking.

Holistic treatment Generally speaking, the holistic perspective on the origin of atherosclerosis is related to an underlying metabolic dysfunction caused by alterations in diet and lifestyle. In other word the origin of atherosclerosis is more of a software issue than a hardware issue, even though it can have very strong hardware implication if it goes to far. This idea is based on sound epidemiological and anthropological research that indicates that the incidence of atherosclerosis is for the most part a disease of people that eat a highly refined modern diet, rich in carbohydrates, plentiful in oxidizing and toxic compounds, and deficient in key nutrients including minerals, vitamins, essential fatty acids, and plant-based antioxidants. Associated factors include a sedentary lifestyle (which promotes insulin resistance) and environmental pollutants, e.g. cigarettes, air pollution etc., some of which are easier to control (i.e. smoking, exercise) than others (i.e. air pollution). The results of this exposure to environmental toxins, a lack of exercise, and a dysfunc-tional eating pattern are metabolic problems such as chronic hyperglycemia, insulin resistance, hyper-insulinemia and dyslipidemia, free radical production, and impaired detoxification. Thus the focus in holistic treatment is to reduce the glycemic load of the diet, and supplement with key nutrients that may be deficient and can enhance antioxidant and detoxification pathways in the body. While the atheroma is fingered as the causal agent of atherosclerosis, and indeed, defines the nature of the condition, a holistic perspective suggests that the atheroma develops as a transient response to endothelial injury, to inhibit further endothelial injury by promoting a local thickening of the endothelial wall: essentially, chewing gum stuck in a crack of a dam about to burst. The transient and reversible nature of the atheroma suggests that if correct measures are taken to eliminate endothelial injury the atheroma will eventually be replaced by normal endothelial tissue. If the factors that cause damage to the endothelium are chronic however, the temporary method the body uses to protect against further endothelial injury



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becomes a secondary source of injury, narrowing the lumen of the vessels, placing stress on the heart, and then eventually, occluding the vessel so as to promote ischemia. The process of atherosclerosis is thus dependent upon chronic, underlying factors that promote the continuance of the atheroma, in much the same way that a scab that is constantly picked will never heal, and will result in a much larger lesion than originally sustained. From a traditional herbal perspective, atherosclerosis can be seen as a dysfunction of blood, specifically, in its constitution and its movement. The constitution of the blood is in large part a manifestation of digestive processes, and thus an assessment of digestion should be carefully undertaken. Specifically, it is the job of the liver to build, replenish and filter the blood, and thus problems relating to the constitution of blood (e.g. blood viscosity, dyslipidemia etc.) demonstrates a need for upregulating liver function with the use of cholagogues, e.g. Berberis, Curcuma, Taraxacum, Buplerum, Chelidonium. In Chinese and Ayurvedic terms an increase in blood viscosity or dyslipidemia relates to the accumulation of phlegm, and thus phlegm-reducing (i.e. kaphahara) remedies such as Commiphora, Zingiber, Capsicum, Rosmarinus, Zanthoxylum and Allium sativum can be used in conjunction with cholagogue remedies. Given the obstructive nature of atherosclerosis the movement of blood is an extremely important consideration, and the nature of the treatment can be implemented based on the presenting signs and symptoms. Generally speaking, it is always wise to include stimulants such as Zingiber, Capsicum and Allium sativum in any therapy directed to atherosclerosis to enhance the processing of blood via the liver, and to dispel the archetypal accumulation of phlegm that underlies the obstructive nature of the atheroma. In many cases however the atherosclerotic patient will present with a substantial deficiency, qi deficiency in Chinese terms, or an increase in vata in Ayuervedic terms. Besides typical symptoms of cold hands and feet, there will be chronic fatigue, poor digestion, and weak pulse. Treatment is orientated to building up the vital essence and restoring the natural heat of the body with nutritive, blood-moving herbs such as Angelica sinensis, Astragalus, Commiphora, Salvia miltiorrhiza, Withania, Panax, Atractylodes, prepared



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Aconitum carmichaeli and the non-toxic Indian species Aconitum heterophyllum. Besides the condition and movement of the blood, attention must also be directed to the integrity of the vessel walls. In Chinese medicine the vessels are said to be regulated by the Spleen, and thus in chronic Spleen qi deficiency the vessels are weak and become susceptible to damage and rupture. Once again, qi-restorative herbs such as those described above are similarly appropriate. Attention should also be directed to using botanicals that have a trophorestorative function on the endothelium. Many of these botanicals are particularly rich in polyphenols such as flavonoids and tannins (e.g. ellagitannins, proanthocyanidins) including Ginkgo, Vaccinium, Terminalia arjuna, Phyllanthus emblica, Curcuma, Centella, Achillea and Vitis vinifera seed. Overall, the holistic approach in the treatment of atherosclerosis is as follows: 1. Reduce the glycemic load of the diet. Adopt a low-

carbohydrate diet, and eliminate all refined carbo-hydrates including sugar, candy, soda pop, cookies and deserts for a minimum period of two to three months. After which time, whole-grain carbohydrates can be rotated back into the diet.

2. Eliminate toxic foods from the diet. Including

hydrogenated and trans-fats (e.g. margarine, deep-fried foods), feed-lot meat and farmed salmon, dairy.

3. Supplement for deficient nutrients. • vitamin B complex, 25 – 50 mg daily • folic acid, 1 g daily • B-12, 1000 mcg daily • vitamin C, 1-5 g bid-tid, to bowel tolerance • vitamin E (d-alpha tocopherol, with mixed

tocopherols), 400-800 IU daily, increase dose gradually (start at 100 IU if recent heart attack)

• EPA/DHA, 2000 – 6000 mg each daily • magnesium, 800 mg daily, in divided doses, with meals • chromium, 200-300 mcg daily • selenium, 100 mcg daily • chelated multimineral, taken with the above minerals;

or high quality kelp (seaweed) supplement (5-15 g

Suggested Program Breakfast Reishi/Cordyceps (3 capsules) Cleansaherb (2 capsules) Garlic (2 capsules) BEVC (2 tablets) B complex (1 tablet) Essential Fatty Acid (2,000 mg) Niacin (50-100 mg) Snack Vitamin C (500 mg). Lunch Vitamin C (500 mg). Snack Same as morning snack. Supper Same as breakfast. Drink 1- 4 cups of Ginger root tea daily.



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daily) • CoQ10, 50 mg daily • Flavonoids (mixed, e.g. quercitin, rutin,

anthocyanidins), 3-5 g daily

4. Support liver, enhance detoxification: Berberis, Curcuma, Taraxacum, Buplerum, Chelidonium, Ganoderma, etc.

5. Promote circulation and blood flow, reduce blood

viscosity (i.e. phlegm, kapha): Commiphora, Zingiber, Capsicum, Rosmarinus, Zanthoxylum, Allium sativum, Piper longum etc.

6. Cardiovascular trophorestoration: Ginkgo,

Vaccinium, Ganoderma, Cordyceps, Crataegus, Terminalia arjuna, Phyllanthus emblica, Curcuma, Centella, Achillea etc.

7. Rebuild the vital essence (i.e. qi, ojas): e.g. Angelica

sinensis, Astragalus, Ganoderma, Cordyceps, Commiphora, Salvia miltiorrhiza, Withania, Panax, Atractylodes etc.

8. Exercise: in particular, anaerobic exercise (muscle-

building) is more effective than aerobic exercise (jumping, running) to reduce insulin resistance, e.g. calisthenics (e.g. pushups, lunges, chin ups etc.), walking or bicycling uphill, hiking, martial arts, weight-lifting; note that any exercise regimen should be implemented gradually

Heart failure Heart failure (HF) is a generalized term that describes a dysfunction in the pumping mechanism of the heart, and a failure to adequately maintain the circulation of blood. Although the term heart failure suggests a rapid cessation of cardiac function, in most cases it refers to a progressive but gradual loss of the efficiency of the heart. A myocardial infarction or heart attack is an ischemic attack of the myocardium, and while it may cause sudden death, it may also lead to progressive heart failure, often with repeated incidents.9,10,11



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Anything that causes the heart to increase its workload for a prolonged period of time can result in heart failure. Heart failure can occur for several reasons, some which are intrinsic to the heart and some that are extrinsic. Intrinsic causes include a loss of the contractile force of the myocardium during systole, a failure of the myocardium to relax during diastole, or a failure of the heart valves to regulate the flow of blood through the heart (e.g. rheumatic fever). A common extrinsic cause of heart failure is hyper-tension (secondary to atherosclerosis), which increases intracardial pressure and promotes pathogenic changes in the pumping mechanism of the heart. Up to 80% of all cases of heart failure relate to an atherogenic process by which the coronary arteries become progressively occluded, causing myocardial ischemia and infarction. The term congestive heart failure (CHF) describes a pathological process that results in a build up of fluid in the lungs and other tissues. It is specifically related to a failure of the ventricles to sufficiently eject blood from the heart, increasing the volume of blood in the ventricles, causing a dilatation of the heart chambers, and elevating the intra-cardial pressure. Overtime the increase in pressure promotes mycocardial hypertrophy (i.e. an “enlarged heart”), a compensatory mechanism that allows the patient to tolerate this state for years. Broadly speaking, CHF can be classified on the basis of which ventricle is more affected, as either left-sided or right-sided heart failure. In most cases CHF relates to a left-sided heart failure, which in turn, can be classified into systolic heart failure or diastolic heart failure. Systolic heart failure refers to a loss of the contractile force of the left ventricle during systole to eject blood into the aorta, resulting in an increase in pulmonary venous pressure and pulmonary congestion and edema. Overtime the result is interstitial fibrosis in the lung, resulting in a loss of pulmonary function. Diastolic heart failure refers to a failure of the left ventricle to relax during diastole, either from a restrictive cardiomyopathy or ventricular tachy-cardia. Right-sided heart failure usually develops as a complication of the former, but can also occur secondary to chronic lung diseases such as lung fibrosis or chronic obstructive pulmonary disease (e.g. emphysema, asthma).



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The resulting pulmonary hypertension places a back pressure on the right ventricle leading to hypertophy, dilatation and an increase in pressure. As a consequence both the right arterial pressure and systemic venous pressure increase, resulting in jugular vein distension, edema of the lower extremities, and congestion of the liver and spleen. The basic signs and symptoms of CHF are as follows: • Dyspnea: Patients with CHF have difficulty breathing,

especially upon lying down, often interrupting normal sleeping patterns. The dyspnea is often associated with a non-production cough, and as the condition progresses the patient may begin to cough up frothy, blood-tinged sputum.

• Exercise intolerance: Patients with CHF experience extreme fatigue and dyspnea, even with day-to-day activities such as sweeping, vacuuming, pushing a lawnmower, or even walking.

• Accumulation of fluid and swelling: With right-sided heart failure patients with CHF often experience a noticeable swelling in their legs, feet, and ankles, which can extend upwards to the waist, with hepatosplenomegaly and ascites.

• Cerebral symptoms: Elderly patients with CHF frequently experience confusion, memory impairment, anxiety, headaches, insomnia, nightmares, or in rare cases, psychosis with disorientation.

The New York Heart Association (NYHA) classifies CHF into four basic groups: • Class I: describes a patient who is not limited in any

normal physical activity by symptoms. • Class II: occurs when ordinary physical activity results

in fatigue, dyspnea, or other symptoms. • Class III: characterized by a marked limitation in

normal physical activity. • Class IV: defined by symptoms at rest or with any

physical activity.

Medical treatment The focus of medical treatment in CHF is three-fold: to decrease pulmonary capillary hydrostatic pressure and fluid



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transudation into the pulmonary interstitium and alveoli; reduce systemic vascular resistance; provide ionotropic and chronotropic support. Typical therapies used to reduce lung congestion and edema include nitroglycerin (mostly for angina), diuretics (e.g. furosemide, bumetanide, torsemide and metolazone) and vasodilators (e.g ACE inhibitors, angiotensin II receptor blockers). Medications used to reduce systemic vascular resistance are mostly comprised of the same vasodilators mentioned above. The most important medications used to provide ionotropic and chronotropic support is digoxin. Digoxin increases the force of myocardial contraction (positively ionotropic) but decreases the heart rate (negatively chronotropic). Beta-adrenergic blockers (e.g. metoprolol, carvedilo) are also sometimes used, as are sympathomimetics such as norepinepherine, dopamine and dobutamine. Antidys-rhythmics are also used to control the rhythm of the heart, particularly in diastolic heart failure, such as amiodarone and flecainide.

Holistic treatment CHF is a condition in which probably many herbalists would decline to treat, given the severity of the condition and the number of medications that the patient is likely to be on, fearing potential drug interactions. It is interesting to note however that the key drug used to treat CHF (i.e. digoxin) is in fact of herbal origin, a glycoside derived from Digitalis pupurea. Medicine attributes the inclusion of this drug in its materia medica to William Withering in 1785. According to Withering, he learned of the use of Digitalis from a Shropshire woman who used it in combination with a variety of herbs to treat cardiac “dropsy.” Withering isolated Digitalis and began to experiment with it, noting its delayed effects and cumulative toxicity, including vomiting, diarrhea, bradycardia, seizures, sweating and a transient loss of consciousness (syncope). Although it would be interesting to observe the effects of the original polyherbal formulation, the natural variance of cardioactive glycosides in the various Digitalis spp. as well as its cumulative, toxic effects, makes Digitalis a difficult herb to prescribe with a great deal of confidence. In Herbal Medicine Rudolf Weiss suggest that a tincture of Digitalis lanata can be used to good effect in small doses in maintenance therapy for CHF, 5-10 drops in water, twice daily, using the smallest dose



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possible. Another important botanical that can be used to good effect in CHF is Convallaria majalis, which also contains cardioactive glycosides. Convallaria is given specifically in bradycardia, particularly in senile hearts which are easily overcome by activity but “perform reasonably well at rest”.12 The primary advantage over Digitalis is that the cardioactive glycosides (i.e. convallatoxin and the cardenolides) have a rapid onset of action and are non-cumulative. Weiss also states that Convallaria is “…effective in mild to medium-severe forms of heart failure, but cannot replace Digitalis when decompensation is severe.” Beyond its cardioactive glycosides Convallaria contains several flavonoids that contribute to the restorative effect that it has upon the heart. Dose of the tincture of the fresh (1:2) or dried rhizome (1:5) is 5-20 drops, bid-tid. Needless to say, neither Digitalis nor Convallaria should be used concurrently with digoxin therapy, although Convallaria may be carefully used to wean the patient off of digoxin. Beyond the use of Digitalis and Convallaria, a number of other botanicals can be of great benefit to control the rate and rhythm of the heart, including: • Selenicereus grandiflorus is described as having a

digitalis-like effect, and in small doses is an excellent heart tonic, increasing the force and regulating the rhythm of ventricular contraction. Dose of the fresh plant tincture (1:2) is 10-20 drops bid-tid.

• Crataegus spp. and Terminalia arjuna are rich in flavonoids and are well-known trophorestorative agents, particularly indicated in senile hearts, helping to strengthen the heart beat while regulating its rhythm. The dose for either Crataegus flower tincture or tincture of Terminalia arjuna is 1-5 mL bid-tid. (fresh plant 1:2; dry plant 1:5). Both plants can also be taken as a powder (2-3 g bid-tid.) or as an aqueous extract (100-150 mL bid-tid.).

• Cytisus scoparius is a cholagogue and diuretic that is used in extrasystole (irregular heart beat), arrhythmia and tachycardia. Dose of the tincture is 15-40 drops bid-tid. (fresh plant 1:2, dry plant 1:5).

• Leonorus cardiaca is an important antispasmodic herb that is particularly useful in tachycardia associated with anxiety and nervousness. Dose of the tincture is 1-4 mL bid-tid (fresh plant 1:2, dry plant 1:5), or it may be



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taken as an infusion, 100-150 mL bid-tid. • Ganoderma and Cordyceps both have cardiac tonic,

blood pressure reducing, lung congestion reducing and qi increasing ability (Reishi/Cordyceps formula 2 – 3 capsules twice daily)

Other important botanicals include Valeriana officinalis, Tilia cordata, and Scutellaria lateriflora. Any botanical that has a cardioactive activity may interact with drug therapy, and thus extreme caution is warranted.

Botanicals that have a particular benefit in reducing hypertensive states include: Ganoderma, Cordyceps, Viscum album, Coleus forskohli, Allium sativum, Viburnum opulus and Tilia cordata. Also called for in CHF are diuretics to relieve pulmonary and venous congestion, such as Petroselinum crispus, Barosma betulina, and Chimaphila umbellata, and expectorants such as Asclepius tuberosa, Verbascum thapsus and Inula helenium. In some cases where the patient does not want alternatives to drug treatment, in particularly severe cases, or where it is difficult to work with the attending physician, it may be impossible to employ any of the above remedies as alternatives. Beyond these specific herbs however, the basic treatment for CHF will be essentially the same as it is for atherosclerosis in the vast majority of cases. Suggested Program

The following guidelines should also be adhered to: 1. Roughage should always be present. 2. Meals should be small and fairly frequent; avoid large

meals. 3. Food should be chewed extremely well. Breakfast A grain with 1 tablespoon of Hemp seed, Chelated Multiminerals (1 tablet), Multivitamins and minerals (1 tablet), B complex (1 tablet), Vitamin C (500 mg), Selenium (100-200 mcg), Chelated Calcium/ Magnesium (1 tablet), Hawthorn (2-3 g bid-tid.), Cayenne (1-2 capsules), Reishi/Cordyceps (3 capsules), Essential Fatty Acids (1 - 2,000mg), Coenzyme Q10 (50mg). Lunch Salad or soup. Vitamin E (start with 100 IU and



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build up to 400 IU), Vitamin C (500 mg). Supper Salad with grains, lightly cooked vegetables and/or some fish or lean poultry. Supplements: same as at breakfast. Before retiring Vitamin E (100 IU, gradually build up to 400 IU).

Varicose veins A varicose vein is an enlarged, tortuous vessel in the venous system filled with stagnant deoxygenated blood. Factors that promote the obstruction of venous flow include tight clothing around the waist and especially pregnancy, which as the fetus grows, compresses the veins that drain legs, causing an increase in pressure and the manifestation of varicosities. Hormones released during pregnancy facilitate this dynamic by making vessels more pliable. Other more serious causes include a thrombosis in the deep veins, and should be ruled out. The most common cause of varicose veins is physical inactivity, especially if it is compounded with the effects of gravity. Thus people who are required to stand for long periods without moving or completely contracting the legs of the muscles are much more prone to varicosities. Researchers have also pointed out the importance of accessory nutrients such as flavonoids that play a key role in the function and repair of venous tissue (e.g. aesculin, derived from Hippocastanum), and thus dietary deficiencies of such nutrient can be seen to promote or exacerbate this condition. While generally not all that serious of a condition, varicose veins can be very painful, and if untreated can eventually ulcerate and become infected. 13 Thrombophlebitis describes the inflammation and secondary thrombosis of the small veins, as part of a local reaction to bacterial infection. Phlebothrombosis is the same as above but is not attributable to inflammation or infection. The term deep vein thrombosis is the formation of a thrombus associated with decreased cardiac output and extended bed rest, typically forming in the deep veins of the iliac and femoral veins. The primary concern in such cases is that the thrombus could embolize to the lungs.

Varicose Vein Lotion for External Use

Hamamelis 80 ml Aesculus tinct 10 ml Symphytum tinct 10 ml Apply liberally to area. You can add Rose water or other floral water to add to the scent.



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Holistic treatment Besides the etiological factors mentioned above, herbalists recognize chronic abdominal and portal congestion as an important cause of an increase in venous pressure. Further, studies show that varicosities often form in childhood. This suggests that not only may the condition have a hereditary link, but may be related specifically to nutritional factors during childhood. Measures are thus taken to correct situations of pelvic congestion and provide the co-factors need to ensure the integrity of the blood vessels. Botanicals that exert a gentle astringing activity, act as pelvic decongestants and are rich in flavonoids are particularly warranted. Examples include Aesculus, Collinsonia, Lamium, Curcuma and Scutellaria baicalensis. Other botanicals that specifically improve blood vessel integrity include Crataegus, Vaccinium, Ginkgo, Phyllanthus and Centella. Circulatory stimulants are also warranted, including Zanthoxylum, Zingiber, and Capsicum. These botanicals can be formulated and taken internally as well as applied externally, twice daily. Where the tissues appear dry and weak, these herbs can be applied as a medicated oil, along with more generalized tropho-restorative botanicals such as Astragalus and Angelica sinensis. In Chinese medicine the health of the vessels directly relates to the strength of the Spleen, and thus Spleen Qi restoratives such as Panax, Astragalus, Atractylodes and Codonopsis can be taken internally. Given that varicosities can relate to thrombus formation, measures should also be taken to inhibit platelet aggregation and reduce the viscosity of the blood. Specific botanicals include Ginkgo, Allium and Commiphora. Trophorestorative nutrients should also be considered, including vitamins A, C, E and zinc, as well as direct supplementation with flavonoids. Hot and cold hydrotherapy can also be helpful (always ending cold), and regular exercise is recommended.

Suggested Program Breakfast Horse Chestnut tincture (20 drops), BEVC (2 tablets), Cleansing Formula (2 capsules), Bioflavonoids (1,000 mg), Essential Fatty Acids (2,000 mg), Zinc (15 mg). Lunch Horse Chestnut tincture (20 drops), Bioflavonoids (1,000 mg). Supper Same as breakfast.



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Action of Herb for Varicose veins ACTION HERBS

Circulatory stimulant Zanthoxylum, Ginkgo Vascular tonic Crataegus, Aesculus,

Achillea Astringent Achillea, Hamamelis Emollient Symphytum Vulnerary Symphytum Anti-inflammatory Aesculus

Anemia

The term anemia refers to a decrease in the number of red blood cells (RBCs) or hemoglobin (Hb) content caused by a limited number of mechanisms that can function independently or occur synergistically. The term anemia is often used incorrectly as a diagnosis, but like hypertension, is really a symptom of an underlying pathology. Thus different types of anemia are defined according to the pathophysiology.

Generally speaking, there are three primary causes of anemia: 1. blood loss 2. deficient erythropoiesis (decreased production of

RBCs) 3. excessive hemolysis (increased RBC destruction) A number of conditions can cause anemia, including: • external blood loss: e.g. trauma, injuries, menorrhagia,

and stomach ulcers • iron deficiency: iron is an important component in the

production of hemoglobin • chronic disease: any long-term disease can lead to

anemia • kidney disease: through decreased erythropoietin

secretion • pregnancy: water gain during pregnancy is thought to

dilute the RBCs (hemodilution); the fetus also robs the



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mother of iron during pregnancy • poor nutrition: inadequate source of dietary iron and

accessory nutrients (e.g. B complex); also common in alcoholism

Signs and symptoms of anemia include: • black and tarry stools (sticky and foul smelling) • maroon, or visibly bloody stools • rapid heart rate • rapid breathing • pale or cold skin • jaundice • hypotension • heart murmur • fatigue • dyspnea (lack of air, air hunger) • chest and/or abdominal pain • weight loss • weakness • vertigo and fainting, especially upon standing Apart from external blood loss from trauma or injury, the two primary metabolic mechanisms of anemia are deficient RBC production and excessive RBC destruction.

Deficient erythropoiesis Anemia is often classified according to RBC morphology, which can give an indication of the cause of the anemia, and thus terms such as microcytic anemia, normochromic-normocytic anemia, and macrocytic anemia are often used. These terms describe the different types of anemias that are caused by deficient erythropoiesis. Microcytic anemia indicates an alteration in heme or globin synthesis, such as in iron deficiency, thalassemia (and related Hb-synthesis defects), and anemia of chronic diseases (e.g. infection, inflammation). Iron-deficiency anemia is the most common anemia, and is a chronic condition characterized by small, pale RBCs and iron depletion. The most common clinical presentation is fatigue, dizziness, headache, insomnia pallor, weight loss and poor immunity. The conjunctiva, buccal mucosa and nail bed may be pale. In severe cases the patient may



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display pica (a craving for dirt, paint, chalk, glue, hair or ice), glossitis (inflammation of the tongue), cheilosis (sores about the lips and mouth), and koilonychias (thinning, concave nails).

Normochromic-normocytic anemia refers to state of the RBCs that appear otherwise normal upon microscopic examination, but are diminished in number. Thus, this type of anemia suggests a failure to produce the necessary number of RBCs to accommodate those that are no longer viable and are removed from circulation by the spleen and liver. In contrast, hypoplastic or aplastic anemia results from a loss of RBC precursors due to a defect in the stem cell pool or an injury to the red marrow from which the RBCs are generated. The cause of such anemias are typically related from exposure to certain industrial chemicals (e.g. benzene, inorganic arsenic), radiation, or drugs (e.g. chemotherapy, antibiotics, NSAIDs, anticonvulsants). In some cases the cause is unknown and termed idiopathic aplastic anemia. Macrocytic or megablastic anemia refers to a state of deficient RBC production, but one in which the RBCs appear unusually large. This results from defective DNA synthesis but with continued RNA synthesis, resulting in an increase in RBC cytoplasmic mass. This form of anemia is typically related to a dietary deficiency or impaired metabolism vitamin B12 and/or folic acid (folate), as well as the use of cytotoxic and immunosuppressant drugs that impair proper DNA synthesis. A vitamin C deficiency can also promote anemia, usually associated with hypochromic anemia, but also normocytic and occasionally microcytic anemia. Vitamin C plays a key role in iron utilization.

Excessive hemolysis Excessive hemolysis refers to the excessive destruction of RBCs, usually by phagocytic cells in the spleen, liver, and bone marrow. A common clinical or laboratory finding for hemolysis is jaundice, occurring when the conversion of Hb to bilirubin exceeds the liver's capacity to form bilirubin glucuronide and excrete it into the bile, promoting unconjugated bilirubinemia. Increased catabolism is also manifested by an increase in stercobilin in the stool and urobilinogen in the urine, as well as pigment-gallstones



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particularly in chronic conditions.

Anemias caused by disorders of red blood cell metabolism relate to a failure of the RBC to use glucose effectively to produce ATP and are rare genetic disorders. Anemias caused by defective hemoglobin synthesis are similarly caused by genetic abnormalities. Sickle cell anemia is a RBC defect that is found mostly in people of African descent, and to a lesser degree those of Mediterranean and Middle Eastern descent.

Holistic treatment The cause of anemia must be carefully ascertained. From a herbal perspective, botanicals that nourish blood are indicated in every kind of anemia, irregardless of cause, including Withania, Asparagus, Phyllanthus emblica, Angelica sinensis, Lycium barbarum, Paeonia alba, Morus alba, and Polygonum multiflorum. Such herbs can be prepared as a strong decoction (1:1), strained well, and preserved with a combination of honey and molasses, taken in tablespoon-full doses bid-tid. Additional helpful herbs include Rumex crispus, Rubus idaeus, and Urtica dioica, as infusion or tincture. • Microcytic anemia relates to an iron deficiency,

caused by a dietary deficiency of iron, malabsorption from intestinal damage (e.g. inflammatory bowel disease or bowel surgery), or from the excess consumption of iron-chelating agents in the diet. Holistic treatment consists of increasing iron containing foods (e.g. meat, yams,g figs, collard greens), botanicals that nourish blood, ascorbic acid and the B vitamins.

• Normochromic-normocytic anemia relates to either hypoproliferative causes (e.g. renal disease, hypothyroidism or protein deficiency), or hypoplastic causes (e.g. industrial chemicals, radiation, chemotherapy, antibiotics, NSAIDs, anticonvulsants). In each case the cause must be treated separately, but can also be treated generally with iron containing foods (e.g. meat, yams, figs, collard greens), botanicals that nourish blood, ascorbic acid and the B vitamins.

g In this case ‘yam’ refers to the true yam (Dioscorea spp.), not sweet potato which many people call a yam (Ipomoea batatas).



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For renal disease see: The Water of Life: Renal function and Botanical Medicine For hypothyroidism see: A Life in Balance: Metabolic Function and Botanical Medicine For chemical intoxication see: The Inner Alchemist: Hepatobiliary Function and Botanical Medicine

• Macrocytic or megablastic anemia refers to a state of

deficient RBC production, related to a deficiency or defective utilization of cobalamin or folic acid, and the use of cytotoxic and immunosuppressant drugs that interfere with DNA synthesis. Supplement with cobalamin (1000 mcg daily), folic acid (1 mg daily), along with the other B vitamins (100 mg daily), vitamin C (2-3 g daily), iron containing foods (e.g. meat, yams, figs, collard greens), and botanicals that nourish blood.

For the hemolytic anemias treatment is once again orientated to the cause, in addition to blood nourishing botanicals. Hemolytic anemias caused by autoimmunity are addressed under Herbal Immunity: Nonspecific Resistance, Immunity and Botanical Medicine, and require the use of anti-inflammatory and immunomodulating botanicals. For sickle-cell anemia specifically, Zanthoxylym bark can be taken continuously as a curative remedy, 20-40 gtt of a 1:5 tincture, bid-tid.



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References Aronson Doron and Elliot J Rayfield. 2002. How hyperglycemia promotes atherosclerosis: molecular mechanisms. Cardiovascular Diabetology. 1:1

Bensky, Dan and Andrew Gale. 1993. Chinese Herbal Medicine: Materia Medica. Rev. ed. Seattle, WA: Eastland Press

Bergner, Paul. 1997. The Healing Power of Minerals, Special Nutrients and Trace Elements. Rocklin, CA: Prima Publishing.

Berkow, Robert ed. et al. 1992. The Merck Manual of Diagnosis and Therapy. 17th ed. Rahway, NJ: Merck and Co.

Despres JP et al. 1996. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med. 334:952-957.

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Govan A, McFarlane, Callander R. 1991. Pathology Illustrated 3rd ed. London: Churchill-Livingstone Haas, Elson. 1992. Staying Healthy with Nutrition: the complete guide to diet and nutritional medicine. Berkeley: Celestial

Kritchevsky D. et al. 1954. Effect of Cholesterol Vehicle in Experimental Atherosclerosis. Am J Physiol July-September. 178:30-32

Mattu, Amal. 2005. 2005. Pulmonary Edema, Cardiogenic. Available from: http://www.emedicine.com/med/topic1955.htm

Moore, Michael. 2002. Herbal Energetics in Clinical Practice. Self-published. Available online from: http://www.swsbm.com

Port S, Garfinkel A, Boyle N. 2000. There is a non-linear relationship between mortality and blood pressure. Eur Heart J 2000 Oct;21(20):1635-8

Price, Weston. 1939. Nutrition and Physical Degeneration. 6th ed. New Canaan, Connecticut: Keats. Priest, A.W. and L.R. Priest. 1982. Herbal Medication. London: L.N. Fowler & Co. Rubin, E. ed. 2001. Essential Pathology. 3rd ed. Philadelphia: J.B. Lippinocott. Rubin, E and J. Farber. 1990. Essential Pathology. Philadelphia: J.B. Lippinocott. Schatz et al 2001. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet. 358: 351–55

Sobel BE et al. 1998. Increased plasminogen activator inhibitor type 1 in coronary artery atherectomy specimens from type 2 diabetic compared with nondiabetic patients: a potential factor predisposing to thrombosis and its persistence. Circulation. 97:2213-2221.

Tillotson, Alan. 2001. The One Earth Herbal Sourcebook. New York: Twin Streams (Kensington) Tortora, G. and S. Grabowski. 2003. Principles of Anatomy and Physiology. 10th ed. New York: Harper-Collins.

Weiss, Rudolf. 1988. Herbal Medicine. Trans. By A.R. Meuss. Beaconsfield, England: Beaconsfield Publishers

Wood, Matthew. 2002. The Six Tissue States: The Energetics of Physiomedicalism. JAHG 3(1):28-33 Zevitz, Michael E et al 2005. Heart Failure. Available from: http://www.emedicine.com/med/topic3552.htm



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1 Wood, Matthew. 2002. The Six Tissue States: The Energetics of Physiomedicalism. JAHG 3(1):28-33 2 Wood, Matthew. 2002. 3 Priest, A.W. and L.R. Priest. 1982. Herbal Medication. London: L.N. Fowler & Co, p19 4 Moore, Michael. 2002. Herbal Energetics in Clinical Practice. Self-published. Available online from: http://www.swsbm.com 5 Bergner, Paul. 1997. The Healing Power of Minerals, Special Nutrients and Trace Elements. Rocklin, CA: Prima Publishing 6 http://en.wikipedia.org/wiki/Obesity_in_Canada 7 Berkow, Robert ed. et al. 1992. The Merck Manual of Diagnosis and Therapy. 17th ed. Rahway, NJ: Merck and Co. 8 Rubin, E and J. Farber. 1990. Essential Pathology. Philadelphia: J.B. Lippinocott p 355 - 369 9 Berkow, Robert ed. et al. 1992. The Merck Manual of Diagnosis and Therapy. 17th ed. Rahway, NJ: Merck and Co 10 Rubin, E and J. Farber. 1990. Essential Pathology. Philadelphia: J.B. Lippinocott 11 Zevitz, Michael E et al 2005. Heart Failure. Available from: http://www.emedicine.com/med/topic3552.htm

12 Weiss, Rudolf. 1988. Herbal Medicine. Trans. By A.R. Meuss. Beaconsfield, England: Beaconsfield Publishers, p 146 13 Berkow, Robert ed. et al. 1992. The Merck Manual of Diagnosis and Therapy



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