The clinical presentation can vary to a large degree, from a mild, itchy rash to severe, red crusting legions that can cover progressively larger regions of the body, and in children can interfere with normal growth and development. With repeated scratching the condition can worsen and secondary bacterial infections can appear. Very often the term eczema is used interchangeably with atopic dermatitis, however, eczema is a less precise term of which atopic dermatitis is a specific form, along with other sub-classifications that include allergic, irritant and seborrheic contact dermatitis. (Berkow 1992; Spagnola 2005)

The pathology of atopic dermatitis relates to a variety of IgE-mediated inflammatory response involving mast cells, lymphocytes, and leukocytes. The most prominent theory for this cause is an imbalance between Th1 and Th2 helper cell activities. Depending upon the antigenic substance, either Th1 or Th2 cells rise from the original T helper cell that interfaces with the antigen presenting cells. Th2 cells secrete cytokines in response to allergens, which in turn promotes the synthesis of immunoglobulin E (IgE). In contrast, Th1 is normally activated during infection with bacteria or parasites – the hygiene hypothesis states that the failure to acquire a normal flora both within and without the body suppresses Th1 response, and allows Th2 activities to function out of control. (Berkow 1992; Spagnola 2005)

Another prominent theory underlying the etiology of atopic dermatitis is either a deficiency of the essential omega-3 and omega-6 fatty acids, or a failure to properly metabolize them. This is clearly demonstrated in bottle-fed infants fed a formula lacking in either omega-6 or omega-3 fatty acids, which have a significantly higher incidence of atopic dermatitis than their breast-fed counterparts. Omega-3 acids specifically also promote the synthesis of eicosanoids that down regulates Th2 activity, and restores a balance between these paired T helper cells. Problems of essential fatty acid metabolism are thought to related to a potential hereditary deficiency of delta-6-desaturase, a key enzyme in the biotransformation of the essential fatty acids. Environmental factors that promote a deficiency of delta-6-desaturase include a diet rich in transfatty acids, aging, chronic disease and emotional stress. True omega-6 deficiencies are not as common as omega-3 deficiencies however, as omega-6 fatty acids are over consumed in the modern diet by a ratio as high as 20:1, when in reality the ratio should be closer to 2:1. (Berkow 1992; Spagnola 2005)

Another important factor to take into consideration is the role of food allergens and food intolerances in atopic dermatitis. Although generally not acknowledged as a major etiological factor by many medical professionals, at least on an anecdotal and clinical basis the removal of common food allergens including dairy, wheat, egg whites, soy, fish, shellfish and peanuts are often accompanied by significant improvements.

Atopic dermatitis can begin during infancy (i.e. ‘infantile eczema’), and can be relatively severe, with red, weeping, and crusting lesions over the entire body, particularly the face and scalp. In children the manifestations are typically less acute, more chronic lesions characterized by erythema and lichenification in typical areas such as inside the elbow or knee. In many people the condition goes into remission during puberty or adulthood, sometimes with periodic exacerbations. In many cases there is a concomitant hypersensitivity to numerous environmental factors, including changes in temperature or humidity, certain fragrances, fabric softeners, and wool. Given the embryonic link between the nervous and integumentary systems it is perhaps no surprise that emotional stress can promote atopic dermatitis. (Berkow 1992; Spagnola 2005)

Medical treatment

The mainstay of the medical treatment of atopic dermatitis are topical corticosteroids, often used in increasing strength after simpler measures such as OTC creams, moisturizers and lotions have been tried to rehydrate the skin and relieve itching. In severe or particularly recalcitrant cases systemic corticoids may be used, and if the condition is refractive to steroids, immunosuppressives such as cyclosporine. Topical and systemic antipuritics are another important component of medical therapy, such as pramoxine, which acts to blocks nerve conduction and impulses by inhibiting depolarization of neurons, and doxepin, which is an antihistamine. Antibiotics are used both topically and systemically to deal with secondary bacterial infection.

Holistic treatment

In Western herbal medicine atopic dermatitis is viewed as a manifestation of skin deficiency, and thus measures are taken to address the underlying cause of such, which includes promoting liver anabolism, peripheral vasodilation, and skin and neuroendocrinal trophorestoration. Modifications are made to the diet on the basis that many of the foods commonly consumed in the modern diet are inherently antigenic, the most common culprits being gluten (e.g. wheat) and casein (dairy protein). Initial herbal therapy consists of a mild eliminatory program, enhancing detoxification through the use of alteratives (e.g. Burdock (Arctium lappa), Red Clover (Trifolium pratense), Ceavers (Galium aparine), Nettles (Urtica dioica)), cholagogues (e.g. Yellow Dock (Rumex crispus), Bearberry (Berberis vulgaris), Black Radish (Raphanus sativus), Turmeric (Curcuma longa)), aperients (e.g. Cascara bark (Rhamnus purshiana), Amlavetasa (Rheum emodi), Trivita (Operculina turpethum), Triphala) and diuretics (e.g. Pipsissewa (Chimaphila umbellata), Buchu (Barosma betulina), Parsley leaf (Petroselinum sativum), Gokshura (Tribulus terrestris)), along with circulatory stimulants that direct that activity of these herbs to the periphery (e.g. Prickly Ash (Zanthoxylum clavaherculis), Ginger (Zingiber officinale), Cayenne (Capsicum minimum), Pippali (Piper longum)). This approach can be followed or used concurrently botanicals that support neuroendocrinal function and down-regulate sympathetic stress (e.g. Licorice (Glycyrrhiza glabra), Damiana (Turnera diffusa), Milky Oats (Avena sativa), Reishi (Ganoderma lucidum), Ashwagandha (Withania somnifera), Skullcap (Scutellaria lateriflora) etc.), as well as botanicals that have a vulnerary activity (e.g. Comfrey (Symphytum officinale), Marigold (Calendula officinalis), Plantain (Plantago spp), Gotu Kola (Centella asiatica) and Yin Chai Hu (Stellaria dichotoma)). Trophorestorative nutrients including vitamins A, B, C and E are important, as well as antioxidants (e.g. grape seed extract, MSM, shilajitu), and omega fatty acids (EPA/DHA). In the case of atopic dermatitis in children of breast feeding mothers attention is directed to removing antigentic foods from the diet, the use of “galacto-purifiers” such as Turmeric (Curcuma longa), and supplementation of essential fatty acids and trophorestorative nutrients.

Soaps and detergents are eliminated and replaced by simply using water, along with oatmeal baths and the topical application of Aloe vera juice to alleviate itching. Lesions can be treated directly with the application of oils and salves medicated with vulnerary and demulcent herbs such as Comfrey (Symphytum officinale), Marigold (Calendula officinalis), Plantain (Plantago spp), St John’s Wort (Hypericum perforatum), Gotu Kola (Centella asiatica) and Yin Chai Hu (Stellaria dichotoma). For weeping, oozing sores a cream prepared with gentle astringents such as Oak (Quercus spp.), Witch Hazel (Hamamelis virginiana) and Walnut bark (Juglans nigra) (3-20% v/v) is applied topically. Secondary bacterial infection can be treated with antibacterial herbs such as Goldenseal (Hydrastis canadensis), Neem (Azadirachta indica), and Purple Coneflower (Echinacea angustifolia), in conjunction with the vulneraries stated above.

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Asthma is another COPD, characterized by inflammation and obstruction of the bronchus and bronchioles, mediated by a hyper-reactivity to a variety of stimuli, including smoke, noxious gases, pollen, animal dander and dust, as well as the heaving breathing that accompanies exercise, laughing, crying or emotional stress. Recently, the role of volatile organic compounds (VOCs) found in carpeting and building materials have been identified in the pathogenesis of asthma. Another factor is a concurrent respiratory infection, such as coryza or pneumonia. With asthma it is thought that these factors or combination of factors initiates the release of inflammatory mediators promoting the release histamine and arachidonic acid metabolism. When activated these inflammatory chemicals promote the smooth muscle spasm of the bronchial wall and edema of the mucosa, enhancing mucus production and bronchial injury by activated immune cells (primarily eosinophils, lymphocytes and neutrophils). It is important to note that production of inflammatory mediators is enhanced by a pre-existing deficiency of vitamins, minerals and accessory nutrients such as n-3 PUFAs and flavonoids that counter or prevent inflammation. (Berkow 1992, 646-47; Rubin and Farber 1990, 329-332)

The frequency and severity of asthma attacks vary to a large degree. Some patients have only occasional episodes that are mild and brief, whereas others experience a chronic cough and mild bronchial congestion that is interrupted by severe episodes of bronchospasm, usually after exposure to some type of stimuli that enhances bronchial hypersensitivity. An asthma attack typically has an acute onset, with sudden wheezing, coughing, and dyspnea, sometimes preceded by pruritis over the neck and chest. The cough of an asthma attack is distinctively tight, hard and sharp, generally unproductive, and accompanied by wheezing, a sensation of chest constriction and the subsequent distress this causes the patient. In less severe attacks a dry cough may be the only presenting symptom. After the attack subsides many patients will produce a thick, tenacious mucus. (Berkow 1992, 647-48; Rubin and Farber 1990, 329-332)

Asthma is classified into four categories according to the severity of symptoms. In many cases a patient will move back and forth between these categories, depending upon treatment and the presence of stimuli that promotes hypersensitivity:

Medical treament

The medical treatment of asthma consists of a consideration for environmental triggers (including animal dander, dust mites, cockroaches, airborne molds, and pollens) and symptomatic drug interventions. Potential allergens are typically identified by the RAST method. Typical interventions include furniture and flooring changes, emphasizing dust covers and hardwood floors. Patients may be counseled to give up a pet, or limit exposure. Pollen allergies however are difficult to control by such methods, and thus densensitization immunotherapy may be recommended, apart from drug therapy.

Drug therapy for asthma consists of bronchodilators, used to control acute symptoms, and corticosteroids, used to inhibit chronic inflammation. Among the bronchodilators used in acute inflammation are ?-adrenergic agonists, often administered in metered doses by inhalation, including epinephrine, albuterol, terbutaline, pirbuterol, metaproterenol, bitolterol, isoetharine and the long-acting (12h) salmeterol. Anticholinergic drugs such as atropine may also be administered in emergency situations to control symptoms. Theophylline is a methylxanthine found in black tea that is administered orally as fast acting bronchodilator, but has a number of severe side-effects including ventricular arrhythmia and even death. Theophylline should be discontinued immediately if there are any symptoms of nausea and vomiting.

Chronic inflammation in asthma is typically treated with corticosteroids, given orally or as an aerosol, the latter of which is also used to treat late responses to inhaled allergens, blocking the subsequent bronchial hyperactivity. Adverse effects of inhaled corticosteroids include hoarseness and mucocutaneous candidiasis. Systemic effects include suppression of the adrenal-pituitary axis, growth suppression in children, osteoporosis in women, thinning of the skin, and easy bruising. Care must be taken when withdrawing corticosteroids as too rapid of a withdrawal can precipitate secondary adrenocortical insufficiency. Other prophylactic drugs used to control inflammation include cromolyn and nedocromil, but are not used in acute scenarios.

Holistic treatment

In Ayurvedic medicine asthma, or svasa, is the result of a worsening cough (kasa), or from similar etiological factors that include the upward movement of apana vayu, which invades the chest and throat, causing a vitiation of Kapha, which causes dyspnea, wheezing, catarrh and distress. Other etiological factors include poor digestion, exposure to poisons, noxious fumes and dust, anemia, chronic fever, wind, injury or from drinking very cold water. The clinical features of svasa are differentiated into five types with different causative factors: Kshudrasvasa (dyspnea), Tamakasvasa (bronchial asthma), Chinnasvasa (anaphylaxis), Mahansvasa and Urdhvasvasa: the latter three are incurable and are premonitory symptoms of death. Kshudrasvasa is a mild form of asthma caused by excessive exertion. Tamakasvasa or bronchial asthma is caused by apana vayu invading the chest and throat, causing a vitiation of Kapha. Tamakasvasa can be further classified on the basis of secondary doshic manifestations, i.e. Pittaja, Vataja, but the condition remains primarily an affliction of Vata and Kapha.

In traditional Chinese medicine asthma is an affliction of the Lungs by one of three etiological agents, including Cold, Heat and Qi deficiency. Dyspnea, wheezing and coughing are clinical features of all three types. Cold-type asthma is more frequent attacks in winter and exposure to cold, identified by a white, moist and glossy coating on the tongue, and taut and tight pulse. Heat-type asthma is identified by its occurrence in hot weather, a yellowish mucoid sputum, thirst, a red tongue with yellow greasy coating, and a slippery and rapid pulse. Deficiency-type asthma is caused by a deficiency of Lung and Spleen Qi and manifests as the chronic form of asthma, with a weak, fragile cough, aversion to wind, debility, a pale tongue a dry coating, and a deep fine, weak pulse.

From the Western herbal perspective asthma is caused by the same etiological factors as the medical perspective, in addition to a more complete analysis of environmental triggers, the role of food allergens, digestive weakness (including hypochlorhydria), nutritional deficiencies (e.g. omega 3 fatty acids), intestinal permeability and dysbiosis. Important considerations are also made for stress and anxiety.

1. Open the airways. This is the most obvious treatment for asthma, and can consist of both short and long term strategies. Generally speaking, botanicals hold no special advantage over ?-adrenergic inhalers, but can be used when such medications are unavailable, e.g. Jimsonweed (Datura stramonium) (oral, inhaled smoke), Belladonna (Atropa belladonna) (oral), Lobelia (Lobelia inflata) (oral, inhaled smoke), Visnag (Ammi visnaga) (oral), Ma Huang (Ephedra sinica). IgE-mediated attacks may respond to freeze-dried Nettles (Urtica dioica), two capsules every five minutes. In a pinch very strong black coffee or black tea given in small sips may be life-saving.

2. Eliminate bronchial congestion and inflammation. A variety of methods are used, including those which ease muscular spasm, promote vasoconstriction of the mucosa, assist in the expectoration mucus, and soothe irritation and inflammation.

• Respiratory antispasmodics, specifically used in cold and dry (Vata) conditions, e.g. Lobelia, Sundew (Drosera rotundifolia), Skunk Cabbage (Symplocarpus foetidus), Grindelia (Grindelia spp), Black Cohosh (Cimicifuga racemosa), Wild Yam (Dioscorea villosa), Thyme (Thymus vulgaris), Wild Cherry bark (Prunus serotina), Mullein (Verbascum Thapsus), Coltsfoot (Tussilago farfara), Elecampane (Inula helenium), Cottonwood (Populus candicans), Sundew (Drosera rotundifolia), Wild Lettuce (Lactuca virosa), Bloodroot (Sanguinaria canadensis) Hingu (Ferula foetida), Vasaka (Adhatodha vasica), Tai Zi Shen (Pseudostellaria heterophylla), Xing Ren (Prunus armeniaca)
• Stimulating expectorants, used in highly congestive conditions with a thick profuse catarrh (Kapha), e.g. Heartsease (Viola spp), Squill (Urginea maritima), Queen’s Delight (Stillingia sylvatica), Cowslip (Primula veris), Daisy (Bellis perennis), Senega (Polygala senega), and Euphorbia (Euphorbia hirta), Guggulu (Commiphora mukul), Cottonwood (Populus candicans), Grindelia, Bibhitaki (Terminalia chebula), Tulasi (Ocimum sanctum), Ban Xia (Pinellia ternata), Jie Geng (Platycodon grandiflorum)
• Mucolytics, digestive stimulants to enhance digestion and decrease viscosity of mucus, e.g. Ginger (Zingiber officinale), Chinese Cinnamon bark (Cinnamomum cassia), Anise (Pimpinella anisum), Cayenne (Capsicum minimum), Prickly Ash (Zanthoxylum clavaherculis), Garlic (Allium sativum), Dong Quai (Angelica sinensis), Ela (Elettaria cardamomum)
• Astringing expectorants, to dry up excessive mucus secretions and constrict mucosal capillaries, e.g. Bayberry (Myrica cerifera), Eyebright (Euphrasia officinalis), Canada Balsam (Abies balsamea), Goldenrod (Solidago virgaurea), Mullein (Verbascum thapsus), Goldenseal (Hydrastis canadensis), Bibhitaki (Terminalia chebula)
• Antiinflammatory expectorants, for symptoms of symptoms of heat (Pitta), Vasaka (Adhatodha vasica), Vamsarochana (Bambusa spp.), Bhumyamalaki (Phyllanthus amarus), Chuan Bei Mu (Fritillaria cirrhosa), Zhe Bei Mu (Fritillaria thunbergii), Gua Lou (Gua Lou Ren, Tian Hua Fen) (Trichosanthes kirilowii)
• Demulcents and vulneraries, used in acute inflammation, heat and dryness (Vata, Pitta), and not in profound catarrh, e.g. Licorice (Glycyrrhiza glabra), St John’s Wort (Hypericum perforatum), Comfrey (Symphytum officinale), Plantain (Plantago spp), Marshmallow (Althaea officinalis), Chickweed (Stellaria media), Mai Men Dong (Ophiopogon japonicus), Shi Di Huang (Rehmannia glutinosa), Shi Hu (Dendrobium nobile)

3. Correct dysfunctional breathing patterns. Assess for dysfunctional breathing patterns. Emphasize meditation, relaxation and stress-reduction techniques. Nervine relaxants and trophoretoratives may be indicated, including Milky Oats (Avena sativa), Wild Passionflower (Passiflora incarnata), Valerian (Valeriana officinalis), Wood Betony (Stachys betonica), Pulsatilla (Anenome pulsatilla), Bugleweed (Lycopus virginicus), Motherwort (Leonorus cardiaca), Chamomile (Matricaria recutita) St John’s Wort (Hypericum perforatum), Skullcap (Scutellaria lateriflora), Ashvagandha (Withania somnifera), Brahmi (Bacopa monniera), Ling zhi (Ganoderma spp.)

4. Support immune function.

• Lymphagogues as supportive, and specifically with lymphadenopathy, e.g. purple Coneflower (Echinacea angustifolia), Redroot (Ceanothus americanus), pokeroot (Phytolacca americana), Cedar leaf (Thuja spp), Cleavers (Galium aparine), Red Clover (Trifolium pratense), Barberry (Berberis spp.)
• Immunomodulants in chronic or recurring conditions, e.g. Amalaki (Emblica officinalis), Ling zhi (Ganoderma spp.), Huang qi (Astragalus membranaceus), Wu Wei Zi (Schizandra chinense), Dong Chong Xia Cao (Cordyceps chinensis)
• Immunosupportive nutrients, including vitamins A (25,000 IU daily), B complex (50 mg daily), C (to bowel tolerance) and E (800 IU daily), as well as zinc (50 mg daily) and selenium (100 mcg daily)

5. Correct inflammatory tendency by addressing nutrient deficiencies.

• Decrease consumption of feed-lot, grain-fed meat and animal products, including beef, pork, chicken and eggs.
• Increase consumption of omega-3 fatty acids, equivalent of 1000 mg of EPA/DHA daily
• Flavonoids and anthocyanidins-rich compounds and foods, e.g. quercitin, grape seed extract, turmeric, berries (e.g. blueberries, strawberries), Rubus, Rosa (hips), Hibiscus, Gingko, Amalaki (Emblica officinalis)
• Magnesium and calcium, 800-1000 mg each daily

6. Detoxification.

• Cholagogues and hepatotrophorestoratives to enhance liver detoxification with cholagogues and supportive nutrients, e.g. Bearberry (Berberis vulgaris), Boldo (Peumus boldus), Milk Thistle (Silybum marianum), Haritaki (Terminalia chebula), Haridra (Curcuma longa), Guduchi (Tinospora cordifolia). Bhumyamalaki (Phyllanthus amarus), Katuka (Picrorrhiza kurroa), Huang Qin (Scutellaria baicalensis),
• Diuretics and lymphagogues, e.g. Celery seed (Apium graveolens), Cleavers (Galium aparine), Nettles (Urtica dioica), Goldenrod (Solidago virgaurea), Horsetail (Equisetum arvense), Pokeroot (Phytolacca americana), Cedar (Thuja spp), Redroot (Ceanothus americanus)
• Hydration and heat: showers, baths, steam baths, sweating under blankets; drinking 2 liters of water daily

7. Eliminate environmental triggers. Patients should be assessed for possible allergens (e.g. dust mites, pollen, animal dander, mold), and then placed on an elimination-challenge diet to determine food allergens. Attention must be directed to the removal of noxious agents including volatile organic compounds (VOCs) and other chemical irritants and toxins found in building materials including paints, flooring, carpets, and pressed wood (e.g. fiberboard, plywood).  Mold is a significant problem. Cessation of smoking (tobacco, cannabis) and avoidance of alcohol is highly recommended. Workplace hazards include recycled air and dust.

8. Specific formulae:

• Compound Tincture of Lobelia (King’s American Dispensatory, 1898), 5 – 10 mL, up to five times daily.
• Nayopayam kvatha, 48 mL bid-tid
• Balajirakadi kvatha, 48 mL bid-tid
• Shiva gutika, 3-6 g bid-tid
• Chaturdasangha churna, 3-6 g bid-tid
• Ma Xing Shi gan Tang (Ephedra Apricot, Gypsum and Licorice decotion), 1 cup thrice daily
• Ding Chuan Tang (Arrest Wheezing decoction), 1 cup bid-tid
• Chuan Ke Ling, 4 pills bid-tid
• Ping Chuan Wan, 10 pills bid-tid
• Ren Shen Ge Jie San (Ginseng and Gecko powder), 3-6 g bid-tid

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Arterial Disease

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 the leading cause of death in North America, a percentage of the population that has been on the rise steadily since that turn of the last century.

Pathogenesis of atherosclerosis

Atherosclerotic plaques form in the tunica intima of elastic and muscular arteries as a result of the proliferation of intimal smooth muscle cells and the accumulation of fat. As the lesion develops smooth muscle cells release cytokines that stimulates the accumulation of mononuclear phagocytes, lymphocytes and neutrophils in the tunica intima. As the lesion progresses the endothelium ruptures and platelets begin to adhere to it. Eventually small capillaries penetrate the vessel wall and supply blood to the plaque, almost like a kind of malignant tumor. (Rubin and Farber 1990, 355-369)

There are a variety of hypotheses that describe the process of atherosclerotic plaquing. While there is good post-mortem evidence of what components comprises a plaque, and now better data on the risk factors for developing atherosclerosis, the actual mechanisms of how the plaque is formed is severely limited by our inability to actually observe this process in vivo. As a result there are several different theories that describe the mechanism of plaquing. Some of these theories are complimentary and some are antagonistic to each other. The most commonly held belief among medical doctors is the insudation hypothesis, which states that the lipid found in plaques is derived from plasma lipoproteins, specifically low density lipoproteins (LDL). This theory states that the atherosclerotic lesion begins with a mutation of a smooth muscle cell, perhaps 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. For some unexplainable reason there is additional damage to the lesion, exposing circulating platelets to subendothelial collagen, which promotes the release of growth factors by the platelets, as well as by local macrophages, that stimulate the proliferation of smooth muscle cells and make the lesion larger. There is the continued insudation of fat into the lesion by macrophages that then undergo degeneration. Eventually the surface of the plaque begins to ulcerate and a thrombus forms on the injured luminal surface. (Rubin and Farber 1990, 355-369)

The initial lesions found in atherosclerosis are thought to be fatty streaks, flat or slightly elevated lesions that contain lipid. Histologically, these streaks are comprised of lipid containing macrophages referred to as foam cells. While these fatty streaks can be found in both young children and the aged, the distribution of these streaks does not correspond with atherosclerotic lesions in adults. Another candidate for the initial lesion of atherosclerosis are intimal cells masses, which are white thickened areas at branch points in the aterial tree, containing smooth muscle cells but no lipid. (Rubin and Farber 1990, 355-369)

Whatever the initial lesion, the characteristic lesion of atherosclerosis is a fibro-fatty plaque consisting of a fibrous cap and an atheroma. The fibrous cap is 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 in the lesion of atherosclerosis include other blood-borne cells including lymphocytes. The complicated plaque of atherosclerosis 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. (Rubin and Farber 1990, 355-369)

The net result of these changes is the occlusion of the blood vessel and the formation of emboli, both of which end up producing ischemia in the tissues supplied by the atherosclerotic or otherwise occluded blood vessel.

It is thought that the process of atherosclerosis begins early in life, with the formation of intimal cell masses and fatty streaks. Regardless, the characteristic lesion of atherosclerosis requires as long as 20-30 years to form, and the clinically important complicated plaques only after several more decades of progressive development. In this respect atherosclerosis is primarily a disease of older adults. (Rubin and Farber 1990, 355-369)

Etiology of atherosclerosis

The causes of atherosclerosis are still not completely understood, with many convoluted and complicated mechanisms described. In this lesson we will examine the most commonly held belief among the medical profession, as well an alternative to this perspective.

Medicine has defined several risk factors for the development of atherosclerosis, some of which may or may not prove to be entirely true. All of these risk factors are based on a statistical analysis of the data called epidemiology, a process that helps to form researcher of associations between certain factors and the incidence of disease. Although this process may identify groups in a population that are particularly vulnerable to a particular disease, it cannot indicate if a particular person will get a particular disease, and thus cannot take the place of an accurate, individualized health assessment.

The vast majority of the approach now utilized in the prevention and treatment of heart disease is based upon the Framingham Heart study, a cohort study over 5000 adult men and women from the town of Framingham, Massachusetts. Begun in 1948, the participants of the study were analyzed for patterns related to the development of cardiovascular disease (CVD). A second generation cohort study was begun in 1971, involving a similar number of participants comprised of the original participants’ adult children and their spouses. A third generation cohort study is now being implemented. Given the duration and number of participants involved in the study, the Framingham Heart Study has proved to be a rich source of data for all kinds of researchers, who use a number of different methods to analyze the data and identify risk factors for CVD, including high blood pressure, high blood cholesterol, smoking, obesity, diabetes, and physical inactivity. The Framingham study has also provided additional information on the effects of factors such as blood triglyceride and LDL/HDL cholesterol levels, age, gender, and psychosocial issues. The Framingham data, the analyses and the theories derived from it has played an important role in the development of the modern medical curriculum, and has been influential in establishing hypertension and elevated serum cholesterol as the most prominent risk factors for the development of CVD.

Hypertension is commonly observed in atherosclerosis, simply due to the increased pressure by which the heart has to pump blood through the narrowed and occluded atherosclerotic vessels. Hypertensive patients are at greater risk of myocardial infarction and stroke. There are several causes of hypertension, such as renal artery stenosis or hyperthyroidism and must be ruled out. Essential hypertension is a term that has been given to hypertension when the cause is unknown, or cannot be directly observed. Designating hypertension as a risk factor for atherosclerosis however appears to be irrational – it is far more logical to suggest that essential hypertension is a symptom of the progressive effects of arterial damage. Unfortunately what may seem to be a fairly simple argument has been for the most part ignored by the medical profession, many of whom still encourage hypertensive patients to use medications to lower blood pressure, even though these same medications have no impact upon morbidity and mortality in hypertensive patients, and may directly interfere with normal physiological processes. (Port et al 2000)

Elevated blood cholesterol and triglycerides are stated as being directly correlated with the development of ischemic heart disease and atherosclerosis. The hypdophobic nature of lipids in the blood means that fats must be transported with protein carriers, including chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL). Chylomicrons are formed by the intestinal villi, and are comprised of globules of triglycerides, phospholipids and cholesterol covered by a protein coating. Chylomicrons are absorbed by the lacteal of a villus, transporting fats through the lymphatic system where they enter into systemic circulation at the left subclavian vein. The triglyceride component of the chylomicron is cleaved by lipoprotein lipase in the blood, where it is taken up by adipose and muscle cells. This leaves a cholesterol-rich lipoprotein remnant that is then taken up by the liver and excreted back into the intestine as bile salts, or repacked with triglycerides into VLDL, where it then reenters into circulation. Once again VLDL is acted upon by lipoprotein lipase, removing triglycerides from VLDL, forming intermediate-density lipoproteins (IDL) that are eventually converted into cholesterol-rich LDL. LDL is then taken up and processed by a variety of cells, leading to the accumulation of cholesterol within these cells. Unlike VLDL and LDL, which functions to transport cholesterol to peripheral cells, high density lipoproteins (HDL) functions to scavenge cholesterol and return it to the liver for excretion. Thus elevated levels of serum VLDL and LDL have been associated with a greater risk of CVD because they deposit cholesterol into peripheral cells, which according to the insudation hypothesis is the primary cause of atherosclerosis, whereas HDL is correlated with a lower risk because it removes cholesterol from cells. (Rubin and Farber 1990, 355-369)

Despite the elegance of this hypothesis and the determination of what are thought of as useful serum markers (e.g. total cholesterol, VLDL, LDL, and HDL) for the risk of cardiovascular disease, a complete analysis of the data suggests that there are a number of problems with the idea that cholesterol is pathogenic in CVD. When it comes to the argument that dietary cholesterol promotes hypercholesterolemia, the Framingham study clearly shows that men who ate the most cholesterol had exactly the same levels of cholesterol in their blood as those who ate the least cholesterol. And while the Framingham study does show that the highest risk of CVD is associated with total elevated serum cholesterol (18% occurrence), those participants with low to normal levels of serum cholesterol continue to be at significant risk (10-12% occurrence). Furthermore, another more recent cohort study called the Honolulu Heart program that examined 3572 Japanese/American men (aged 71–93 years) found that low serum cholesterol levels in the elderly is an indicator of increased mortality (Schatz et al 2001). All of this becomes extremely confusing.

Much of the impetus behind the cholesterol hypothesis is based on animal experimentation, such as the landmark study published by David Kritchevsky in 1954, who described the effects of feeding cholesterol to rabbits causing the formation of atheromas (Kritchevsky et al 1954). In another study published the following year Kritchevsky published a paper that described the benefits of consuming polyunsaturated fatty acids for lowering cholesterol levels. Some researchers criticized Kritchevsky’s research – after all, rabbits are herbivores and don’t normally eat cholesterol, unlike humans, who are omnivores and have a long history of eating cholesterol and saturated fat. Kritchevsky’s research marks the beginning of a drawn out campaign to get North American consumers to substitute traditionally-consumed cholesterol-rich foods such as butter for low cholesterol innovations such as refined corn oil. This marketing campaign had already begun much earlier in the century, but with a highly selective presentation of the preliminary scientific evidence, the industry-funded American Heart Association began to encourage the North American public to substitute butter, lard, beef and eggs with corn oil, margarine, chicken and cold cereal (Enig and Fallon 2003). Unfortunately these changes have been marked by an increasing incidence of cardiovascular disease in North America, which from 1900 to the mid 1960’s increased by 300%, and is now the single leading cause of death (Bergner 1997, 202-03)

The reason for the exclusion of data such as these from conventional medical thinking on CVD risks is unknown, but when considered it radically alters the perception that cholesterol-rich foods are responsible for elevated serum cholesterol, or that elevated serum cholesterol is an important a risk factor CVD. Of particular concern is the relatively recent use of a new class of drugs called statins, derived from red rice yeast, which are used to interrupt the synthesis of cholesterol and reduce LDL/cholesterol levels in the blood. Unfortunately, while statins indeed have been shown to reduce the risk of cardiovascular disease in patients with a history of myocardial infarction, they have also been shown to have number of adverse effects that make them unsuitable for general prevention in patients presenting with dyslipidemia. Some researchers have stated that the benefit of statins has nothing to do with the benefits of lowering cholesterol, but of promoting the stabilization of the lesion.

Hyperglycemia and atherosclerosis

Prolonged exposure to hyperglycemia has also been recognized another factor in the pathogenesis of atherosclerosis. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerate the atherosclerotic process. Animal and human studies have indicated three major mechanisms that encompass most of the pathological alterations observed in the atherosclerosis:

1. nonenzymatic glycosylation
2. oxidative stress
3. protein kinase C (PKC) activation (Aronson and Rayfield 2002)

One of the important mechanisms responsible for the accelerated atherosclerosis in diabetes is the nonenzymatic reaction between glucose and proteins or lipoproteins in arterial walls, collectively known as Maillard, or browning reation. Glucose forms reversible early glycosylation products with reactive amino groups of circulating or vessel wall proteins to form advanced glycosylation end products (AGEs). AGEs normally accumulate with normal aging and at an accelerated rate in diabetic patients. In situations in which the local redox potential has been shifted to favor oxidant stress, AGEs formation is increased substantially, and can accelerate the atherosclerotic process (Aronson and Rayfield 2002).

Oxidative stress is another commonly described pathogenic mechanism for atherosclerosis. Hyperglycemia can increase oxidative stress through several pathways promoting the intracellular production of reactive oxygen species (ROS). There is also evidence that hyperglycemia may compromise natural antioxidant defenses. Reduced glutathione as well as reduced vitamin E have been reported in diabetic patients. Plasma and tissue levels of vitamin C are 40–50% lower in diabetic patients compared with nondiabetic subjects (Aronson and Rayfield 2002).

High glucose concentrations have been shown to activate the protein kinase C, a family of at least 12 isoforms of serine and threonine kinases. In vascular smooth muscle cells, PKC activation has been shown to modulate growth rate, DNA synthesis, and growth factor receptor turnover. Hyperglycemia-induced PKC activation also results in increased platelet derived growth factor-beta receptor expression on smooth muscle cells and other vascular wall cells, and increases the expression of transforming growth factor-beta (TGF-beta), which is thought to lead to thickening of capillary basement membrane (Aronson and Rayfield 2002).

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:

• diuretics: promoting diuresis, decreasing plasma volume and edema, thereby decreasing cardiac output and blood pressure. Major drugs include thiazides (e.g. hydrochlorothiazide, 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 depolarization (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) (Berkow 1992)

Hyperlipidemia is generally perceived as a risk factor for 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 (1), 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 more than 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, transfats 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 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 spirits.

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. 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. Concomitant 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 result this exposure to environmental toxins, a lack of exercise, and a dysfunctional eating pattern are metabolic problems such as chronic hyperglycemia, insulin resistance, hyperinsulinemia 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 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 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. Barberry (Berberis vulgaris), Turmeric (Curcuma longa), Dandelion (Taraxacum officinale), Chai Hu (Buplerum falcatum), Celandine Poppy (Chelidonium majus). 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 Guggulu (Commiphora mukul), Ginger (Zingiber officinale), Cayenne (Capsicum frutescens), Rosemary (Rosmarinus officinalis), Prickly Ash (Zanthoxylum clavaherculis) and Garlic (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 Ginger, Cayenne and Garlic 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 Dong Quai (Angelica sinensis), Huang Qi (Astragalus membranaceus), Guggulu (Commiphora mukul), Dan Shen (Salvia miltiorrhiza), Ashwagandha (Withania somnifera), Ren Shen (Panax ginseng), Bai Zhu (Atractylodes macrocephala), prepared Fu Zi (Aconitum carmicheli) and purified Ativisha (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 Gingko (Ginkgo biloba), Bilberry (Vaccinium myrtillus), Arjuna (Terminalia arjuna), Amalaki (Phyllanthus emblica), Turmeric (Curcuma longa), Gotu Kola (Centella asiatica), Yarrow (Achillea millefolium) and Grape (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 carbohydrates 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, 100 mg daily
• folic acid, 1 g daily
• cobalamin, 1000 mcg daily
• vitamin C, 1-5 g bid-tid, to bowel tolerance
• vitamin E (d-alpha tocopherol), 400-800 IU daily, increase dose gradually
• EPA/DHA, 1000 mg each daily
• magnesium, 800 mg daily, in divided doses, with meals
• chromium, 200-300 mcg daily, in divided doses, with meals
• selenium, 100 mcg daily
• chelated multimineral, taken with the above minerals; or high quality kelp (seaweed) supplement (5-15 g daily)
• CoQ10, 50 mg daily
• Flavonoids (mixed, e.g. quercitin, rutin, anthocyanidins), 3-5 g daily

4. Support liver, enhance detoxification: Barberry (Berberis vulgaris), Turmeric (Curcuma longa), Dandelion (Taraxacum officinale), Chai Hu (Buplerum falcatum), Celandine Poppy (Chelidonium majus) etc.

5. Promote circulation and blood flow, reduce blood viscosity (i.e. phlegm, kapha): Guggulu (Commiphora mukul), Ginger (Zingiber officinale), Cayenne (Capsicum frutescens), Rosemary (Rosmarinus officinalis), Prickly Ash (Zanthoxylum clavaherculis), Garlic (Allium sativum), Pippali (Piper longum) etc.

6. Cardiovascular trophorestoration: Hawthorn (Crataegus spp.), Bilberry (Vaccinium myrtillus), Arjuna (Terminalia arjuna), Amalaki (Phyllanthus emblica), Turmeric (Curcuma longa), Gotu Kola (Centella asiatica), Yarrow (Achillea millefolia) etc.

7. Rebuild the vital essence (i.e. qi, ojas): e.g. Dan Gui (Angelica sinensis), Huang Qi (Astragalus membranaceus), Guggulu (Commiphora mukul), Dan Shen (Salvia miltiorrhiza), Ashwagandha (Withania somnifera), Ginseng (Panax ginseng), Bai Zhu (Atractylodes macrocephala) 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

Amenorrhea refers to the absence of menstruation and is of two types: primary amenorrhea, in which menstruation has not begun by late puberty, even if other signs of physical maturation are present; and secondary amenorrhea, which is the cessation of menstruation for more than 3 cycles in a post-pubescent woman. There are many possible causes of amenorrhea, including:

• intrauterine adhesions
• cervical stenosis
• obstruction of menstrual flow
• hypothalamic dysfunction
• GnRH inhibition
• weight loss
• rigorous exercise
• severe chronic illness
• drugs such as the phenothiazines (antiemetics), antihypertensives and antipsychotics
• after using oral contraceptives
• polycystic ovarian disease
• breast feeding
• hypothyroid conditions (leads to decreased SHBG and thus increased estrogen)
• hyperthyroid (conversion of androgens to estrogens)
• excessive glucocorticoids (e.g. Cushing’s syndrome)
• premature ovarian failure (perhaps an autoimmune disease?)
• ovarian damage or destruction (from ischemia) (Trickey 1998, 209-212; Berkow 1992, 1798, 1802)

The most common causes of amenorrhea are hyperprolactinemia, and a relative androgen excess. Hyperprolactinemia is a condition in which there are increased levels of prolactin in the bloodstream. The signs and symptoms include galactorrhea (breast milk production), menstrual irregularities, decreased GnRH and LH levels, elevated androgens (with decreased 5-alpha-reductase activity), decreased SHBG, and decreased bone density. Possible causes of hyperprolactinemia include pituitary tumors, hypothyroidism, prolonged stress, excessive breast stimulation (Chinese “Deer” exercises), excessive exercise, drugs (phenothiazines, dopamine antagonists, antihypertensives, antiulcer drugs, estrogen oral contraceptives, opiates, cocaine) and alcohol (especially beer because of the Hops, which is a galactagogue). (Trickey 1998, 213-216)

The primary treatment of hyperprolactinemia involves the usage of progesterogenic botanicals such as Chasteberry (Vitex agnus castus) that has a dopaminergic activity, and other herbs to support the hypothalamic-pituitary axis such as Peony root (Paeonia lactiflora), Rehmannia (Rehmannia glutinosa), and Licorice root (Glycyrrhiza glabra). The supplementation of zinc and vitamin B6 are useful as both are cofactors in dopamine synthesis and can be included in the treatment. Important also is weeding through the various medications that could be causing this condition, as well as eliminating alcohol from the diet. Other lifestyle regimens that need to be addressed are stress management skills and physical exercise.

Androgen excess is another possible cause of amenorrhea, and describes a condition in which there are higher than normal levels of circulating androgens. Possible causes include PCOD (polycystic ovarian disease), an androgen-secreting adenocarcinoma of the adrenal gland, adrenal hyperplasia, steroidal drugs (synthetic progesterone, cortisone), post-menopause, and obesity. The signs and symptoms of androgenization include hirsutism, alopecia, acne, and elevated blood pressure. Other, more rare symptoms include the deepening of the voice, clitoral enlargement, and decreased breast size. Laboratory evidence will typically show elevated serum testosterone and DHEA. Some cases of androgenization are the result of an increased sensitivity to androgens rather than an androgen excess, and thus will not show up with lab tests. (Trickey 1998, 217-219; Berkow 1992, 1800)

The treatment of androgenization is difficult, and the primary thrust of the treatment is symptomatic, with the attention being placed upon the cause or causes. Important botanicals are those that nurture and enhance the “feminine essence” such as Peony root (Paeonia lactiflora) and Licorice (Glycyrrhiza glabra), both of which have been shown increase the enzymatic conversion of testosterone to less potent androgens. Phytoestrogens too, such as Red Clover blossoms (Trifolium pratense), True Unicorn root (Aletris farinosa), and Black Cohosh (Cimicifuga racemosa) are important as they increase the levels of SHBG that deactivate androgens. Especially important are herbs that have the ability to competitively inhibit androgenic activity, such as Damiana (Turnera diffusa), Saw Palmetto (Serenoa serrulata), and Sarsaparilla (Smilax spp.). In regard to diet, animal products and saturated fat should be decreased, replaced by increasing fiber, fermented legumes, and whole foods. Additionally, the importance of treating obesity should not be underestimated. This treatment of this condition is truly a challenge, complexed with the fact that herbal therapies are slow to take effect in established syndromes.

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is a degenerative condition of the brain that destroys memory, disrupts personality and accelerates death. The disease was first described in 1907 by Dr. Alios Alzheimer, who had a 51-year-old female patient suffering from a severe form of dementia. Upon autopsy, he noticed the deposition “of a peculiar substance in the cerebral cortex,” which has since been determined to be a 40 amino acid long protein fragment called amyloid beta-protein. Alzheimer’s disease affects more than 4 million people in the US, with an estimated 250,000 new cases every year. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996)

The tendency to develop AD is probably multifactoral rather than a case of simple genetics or infection: in the case of familial prevalence, this may or may not be genetic, but rather, evidence of similar predisposing factors. Above all, AD appears to be a 20th century disease, resulting from the combined effect of dietary and environmental changes with genetic and immunological factors. The clinical features of AD include dementia, disturbances in comprehension and language, as well as several other behavioral clues. Dementia refers to an impaired ability to pursue one’s occupation and social activities. This may include confusion, difficulty in memory recall, difficult speech, altered judgment and impaired abstract thinking. There may also be a feeling of “not being oneself,” a loss of interest in favourite pastimes, diminished creativity and a diminished ability to express affection. Language disturbances include the inability to find the correct word or the use of “filler” words in conversation, circumlocation (talking around the subject), an inability to express one’s thoughts in a written form or comprehend the written word, and difficulties in performing everyday physical tasks such as dialing the telephone or unlocking the door. Concomitant behaviours may include a deterioration of personal hygiene, inappropriate dress, a loss of social graces, losing and misplacing items, repeated traffic accidents, irritability, stubbornness, suspiciousness, a short attention span, an inability to perform simple instructions and an obsessive attention to trivial matters. The diagnosis of probable Alzheimer’s disease (PAD) occurs when other possible causes of the above clinical features have been ruled out. This includes multi-infarct disease, Parkinson’s, depression, alcoholic dementia, hypothyroidism, adverse reactions to pharmaceuticals, vitamin B12 deficiency, hydrocephalus (increased CSF in the brain’s ventricles) and infections such as syphilis. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996)

There are characteristic changes to the morphology of selective brain structures in AD, specifically of the hippocampus and cerebral cortex, which can be detected by MRI (multiple resonance imaging). The characteristic findings in AD are amyloid plaques, neurofibrillary tangles and the loss of nerve cells and synapses. Amyloid plaques are spherical structures that have a central core of beta-amyloid and varying degrees of inorganic aluminum. The number of these plaques directly corresponds with the severity of the disease. Beta-amyloid is cleaved from a much larger protein called amyloid precursor protein (APP), which is encoded on the 21st human chromosome, which in Down’s syndrome is triplicated (trisomy 21). The production of beta-amyloid is not limited to the brain however, but also occurs in the walls of peripheral blood vessels. Thus, the gradual production and accumulation of amyloid plaques may occur well before neuronal degeneration in the brain: thus, AD may begin in early adulthood. The enzyme which cleaves APP has a genetic determinant and current research is focused on finding substances that block the activity of this enzyme. Neurofibrillary tangles are the twisted ends of dead nerve cells, and although not specific to AD, large quantities of them have been correlated with severe dementia. These tangles slow down nerve transmission and impair cellular function. There is a significant loss of brain cells and nerve synapses in AD, within the cerebral cortex and subcortical structures, the major suppliers of acetylcholine, norepinepherine and serotonin that serve the higher cortical centres. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996)

In cases of AD a marked depletion of acetylcholine has been noted in an area of the brain called the nucleus basalis of Meynert, in contrast to other neurotransmitters such as dopamine and GABA which remain normal. This has lead to the theory that AD is a degenerative nerve cell disorder that targets cholinergic neurons. Acetylcholine is a neurotransmitter that binds with M-1 muscarinic receptors to evoke changes in that tissue, and is quickly broken down by acetyl cholinesterase. It has been suggested that there may be a deficiency of acetyl-L-carnitine, which provides acetyl groups for the production of acetylcholine. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996; Mitchell 1996)

The average adult brain requires 112 grams of glucose to maintain proper brain function and impaired glucose levels can alter brain cells, initiate the induction of a neurotoxin called glutamate and cause dramatic alterations in the synthesis and metabolism of acetylcholine. The areas of the brain that seem to be highly vulnerable to glucose deprivation are the same regions of the brain that are affected by AD. Reactive hypoglycemia, caused by the overconsumption of refined carbohydrates, the usage of exogenous insulin in the absence of dietary precautions, calorie restriction, as well as the chronic usage of caffeine, alcohol and tobacco, are all possible cause of impaired glucose metabolism in the brain. (Roberts 1996; Mitchell 1996)

Reduction in the levels of brain oxygen, necessary for the production of ATP in oxidative phosphorylation, may affect various neurotransmitters, acetylcholine and nerve growth factor and is another possible contributing factor in AD. Factors that limit brain oxygen include smoking, lung and heart disease, anesthesia, air travel, excessive sleep, poor breathing habits, migraine related brain blood vessel spasm and cerebral atherosclerosis. The latter of these factors may be caused by chronic states of hyperinsulinemia. (Roberts 1996; Mitchell 1996)

Certain food additives have been implicated in the development of AD, such as MSG and aspartame (NutraSweet®). Increased concentrations of glutamate and aspartate have been found in the CSF of AD patients. When MSG was tested on young experimental animals it lead to the rapid destruction of brain cells, leading it to be banned in baby foods. Aspartame consists of 50% phenylalanine, 40% aspartic acid and 10% methyl ester. Upon entering the stomach the methyl ester is transformed in free methyl alcohol, which in small amounts can cause blindness, permanent neurological damage and even death. There is increasing evidence that mutation involving a single amino acid may be the cause of the production of amyloid precursor protein (APP). In a family with three generations of early onset autosomal dominant AD, DNA sequencing revealed the substitution of phenylalanine for valine in the transmembrane domain of APP. Excessive amounts of D-aspartate and other stereoisomers have been found in the neurofibrillar tangles of AD patients, as well as in the amyloid plaques. (Roberts 1996)

A substantial amount of evidence has indicated that aluminum plays a role in Alzheimer’s disease. As much as four times the amount of aluminum as normal has been found in the brain of AD patients. Aluminum is known to interfere with essential enzymes needed to metabolize glucose for ATP production, cause the destruction of the blood brain barrier and transform L-aspartic acid into the neurotoxic D-aspartic acid. (Roberts 1996)

Demographic studies have found a greater preponderance of AD in women, possibly due to a higher incidence of excessive sugar consumption, fad dieting (causing reactive hypoglycemia), and greater longevity. On average, men have a higher metabolic activity in the temporal and limbic regions of the brain than women, which may confer a preventative benefit. (Roberts 1996)

Holistic treatment of AD

The treatment of AD disease is similar in scope to other neurodegenerative conditions such as PD. As AD is likely a condition that progresses slowly from repeated insult and damage to the brain, preventative measures based in eating a healthy diet and following a healthy lifestyle are highly recommended for anyone with a family history of AD.

Botanicals

• Cerebrovascular stimulants: Rosmarinus, Vaccinium, Ginkgo, Vinca, Crataegus, Capsicum, Zingiber, Zanthoxylum
• Nervine trophorestoratives, to protect neurons: Centella, Bacopa, Acorus, Withania, Rosmarinus, Avena Hypericum, Ganoderma, Eleuthrococcus, Turnera, Sida cordifolia, Phyllanthus emblica, Panax spp., Polygonum, Angelica sinensis, Cordyceps, Grifolia, Coriolus
• Antioxidant botanicals: Curcuma, Boswellia, Commiphora, Crataegus, Phyllanthus emblica, Bacopa, Tinospora, Shilajitu, Ginkgo, Rosmarinus, Centella, Silybum, Buplerum, Astragalus, Spirulina, Ganoderma
• M1-mimetics, to provide cholinergic stimulus in the nucleus basalis of Meynert: Pilocarpus, 10-30 gtt b.i.d.
• Acetyl cholinesterase inhibitors, to inhibit the enzymatic degradation of acetylcholine: Physostigma venenosa, 5 gtt b.i.d.

Supplements

• vitamin A, 20,000 IU daily
• vitamin B complex, 100 mg b.i.d.
• vitamin C, to bowel tolerance
• vitamin E, 800-1200 IU daily
• EPA/DHA, 1000 mg each daily
• phosphotidylserine, to support biosynthesis of acetylcholine, 100 mg t.i.d.
• L-acetylcarnatine, to support biosynthesis of acetylcholine, 500 mg t.i.d.
• iron, 20 mg b.i.d.
• calcium/magnesium, 1:1, 800 mg each b.i.d.
• chromium, 200 mcg t.i.d.
• selenium, 200 mcg b.i.d.
• zinc, 50 mg daily
• CoQ₁₀, 50 mg t.i.d.
• grapeseed extract, 50 mg t.i.d.
• superoxide dismutase, 100 mg b.i.d.
• bioflavonoids, 3-5 g daily

Diet

• Paleolithic diet, low carbohydrate diet to prevent CVD
• emphasize antioxidant foods, e.g. garlic, onions, cruciferous vegetables; foods rich in anthocyanidins, e.g. blueberries, huckleberries, elderberries, red and black grapes
• emphasize foods rich in the biochemical building blocks of acetylcholine, e.g. free-range eggs, lecithin
• avoid transfatty and hydrogenated fats
• avoid all aluminum containing foods or foods packaged in aluminum (e.g. various antacids, dolomite; aluminum cans, foil and cookware),
• emphasize artichokes to enhance liver metabolism

Topical

• Brahmi taila abhyanga, Brahmi or Vacha nasya

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ALZHEIMER’S DISEASE:
TREATMENT WITH CHINESE HERBS

by Subhuti Dharmananda, Ph.D., Director, Institute for Traditional Medicine, Portland, Oregon

BACKGROUND

Alzheimer’s disease is currently thought to contribute to about 75% of all cases of senile dementia that occur in the U.S. The disorder is marked by reduced levels of acetylcholine, development of amyloid plaques, and degeneration of brain tissue. It produces cognitive and coordinative dysfunctions with notable loss of memory. From the modern medical viewpoint, the cause of Alzheimer’s disease is not yet established. There is a genetic component, since the frequency of the disease is higher in an identical twin or a child of a person with Alzheimer’s disease, and the disease occurs with higher frequency in persons with the genetic disorder producing Down’s Syndrome. But other factors, as yet unidentified, seem to be at least as important as genetics, based on the distribution of the disease. No infectious agent that might cause the disease has been identified, and there is no current evidence suggesting that an infection is involved.

Except for one of the rare genetic forms of the disease that causes early dementia, Alzheimer’s usually does not occur in clinically obvious form before age 60. The incidence of the disorder increases with age, such that up to 30% of those over age 80 are believed to suffer from some degree of Alzheimer’s disease. A recent study has suggested that early subtle signs-such as limited linguistic complexity-reveal the tendency to develop Alzheimer’s disease. Such indicators may be detected before age 30. This would support the idea that the disorder has a genetic basis which yields an evident mental disease under the influence of the aging processes. It is possible, though not proven, that chemical pollutants, high fat diet, and sedentary life style may lead to the severe form of the disease.

Current orthodox medical treatment involves use of hydergine, dexedrine, and a variety of antidepressant drugs, all of which can produce modest improvements, especially in early stages of the disease. There are several experimental drugs in various stages of clinical trials that may improve the outcomes. Because of the advanced age of most sufferers, it is unlikely that even the most effective treatments would be able to produce complete remission.

In Europe, one of the main therapies for Alzheimer’s disease is Ginkgo biloba leaf extract, which is a widely-used plant drug sold in pharmacies. This flavonoid-rich extract promotes blood circulation to the brain as well as to other parts of the body. Because a large investment in research dollars has been made in testing ginkgo extract, many people do not realize that the same or similar effects may be attained by using other herbs that are a source of circulation-promoting flavonoids.

THE CHINESE MEDICAL APPROACH

Currently, there are two treatment approaches to Alzheimer’s disease in China: use of complex herbal formulas based on the traditional methods of Chinese medicine, or administration of an alkaloid drug, called huperzine A, derived from the herb huperzia. This drug inhibits the breakdown of the neurotransmitter acetylcholine, allowing more of it available for brain functions, including memory. Huperzine A has passed Phase I trials in the U.S. and it may become available as a prescription drug at the end of this decade. It is not possible to get sufficient quantities of huperzine A by simply consuming the whole herb from which it is derived, nor its crude extract in reasonable dosage. There are, however, numerous Chinese herbal formulas that may significantly increase levels of acetylcholine.

In analyzing the Chinese medical therapies for Alzheimer’s, it is important to recognize the difficulty in distinguishing this condition from other cases of senile dementia, mainly atherosclerotic dementia. A firm diagnosis of Alzheimer’s is made by extensive procedures that might include a CT scan, MRI, and EEG. In most cases, such procedures are not routinely done in China; therefore, the symptom pattern is used as the diagnostic criteria. Some reversible diseases produce dementia and even severe depression may produce dementia, so the treatments that are reported to be successful for dementia might not succeed in actual cases of Alzheimer’s disease.

HISTORICAL DEVELOPMENT OF IDEAS ABOUT SENILE DEMENTIA

According to the fundamental ideas of Chinese medicine, the brain is an outgrowth of and is nourished by the kidney. Therefore, brain defects and deterioration of the brain may be prevented, limited, or halted by the ingestion of kidney tonics. Rich nourishing agents such as placenta, rehmannia, and cistanche; kidney essence astringents, such as rose fruit and schizandra; and qi and blood tonics that ultimately help nourish the essence, such as astragalus, polygonatum, and tang-kuei, are frequently recommended to benefit the brain. The cognitive functions of the brain are said to be regulated by the heart: the kidney provides the substance, the heart the regulation of activity. Memory, cognition, and wisdom are believed to become disordered if the heart is agitated or if the influence of the orifices that connect the heart and brain are blocked by phlegm obstruction of the channels. The herbs zizyphus, biota, polygala, and acorus are considered important for treating heart disorders affecting memory and cognition. To benefit the function of the heart, qi tonic herbs are also used, as they enhance the energy or qi of the heart. Formulas based on the combination of heart-regulating herbs coupled with kidney and qi tonic herbs are sold in China as Bu Nao Wan (Brain Tonic Pills) or Jian Nao Wan (Healthy Brain Pills).

In the book Jingyue Quanshu (Collected Works of Zhang Jingyue; 1637 A.D.), a chapter on dementia (chidai) describes the problem as a combination of collapse of original qi (yuanqi) and the presence of impure qi in the meridians and heart orifices. Tonification therapy is the proposed solution, as the restoration of normal qi will help to dispel the pathological qi. A formula developed by Zhang for dementia is Qi Fu Yin, comprised of ginseng, cooked rehmannia, tang-kuei, atractylodes, zizyphus, baked licorice, and polygala. The latter herb helps to clear the phlegm obstruction of the orifices.

In the book Bianzheng Lu (Manual of Medical Differentiation; 1690), Chen Shiduo proposed that the first step in development of dementia is depression of liver qi, which is usually caused by emotional problems. This liver qi disorder might eventually lead to exhaustion of the stomach qi because the pathological qi from the liver is easily transmitted to the stomach, where it disrupts normal digestive functions. The resulting undigested food in the stomach can produce obstructive phlegm. He said that “treating phlegm is treating dementia.” To accomplish the goal, he suggested that one would tonify the spleen and stomach, resolve phlegm, and clear the orifices of the heart. A formula that Chen developed is Su Xin Tang, comprised of ginseng, hoelen, pinellia, bupleurum, coptis, evodia, gardenia, aconite, tang-kuei, peony, and zizyphus. Bupleurum invigorates the flow of liver qi; coptis and gardenia purge the pathologic qi of the liver, while evodia disperses the liver qi that is damaging the stomach functions; pinellia and hoelen resolve phlegm. Chen devised some alternative formulas for dementia, including ingredients such as shen-chu to enhance the stomach’s digestive activity, arisaema to cleanse the accumulated phlegm, and acorus to open the clogged orifices.

At the end of the 19th century, Wang Qingren, who is famous for developing the use of blood-vitalizing therapies, proposed that dementia was caused by an emptying of the material substance making up the marrow and brain, and by stagnant blood clogging the orifices. A formula he developed for this purpose is Tong Qiao Huo Xue Tang, comprised of red peony, cnidium, persica, carthamus, onion, musk, jujube; rice wine is added to the water when preparing the decoction. Onion and musk help to clear out the clogged orifices. The wine helps activate the blood-vitalizing properties of the formula.

The modern (post-1950) Chinese approach to Alzheimer’s follows closely the ideas of Wang Qingren. Degenerative changes in tissues are usually treated by herbs that promote blood circulation-often relying on salvia in place of persica and carthamus used in Wang’s time-plus tonics to treat the deficient organ. The brain is nourished with kidney tonics and qi tonics, such as rehmannia and ginseng. Many physicians still pursue the method of differential diagnosis, and the treatments may vary rather than follow a set pattern based on the disease description.

In China, a patent remedy, Nao Li Kang (Restore Brain Power Granules) has recently been developed. In the patent remedy application to the Sichuan Ministry of Health, it was reported that the formula was carefully tested in 31 patients with Alzheimer’s disease and atherosclerotic dementia confirmed by CT scans. The formula ingredients include rehmannia, salvia, polygala, and polygonatum. Three months treatment with the formula resulted in improvements in 40% of the Alzheimer’s patients and in 86% of the atherosclerotic patients. Although the improvement rate for Alzheimer’s was relatively low, because this disease is so difficult to reverse, the result is still of interest.

The treatment of Alzheimer’s should begin at its earliest signs, since any brain cells that have been destroyed cannot be regenerated and the fibrous and mineralized plaques that form in the brain are unlikely to be removed as a result of the ingestion of herbs. Chinese herbs can still prove useful in later stages, by preventing further degeneration or optimizing the function of the intact brain cells, but attempts to more fully resolve the disease could only meet with success in the early phases. During this earlier period, a definitive diagnosis of Alzheimer’s is not always possible, but one can safely administer the Chinese tonic herbs and blood circulation agents.

USING DIFFERENTIAL DIAGNOSIS

Despite the fact that brain disorders can be described generally by the theoretical framework of traditional Chinese medicine, many physicians working in China continue to rely on differentiating cases. The particular disorder, Alzheimer’s disease, may occur either from a variety of different causes or from a basic cause in a variety of constitutional situations. The primary differential categories used by Chinese doctors to describe senile dementia are:

1. Spleen qi deficiency, with phlegm and stagnating blood obstructing the orifices to the brain.
2. Liver qi stagnation, with entanglement of qi, accumulation of phlegm, and stagnating blood.
3. Hot phlegm clogging the orifices.
4. Spleen and kidney yang deficiency, with phlegm and stagnating blood obstructing the orifices to the brain.
5. Deficiency of liver and kidney yin, with phlegm and stagnating blood obstructing the orifices and with generation of internal wind.
6. Qi and blood stagnation, obstructing the orifices to the brain.

According to the category that seems most appropriate, one may tonify qi, yin, and/or yang, disperse qi and blood, and resolve phlegm accumulation. The tonic herbs to be used are the same as those commonly found in traditional formulas to treat problems of aging: ginseng, astragalus, atractylodes, dioscorea, rehmannia, lycium fruit, cistanche, and morinda. For unclogging the orifices, acorus, polygala, arisaema, typhonium, and alum are used in various combinations. Acorus and polygala are said to restore proper communication between the kidney and heart;. Alum (an aluminum sulfate compound) and arisaema are considered remedies for “mental phlegm.” Sedative herbs are sometimes included in prescriptions for dementia, including zizyphus, fu-shen, biota, dragon bone, and oyster shell.

According to traditional Chinese medicine, the depletion of kidney-which is the dominant cause of symptoms associated with aging-can be largely overcome by regular ingestion of either Rehmannia Six Formula (Liu Wei Di Huang Wan) or Rehmannia Eight Formula (Ba Wei Di Huang Wan). Stagnation of blood can be limited by daily ingestion of salvia wine, or some other salvia-based herbal preparation. The obstruction by phlegm can be largely overcome by reducing fat in the diet (a health-promoting strategy that is recommended by all physicians today) and by using herbal formulas that aid the digestive process, such as Six Major Herbs Combination (Liu Jun Zi Tang) or a formula that contains herbs such as crataegus and shen-chu. Saponins from ginseng (and from several traditional anti-aging tonic formulas) have been shown to improve memory function. Sleep disorders-which may respond to the use of herb therapies-are commonly reported among the elderly and may contribute to worsening mental function.

A report in the Shanghai Journal of Traditional Chinese Medicine (1991) describes a study with 60 patients divided into a Chinese herb group and a control group (both used Western medications as needed). Six different herb formulas were used for the study, given according to the diagnosis of the patients’ underlying conditions. Eighteen symptoms other than memory functions were monitored, including headache, dizziness, tinnitus, and head fullness; poor appetite and constipation; fatigue and leg weariness; fever and sweating; and so on. The Chinese medical treatment group showed improvements in all of the symptoms except tinnitus. There were also changes in the tongue (less redness) and tongue fur (less greasiness). When the symptom changes related to mental condition were compiled, 7 of 30 in the Chinese medical group showed marked improvement and 16 more showed some improvement. Thus, about 77% showed some degree of improvement, but there was no notable difference between these results for mental capabilities and those of the Western medical control group. The patients in this study were treated with herbs in capsules or tablets, in order to obtain good compliance, not higher-dosage decoctions as would have been preferred by the physicians. The dosage used began low and was increased gradually. Treatment time was six months, and the treatment then needed to be continued to maintain the benefits.

Based on a review of the literature on Alzheimer’s disease and senile dementia, a general formula would be acorus, polygala, platycodon, ginseng, atractylodes, licorice, astragalus, citrus, pinellia, crataegus, shen-chu, curcuma, gastrodia, salvia, cnidium, red peony, zizyphus, rehmannia, lycium fruit, tang-kuei, cistanche, morinda, aconite, dioscorea, and hoelen (or fu-shen). Certain herbs could be deleted or added to focus the formulation on the exact needs of the patient.

Among the contributors to aging disorders are the cumulative impact of oxidation reactions (including the accumulation of lipofuscin) and the decline of hormones (it was recently shown that estrogen aids memory in women). Numerous antioxidants have been identified and are readily available in convenient tablet or capsule form (flavonoids, carotenes, Vitamins C and E, and certain minerals, such as selenium, and amino acids, such as glutathione). Several Chinese herbs have been shown to have antioxidant effects and reduce levels of lipofuscin; these include the tonic herbs ligustrum, lycium, cuscuta, psoralea, atractylodes, codonopsis, epimedium, ganoderma, polygonatum, and ho-shou-wu. Some of these herbs function by increasing levels of antioxidant systems, such as SOD (super oxide dysmutase). In addition to using Chinese kidney tonic herbs to enhance the body’s production of hormones, exogenous sources of many hormones are now available, including growth hormone, DHEA (dehydroepiandrosterone), and melatonin, which could be administered along with the herbs initially to obtain more obvious early effects from the treatment.

NEW PLANT DRUG FOR ALZHEIMER’S: HUPERZINE

Huperzine, an anticholinesterase alkaloid, is divided into two chemical species, huperzine A and huperzine B, which have similar effects but differing activity levels (huperzine A being about 10 times as strong as huperzine B). Huperzine A was first isolated from the Chinese herb Lycopodium serratum in 1980 at the Zhejiang Academy of Medical Sciences and the Shanghai Institute of Materia Medica of the Chinese Academy of Sciences. Huperzine B was isolated five years later. The plant source, originally called Qian Ceng Ta, meaning thousand-layers pagoda (referring to the tall multi-leafed appearance of the plant), is also known in China as Jin Bu Huan, a term meaning “more valuable than gold,” usually applied to plants that have potent analgesic actions. This herb should not be confused with the patent remedy called Jin Bu Huan made from tetrahydropalmatine. The plant has been reclassified botanically as Huperzia serrata from the new family Huperziaceae, rather than from the closely related family Lycopodiaceae. It is reported that the Lycopodiaceae have two medicinal genera: Lycopodium (now Huperzia) and Phlegmariurus. A common constituent is the alkaloid fordine, which is found in 14 species of Huperzia and has similar action to the huperzines.

Huperzia, as it is now called, contains a wide variety of alkaloids, including lycodoline, lycoclavine, and serratinine, as well as the huperzines. The alkaloids are of a unique structure and have been called Lycopodium alkaloids. In general, they are comprised of four rings, though one of the rings may be opened. The huperzines, like many of the other lycopodium alkaloids, contain a nitrogen within one of the rings and an NH2 group attached to the ring structure (some of the Lycopodium alkaloids contain only a nitrogen within the ring structure).

Huperzia is not much used as a crude herb in Chinese medicine: the dominant application is for blood disorders caused by trauma or acute ailment, such as hematamesis caused by overstrain, bruises, hemorrhoids, and lung abscess. In addition to alkaloids, it contains triterpenoids. Huperzines and other isolated alkaloids are increasingly used in Chinese medicine as an alternative to crude herb preparations.

PHARMACOLOGY AND CLINICAL APPLICATIONS OF HUPERZINE

Huperzines A and B reversibly inhibit cholinesterase; huperzine A has a stronger action than huperzine B, which in turn has a stronger action than galanthamine (an alkaloid from Lycorus radiata that has been used for its anticholinesterase activity). Huperzine A has substantially stronger anticholinesterase activity than physostigmine or neostigmine (chinchona alkaloids obtained from Physostigma venenosum; neostigmine is a common drug for treatment of myasthenia at a dose of 1-2 mg by IM or 0.5 mg IV; physostigmine is also an approved anticholinesterase drug), but huperzine B is three to five times weaker than physostigmine. Huperzines A and B have greater effect on acetylcholinesterase (AChE) than on butyrocholinesterase (BuChE). Huperzine A, because of its cholinesterase inhibiting activity, has been used in myasthenia gravis patients in China, with apparent success.

Both huperzine A and B have been shown to have memory-enhancing activities in animals. At 0.075 mg/kg for huperzine A or 0.5 mg/kg for huperzine B, IP administration to mice significantly facilitated spatial discrimination learning in a Y-maze study. At slightly higher doses (0.075-0.125 mg/kg for A and 0.6-0.8 mg/kg for B) the huperzines given prior to exposure of mice to carbon dioxide prevented hypercapnia-induced impairment of learning. Memory retention and retrieval could be enhanced in animals when the alkaloids were given immediately or 6-12 hours after training. Substantially lower or higher doses of huperzines are not effective. Huperzine has been used for Alzheimer’s and senile dementia with positive results. In a double-blind trial with a group of 56 patients suffering from multi-infarct dementia or senile dementia and a group of 104 patients with senile and presenile memory loss, huperzine A was demonstrated to be effective for improving memory. It was given by intramuscular injection, 0.05 mg twice daily for four weeks to the first group and 0.03 mg twice daily for two weeks to the second group. The only side effect was slight dizziness experienced by a few patients. In rats, fordine, at 0.01-0.04 mg/kg IP, speeds up conditioned avoidance responses, reverses impairment of conditioned avoidance response, and antagonizes hippocampal and cortical EEG changes induced by quinuclidinyl benilate.

Huperzine A has been evaluated at the Mayo Clinic in Jacksonville, Florida. According to Alan Kozikowski, a chemist who is heading the research there, Huperzine A is more effective and more specific than tacrine, another anticholinesterase drug. Interneuron Pharmaceuticals in Lexington, Mass. is testing Huperzine A in human clinical trials.

OTHER CHOLINESTERASE INHIBITORS FROM CHINESE HERBS

Lycorus radiata (shisuan) contains the alkaloids lycorine, lycoramine, lycoreine, and galanthamine. Both lycoramine and galanthamine have been shown to be reversible cholinesterase inhibitors. Lycoramine is weaker than galanthamine, but equivalent to Nivalin. Galanthamine easily crosses the blood-brain barrier. It decreases cholinesterase activity of the cerebral cortex and medulla oblongata, and at high dosage shows an anticholinesterase activity in the thalamus. Lycorine produces a marked sedative action in mice and rats, and it prolongs sleep time in animals treated with pentobarbital. Lycorine could also potentiate the analgesic effects of morphine and corydalis.

Macleaya cordata (boluohui) in the Papaveraceae family, contains several alkaloids including sanguinarine, chelerythine, protopine, and allocryptopine. The sulfates of these alkaloids have a more potent local anesthetic action than procaine. Sanguinarine inhibits cholinesterase. The herb is mainly used for bacterial infections and trichomonas, and for killing maggots (the alkaloids cause excitation and then paralysis and death of larvae).

Coptis chinenses (huanglian) contains berberine alkaloids, mainly berberine, but also coptisine, worenine, palmatine, and columbamine. Berberine is a cholinesterase inhibitor. When given to mice at 0.250 mg/kg, berberine enhances establishment of positive conditional reflex, but high dosages (10 to 20 times higher) inhibit it. Berberine exerts a dose-dependent biphasic effect on acetylcholine in animals and their isolated organs. Berberine antagonizes acetylcholine-induced bradycardia and ST segment depression in rabbits. Tetrahydroberberine, a berberine derivative, produces analgesia, sedation and muscle relaxation, with an effect that is three times more potent than that of meprobamate. Its action may be similar to that of tetrahydropalmatine; l-tetrahydroberberine, like l-tetrahydropalmatine, appears to be a more potent tranquilizer than the d-isomer.

Berberis species (sankezhen) are another source of berberine and also provide berbamine, palmatine, isotetrandrine, and jatrorrhizine. Palmatine was shown to have strong anticholinesterase activity. Isotetrandrine (also found in Stephania species), antagonizes ileal contraction induced by histamine or acetylcholine. Jatrorrhizine reduces spontaneous activity of mice and prolongs the animals sleep elicited by pentobarbital; it also induces sleep in mice given subthreshold doses of pentobarbital.

Securinega suffruticosa (yiyiqiu) contains many alkaloids, mainly securinine and its derivatives. Securinine is a CNS stimulant that antagonizes the inhibitory action of meprobamate. Securinine inhibits cholinesterase activity, but it is weaker than galantamine. Solanum nigrum (longkui), contains solanine, salasodine, and related alkaloids. Salasodine reduces sensitivity of animals to pain. Solanine markedly decreases spontaneous activity of mice and prolongs the sleeping time induced by pentobarbital. Solanine has a strong anticholinesterase action that is attributed to its aglycone solanidine.

Most of the herbs mentioned in this section inhibit bacterial growth and are used in tumor therapy. The isolated alkaloids often have the same effect as the crude herbs for these applications and are increasingly used in clinical practice. Clearly, there is reason to hope that one or more of the plant alkaloids will prove helpful to those with Alzheimer’s and that these alkaloids might be administered with the herbs used by traditional doctors for the treatment of memory disorders so as to attain superior results.

SOURCES

Except for the general information about the nature of Alzheimer’s disease and its treatment with Western medicine, which is available from many sources, the information for this article was derived from three sources:

Chang HM and But PPH, Pharmacology and Applications of Chinese Materia Medica, (2 vols.) 1987 World Scientific, Singapore (USA office: Teaneck NJ).

But PPH, et al., (eds.), Abstracts of Chinese Medicine, 1986-1995, Chinese University of Hong Kong, Shatin, N.T., Hong Kong. This is a quarterly journal.

Fu KZ and Fruehauf H, Senile Dementia and Alzheimer’s Disease, 1995 Institute for Traditional Medicine, Portland, OR. This is a collection of unedited papers produced for ITM from a review of Chinese language literature.

July 1996

Distance Learning Fair Use Source: http://www.itmonline.org/arts/alzheimers.htm

Alzheimer’s And Dementia

Currently, more than 4 million people in the United States suffer from Alzheimer’s disease (AD) or other dementias. AD affects 47% of people over the age of 85. In AD, in addition to degenerative changes and atrophy, individual brain cells begin to produce a sticky proteinous substances which swell the interior of the cell (neurofibrillary tangles) and “gum up” the exterior (amyloid plaques). In essence, the brain petrifies.
Causes of dementias include hardening of the arteries and mini-strokes.  Inflammation is a major contributor to neuronal damage in neuro-degenerative disorders such as AD, Parkinson’s disease, multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS) (Torreilles F et al.  1999). Nitric oxide inflammation has been shown to play a specific role in neuro-degeneration (Strijbos 1998). Blood flow to neural tissue is another important consideration.
The historical use of herbal medicines to treat dementia diseases like Alzheimer’s varies according to the different traditions.  According to TAM and TCM theories, dementias result from multi-systemic decline and brain destruction due to aging, and thus can be prevented or slowed by maintaining overall health and using tonics. Consequently, our preventive and treatment goals are the reduction of oxidative damage, reduction of cellular toxins and inflammation, and improvement of cerebral circulation and oxygen and glucose transport.

• Neural circulation can be improved with blood moving herbs, especially corydalis rhizome (yan hu suo), which slows the breakdown of choline.  (Kim 1999)

• According to studies of the pharmacological properties of gingko leaf, gingkolides exhibit anti-oxidant, neuro-protective and cholinergic activities relevant to Alzheimer’s disease mechanisms (DeFeudis, 1991).

• In numerous well-controlled clinical studies in Europe and the US, extracts of ginkgo leaf have proven “effective therapy for a wide variety of disturbances of cerebral function, including multi-infarct dementia, early cognitive decline, and mild-to-moderate cases of the more severe types of senile dementia including Alzheimer’s disease (Clostre 1999).

• Tonics that can prevent mental and neurological decline include flaxseed oil, DHA (Docosahexanoic acid from fish oils – more info), guggul gum, rehmannia root, amla fruit, American ginseng root, ginseng root, ashwaghanda root, dang gui root, garlic bulb, gotu kola, guduchi stem, shou wu root, maitake mushroom, milk thistle seed, ganoderma mushroom, shilajatu, and Siberian eleuthero root bark.

• Anti-oxidant protection comes from eating lots of fresh fruits and vegetables, and using herbs like amla fruit, triphala and wheat sprouts.

• Because neurotransmitters and other brain chemicals are formed from amino acids, and digestion declines with age, digestion-strengthening herbs like bromelain or trikatu can be used to ensure proper protein and nutrient assimilation.

Learning Therapy and Alzheimers

cannabis may help Alzheimers

excellent article on Alzheimers prevention

Distance Learning Fair Use Source:

http://oneearthherbs.squarespace.com/diseases/alzheimers-and-dementia.html

Alcohol consumption has a long history in human civilization, dating back to the early neolithic, with references to the problem of alcoholism noted in the ancient medical texts of India and other cultures. At one time it was thought that alcoholic liver disease (ALD) was solely related to the nutritional deficiencies caused by using alcohol as the primary source of dietary calories, but it is now understood that excessive alcohol consumption promotes specific degenerative changes in the liver that are responsible for the clinical manifestations of ALD, which progresses from fatty liver, to alcoholic hepatitis, and finally cirrhosis. Only about 15% of people with alcoholism however will go on to experience cirrhosis of the liver. (Berkow 1992; Rubin and Farber 1990, 412-415)

The pathogenesis of ALD relates primarily to the quantity of alcohol consumed and the duration of consumption, as well as the patient’s overall nutritional status and a number of genetic and metabolic characteristics. Consuming as little as 20 grams of ethanol, equal to 60 mL of 40% whiskey, 200 mL of 12% wine, or 500 mL of 5% beer can produce liver injury when consumed daily over a period of years. In cases of alcoholic hepatitis a patient will consume up to 80 grams of alcohol daily for almost a decade, whereas cirrhosis is typically seen with the consumption of 160-200 g daily over the same period. (Berkow 1992; Rubin and Farber 1990, 412-415)

Alcohol is a potent source of carbohydrates, and thus decreases the appetite, promoting malabsorption through its toxic effects on the gut and pancreas. The net result of this is malnutrition, which tends to hasten the negative effects of alcohol, and promoting aging and susceptibility to other diseases. (Berkow 1992; Rubin and Farber 1990, 412-415)

When ingested alcohol is quickly absorbed from the GI tract, and directed to the liver where it is metabolized by oxidative mechanisms that involve alcohol dehydrogenase and the microsomal ethanol oxidizing system. Alcohol dehydrogenase produces acetaldehyde as the major catabolite, which is toxic to both the liver and other organs, and is further oxidized to acetate. This process increases the redox state of the liver, which interferes with normal functions, inhibiting gluconeogenesis and protein synthesis, and increasing fatty acid synthesis and lipid peroxidation (seen in fatty liver). Alcohol metabolism also induces a local hypermetabolic state that promotes hypoxic damage, as well as induces microsomal P-450, which is involved in drug metabolism. As a result of this, alcoholics tend to acquire an increased tolerance to alcohol and drugs, often leading to multiple drug abuse patterns. Women in particular appear to be more susceptible to alcohol, thought to be because females tend to produce less alcohol dehydrogenase in the gastric mucosa than males. (Berkow 1992; Rubin and Farber 1990, 412-415)

Fatty liver or steatosis is the initial manifestation of acute or chronic excess alcohol consumption, the liver becoming enlarged and yellowed from the accumulation of fat droplets that can coalesce as larger cysts. These fatty changes to the liver however are completely reversible, and usually presents no more symptoms that the malaise and discomfort of the typical symptoms of ‘hangover’ experienced the next day. (Berkow 1992; Rubin and Farber 1990, 412-415)

If ethanol is consumed on a regular basis and to excess however, the injury to the liver persists and the result is alcoholic hepatits, which is usually superimposed upon the fatty changes. The swollen and injured hepatocytes undergo degeneration and a localized inflammatory reaction develops in response. Cellular necrosis and hypoxia stimulates fibrosis, often around the central vein, and in severe cases can be totally obliterated, surrounded by dense fibrous tissue called central hyaline sclerosis. Clinically, the effects of alcoholic hepatitis are noted by malaise, anorexia, right upper quadrant pain and jaundice, with laboratory investigation revealing leukocytosis and elevated serum aminotransferase activity. In about 10-30% of the cases the result is death. In those that survive and persist in drinking the acute illness will eventually be followed by chronic hepatitis, usually resulting in cirrhosis within a few years. Even for those patients that abstain from drinking at this point only about 25% fully recover by 6 months, and 20% will continue on to experience cirrhosis regardless of abstinence. For most patients recovery is very slow, and will show some degree of liver disease even after a year of abstinence. (Berkow 1992; Rubin and Farber 1990, 412-415)

Cirrhosis represents the end-stage disease of ALD, with hepatocellular necrosis and generalized fibrosis that surrounds the few remaining hepatocellular nodules. Essentially, the liver becomes shrunken and fibrotic, and patients will often die from esophageal hemorrhage (secondary to portal hypertension) or from complete hepatic failure. (Berkow 1992; Rubin and Farber 1990, 412-415)

Treatment of alcoholism

There are a variety of approaches undertaken in the treatment of alcoholism, but none are effective until the patient is faced with the realization of the impact of the disease, and fortified with the resolve to make healthy changes. This process is greatly assisted by a loving, compassionate and respectful group of peers that the patient can turn to for advice, reassurance, and encouragement. In many cases the 12-Step program initiated by Alcoholic Anonymous is undertaken:

Step 1. We admitted we were powerless over alcohol – that our lives had become unmanageable.

Step 2: We came to believe that a Power greater than ourselves could restore us to sanity.

Step 3: We made a decision to turn our will and our lives over to the care of God, as we understand him.

Step 4: We made a searching and fearless moral inventory of ourselves.

Step 5: We admitted to God, to ourselves and to another human being the exact nature of our wrongs.

Step 6: We were entirely ready to have God remove all these defects of character.

Step 7: We humbly asked Him to remove these shortcomings.

Step 8: We made a list of all the persons we had harmed, and became willing to make amends to them all.

Step 9: We made direct amends to such people wherever possible, except when to do so would injure them or others.

Step 10: We continued to take personal inventory and when we were wrong promptly admitted it.

Step 11: We sought through prayer and meditation to improve our conscious contact with God as we understand him, praying only for knowledge of his will and the power to carry that out.

Step 12: Having had a spiritual awakening as a result of these steps, we tried to carry this message to others, and to practice these principles in all our affairs.

While many have found the 12-Step promulgated by Alcoholic Anonymous (AA), which is supported by a large community that maintains regular meetings in almost every city and town, not all people find the 12-Steps outlined to be necessarily helpful. The 12-Step program has a fairly strong Judeo-Christian ethic, and thus may discourage participation by people of other faiths, rationalists and agnostics. Some people are able to give up alcohol simply through the act of gumption, others with fairly intensive psychotherapy, or some with the help of family and friends. Former alcoholics often believe that alcoholism is a disease, a perspective which is fostered by the AA and has now more or less become enshrined as truth. Some critics perceive this notion has divested alcoholics of personal responsibility, and therefore the need for balance and moderation in all activities. For example, many former alcoholics continue to abuse their bodies, such as by smoking or drinking large volumes of coffee: in such cases the addictive response has not been addressed. Some former alcoholics that have learned to control their desires find that they can continue to drink in small amounts on special occasions, after a period of abstinence and self-reflection, without guilt or depression. In large part the success of either method entirely depends upon the patient.

It is important when initiating a program for an alcoholic patient to ensure that alcohol consumption is tapered off slowly, over a period of a week. Quitting alcohol “cold turkey” may give rise to delirium tremens, a potentially fatal form of ethanol (alcohol) withdrawal. Symptoms include tremors, irritability, insomnia, nausea/vomiting (frequently secondary to gastritis or pancreatitis) hallucinations (auditory, visual, or olfactory), confusion delusions, severe agitation, and seizures, which can begin between 6 to 48 hours after the last drink. The condition appears to be caused by the direct effect that ethanol has on the benzodiazepine-GABAa-chloride receptor complex, leading to the down-regulation of GABA and an unopposed increase in sympathetic activity. Ethanol also acts as an N-methyl D-aspartate receptor antagonist.

Beyond specific treatments to the hepatobiliary system, the treatment of alcoholism in herbal medicine consists of:

1. Restoring proper nutrition. The high carbohydrate, high calorie nature of regular alcohol consumption can have a major effect upon metabolic and cardiovascular health. Furthermore, an assessment of hepatic detoxification should also be undertaken at some point to establish guidelines for hepatotrophorestoration, or at least, the usage of hepatorestorative botanicals. A variety of nutrients in supplemental form can be seen to be helpful, including:

• Vitamin A, 25,000 IU daily
• Vitamin B complex, 100 mg daily
• Vitamin C, 2-3 g daily
• Vitamin E, 400 IU daily
• Magnesium, 250 mg twice daily
• Selenium, 200 mcg daily
• Zinc, 30 mg daily
• EFAs, EPA/DHA, 1000 mg each daily
• Glutamine, 1 g daily
• MSM, 2-3 g daily
• Probiotics

2. Addressing symptoms of withdrawal.

• Oral rehydration
• Antispasmodics, e.g. Black Cohosh (Cimicifuga racemosa), Wild Yam (Dioscorea villosa), Cramp Bark (Viburnum opulus), Hing (Ferula foetida)
• Relaxing nervines, e.g. Milky Oats (Avena sativa), Valerian (Valeriana officinalis), Skullcap (Scutellaria lateriflora), Passionflower (Passiflora incarnata)
• Trophorestoratives, e.g. Damiana (Turnera diffusa), American Ginseng (Panax quinquefolium), Ren Shen Ye(Panax ginseng leaf), Bai Shao (Paeonia lactiflora), Ashvagandha (Withania somnifera), Amalaki (Phyllanthus emblica), Draksha (Vitis vinifera), Punarnava (Boerhavia diffuse)
• Sedatives, e.g. California Poppy (Eschscholzia californica), Himalayan Blue Poppy (Meconopsis spp), Yan Hu Suo (Corydalis yanhusuo)
• Aromatherapy, e.g. EO of lavender, rose, geranium, neroli, vetivert, rosemary, lemon balm, peppermint, basil, sweet marjoram, bergamont, hyssop, lemon, clary sage, myrrh, frankincense, sandalwood
• Massage
• Steam bath, sweat lodge, after weaning and no indication of delirium tremens

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Addison’s disease is a chronic, progressive disease caused by a failure of adrenocortical secretion, characterized by a deficiency of glucocorticoids, mineralcorticoids and androgens. The etiology of Addison’s disease in most patients (75%) is unknown, but is thought to be related to an autoimmune process, as patients typically present with other autoimmune endocrinal diseases. Immune mechanisms include The remainder of cases relate to granulomatous conditions from infection (e.g. tuberculosis), as well as amyloidosis, cancer, adrenal hemorrhage, sarcoidosis, and the treatment of fungal infections with ketoconazole. (Rubin 2001, 615-16; Berkow 1992, 1088)

Clinically apparent indications of Addison’s only occurs after 90% or more of the adrenal gland is destroyed. The initial symptoms are insidious, including weakness, poor appetite, and asthenia. As the condition progresses there is increased pigmentation, caused by increased melanocyte-stimuliting activity of pituitary pro-opiomelanocortin, which is commensurate with an increase in ACTH secretion. This is characterized by a diffuse “tanning” of both exposed and unexposed portions of the body, including on bony regions, skinfolds, and scars. Another common feature is the appearance of blackish freckles over the forehead, face, neck, and shoulders, as well as bluish-black discolorations of the areolae and mucous membranes. In some cases vitiligo may be present. Hypotension (e.g. 80/50 mm Hg) occurs as the result of mineralcorticoid insufficiency, from the resulting low serum sodium. As the condition progresses signs and symptom include nausea, vomiting, diarrhea, and cold intolerance. (Rubin 2001, 616p; Berkow 1992, 1088)

An adrenal crisis is a life threatening emergency that results from an abrupt loss of adrenocortical function. Symptoms typically relate to a deficiency in mineral corticoid secretion, and are characterized by hypotension and shock, commensurate with profound weight loss, abdomen pain, and lower back and leg pain. If untreated renal failure with azotemia is a result. The crisis can be caused by the stress of acute infection or surgery, and in some cases from sodium loss due to excessive sweating. Waterhouse-Friederichsen syndrome relates to the acute injury of the adrenal glands secondary to meningococcal or pseudomonal infections of the blood, usually occurring in young patients and typified by sudden vascular collapse, hypotension, fever, myalgia and pupura. In most cases an adrenal crisis is caused by the abrupt withdrawal of corticosteroid therapy. (Rubin 2001, 616p; Berkow 1992, 1088)

Medical treatment

The primary medical management of Addison’s disease consists hormone replacement with synthetic cortisone, hydrocortisone and fludrocortisone. Although these drugs can promote significant changes in the course of the disease, they also have a simultaneous immunosuppressant activity thus making the patient more susceptible to secondary infection. Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves Dehydroepiandrosterone (DHEA) is an adrenal steroid hormone that is a precursor to cortisone and has recently undergone recent investigation in Addison’s disease, used in conjunction with glucocorticoid and mineral corticoid therapy, and was demonstrated to have a benefical effect upon mood and fatigue (Hunt et al 2000).

Patients with Addison’s are advised to not restrict salt in their diets, and in patients that live in warm climates or exercise regularly to increase their salt and electrolyte intake because of an increased loss of sodium as a result of sweating.

Holistic treatment

The holistic treatment of Addison’s disease is complimentary, using herbs and supplements to support adrenal function and prolong the half-life of the glucocorticoids. Perhaps the best studied herb for this is Licorice (Glycyrrhiza glabra), which was studied in the 1950’s for its synergistic activity with corticoids in the treatment of Addison’s (Borst et al 1953). Other botanicals to consider include Ashwagandha (Withania somnifera), Siberian Ginseng (Eleutherococcus senticosis), and American Ginseng (Panax quinquefolium). Adequate amounts of vitamins B and C should also be considered. The holistic treatment of Addison’s disease should occur under proper medical supervision to monitor the effects of treatment on glucocorticoid and mineralcorticoid levels.

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There is perhaps no disease that is as close to the human condition as arthritis, or joint pain. It is among the earliest diseases described in the ancient medical literature, and is clearly found throughout the anthropological record, such as in bone and fossil remains. Researchers from many fields tell us that it is a disease we share with a great many animals, including our fellow mammals, as well as birds, reptiles and fish. For all of us, the sad commonality is that it is apparently inevitable: a simple process of wear and tear to joints over a lifetime of use. Interestingly enough, some mammals that hang upside down such as bats and sloths don’t seem to experience this kind of joint damage, although mammals supported by water such as whales do (Berkow 1992). In yogic tradition this might be seen as evidence that inverse postures (asanas) such as headstands promote the proper flow of energy that overcomes stagnant energy… in the philosophical tradition of ancient India this is represented by Bodhi, or Enlightenment tree, which as it grows sends its branches back down into the earth…

Broken down, busted up and good ol’ fashioned deee-generating joint problems got a high falootin’ name in western medicine: osteoarthritis (OA). It nonetheless has a precise definition, to differentiate it from the other forms of arthritis such as the rheumatoid, gouty, or bacterial arthritides (plural of arthritis). OA is characterized as a mild inflammatory joint disease with a gradual loss of articular cartilage and the subsequent hypertrophy of bone producing osteophytes. Its prevalence increases with age, as does its severity, with a usual onset of it more symptomatic forms in the fourth to fifth decades of life (or usually earlier with sports injuries). Men typically have an earlier onset than women, but women get it at an increasing frequency with age. (Berkow 1992; Rubin and Farber 1990, 723)

OA is classified as either primary (idiopathic) or secondary to some identifiable cause. Primary OA involves the distal and proximal interphalangeal joints, the first carpometacarpal joint, the intervertebral disks and zygapophyseal joints in the cervical and lumbar vertebrae, the first metatarsophalangeal joint, the hip, and knee. Secondary OA may present as above, but has a known underlying cause, including congenital joint abnormalities, genetic defects, crystal deposits, infection, metabolic diseases, endocrinopathies, inflammatory disease (e.g. RA, gout), and trauma from fracture or simple “wear and tear.” (Berkow 1992; Rubin and Farber 1990, 723)

Joints are an amazing feature of anatomical mechanics. Cartilage is a spongy, dense tissue covering the articular surfaces of bones, comprised mostly of extracellular matrix managed by a small number of very long-lived chondrocytes. This spongy surface is bathed in an extremely slippery synovial fluid filled with nutrients to feed the chrondrocytes and support cartilage health. Surrounding the synovium is a series of tough fibrous tissues and muscles to unite the joint, and maintain stability. As the cartilage is compressed with movement, fluid is pumped out of it and into the joint space. In essence, this action squeezes the wastes from out of the spongy cartilage, to be absorbed by the capillaries and then venules of the muscosa. As the cartilage is released the cartilage expands, swelling back up with nutrient-rich, slippery synovial fluid. As a result, normal joint movement is essential to joint health, and because joints have a very coefficient of friction, they should maintain themselves almost indefinitely with normal activity. The primary pitfall with cartilage is that it is an avascular tissue, as well as both aneural and alymphatic: or in other words, a part of the body that we have an inherent capacity to take for granted (aneural), but can take a very long time heal (avascular, alymphatic). (Berkow 1992; Rubin and Farber 1990, 723)

The earliest changes of osteoarthritis are the loss of proteoglycans and type II collagen, which is the principal structural elements of cartilage, from the surface of the articular cartilage, followed by the death of the chondrocytes. This process may take several years. Overtime, the articular surface develops microfractures, and the synovial fluid works its way down into these fissures, extending the cracks deeper. Neovascularization from the epiphysis and subchondral bone extends into the areas of the fissures, inducing subchondral osteoclastic bone resorption. Adjacent osteoblastic activity occurs simultaneously, resulting in a thickening of the subchondral bone plate in the area of the crack. Fibrocartilage plugs then form as a substitute for the articular cartilage, and the subchondral bone becomes exposed as it grinds against the opposite joint surface, which is usually undergoing a similar process. These thick, shiny smooth areas or subchondral bone are described as eburnated, or “ivory-like.” This eburnated bone then cracks, allowing synovial fluid to extend into the subchondral bone marrow, leading to a subchondral bone cyst. An osteophyte or bone spur then develops, consisting of bone and a mixture of connective tissues with a coating of fibrocartilage and sometimes islands of hyaline cartilage within the osteophyte. The degree of formation of these spurs varies among the joints, in proportion to the underlying cause. Finally, bony cysts (pseudocysts) form in the marrow below the subchondral bone, resulting from extrusion of joint fluid through the hyaline cartilage into the marrow, with a fibroblastic and osteoblastic cellular reaction. The gross pathology includes a roughening, pitting, and irregularity of the hyaline cartilage surface, proceeding to gross ulceration with focal and then diffuse areas of complete loss of cartilage, leaving only eburnated bony surfaces. By the time symptoms appear, synovial proliferation and some mild synovitis are virtually always present. (Berkow 1992; Rubin and Farber 1990, 723)

The signs and symptoms of OA are insidious and gradual, usually involving one or only a few joints. Pain with movement and morning stiffness are among the earliest symptoms of OA. As the condition progresses joint movement is impaired, with crepitus, tenderness, grating sensations or muscle spasm. Overtime the joint can become edematous and swollen, with the proliferation of the various joint tissues. With improper treatment and repeated injury the chances for recovery become progressively less and less. (Berkow 1992; Rubin and Farber 1990, 723)

Medical treatment

The primary focus in the medical treatment of osteoarthritis is upon eliminating risk factors and treating symptoms such as pain and immobility. Thus patient education, physical and occupational therapy, weight reduction, exercise, and corrective devices such as orthotics may be recommended. Initial medications include OTC analgesics such as ASA, acetaminophen and NSAIDs. Prescription NSAIDs may be recommended when OTC medications are ineffective, including the newer generation COX-2 inhibitors that include valdecoxib, celecoxib and rofecoxib. COX-2 inhibitors are believed to exert their anti-inflammatory effects by inhibiting the enzyme cyclooxygenase-2 (COX-2) and thus the synthesis of proinflammatory prostaglandins from arachidonic acid. The stated benefits of COX-2 inhibitors over other non-selective NSAIDs that inhibit both COX-1 and COX-2 is that they do not inhibit COX-1, which plays an important role in prostaglandin-dependent mucosal protective mechanisms. Clinical studies have shown that patients taking selective COX-2 inhibitors have a lower incidence of gastrointestinal irritation and inflammation than patients taking non-selective NSAIDs. Despite being heavily marketed as a safe and important alternative to manage pain in osteoarthritis however, recent research indicates that COX-2 inhibitors also inhibit angiogenesis through direct effects on endothelial cells, and interfere with normal healing (Jones et al 1999). Furthermore, a series of studies published in the New England Journal of Medicine (Mar 17, 2005) have shown an increased risk of cardiovascular complications in patients taking various COX-2 inhibitors, including celecoxib, parecoxib, valdecoxib and rofecoxib. These studies and others initially caused the US FDA to ban these drugs, although in what was seen as a politically motivated move they have been placed back on the market, albeit for more limited indications, and not for sustained periods of time.

Surgical procedures in OA include arthroplasty (joint surfaces are replaced with artificial materials, usually metal or plastic), chondroplasty (surgical repair of the damaged cartilage) and arthrodesis (surgical fusion of the articular surfaces, which prevents movement-induced pain). In some cases joint replacement is recommended, in which the diseased or damaged joints are replaced with an artificial joint composed of a combination of metal and plastic. Knee and hip replacement are among the most common joint replacement procedures, but some joints such those of the spine cannot be replaced with the present technology.

Holistic treatment

It is fairly well-established that osteoarthritis is better prevented than treated, as effective treatment is hampered by the relatively poor circulatory supply to cartilage. Thus proper attention to preventing joint injury is key to preventing the later development of OA. Nutritional status however is key in the pathogenesis of OA, and care should be taken to supply the body with an optimal volume of key vitamins, minerals, and accessory nutrients involved in joint repair. To control pain and inflammation medicinal plants are used along with essential fatty acids that can help to down-regulate the production of pro-inflammatory eicosanoids.

Both Ayurvedic and Chinese medicine view osteoarthritis as an evolution of chronically poor circulation, and thus treatments are undertaken to restablish the proper flow of blood to the affected area. In Ayurvedic medicine osteoarthritis is called Sandhigata vata, of which Vata and ama are the primary the pathogenic factors taken into account.

1. Ensure proper nutrition. See the Paleolithic diet listed under The Fire Within: Digestive function and Botanical medicine. Care should be taken to remove foods that are associated with inflammatory symptoms, including red meat (i.e. feed-lot beef, pork), grains, dairy, sugar, fried foods, transfatty acids and solanaceous foods (e.g. potatoes, tomatoes, eggplant etc.). The diet should be optimized to provide the body with all the nutrients needed for proper bone and joint health, including generous amounts of cartilage and bone soups that contain chondroitin and glucosamine sulfate. In particular, chondroitin and glucosamine promote an increase in the synthesis of collagen and proteoglycans that form joints, as well as exert antiinflammatory effect.

• Calcium citrate or malate, 800-1200 mg daily
• Magnesium citrate or malate, 400-600 mg daily
• Manganese, 15-30 mg daily
• Boron, 3 mg daily
• Zinc, 15-20 mg daily
• Copper, 1.5-3 mg daily
• Folic acid, 400-800 mcg daily
• Vitamin A, 20,000 IU daily
• Niacin, 250 mg up to six times daily (taken with a B complex formula, 100 mg daily)
• Vitamin C, to bowel tolerance
• Vitamin D₃, 1000-1200 IU daily, taken all year in temperate climates
• Vitamin E, 800 IU daily
• Vitamin K, 200 mcg daily
• Chondroitin, 0.5-3 g bid-tid
• Glucosamine sulfate, 0.5-3 g bid-tid

2. Decrease pain and inflammation. The focus should be on restoring joint function and limiting the production of proinflammatory eicosanoids.

• antiinflammatory botanicals, e.g. Black Cohosh (Actaea racemosa), Wild Yam(Dioscorea villosa), Ash (Fraxinus excelsior), Licorice (Glycyrrhiza glabra), Lignum Vitae (Guaiacum officinale), Devil’s Claw (Harpagophytum procumbens), Buckbean (Menyanthes trifoliata), Trembling Aspen (Populus tremuloides), Salix, Yucca spp., Smilax spp., Tanacetum,, Huang Qin (Scutellaria baicalensis), Ashwagandha (Withania somnifera), Guggulu (Commiphora mukul), Amalaki (Emblica officinalis), Huang Bai (Phellodendron amurense), Mandukaparni (Centella asiatica), Fang Feng (Ledebouriella divaricata), Kushta (Saussurea lappa)
• analgesic botanicals, e.g. Arnica, Hypericum, Populus, Salix, Lactuca, Gelsemium, Piscidia, Ashwagandha (Withania somnifera), Guggulu (Commiphora mukul), Han Fang Ji (Stephania tetrandra), Yan Hu Suo (Corydalis yanhusuo), Jatiphala (Myristica fragrans)
• EPA/DHA, 1000 mg each daily
• MSM, 2-3 g bid-tid; also MSM cream applied topically
• antioxidants, e.g. vitamins A, C, E; minerals such as zinc and selenium

3. Ensure proper digestion.

• Digestive enzymes, full spectrum, 2-3 capsules with each meal
• Bitters (e.g. Berberis, Gentian,etc.) to enhance gastric and hepatic secretions
• Dipanapachana dravyas, to enkindle agni, e.g. Yavani (Trachyspermum spp.), Shunthi (Zingiber officinalis), Pippali (piper longum), Hingu (Ferula foetida)
• Botanicals to relieve Food Stagnation and strengthen the Spleen Qi, e.g. Chen Pi (Citrus reticulata), Shan Zha (Crataegus pinnatifida), Huang Qi (Astragalus membranaceus), Dang Shen (Codonopsis pilosula)
• Probiotics and synbiotics to restore the ecology of the gut

4. Promote alterative changes and enhance elimination. Conduct a proper review of eliminative function, with particular attention paid to kidney, liver and bowel function.

• alteratives, e.g. Smilax, Apium, Rumex, Guaiacum, Galium, Chimaphila, Berberis, Trifolium, Haritaki (Terminalia chebula), Amritbhallataka (Semecarpus anacardium milk extract), Guduchi (Tinospora cordifolia), Haridra (Curcuma longa), Guggulu (Commiphora mukul), Manjishta (Rubia cordifolia)
• alkalizing diuretics, e.g. Celery seed or juice (Apium graveolens), Nettle (Urtica dioica), Cleaver (Galium aparine), Pipsissewa (Chimaphila umbellata)
• Triphala churna, 2-3 g bid-tid, with equal parts laxative herb, e.g. Trivrit (Operculina), Turkey Rhubarb (Rheum) in chronic constipation

5. Enhance systemic and local circulation.

• steam baths, sauna
• circulatory stimulants, e.g. Prickly Ash (Zanthoxylum), Ginger (Zingiber), Cayenne (Capsicum), Tvak (Cinnamomum cassia)
• rubefacients, applied topically, used as a poultice, medicated oil, or volatile oil in joint edema with pain, but little indication of active inflammation, e.g. Ginger (Zingiber), Cayenne (Capsicum), Mustard seed (Brassica spp.), Peppermint (Mentha piperita), Jimsonweed (Datura), Nirgundi (Vitex negundo), Yavani (Trachyspermum spp.), Pippali (Piper longum)
• low impact weight bearing exercise
• niacin, 250 mg up to six times daily
• massage therapy, e.g. with rubefacient medicated oils (see above), or Ayurvedic tailam such as Narayana taila, Balashvagandhalakshadi taila, Pinda taila, Balaguduchyadi taila
• moxibustion
• acupuncture

6. Joint trophorestoratives, to rebuild the integrity of the joint. Many of these botanicals are rasayanas in Ayurvedic medicine, and in Chinese medicine, function to support Kidney and Jing.

• Western botanicals, e.g. Milky Oats (Avena sativa), Horsetail (Equisetum arvense), Nettle (Urtica), Bladderwrack (Fucus spp), Hawthorn (Crataegus), Bilberry (Vaccinium), Comfrey (Symphytum), Irish Moss (Chondrus), Alfalfa (Medicago)
• Ayurvedic botanicals, e.g. Ashwagandha (Withania somnifera), Gokshura (Tribulus terrestris), Amalaki (Emblica officinalis), Brahmi (Bacopa monniera), Mandukaparni (Centella asiatica), Guggulu (Commiphora mukul), Bala (Sida spp.), Shilajitu, Shuktibhasma (purified oyster shell ash), Shringaputa (deer horn ash)
• Chinese botanicals, e.g. Ren Shen (Panax spp.), Shan Yao (Dioscorea opposita), Huang Jing (Polygonatum sibiricum), Shu Di Huang (Rehmannia glutinosa), He Shou Wu (Polygonum multiflorum), Gou Qi Zi (Lycium chinense), Sang Shen (Morus alba), Lu Rong (Deer or Elk velvet), Dong Chong Xia Cao (Cordyceps sinensis), Yin Yang Huo (Epimedium grandiflorum), Bai Ji Tian (Morinda officinalis), Bu Gu Zhi (Psoralea coryfolia), Du Zhong (Eucommia ulmoides)
• Bone and seaweed soups

7. Specific formulations.

• Yogaraja guggulu, 2-3 g bid-tid
• Kaishora guggulu, 2-3 g bid-tid
• Feng Shih Xiao Tong Wan, 10 pills bid-tid
• Guan Jie Yan Wan, 8 pills bid-tid
• Feng Shi Pian, 2 pills bid
• Te Xiao Yao Tong Ling (Specific Lumbaglin), 2 caps bid-tid

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Osteoarthritis is a degenerative disease of the joints associated with aging. The disease mostly affects the spine and large weight-bearing joints, and is often characterized more by degeneration of the articular cartilage than by inflammation. The absolute first thing to do is to make sure the digestive system is working properly, especially in the elderly. Look for signs like poor digestion, low appetite etc.

I have found the herb devil’s claw root (Harpagophytum procumbens) helpful in many cases of arthritis with inflammation and pain, taken either by itself or as part of a combination formula, about 2 grams twice a day as a crude powder, or 60 drops of tincture 3 times per day.  Boswellia gum is also very effective. Both of these are free of the side effects caused by many NSAIDS because they do not cause bleeding.

Herbs from the blood-nourishing group are also essential to slow, and hopefully reverse, joint degeneration. They act on the structural components of ligament and bone.  TCM doctors frequently use raw rehmannia root, dang gui root, shou wu root, millettia stem, eucommia bark (du zhong or E. ulmoides), drynaria rhizome (gu sui bu or D. fortunei), psoralea seed (bu gu zhi or P. corylifolia) and deer antler.

Glucosamine sulfate is extraordinarily effective in most cases so I always use it to treat this disease. This substance is an amino-sugar extract derived from the exoskeletons of shrimp, lobsters and crabs.  As people age, they lose the ability to manufacture their own supply of glucosamine sulfate.  More than 300 scientific investigations and 20 double-blind studies have shown that patients treated with this nutrient experience an improvement rate between 72% and 95% in various forms of osteoarthritis (reported in Murray 1996). The recommended dosage is 750 mg twice per day. It takes up to six weeks to see results, at which point patients often experience pain relief that exceeds the results from aspirin treatment. Japanese research shows that it works better when combined with MSM.

Glucosamine sulfate is not a painkiller—it literally repairs the joint tissue.  This translates into dramatic and long-lasting results. However, in spite of the treatment’s effectiveness, we must remember that it does not reverse or cure the underlying degenerative process that causes the disease.

Traditional Ayurvedic medicine (TAM) doctors consider osteoarthritis (sandhigatavata) to be a degenerative process caused by any food, behavior or condition which results in poor blood circulation, dryness (Vata) or low nutrient supply to the joint.  Their treatments emphasize use of the following strategies:

• Gentle and slow oil massage (do not disturb the joint), using the standard tonic oil narayana taila, which contains wild asparagus root as a main component.
• The oil massage is followed by application of a warm compress soaked in a warm decoction made from bala, using gentle range-of-motion manipulation.
• The well-known tonic yogarajaguggulu, which contains guggul gum, is a standard Ayurvedic medicine for osteoarthritis, used for several months.
• A second general tonic should also be prescribed to supply nutrition, such as the ones mentioned in the immune/longevity group.
• Use the diet to reduce wind, along with carminative (gas-expelling) spices, especially celery seeds. Other carminatives include cloves, caraway, and fennel (Bajracharya, 1979).

To control arthritic inflammation (as opposed to degeneration), it is often important to use herbs from the heat-reducing group.   TCM doctors use phellodendron bark and scute root to control inflammation, in combination with other herbs like myrrh gum, fang feng root (Ledebouriella species), and qin jiao root (Gentiana macrophylla).  They also use a relative to boswellia gum called ru xiang gum (B. carterii).

Except for short term use, beware of NSAIDs—aspirins and aspirin-like compounds including acetaminophen.  Unlike many natural anti-inflammatory herbs, these pharmaceutical products cause damage to mucosa, kidney and heart, and worsen progression of damage to cartilage and joints. One would therefore expect that herbs containing salycilate compounds would cause the same problems. Interestingly, I have used the European prescription herbal tincture Phytodolor--which contains three such herbs, common ash bark (Fraxinus excelsior), aspen leaf/bark (Popuolus tremula), and goldenrod aerial portions (Solidago virgaurea), and it does not seem to cause stomach upset or bleeding, as correctly stated in the promotional literature. This may be because of the slow onset of action (several days) creates less concentrated action on the stomach mucosa. Another trick is to use DGL licorice to protect the mucosa.

Most herbal anti-inflammatories do not cause stomach problems.  Turmeric root, for example, has not been reported to cause bleeding, nor has boswellia gum, even in high doses. Such medicines seem not to damage the mucosa because they work in a different biochemical way.

A good base herbal anti-inflammatory formula might start with boswellia gum, myrrh gum, scute root and turmeric root. Add other herbs as discussed, and adjust as follows:

• If the patient tends toward coldness, try adding ginger root or prickly ash bark.
•  If heat and inflammation are severe, add phellodendron bark.

Thus our typical osteoarthritis treatment program consists of:

1. Glucosamine sulfate/MSM supplements: 750 mg, twice per day.
2. An herbal formula for inflammation.
3. Additional nourishing tonic herbs and basic vitamins to slow degeneration.
4. A healthy diet, bodywork, oil/herb massage, exercise and vitamin supplements.

The relative proportion of the formula that tonifies and the formula that reduces inflammation depends on signs and symptoms. In elderly patients, for example, tonification and digestion are usually emphasized.

The following therapies can also be useful additions to your treatment protocol.

• Some patients, especially those over the age of 60, require digestive aids to ensure proper absorption of nutrients. Digestive herbs like bromelain, white atractylodes, and ginseng root can be added to the formula in these cases.
• Essential fatty acids (EFA’s) are essential to control deficiency-based inflammation, so I use fish oils along with borage oil or evening primrose oil.
• Acupuncture can help alleviate pain and stimulate natural healing powers.
• Women must remain aware hormonal changes that can affect arthritis and bone loss. In cases of hormone involvement, collateral treatment may be necessary

You can also treat bursitis and Sjogren’s syndrome with these same methods

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AN ANALYSIS OF CHINESE HERB
PRESCRIPTIONS FOR RHEUMATOID ARTHRITIS

by Subhuti Dharmananda, Ph.D., Director, Institute for Traditional Medicine, Portland, Oregon

INTRODUCTION

Arthritis is a general term for joint (Greek: arthron) inflammation (Greek: itis). The main symptoms are pain, swelling, and stiffness. The cause of the disorder is an immune-based disturbance primarily affecting the joint fluids. There are several types of arthritis, but there are two basic forms mentioned in modern literature that occur frequently: rheumatoid arthritis and osteoarthritis. Rheumatoid arthritis is characterized by autoimmune attacks that usually come and go, and it may be influenced by numerous factors that alter the immune functions, including infections, dietary components, and stress. Osteoarthritis also involves some autoimmune responses, but is characterized by a gradually worsening degradation of the joint spaces, leading to sharp, fixed pain that persists. Although both disorders can begin at any of the joints, rheumatoid arthritis most often affects the upper body first (fingers are frequently the first site), while osteoarthritis most often affects the lower body first (hips and knees are commonly affected). Rheumatoid arthritis tends to be felt for the first time at a somewhat earlier age than osteoarthritis, with rheumatoid arthritis usually starting before age 50 and osteoarthritis usually starting after age 50. Women are more likely than men to suffer from arthritis of both types.

Arthritis has been a recognized medical condition since ancient times, and the Chinese had developed numerous formulas for its treatment. Chinese herbal formulas were not specifically designed for either of the two major types of arthritis defined today. The basis for Chinese doctors differentiating arthritis into subgroups was not the microscopic details of the pathology. Instead, arthritis was divided into traditional medicine categories: hot and cold types, upper and lower body involvement, deficiency or excess syndrome, pain characteristics (such as variability and severity), and whether the site of the arthritis was fixed or “moving.” Both rheumatoid arthritis and osteoarthritis fall under the heading of bi syndrome, a disorder of qi and blood circulation that leads to symptoms of pain, numbness, swelling, and stiffness. Rheumatoid arthritis fits most closely those syndromes characterized by the Chinese as wind-damp invasion affecting the joints. Osteoarthritis more closely fits the syndrome of liver/kidney deficiency syndrome causing weakness and stiffness in the legs with painful joints.

In China, syndromes similar to rheumatoid arthritis were an area of special concern, generating considerable literature on the subject, since the condition could arise suddenly and could rapidly become severely debilitating. Osteoarthritis, on the other hand, tended to be lumped together with other disorders of aging, in which stiffness and pain, especially of the legs, was considered just one part of the gradual deterioration of body functions that occurs with old age. As such, it is usually not the subject of much discussion separate from antiaging therapies. The formulas described in this article mainly fit the category of rheumatoid arthritis treatments.

There are three key pathological factors addressed by the formulas: wind, damp, cold:

• Wind (feng) refers to the sudden onset of the disease, mobility of the affected site (mobile bi syndrome), variability of the manifestation of symptoms, and sensitivity to changes in the environment (see: Drawing a concept: feng). Wind-dominant arthralgia most often affects the upper body and corresponds to the early stage of rheumatoid arthritis. Deficiency of qi and blood allows wind to more easily penetrate the body and cause pain.
• Damp (shi) refers to the worsening of the symptoms in damp weather, the initiation of the disease or worsening of symptoms after spending time working in a wet environment (such as wading in water or sleeping on damp ground), and the accumulation of fluid in the joints and/or nearby areas of the limbs (see: The six qi and six yin). Dampness-dominated arthralgia most often affects the lower part of the body and is characterized by swelling and stiffness of the joints, and accompanying sensations of numbness; it may correspond to a middle stage of rheumatoid arthritis (that is, after the disease has become chronic, with less variability of affected joints). Disorders of fluid metabolism, especially a weakness of spleen function, will aggravate dampness and the resulting joint dysfunction.
• Cold (han) refers to the worsening of symptoms with exposure to cold, improvement by applying heat (including liniments that cause increased local circulation), and impaired circulation associated with declining kidney yang that most often occurs with aging (see: Exploring yin/yang #6: cold and heat). Cold-dominated arthritis especially affects the extremities (hands and feet) where circulation is poorest, as well as the lower back-the site of the kidneys. The kidney yang, if deficient, is unable to dispel chilliness. Exposure to cold may initiate arthritis; however, the more common association is with advanced arthritis in which the internal metabolism (qi and yang aspects) are debilitated by chronic disease and aging, yielding a cold syndrome. More rarely, there can be a hot type arthralgia, initiated perhaps by excess exposure to the hot sun during the summer, and manifesting with redness of the joints.

The closest traditional Chinese medicine term to rheumatoid arthritis is fengshi bing which literally means wind-damp disease. The wind and damp factors can complex with either cold or heat factors to yield arthralgia. Almost all of the traditional approaches apply to the complex involving cold factors rather than heat. Gout, which has some characteristics in common with arthritis, usually fits the cold-dominated category or the cold-damp category of bi syndromes.

Cold, wind, and dampness cause stagnation of circulation within the channels (meridians; blood vessels). According to the Chinese medical concept, when these pathological factors are dispelled, the circulation returns to normal and the disease goes into remission. If the disease has been experienced for a long period of time, the blood becomes static (a more severe condition than poor circulation). Eventually, the initiating factor (wind) becomes less prominent and the stagnation dominates, with blood stasis an increasing concern. Therefore, in the treatment of the chronic and advanced disease, there is more emphasis on overcoming static blood than when treating an earlier and more variable phase of the disease.

BASIS OF THE ANALYSIS

One can use the traditional Chinese description of arthritis to suggest herbs and formulas to use for each patient. However, rather than devising unique formulations for each patient, it is common practice throughout the Orient to make use of a relatively small group of arthritis formulas that are believed be very successful. In this article, 31 such formulas that are in the current literature and based on the traditional approach are analyzed to reveal their commonly used ingredients and the patterns of formulation that have been relied upon. The sources of the prescriptions were as follows:

1. Two publications of the Oriental Healing Arts Institute (OHAI): the compendium Commonly Used Chinese Herb Formulas with Illustrations (1) and the journal articles in OHAI Bulletin devoted to rheumatism and gout and their Chinese herb treatment (2).
2. The English-language rheumatology books Bi Syndromes (3) and Rheumatology in Chinese Medicine (4) based on traditional Chinese herb prescriptions.
3. The formula reference books Thousand Formulas and Thousand Herbs of Traditional Chinese Medicine (5) and Chinese Herbal Medicine Formulas and Strategies (6).
4. The books on patent remedies available in English, Chinese Herbal Patent Formulas (7), Handbook of Prepared Chinese Herbal Formulas (8), and Chinese Patent Medicines (9). In addition, one Japanese patent remedy based on a popular Chinese patent and approved by the Japanese Ministry of Health, was also included in the listing (10).

Formula selection was based on two main factors:

• The indications for the prescription suggest that it could be used in the treatment of arthritis associated with any combination of wind, damp, and cold factors. Formulas specifically designed for unusual cases of arthralgia, such as heat-dominated arthritis, were not included.
• The presence of common Materia Medica items in the prescriptions, with non-toxic ingredients being the dominant components of the formulas.

The selection of formulas will have some influence on the outcome of the analysis, so an effort was made to include formulas that were described in several different texts, indicating their importance to the study of traditional Chinese medicine.

Table 1: Arthritis Formulas. This table displays the names of the formulas, the list of ingredients, and some comments about each of the formulas. In the first column, the pinyin transliteration of the Chinese formula name is given first, followed by the common name (OHAI system) if available, and then the references to the source texts (which have been listed above). In the ingredients column, the herbs have been listed in order from the most frequently used to the least frequently used (see Tables 2 and 3), followed by a short list of some rarely used items (after “plus”). The final column gives the Chinese traditional source text (STNA denotes source text not available) and some comments about the use and application of the formulas.

MAIN HERBS IN THE SELECTED FORMULAS

Table 2 lists 8 herbs as “standard herbs” for arthralgia syndromes. They are broadly used in constructing arthralgia formulas and were included in at least half of the formulas listed in Table 1. There were another 21 herbs, listed in Table 3, that serve as adjunctive therapies; they each were present in at least 4 of the formulas. Each of these 29 herbs are described in some detail below, with the herbs presented from most frequently mentioned (21 times for tang-kuei and siler) to least frequently mentioned (4 times for coix, persica, scute, and phellodendron). In both Tables, the common name and pinyin name for the herb is given in the first column, followed by the botanical name and the plant family (in parentheses) in the second column. Traditional actions are from Oriental Materia Medica (11) and only include those that are related in some way to treatment of arthralgia.

Table 2: Standard Herbs. The following herbs are routinely used in arthritis treatments and are not specific for a location or type of arthritis. In some cases, more than one variety of an herb can be used. For example, with cinnamon, the twig is most often utilized, but cinnamon bark, considered more warming, is included in some formulas; white atractylodes, which serves as a qi tonic, is more often used than red atractylodes (for clearing dampness), but sometimes both are included in the formulation; white peony, the blood-tonifying herb, is more often used than red peony, which may be substituted when a stronger blood-vitalizing action is desired.

Table 3: Adjunctive Herbs. The herbs in this section are used for particular types of arthralgia or particular constitutional conditions of the patient. The herbs may be selected to address the dominance of one of the three factors contributing to bi syndromes: wind (e.g., use ma-huang or angelica); damp (e.g., use tu-huo, hoelen, clematis, stephania, or coix); or cold (use aconite or asarum). Further, the herbs may be selected for deficiency syndromes: for weakness add astragalus; for kidney/liver deficiency add rehmannia, eucommia, and achyranthes; for blood-stasis syndrome add persica and carthamus; for stiffness add chin-chiu and chaenomeles; for underlying heat syndrome, add scute and phellodendron.

CHARACTERISTICS OF THE COMMONLY USED HERBS

There are at least three important characteristics of the herbs listed in Tables 2 and 3 in relation to treatment of arthritis: the common nature and taste of most of the herbs; the fact that several of the listed herbs are components of widely used traditional tonic formulas; and the reliance on herbs from a particular plant family with a similar group of active constituents.

As to the nature and taste of the herbs, nearly all are warming, or at least neutral (exceptions: peony, stephania, coix, scute, and phellodendron are cold-natured), and most are spicy (exceptions: licorice, peony, achyranthes, hoelen, rehmannia, eucommia, stephania, astragalus, chaenomeles, coix, persica, scute, and phellodendron). Even among the herbs that stand as exceptions to this rule, only very few of these are used frequently in the formulas that were analyzed, namely: licorice, peony, and achyranthes, all of which serve the role as tonics. The warm quality dispels cold, and the spicy quality dispels wind; the warm-spicy action disperses dampness accumulation and resolves stagnation at the surface (i.e., limbs, skin, flesh; not internal organs).

As to the correspondence of several key herbs to traditional base formulas, the following two formulas contribute several of the herbs that are used with high frequency:

1. Tang-kuei Four Combination (Si Wu Tang), which contains tang-kuei, peony, cnidium, and rehmannia; Tang-kuei Four Combination nourishes and vitalizes blood circulation; and
2. Four Major Herbs Combination (Si Junzi Tang), which contains ginseng, atractylodes, licorice, and hoelen. Four Major Herb Combination invigorates the stomach/spleen functions, tonifies qi, and promotes moisture circulation.

Deficiency of qi and blood flowing through the meridians makes the body susceptible to external pathological factors, such as wind, cold, and dampness. Qi deficiency further makes the body susceptible to developing internal chilliness or moisture accumulation that will merge with external cold and damp factors to worsen arthralgia. Blood deficiency will allow the development of internal wind secondary to liver dryness, which will merge with external wind to worsen arthralgia. The herbs in these two formulas are not specific for arthralgia, but, instead, are aimed at treating internal deficiencies that contribute to susceptibility to this and other diseases and that allow further progression of the diseases rather than spontaneous remission.

The plant family that dominates this group of herbs is the Umbelliferae, sometimes known as the “celery family” because it includes this well-known plant. The herbs in this family mentioned in Tables 2 and 3 are: tang-kuei (see Figure 1), siler (see Figure 2), chiang-huo, cnidium, tu-huo, and angelica. In all cases, the root material is used. The roots are fragrant, and there is a certain similarity in their odor that is attributable to the common active constituents. By contrast, the three Ranunculaceae herbs (peony, aconite, and clematis), the two Rosaceae herbs (chaenomeles and persica), and the two Leguminoseae herbs have only remotely related substances within each family group that contribute to their actions in the arthritis formulas (i.e., it is a coincidence that they fall into the same plant family).

The common active constituents of interest belong to the chemical category of benzopyrone derivatives, mainly the coumarins (e.g., osthenol) and the furanocoumarins (e.g., bergapten). These compounds have been claimed to reduce protein-rich edematous swellings (see: Chinese herbs for lymphedema) and they have some antiinflammatory actions that have been revealed in laboratory animal experiments. Of the formulas listed in Table 1, all but one formula contains at least one of the Umbelliferae herbs (Da Qinjiao Tang contains all six of them); the exception is Stephania and Astragalus Combination, an ancient formula for leg edema that has been adopted to treat arthralgia of the knee.

REPRESENTATIVE FORMULAS

There are five formulas presented in Table 1 (the first five listed) that are comprised almost entirely of the commonly used herbs for treatment of arthralgia and might be considered representative formulas:

1. Sanbi Tang (Chin-chiu and Tu-huo Combination)
2. Shujing Huoxue Tang (Clematis and Stephania Combination)
3. Duhuo Jisheng Tang (Tu-huo and Loranthus Combination)
4. Da Qinjiao Tang (Major Chin-chiu Combination)
5. Da Fangfeng Tang (Major Siler Combination)

Each of these formulas contains at least 14 ingredients from Tables 2 and 3, but few additional ingredients not listed in the Tables. All of these formulas contain Tang-kuei Four Combination (Siwu Tang: tang-kuei, peony, cnidium, and rehmannia) plus siler and licorice. Of these, Sanbi Tang and Duhuo Jisheng Tang are the most commonly referenced formulas in the modern literature devoted to traditional herb formulas for treatment of arthritis.

RESEARCH EFFORTS

The most recent Chinese medical literature on rheumatoid arthritis treatments, including English language publications as found in the Journal of Traditional Chinese Medicine and the Journal of Integrated Western and Traditional Medicine, reveal that there is much experimentation still going on with herbal recipes for rheumatoid arthritis. The new formulas may treat heat syndrome, blood stasis, phlegm accumulation, or other disorders that were not the principal targets (wind, cold, damp) of the more traditional approaches. In addition, they may utilize ingredients that are toxic and cannot be used in Western practice, such as the immune-inhibitor tripterygium or the powerful muscle stimulant strychnos. Such ingredients may have a more profound effect than the commonly used and gentle components of the formulas described above. Since Western patients are usually seeking treatments to substitute for the modern drugs that cause unacceptable side effects, the herbal prescriptions used must be essentially non-toxic.

Due to concerns about the quality of design, conduct, and reporting of clinical trials for Chinese herbs, rather than reviewing the broad range of reports that can be found by searching the literature, an example will be provided here to illustrate the claimed results and the duration of therapy that was indicated as sufficient to yield those results. The study was selected for its large number of patients enrolled.

The tableted formula Fengshi Hantong Pian (Rheumatism Cold Pain Tablets) was given to 310 patients suffering joint pain (12). The prescription included tang-kuei, chiang-huo, cinnamon, red peony, aconite, astragalus, clematis, coix, scute, sinemonium, deer antler, lycium, and corydalis. According to the report, after a course of treatment lasting ten days, marked pain relief was experienced by about 70% of the patients, with pain being the main arthritic symptom of concern. A 30 day course of this therapy produced normalization of ESR (erythrocyte sedimentation rate) and RF (rheumatoid factor) values in about half of the patients that were followed up (31 of 61 had normal ESR; 24 of 38 had RF turn from positive to negative).

This report, and information garnered from other Chinese studies, suggest that alleviation of pain may be expected during the first week of treatment, blood chemistry changes may be expected as early as the first month of treatment, and remission may occur from one month to several months after treatment begins in some patients. Since rheumatoid arthritis can have periods of spontaneous remission, the possibility that the herbs bring on an earlier or more complete remission can only be determined by very careful testing with large treatment and control groups.

Unlike steroid drugs that powerfully inhibit the immunological component of the disease and can produce results within 24 hours, the herbal compounds may need to first reach a certain blood concentration that requires two or three days of regularly consuming the herbs, and then there may be another few days in which the changes in metabolism and immune function eventually result in a reduction of the inflammatory process. Still, if given in adequate dosage and if the formula ingredients are suited to the individual, some improvements (most alleviation of severe pain) could be reasonably expected in the first 3-7 days. Patients should not need to pursue the therapy for several weeks to determine if it has any influence on their condition. Other effects may take longer. For example, with benzopyrones in the treatment of protein-rich edemas, it has been indicated that a treatment time of several months is required to markedly reduce the swelling. Typically, Chinese herbal therapies for chronic diseases, such as rheumatoid arthritis, are given for several weeks or several months to attain substantial improvements. This duration of time is consistent with traditional Chinese theories of treatment of deficiency syndromes that underlie the disorder: it simply takes time to overcome the visceral weaknesses so that pathologic factors can be expelled.

MECHANISM OF ACTION

Chinese researchers have attempted to elucidate how the herbs used in traditional arthritis formulas alleviate the symptoms-from the modern viewpoint-by carrying out numerous studies of the blood constituents of patients. According to studies that have been carried out recently (13, 14, 15), the mechanism of action that may be dominant in the situations with good therapeutic results is a reduction in the levels of pro-inflammatory cytokines, such as interleukin-1 (IL-1). The effect is then to alter the levels of T-cells and the production of activated antibodies and other components. In addition, or as a result, the properties of the blood and its circulation also change, with lowered sedimentation rate and improved circulation to the extremities. The herbs may also act on the prostaglandin synthesis and degradation pathways, yielding a lower level of pro-inflammatory prostaglandins.

REFERENCES

1. Hsu HY and Hsu CS, Commonly Used Chinese Herb Formulas with Illustrations, 1980 rev. ed., Oriental Healing Arts Institute, Long Beach, CA.

2. Hsu HY, Neuralgia, rheumatism, and gout and their Chinese herb treatment, Bulletin of the Oriental Healing Arts Institute, 1979; 4(4): 16-27.
3. Vangermeersch C, and Sun Pei-lin, Bi-Syndromes, 1994 SATAS, Belgium.
4. Guillaume G and Chieu M, Rheumatology in Chinese Medicine, 1996 Eastland Press, Seattle, WA.
5. Huang Bingshan and Wang Yuxia, Thousand Formulas and Thousand Herbs of Traditional Chinese Medicine, vol. 1, 1993 Heilongjiang Education Press, Harbin.
6. Bensky D and Barolet R, Chinese Herbal Medicine: Formulas and Strategies, 1990 rev. ed., Eastland Press, Seattle, WA.
7. Fratkin J, Chinese Herbal Patent Formulas: A Practical Guide, 1986 Shya Publications, Santa Fe, NM.
8. Chun-Han Zhu, Clinical Handbook of Chinese Prepared Medicines, 1989 Paradigm Publications, Brookline, MA.
9. Chen Keji (editor), Chinese Patent Medicines, 1997 Hunan Science and Technology Press, Hunan, China.
10. Tsung PK and Hsu HY, Arthritis and Chinese Herbal Medicine, 1987 Oriental Healing Arts Institute, Long Beach, CA.
11. Hong-Yen Hsu, et al., Oriental Materia Medica: A Concise Guide, 1986 Oriental Healing Arts Institute, Long Beach, CA.
12. Wang Zhaoming, et al., A report on 310 cases of articular rheumatism treated with Fengshi Hantong Pian, Chinese Journal of Integrated Traditional and Western Medicine 1985; 5(5): 284-285.
13. Zhou Xueping, et al., Clinical and experimental study on treatment of mid-late stage rheumatoid arthritis with Shuguan Granules, Chinese Journal of Integrated Traditional and Western Medicine 1999; 5(3): 165-170.
14. Xu Desheng, et al., Clinical and experimental study on RA Mixture in treatment of rheumatoid arthritis, Chinese Journal of Integrated Traditional and Western Medicine 1996; 2(3): 178-183.
15. Li Shangzhu, et al., Changes in blood flow in the extremities in patients with rheumatoid arthritis and treatment with integrated traditional and western medicine, Chinese Journal of Integrated Traditional and Western Medicine 1996; 2(2): 115-116.

August 2000

Figure 1. Angelica sinensis; tang-kuei.

Figure 2. Ledeborella divaricata; siler.

Distance Learning Fair Use Source: http://www.itmonline.org/arts/arthritis.htm

We have already discussed single cell immune response to foreign antigens in the immune system players article. The whole process is that antigen processing cells present the antigen to T-cells, which then help B-cells to change form into IgE-secreting  cells (called plasma cells). The newly formed IgE attaches itself to mast cells, which are found in large quantities in the respiratory tract, sinus, GI tract and skin. This is why allergy occurs mostly in these locations. When the antigen gets into your system again, it links to the mast cells, which then release histamine, leukotrienes and other irritating cytokine chemicals, which cause the initial allergy symptoms to occur. The later reactions occur because Th2 cells are activated by the processed allergen, then release interleukins, which cause eosinophils, basophils and neutrophils to release more allergy-causing cytokines.

Allergy Symptoms

The classic respiratory symptoms are sneezing, secretion of watery mucus, and membrane swelling that blocks the nasal passageways. In chronic cases dark circles develop under the eyes, as well as fatigue and hacking due to an itching sensation in the roof of the mouth.  Over time, respiratory allergy and sinusitis moves toward asthma, discussed in another section of this website.

•  Gastrointestinal symptoms develop from allergens in foods. This can cause itching and burning in the mouth, nausea, vomiting, intestinal inflammation and increased permeability, gas and bloating, and diarrhea or constipation. In severe cases anaphylaxis can develop, with lowered blood pressure, tracheal edema and cardio-respiratory distress. In infants and children, food allergies can cause projectile vomiting, eczema or failure to thrive.

• Cutaneous symptoms can develop from external sources such as chemical or insect venom. If the allergen is strong, it can lead to anaphylaxis. More often, there is a late-phase redness and swelling at the site of injury or bite.

• When allergens or secondary by-products of intestinal allergy are absorbed into the blood, it can lead to hives, fatigue, heat sensations, chronic inflammatory diseases, depression, emotional imbalance, itching skin, edema, headaches, joint pain and swelling, smooth muscle contraction etc.  These are more common as patients increase in age.

• Acute symptoms occur within minutes of exposure to an allergen and typically recede over the next 30-90 minutes. Symptoms can recur a few hours later and last for several hours. If exposure to the allergen is continuous, such as with food allergies or pollutants in the home or work environment, late phase reactions occur. Over time, tissue damage can occur.

Allergy is a difficult nut to crack. Originally it was enough to keep people away from triggering substances, such as chemical, bacteria, parasites, dust, mold, foods and pollen spores. Think of my friend, the caveman Og. Og lives a few miles from a sulfur pit surrounded by a giant fungus. One day Og walked close to the pit, and the sulfur/fungus fumes got into his eyes, which began to burn and itch. Of course, Og got out of there. Unbeknownst to him, however, his B-cells were releasing signals that created sulfur and/or fungal remembering mast cells that lay in wait for the next appearance of the chemicals.  Next week, OG takes his wife Mrs. OG out for a walk. About a mile from the pit, Og begins to sniffle, itch and burn, rubbing his eyes. He say, “Air bad. Go this way,” as he turns and leaves the area. Mrs. Og says, “Air not bad. Og crazy.”  Mrs. Og did not react because she had not developed reactivity.

Og had it easy, all he had to do was stay away from the sulfur pit. Today, however, we face the problem of inundation of thousands and thousands of invisible chemicals, many undetectable until an allergy develops and we have symptoms. It is difficult if not impossible to completely turn off allergies without incapacitating the immune system. This is what happens when immunosuppressant drugs are used. Antihistamines are a bit better because they have fewer side effects, but they tend to wear off. This is because they do not extinguish the causes, and the immune system will simply find another way to do what it thinks it should to cope.

Our best approach is to try to take advantage of three facts:

•  Reactions depend upon exposure and we can modify our environment
• The strength of our barrier defenses can limit entry even when exposed
•  We can modify our immune response can be modified with herbs and nutrients

I employ several approaches:

• Purify the home atmosphere to reduce exposure to allergen triggers.  This works even though all triggers cannot be avoided, because when the total allergy load is decreased, the response is often far less. This is especially true for food allergies.

• Test for and reduce exposure to food allergies.  The method for doing this, as well as strengthening the intestinal membranes (to reduce allergen absorption) is covered in the section on hidden food allergies. Although many allergists limit identification to IgE antibodies, holistic physicians include IgG, IgM and sometimes IgA (Marinkovich, 1996). It may be important to have your health care provider test for elevated IgG antibodies if you are having trouble with identification.

• Prescribe specific herbs and nutrients to tone down the allergy response and make it less aggressive.

Treatment of Allergies

•  The severity of the general inflammatory response can be decreased by using healthy fats and oils, and supplementing with borage oil, fish oils etc.

• Some herbs that have specific anti-allergy effects are listed under the antibody, IgG, IgE, eosinophil, basophil and mast cell headings in the immune system articles. Choose based on signs and symptoms.

• TCM herbs with anti-allergy effects include scute root, chrysanthemum flowers, schisandra berries, er bu shir tsao herb (Centipeda minima), magnolia flower, honeysuckle flower, and forsythia fruit. Most of these are contained in Pe Min Kan Wan pills, commercially available (see safety section). If there are signs of mucus, add pinellia tuber, tangerine peel and ginger root.

• Ayurvedic herbs with anti-allergy effects include neem leaves, turmeric root, eclipta, tulsi,  boswellia gum, aguru wood, karchura root (Curcuma zedoaria), tamalaki (Phyllanthus nururi),  karkatashingi gall (Pistacia intergerrima), katphalam bark (Myrica nagi), coleus (C. forskohlii), Malabar nut (Vasaka or Adhatoda vasica) and anthrapachaka leaf (Tylophora indica).

•  Western herbs used for allergy include lobelia, feverfew, echinacea, eyebright flowering herb (Euphrasia officinalis), stinging nettle, ginkgo leaf, and garlic bulb. The combination of the flavonoid quercetin with bromelain is also useful.

See sinusitis and asthma

Distance Learning Fair Use Source: http://oneearthherbs.squarespace.com/diseases/allergy.html

The term anemia refers to a decrease in the numbers 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.

The rate by which RBCs develop in red bone marrow is dependent upon the status of hemoglobin, which ensures the proper oxygenation of the tissues. This process is maintained by a negative feedback mechanism that is stimulated by hypoxic conditions in the affected tissues, which in turn, promotes an increase in RBC synthesis until tissue oxygen levels are restored to normal. RBCs develop from pluripotent hematopoietic stem cells to progenitor cells, when then form into proerythroblasts, reticulocytes and then erythrocytes (RBCs) in a process requiring a variety of growth factors and cytokines including erythropoietin. Once formed, RBC precursor cells are released into circulation as reticulocytes where they remain in circulation for about one day until they lose their nucleus. This causes the center of the cell to indent and form the distinctive concave shape of a mature RBC. Since erythrocytes have no nucleus they rely upon anaerobic and aerobic glycolytic pathways for energy, and as the cell ages the levels of these enzymes gradually decrease. After 120 days worn and damaged RBCs are destroyed by phagocytic cells in the liver and spleen. Thus the body requires that at least 1/120 the number of RBCs are produced on a daily basis to maintain homeostasis and prevent hypoxia. (Berkow 1992; Rubin and Farber 1990, 553-563)

The unique concave shape of an RBC functions to increase the surface area for gas exchange. This shape also ensures that RBCs are highly deformable, and can bend in upon themselves allowing them to squeeze through the narrow openings of capillaries into the tissues. Each RBC contains approximately 280 million molecules of hemoglobin (Hb), contained in a lipid membrane and supported by a cytoskeletal network. (Berkow 1992; Rubin and Farber 1990, 553-563)

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 mother of iron during pregnancy
• poor nutrition: inadequate source of dietary iron and accessory nutrients (e.g. B complex); also common in alcoholism (Berkow 1992)

More uncommon causes of anemia include bleeding disorders, liver disease, thalassemia, infection, cancer, arthritis, enzyme deficiency, sickle cell disease, hypothyroidism, toxins, or hereditary conditions.

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
• 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. (Berkow 1992; Rubin and Farber 1990, 553-563)

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 kinds 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 cause is blood loss, from chronic bleeding (e.g. erosive gastritis), excessive menstruation, or from a developing fetus. Other prominent causes include 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 diet (e.g. phytates in cereals and legumes, tannins and oxalates in certain plants, etc.). 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 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 koilonychia (thinning, concave nails). (Berkow 1992)

Normochromic-normocytic anemia refers to state of the RBCs that appears 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. Normochromic-normocytic anemia is either hypoproliferative or hypoplastic. Hypoproliferative anemia is caused by a deficient production of erythropoietin (EPO), commonly associated with renal disease (which produces EPO), hypometabolic states (e.g. hypothyroidism), and protein deficiency. 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. (Berkow 1992)

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. (Berkow 1992)

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. (Berkow 1992)

Excessive hemolysis

Excessive hemolysis refers to the excessive destruction of RBCs, usually by phagocytic cells in the spleen, liver, and bone marrow. There are a variety of factors that promote the destruction of RBCs including defects in the RBC itself, or external factors such as the presence of anti-RBC immunoglobulins, trauma or infectious disease. Depending upon the cause, excessive hemolysis can be acute, chronic, or periodic.

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, promotiong 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 particularly in the course of the condition is chronic.

Abnormalities within the RBC that promote hemolysis are either related to some dysfunction within the cell or the cell membrane. There are a number of rare, congenital red cell membrane disorders including hereditary spherocytosis, congenital hemolytic jaundice, chronic acholuric jaundice, familial spherocytosis and spherocytic anemia. Acquired red cell membrane disorders include as stomatocytosis (caused by alcoholism) and hypophosphatemia (caused by several factors including starvation, diabetic acidosis, diuretics, vomiting, corticosteroids etc.), the latter of which results in RBC ATP depletion. ((Berkow 1992; Rubin and Farber 1990, 553-563)

Anemias caused by disorders of red 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 extent those of Mediterranean and Middle Eastern descent. It characterized by a sickle-shaped RBC caused by the homozygous inheritance of Hb S, an abnormal form of hemoglobin that clumps together, making RBCs sticky, stiff, and more fragile, causing them to assume a curved, sickle shape. The distorted and inflexible RBCs adhere to vascular endothelium and end up plugging small arterioles and capillaries, leading to occlusion, hypoxia and local cell death. There are a variety of other congenital diseases that relate to impaired or improper hemoglobin synthesis and cause anemia, including hemoglobin C disease, hemoglobin S-C disease, and hemoglobin E disease. Of note is the relatively common thalassemia major and thalassemia minor, a group of chronic, inherited, microcytic anemias characterized by defective Hb synthesis and ineffective erythropoiesis resulting from decreased production of beta, alpha, gamma, or delta polypeptide chains. Thalassemia is particularly common in persons of Mediterranean, African, and Southeast Asian ancestry. (Berkow 1992; Rubin and Farber 1990, 553-563)

Hemolysis caused by defects external to the red cell is determined when no intrinsic RBC abnormality can be identified. Causes include:

• Hypersplenism: characterized by a mechanism that produces splenomegaly (splenic enlargement) with increased filtering of RBCs and phagocytic function. Mechanisms include infection (e.g. bacterial endocarditis, mononucleosis), hereditary conditions (e.g. spherocytosis, thalassemia major), congestive conditions (e.g. splenic vein thrombosis, portal hypertension), myeloproliferative disease (e.g. chronic myeloid metaplasia), infiltrative diseases (e.g. sarcoidosis) and cancer (e.g. chronic lymphocytic leukemia, lymphomas).
• Autoimmune hemolytic anemia (AIHA): identified by the presence of anti-RBC immunoglobulins. More frequent in women than in men, usually with an abrupt onset, producing a severe and potentially fatal anemia.
• Traumatic hemolytic anemia: caused by some kind of trauma such as hand-drumming or karate, or from roughened endothelial surfaces in the heart (e.g. calcific aortic stenosis) or arterioles (atherosclerosis); in the latter case, increases in blood pressure can also promote RBC damage
• Infectious hemolytic anemia: from reacting to toxins produced by infectious organisms in the body (e.g. Clostridium perfringens, hemolytic streptococci, meningococci), or when RBCs are actually infected themselves (e.g. Plasmodium and Bartonella spp.). (Berkow 1992; Rubin and Farber 1990, 553-563)

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, regardless of cause, including Ashwaganda (Withania somnifera), Asparagus (Asparagus officinalis), Amalaki (Phyllanthus emblica), Dong Quai (Angelica sinensis), Gou Qi Zi (Lycium barbarum), Bai Shao (Paeonia lactiflora), and He Shou Wu (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 Yellowdock (Rumex crispus), Raspberry (Rubus idaeus), and Nettle (Urtica dioica), as infusion or tincture.

• Microcytic anemia relates to an iron deficiency, caused by dietary 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 diet. Holistic treatment consists of increasing iron containing foods (e.g. meat, yams,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.
• Macrocytic or megablastic anemiarefers 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 require the use of anti-inflammatory and immunomodulating botanicals. For sickle-cell anemia specifically, Prickly Ash (Zanthoxylym clavaherculis) bark can be taken continuously, 20-40 gtt of a 1:5 tincture, bid-tid.

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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The traditional Chinese medicine view of blood deficiency (xuexu) doesn’t correspond completely to the modern medical concept of anemia. This divergence in interpretation often leads to difficulty in discussing the matter with patients. Although there are many types of anemia described in modern medicine (some of them related to rare deficiencies of blood cell production or altered hemoglobin formation), by far the most common type-and the one that might come closest to the usual description of blood deficiency in Chinese medicine-is iron deficiency anemia. The causes, such as excessive menstrual bleeding, are the same in the two systems. Iron deficiency is easily measured by taking a blood sample and evaluating its iron constituents, such as hematocrit (red blood cell proportion), hemoglobin (iron-based blood component), and serum ferritin (iron storage protein). From a symptomatic point of view, there are typical indicators of blood deficiency, which sometimes overlap and sometimes differ in the two medical systems, as shown in Table 1.

TABLE 1: Iron Deficiency Symptoms.
Symptoms that have some overlap or similarity are listed in the same row, those which differ are in separate rows. The modern medicine indications are taken from University of Maryland Medicine (1) and MedLine Plus (2); Chinese indications are from the Advanced Textbook of Traditional Chinese Medicine and Pharmacology (3) and New Practical Syndrome Differentiation of TCM (4).

The primary overlap is in the pale complexion. Easy fatigue is attributed to qi deficiency in the Chinese medicine texts referenced here, and a swollen tongue and shortness of breath may also correspond to qi deficiency. It should be noted that tachycardia is not the same as palpitation, the latter referring to the experience of feeling the heart beat, which seems fast; speeded up heart rate may occur with palpitation. Irritability is sometimes associated in Chinese medicine with a liver qi stagnation syndrome, which, according to doctrine, can arise with liver blood deficiency, but irritability is not considered a typical symptom within the general blood deficiency pattern. Potentially, iron deficiency anemia might correspond to a diagnosis of deficiency of qi and blood in the Chinese system.

While blood deficiency is a commonly treated syndrome in traditional Chinese medicine, few texts devote much space to discussing the basic concept of blood deficiency. In a compilation of information from four Chinese language sources, an article in the Journal of the American College of Traditional Chinese Medicine laid out some of the basic dogma (5). Blood deficiency is described as occurring from excessive blood loss (with insufficient replacement) and by “inadequacy of the blood factors and components required in blood formation due to spleen and stomach dysfunction.” It was also pointed out that blood deficiency could arise secondary to blood stasis. This problem is usually attributed to the idea that generation of new blood requires getting rid of old blood, and blood stasis indicates old blood that is retained.

In addition to the signs of systemic blood deficiency as outlined in Table 1, blood deficiency syndromes can be elaborated as belonging to one or more of the major organs, adding certain symptoms, specifically:

• heart blood deficiency, add symptoms of restlessness, agitation, disturbing dreams, and forgetfulness;
• spleen blood deficiency, add anorexia and mental fatigue; and
• liver blood deficiency, add spasms, dry and withering nails.

According to the central doctrine, blood is governed by the heart, stored by the liver, and generated and controlled by the spleen.

Modern medical treatment of iron deficiency anemia is straightforward and easy: the main thrust is to recommend a diet rich in iron. Then, if necessary, iron supplements can be administered (many of these are available over-the-counter). The Chinese treatment of anemia most often revolves around the use of a small number of herbs, with tang-kuei (see Figure 1, last page) as the central one. This herb is an ingredient in the principal blood nourishing formulas of Chinese medicine, such as Siwu Tang, Danggui Buxue Tang, Guipi Tang, and Bazhen Tang. Tang-kuei is not particularly rich in iron, nor are these formulas.

Iron compounds, primarily hematite, pyrite, and magnetite, are used in Chinese medicine, yet these mineral ingredients do not appear in any of the commonly-used blood nourishing prescriptions. However, an important aspect of traditional Chinese medicine in China is combining herbs with food therapies or directly with foods. For example, tang-kuei (or the full formula Siwu Tang) is often administered in a base of chicken soup, providing some iron from the chicken (if the chicken liver is included, that is the source of most of the iron). Siwu Tang, and its expanded form Bazhen Tang (which adds tonics for spleen qi), are usually recommended for recovery from blood loss due to menstruation; for most women, this blood loss is limited. The main formula recommended for treating severe blood loss is Danggui Buxue Tang, comprised of two herbs: a high dose of astragalus (30 g), with a standard dose of tang-kuei (6 g), a formula made without any iron compounds. Another prescription, made with just fresh ginger (15 grams) and a high dose of tang-kuei (9 grams), is cooked with mutton (48 g), a red meat that is high in iron, though not quite as much as in beef. That formula is used for the blood loss associated with childbirth, which can be significant. Evidently, Chinese herbs prescribed for blood loss are not good sources of iron even when treating severe blood loss, though when prepared with chicken or mutton or other meat products, the combination becomes at least a moderate source of iron. It is possible that the herbs promote some aspect of red blood cell production or iron metabolism leading to better retention of iron in the blood; this interpretation remains to be evaluated.

Therefore, within the realm of standard herbal practice, given the ready availability of iron compounds used in making formulas and their absence in blood tonic formulas, one may suspect that iron deficiency anemia is not a significant target of Chinese medicine therapy for blood deficiency. With our modern knowledge of the blood and its constituents and functions, practitioners may wish to find out about the patient’s blood test results regarding iron to determine whether iron deficiency is a part of a broader diagnosis of blood deficiency. If it is, dietary recommendations related to adequate iron consumption and consideration of iron supplements might be appropriate, since most patients will not be cooking their herbs with meats in order to get additional iron. The issue of dietary and supplemental iron may be an important one for practitioners who prescribe herbs. It is common for patients who seek herb therapies to pursue vegetarian or near-vegetarian (e.g., no red meat) diets that are low in iron. Further, excessive menstrual bleeding due to fibroids is a frequently presented disorder for treatment by herbs therapies.

GETTING IRON FROM THE DIET

It has been determined that most adults can maintain a healthy level of iron in the blood by consuming a total of about 10 mg of iron each day, with 15 mg per day for menstruating women. According to USDA recommendations, the allowances of dietary iron intake are as follows:

• Young children – male and female: 6 months to 10 years: 10 mg
• Males: 11 to 18 years: 12 mg; 19 and older: 10 mg
• Females: 11 to 50 [menstruating]: 15 mg; 51 and older [non-menstruating]: 10 mg; Pregnant: 30 mg; Lactating: 15 mg

There are three primary dietary sources for iron (see Tables 2 and 3, for specific examples and quantities):

• consumption of meat, usually providing 1-5 mg in a modest serving of about 3 ounces (an amount currently recommended for a single meal portion to minimize consumption of saturated fats);
• dried fruits, fruit juices, vegetables, legumes, and certain nuts usually providing 1-3 mg per serving of about half a cup (these are items that are encouraged to be consumed with higher frequency to assure adequate intake of vitamins, flavonoids, and other beneficial plant components); and
• wheat products, which are usually made with iron-fortified flour, providing, for example, 1-2 mg of iron in two sandwich slices or a cup of pasta.

In a typical diet of three meals per day, one needs about 3-4 mg of iron per meal, which is easily obtained by most people. Some individuals, particularly women, suffer from low iron levels in the blood as a result of: low intake of foods (e.g., low calorie diets); losses of iron from bleeding (e.g., menstrual bleeding; see appendix for further details); and problems with iron uptake or distribution to iron carriers and reservoirs.

TABLE 2: Iron-rich foods arranged from largest to least amount of iron in a typical serving size (1). The quantities of iron may differ slightly from those in the table below based on different samples of the foods (variation is usually not more than 25%).

TABLE 3: Iron content of some common foods rich in iron, divided by heme-iron (more easily absorbed) and non-heme iron (less easily absorbed, by a factor of about 10). These are also grouped according to type of source; note the variation in iron content among different varieties of a food type (6).

IRON SUPPLEMENTS

Iron supplements are readily available, and can provide quantities of iron that range from 10 to 40 mg per daily dose. There are potential problems with some iron supplements, of which the greatest is getting too much iron. Excess intake of iron can cause constipation, impair the uptake of essential trace minerals, and contribute to a higher state of oxidative stress (iron is one of nature’s most potent oxidants). Children who accidentally consume large amounts of iron are most susceptible to the adverse effects and the single most commonly reported poisoning from supplements is due to children getting into packages of iron supplements (all supplements providing iron are now required to have child-proof caps). In 2001, the Institute of Medicine set a tolerable upper intake level of 40 mg per day for infants and children through age 13 and 45 mg per day for ages 14 and over. Generally, supplement recommendations, even for severe iron deficiency anemia, are for less than 40 mg/day, because at that level people can experience nausea and other immediate reactions. In an attempt to maximize iron supplementation without evident side effects, many suppliers of supplements for prescription by nutritionists provide 27 mg/day, the highest amount that is associated with a low incidence of complaints. In addition to maximizing iron levels in the supplements, the manufacturers also attempt to maximize its absorption by using iron glycinate and by including vitamins (mainly vitamin C and several B vitamins) that enhance the absorption of iron.

Maximizing iron dosage and promoting efficient absorption together may not be ideal because it involves adding as much iron as possible to the system. An alternative is to provide a more modest amount of iron within a blood nourishing herb formulation that may have other benefits to the blood system.

APPENDIX. THERAPIES FOR EXCESSIVE MENSTRUAL BLEEDING

The base RDA for iron is set at 10 mg, but rises to 15 mg (some suggest 18 mg) for menstruating women to compensate for the monthly blood loss. Dietary sources may prove inadequate to attain this level, especially for those who rely on non-heme sources. A supplement is often indicated, particularly for women who have heavy blood flow during menstruation. By adding about 10 mg of supplemental iron to the daily diet that should already provide 10 mg, a sufficient level (e.g., about 20 mg/day) is attained for most women. There appears to be some correlation between low iron levels and increased blood flow during menstruation, so that a low iron state can end up being maintained easily: the low iron promotes more bleeding, while the bleeding keeps the iron levels low. This situation may be remedied in some cases by the addition of iron supplements to the dietary intake.

Increased menstrual blood flow is a common result of uterine fibroids, a condition that brings many women to seek natural health care alternatives to surgery. Herbs used to reduce uterine bleeding from various causes include tien-chi ginseng (sanqi); lotus (seed, node, and other parts); gelatins (deer antler, tortoise shell, donkey skin); and certain traditional formulas, mainly Guipi Tang (Ginseng and Longan Combination) and Bazhen Tang (Tang-kuei and Ginseng Eight Formula), and patent medicines (mainly Yunnan Bai Yao and Wu Ji Bai Feng Wan).

The low point of blood iron levels occurs as the menstrual period is completed, with maximum cumulative blood loss. Thus, Chinese herbalists emphasize the use of tonic formulas to begin immediately following cessation of menstrual bleeding, and continuing for several days afterward. In some cases, the blood tonics are continued throughout the month, rather than used for just a few days. The decision to purse this routine use of tonics is based on the constitutional analysis, to determine whether tonification is the most appropriate therapy during the rest of the menstrual cycle, as opposed to a possible alternative therapy, such as regulating liver qi.

Similarly, the decision to continue iron supplementation throughout the month, or only during the days following menstruation (and during menstruation, to help control excessive blood flow), would depend primarily on blood tests showing low levels of iron.

REFERENCES

1. University of Maryland Medicine, Iron-deficiency Anemia, 2003 University of Maryland Medical System, http://www.umm.edu/blood/aneiron.htm
2. Medline Plus, Iron in diet, 2003 U.S. National Library of Medicine and National Institutes of Health http://www.nlm.nih.gov/medlineplus/ency/article/002422.htm
3. State Administration of Traditional Chinese Medicine, Advanced Textbook on Traditional Chinese Medicine and Pharmacology, (vol. 1) 1995-6 New World Press, Beijing
4. Wang Qi and Dong Zhi Lin, New Practical Syndrome Differentiation of T.C.M., 1992 China Ocean Press, Beijing.
5. Cheung CS and Belluomini J, Blood, Journal of the American College of Traditional Chinese Medicine 1982 (2): 48-54.
6. McKinley Health Center, Dietary Sources of Iron, 2001 University of Illinois; http://www.mckinley.uiuc.edu/handouts/dietiron.html
7. Dharmananda S, Bag of Pearls, 2002/2003 Institute for Traditional Medicine, Portland, OR.

Figure 1. Tang-kuei (danggui) pressed slices as found in Hong Kong pharmacies. These are made by slicing the roots, putting several root slices next to each other, and then pressing them, to make one large “palm” slice. They are usually soaked in Chinese wine, which makes the active constituents more mobile when cooking as a decoction or when using consuming the ground herb powder.

May 2003

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by Subhuti Dharmananda, Ph.D., Director, Institute for Traditional Medicine, Portland, Oregon