Skin Deep: the Integumentary System and Botanical Medicine

Applied Phytotherapeutics I Skin Deep By Terry Willard ClH, PhD; Todd Caldecott ClH Lesson 7 – Integumentary System

Skin Deep: The Integumentary System and Botanical Medicine

Introduction

The Skin is the largest organ in the body and takes up considerable attention by many people. Our skin is the interface between the internal structures of our body and environments. It is also an interface between our consciousness and the world, through expression, and adornments. The psychological relationship a person has with their skin can be quite complex. It is often wrapped up in ones own self-image.

When we refer to the skin, we are referring to a group of tissues that make up the integumentary system. Of all the body organs, none is more easily assessed in a clinical environment than the skin. The skin is derived from the embryonic ectoderm, as is the nervous system, and thus many skin conditions are partially influenced by the underlying state of the nervous system.

In Ayurvedic medicine skin relates to the sensation of touch (sparsha) and the element of wind (vayu), the latter of which forms the humoral division of vata, which functions to control the nervous system. Thus the correlation between the skin and the nervous system in Ayurvedic medicine bears remarkable similarity to the scientific concept that the skin and nervous tissue are similar tissues.

In the formation and ongoing regeneration of skin however, Ayurvedic medicine considers the skin to be derived from blood, in much the same that milk when heated forms a scum on its surface. Blood is primarily a nutrient delivery and waste removal system, and is routed through the spleen and liver to be filtered. Borrowing from the analogy of Ayurvedic medicine, many skin disorders are thus thought to arise from “bad blood,” which is treated by promoting and normalizing spleen and liver function.

The skin also tells us about the state of blood circulation and the oxygenation of tissues, and a bluish skin color, for

example, may be an indicator of heart failure.

As a protection agent the skin has many jobs, from simple mechanical injury, to attacks by bacteria, fungi, viruses and parasites. The skins pigment provides protection from the sun’s ultraviolet radiation. To this we must remind ourselves that it is one of the major elimination organs, with sweating and the sloughing off of dead skin cells. The skin also plays a role in temperature regulations.

The skin serves as a primary sensory organ. The five major sensation that the skin (and nerves) can react to are: touch, pain, heat, cold and pressure. There are other sensations, like vibration that can be seen as composites of these basic sensations.

I. Anatomy of skin Information on the Integumentary System can be found in previous courses you have taken, or in your mandatory text: Principles of Anatomy & Physiology by Tortora and Grabowski.

T h e

s k i n

c o v e r s

a b o u t

square meters of body tissue, weighing about 4.5-5 kg, and ranging in thickness from 0.5 to 4 cm. It is comprised of two principle parts, the epidermis and the dermis. Beneath the dermis is the subcutaneous tissue or hypodermis, that in turn is attached to the underlying connective tissue.

The epidermis

The epidermis is composed of stratified squamous epithelium, and contains four principal cell types:

Keratinocytes: protein keratin, waterproofs and protects, desmosomes. Melanocytes: pigment called melanin, protects the underlying tissues from UV radiation. Langerhans cells: arise from bone marrow and migrate to the epidermis, interact with helper T cells, easily damaged by UV radiation. Merkel cell: deepest layer of the epidermis (stratum basale) in hairless skin, make contact with sensory neuron endings, functioning in the sense of touch.

There are five layers of epidermis, and from deepest to superficial, they are the:

Stratum basale: a single layer cuboidal cells that contain stem cells capable of continued cell division, and melanocytes. Stratum spinosum: containing 8-10 rows of tightly packed polyhedral cells with spine-like projections. Long projections of melanocytes extend among the keratinocytes, which take in melanin by phagocytosis. Stratum granulosum: consisting of 3-5 layers of flattened cells that are undergoing apoptosis (cell death), contain keratohyalin, precursor of keratin, in various stages of degeneration. Stratum lucidum: consisting of 5 rows of flat, clear dead cells that contain intermediate substances between keratohyalin and keratin, thickened skin of palms and feet have this layer. Stratum corneum: consisting of 25 - 30 layers of flat dead cells completely filled with keratin, and are an effective barrier against water, microbes, heat and UV radiation.

Epidermal growth factor (EGF) is a protein hormone that stimulates growth of epithelial and epidermal cells during tissue development, repair and renewal. Certain kinds of proto-cancer genes called oncogenes can cause tumors by permanently activating EGF, which then causes epidermal cells to proliferate out of control.

The Dermis

The dermis is composed of connective tissue containing collagen and elastic fibers, and certain cells such as macrophages, fibroblasts and adipocytes. The dermis is thickest in the soles and palms, and thin in the eyelids, penis and scrotum. Generally it is thicker on dorsal and lateral aspects of the body, rather than on the ventral and medial parts of the body.

Outer portion of the dermis is the papillary region: areolar connective tissue, fine elastic fibers, surface area increased by the dermal papillae, fingerlike projections that indent the overlying epidermis, contain loops of capillaries and a few corpuscles of touch, nerve endings sensitive to touch, produces the characteristic ridges seen in fingerprints.

Deepest portion of the dermis is called the reticular region: dense irregular tissue, interlaced bundles of collagen and coarse elastic fibers, provides skin with strength, extensibility and elasticity, small tears occur with stretching are called striae, or stretch marks.

Subcutaneous layer: lamellated corpuscles, nerve endings sensitive to pressure and cold are located just below the dermal layer, and those that are sensitive to heat are located in the medial and superficial regions of the dermis.

Skin Colour There are three pigments found in the skin: melanin, carotene and hemoglobin. Melanin is produced by melanocytes, most abundantly in the mucous membranes, penis, areola, nipples, breasts, face and extremities, number of melanocytes is the same in all people, and the difference in skin colour is relative to the amount of melanin produced synthesized by melanocytes from tyrosine by the enzyme tyrosinase in an organelle called a melanosome, exposure

to UV radiation increases the enzymatic activity of tyrosinase, and as a result, stimulates the production of melanin, tanning. Carotene: is a yellow-orange pigment found in such foods as carrots and egg yolks, precursor of vitamin A, Asian descent carotene is also present in stratum corneum, fatty areas of dermis and subcutaneous layer, giving Asian skin its characteristic yellowish hue. Hemoglobin: pigment contained within red blood cells, Caucasian skin is mostly translucent, due to the small amount of melanin, blood within the capillaries of dermis provides the characteristic pinkish-red colour of Caucasian skin. Albinism is an inherited defect, inability to produce the enzyme tyrosinase. Vitiligo is a disease in which there is a complete loss of melanocytes in the areas affected, producing a pattern of white blotches on the skin.

Epidermal Ridges Epidermal ridges are ridges and grooves on the digits of fingers and toes, appearing as a series of straight lines or a pattern of loops and whorls. By the third or fourth month of fetal development the developing epidermis conforms to the underlying structure of the dermal papillae. One of the functions of epidermal ridges is to increase grip of the hand and foot by friction, by acting as tiny suction cups. Epidermal ridges are genetically determined and are lifelong: it is thought that each individual has a unique pattern, which is the basis of using fingerprints in criminology.

III. Accessory skin structures

Accessory structures in skin include hair, nails and glands. Hair: or pili, projections of epidermis, growth and distribution is largely determined by location, sex, genes, and hormonal activity, protects against UV radiation, decreases heat loss, guards against foreign particles. Normal hair loss is between 70-100 hairs per day, rate of replacement is dependent upon illness, surgery, diet, fever, blood loss, emotional stress, severe weight loss, chemotherapy and childbirth.

Glands: sudoriferous (eccrine and apocrine), sebaceous (oil glands), mammary glands and cerminous glands. Perspiration: watery substance produced by eccrine glands, water, salts (mostly NaCl), urea, uric acid,

ammonia, sugar, lactic acid, and ascorbic acid, cooling mechanism and in the elimination of wastes. Ceruminous glands: modified sweat gland that produces cerumen (ear wax) in auditory canal.

Nails: tightly packed keratinized cells, forming a clear covering; nail body, free edge, nail, lanula, or moon, nail matrix, eponychium or cuticle occupies the margin of the nail, ability to grasp objects and for protection shield.

II. Physiology of skin

The skin has several distinct functions, including: regulation of body temperature, protection, sensation, excretion, immunity, blood reservoir, synthesis of vitamin D.

Skin and homeostasis

There are two basic repair mechanisms for skin damaged by injury, depending upon the depth of the wound: abrasion occurs, or a first to second degree burn, damage to just the epidermal layer, basal epidermal cells break contact with basement membrane, contact inhibition, completely replaced by new cells, over a period of 24 to 48 hours, occurs only among the same kind of cells, stimulated by epidermal growth factor (EGF).

Deeper wound healing: inflammatory phase, vasodilation, an immune response, and blood clotting, migratory phase, clot is replaced by a scab, epithelial cells bridges wound, fibroblasts synthesize scar tissue and blood vessels regrow, granulation tissue, proliferative phase, extensive growth of epithelial cells and regrowth of blood vessels, maturation phase, scab is sloughed off and the blood vessels are restored to normal.

When the injury is severe enough: form a scar, fewer melanocytes, making the scar look lighter, formation is called fibrosis, limited by the margins of the original wound it is called a hypertrophic scar, If the scar extends beyond the original boundaries, called a keloid scar.

Part Two: Traditional Herbal Perspectives on Skin Disease

Ayurvedic perspectives on skin diseases

Ayurvedic medicine states that the skin is formed by the metabolic activity of blood just as a layer of scum forms on the surface of milk when it is heated. Thus the skin is intimately connected to the activity of the blood in every respect, and can be seen to represent a grosser, more stable phase of blood, in which changes to it occur much more slowly.

According to Ayurvedic theory, ‘blood’ or rakta, is formed by the processes of digestion, of which the first component formed is ‘plasma’ (rasa), which in turn gives rise to blood. As an extension of blood the skin records upon itself the health of the blood, which in turn is reflective of digestion, and thus the skin forms a useful and easily accessible indicator of both the blood and digestive health.

When digestion is poor the result is ama or ‘toxins,’ which are transferred to the blood, and if these toxins overwhelm the body’s capacity to immediately process and eliminate them, the ‘toxins’ remain in the blood and eventually manifest in the skin. Unlike the blood, which undergoes constant filtering and purification by the liver and spleen, the skin is only cleansed or purified by the activities of blood. Thus it is something of a primary tenet in Ayurveda that in order for a skin condition to improve the blood must first be purified, after which the toxins present in the skin can be received by the blood and returned to the koshta (digestive tract, via the liver) to be eliminated.

A number of factors indirectly or directly promote the vitiation of the doshas to produce skin disease, including:

1. overeating, or eating before the previous meal has been digested 2. eating contradictory foods (see Appendix I) 3. eating improperly cooked or prepared foods

4. eating excessively heavy or greasy foods 5. eating excessively acidic, salty or spicy foods 6. eating excessive amounts of foods such as freshly harvested grains, curd, fish, masa (Phaseolus mungo), radish, pastries, sesame seed, milk, and jaggery 7. suppression of bodily urges such as vomiting 8. excessive fear, anxiety or worry 9. excessive exposure to heat 10. excessive exercise in hot weather 11. exercise after a heavy meal 12. sleeping during the day or immediately after eating 13. application of cold water immediately after exposure to extreme heat 14. improper administration of pancha karma (cleansing and rejuvenation plan) 15. suddenly implementing a fasting regimen, or eating a large meal immediately after a fast

Western herbal perspectives on skin disease

The skin forms an important physical barrier to microbial infection, and also protects the tissues from the oxidizing effects of the atmosphere. The skin is the metabolically active organ in the body, and undergoes changes that are dependent upon the underlying factors that support its activities.

As in Ayurvedic medicine, the skin in Western herbal medicine is seen to maintain an important relationship with blood, and hence the importance of alterative remedies that enhance the processes of intermediate metabolism and the discharge of cellular wastes into the blood.

One common mistake in treating skin conditions is to do nothing more than promote alterative changes, without at the same time up-regulating the function of the other eliminatory organs (liver, bowels and kidneys) to cleanse and purify the blood. Using alterative herbs is an important tool to mobilize wastes and toxins in the body, but if attention is not also directed to the organs of elimination the end result is to simply aggravate the blood, and in turn, aggravate the skin. Thus, alterative changes must be accompanied by up-regulating the eliminatory function, such as using cholagogues, aperients, and diuretics simultaneously with alteratives. While some alteratives

such as Rumex and Berberis do up-regulate eliminatory function (i.e. an insufficient liver), others herbs such as Arctium and Galium lack this activity, and are notorious for worsening skin conditions when used in physiologic doses without proper eliminatory support.

David Hoffmann has a simple generalization he uses for direction of alteratives. As he says it doesn’t always work, but it is a great generality.

Plant Part used Primary elimination Herbal examples path/action Galium aparine, Leaf Kidney/diuretic Trifolium pretense, Urtica dioica Root, rhizome, Acticum lappa, wood Liver/hepatics Mahonia aquifolium, Rumex crispus

Despite its role as a physical barrier to protect the underlying tissues and as an eliminatory organ (sweat, sebum), the skin is also an important sensory organ, housing receptors of touch but also temperature, pressure and pain.

During the third week of development in a process called gastrulation, the embryo differentiates into three primary germ layers called the endoderm, mesoderm and ectoderm. Both the skin and nervous system arise from the embryonic ectoderm and thus these tissues maintain a strong embryonic link. Western herbalists recognize this link between the skin and nervous system such that the skin can reflect dysfunction within the nervous system. For example, during a period of emotional stress, such as that experienced by a student during a week of exams, the skin may manifest acne, a transient rash or wheals (hives). In this case, traditional alterative remedies directed to removing an obstruction to elimination will invariably fail, or can even make the situation worse by further irritating the nervous system. (Alteratives and eliminatory agents act, by promoting an immunological response appropriate to a toxic exposure, albeit with a benign agent, i.e. the herb.) Thus it is important that the underlying cause of the skin disorder be accurately ascertained before treatment is implemented.

In some cases the worsening of a skin condition during the initial phases of treatment may be referred to as a kind of healing crisis, but this should only be reserved for chronic, poorly manifested conditions. Despite the fact that the skin is an eliminatory organ, it is relatively inefficient and generally speaking toxins and wastes are best eliminated via the liver, bowels and kidneys. In most cases any worsening or aggravation of a skin condition during treatment is indication to stop or change the strategy.

Based on the constitutional model presented by Michael Moore in his Herbal Energetics in Clinical Practice (2002), the skin can manifest symptoms of deficiency or excess. With this model Moore builds a correlation between the skin and mucosa, which are continuous structures (although derived from different embryonic tissues), inferring that a derangement in one is often manifested in the other:

Skin/mucosa deficiency Moore states that skin and mucosal deficiency symptoms are often caused by a liver deficiency (see The Inner Alchemist: Hepatobiliary Function and Botanical Medicine). Commensurate with a liver deficiency, the circulation of blood and glandular secretions in these tissues is deficient, manifesting as dry flaking skin, with cracking and fissures, in focal areas or more or less systemically. In many cases the mucosa of the mouth, rectum and vagina are irritated and sore. Often the entire pattern of skin and mucus membrane deficiency plays into the dynamic of neuroendocrinal stress, with excessive sympatheticotonia (‘fight and flight’ responses), and thus needs to be addressed as well.

Botanicals that are used to stimulate deficient skin conditions act to enhance blood circulation to the periphery and support liver function, promoting the anabolism of nutrients that supply and nourish the skin. Given the need for trophorestoration, botanicals that promote anabolic processes generally can also be used, as well as those targeted towards the neuroendocrinal system to support the adrenals and down-regulate sympathetic stress:

e.g. vascular stimulants: Asclepias, Capsicum, Zanthoxylum

e.g. cholagogues, portal stimulants: Berberis, Rumex, Chelidonium, Iris, Leptandra, Mahonia, Menyanthes, Silybum, Rumex e.g. trophorestoratives, anabolics: Panax, Aralia, Avena, Turnera, Glycyrrhiza e.g. parasympathetics, sympatholytics: Scutellaria, Passiflora, Valeriana, Nepeta, Avena, Anenome

In addition to the above, topical therapies such as dry skin brushing, wet sauna and oil massage can be useful adjuncts. In regard to dietary therapies, it is important to look for potential deficiencies in fat soluble nutrients (i.e. vitamins A, E, D, EFAs, etc.).

Skin/mucosa excess Symptoms of skin and mucosa excess are moist, greasy and oily skin, not too dissimilar from what most people experience during puberty, but equally distributed all over the body. There may be a tendency towards acne, boils, ingrown hairs, and sebaceous cysts, and generally speaking, the skin is warm and moist to the touch, sweating is easy and profuse and the body odor is strong and pungent.

Skin and mucosa excess is usually related to liver and reproductive excess, and a tendency towards excessive anabolism. In most cases the patient has a tendency to excessive weight gain, and/or is directly related to dietary factors such as excessive animal products and an avoidance of alkalizing, high fiber foods (e.g. leafy green vegetables), and nutrient chelating foods such as legumes and grains.

Moore states that this is a difficult condition to treat directly, and apart from dietary changes, is treated by focusing on liver and reproductive excess (see The Inner Alchemist: Hepatobiliary Function and Botanical Medicine and The Human Flower: Reproductive Health and Botanical Medicine).

Traditional Chinese perspectives on skin disease

According to the Huang Ti Nei Jing Su Wen (Yellow Emperor’s Classic of Internal Medicine), the skin (and hair) is governed by the Lungs. Using the metaphor of “the steam that rises from a boiling cauldron”, the Lungs receive the purified fluids obtained from the ‘cooking’ of digestion as a kind of ‘mist.’ The mist-like nature of the Lungs represents the foundation of phlegm, the viscosity and turbidity of which is dependent upon the strength of digestion, whose job it is to separate nutrient from waste. Thus when digestion is weak the ‘mist’ of the Lungs becomes turbid and laden with toxins, which increases the viscosity of phlegm. In its role as a moisturizing, phlegm- producing organ, the Lungs support the mucosa and also the skin, and to some extent the skin could be visualized as a form of ‘solidified phlegm.’

The Lungs can transfer wastes and toxins inherited from poor digestive function to the skin, and thus a weakness in digestion represents an underlying causative factor in certain skin diseases. Thus skin diseases marked by itching and weeping lesions are treated with spicy herbs that dispel phlegm, such as Cang Er Zhi (Xanthium sibricum) and Bai Jie Zi (Brassica alba seed). Similarly, when the Lungs are dry and deficient, exemplified by a dry cough or when the humidity of the air is very low (as in a desert), the skin will reflect this dryness, and are thus treated with herbs that are moistening and nurture the lungs, such as Huang Qi (Astragalus membranaceus) and Sha Shen (Adenophora tetraphylla)

Apart from its moisturizing activity in the body, the Lungs are also the site of the zheng qi or ‘true’ qi, the final refinement of all types of qi. Zheng qi is formed from a combination of the original qi (xian tian zhi qi), the qi obtained from food (gu qi, ‘food’ qi, as the rising ‘mist’), and the ‘air’ qi (ta qi), obtained through breathing. Through its rhythmic, bellows-like activity, the Lungs are responsible for directing the zheng qi throughout the body, and in particular, directs a subset of zheng qi called the ‘defensive’ qi or wei qi. Wei qi is specifically directed to

the skin where it controls the opening and closing of the ‘pores’ (sudoriferous glands), expelling and preventing the entry of external pathogenic influences (i.e. the ‘six evils’).

In feverish conditions, which are usually caused by a pathogenic influence attacking the Lungs (in medical terms, an upper respiratory tract infection), the wei qi is mobilized in the skin to push the pathogenic influence out of the body. This process is very much likened to a battle, the resolution of which is the crisis of a fever in which the fever overcomes the pathogen, and forces the pathogenic influence out of the body as sweat. The relationship between the Lungs, skin and the wei qi elegantly describes the role of skin as a mechanism of non-specific resistance.

The relationship of the Lungs and skin does not completely describe the entire spectrum of skin disease, and thus Chinese medicine also relies on the notion that skin diseases can be manifest from dysfunctions in Liver and Blood. Although the specific relationships and mechanisms are not as clearly described, it is important to note that the Liver (as the storehouse of Blood) can easily overpower the Lungs, resulting in a compromise of Lung function that can extend to the skin.

Generally speaking, skin diseases in Chinese medicine relate to some kind of pathogenic influence in the body, which apart from dryness, usually relates to the pathogenic influence of wind, dampness, heat or toxins. These influences may extend themselves from the Liver or manifest within the Blood, or maybe part of a general syndrome associated with each of these pathogenic influences.

Part Three: Diagnosis of Skin Disease

It is important for the clinician to recognize and distinguish the different skin lesions, not only to describe them accurately in the case history, but as a diagnostic guide. The following are the basic, primary and secondary types of skin lesions most commonly seen in clinical practice.

Primary skin lesions

The following clinical descriptions of primary skin lesions are taken from the Merck Manual of Diagnosis (1992):

Macule: a macule is a flat, variably shaped, discolored lesion that can be large or small, including freckles, flat moles, tattoos, port-wine stains, rickettsial rashes, rubella, measles, and some allergic drug eruptions.

Papule: a papule is a solid, elevated lesion usually less than 10 mm in height. A plaque is a plateau-like lesion greater than 10 mm in height, or a group of confluent papules. Examples include warts, psoriasis, syphilitic chancre, lichen planus, some drug eruptions, insect bites, seborrheic keratoses, some lesions of acne, and skin cancers.

Nodule: a nodule is a palpable, solid lesion greater than 5 to 10 mm in height, or may not be elevated. Larger nodules greater than 20 mm in height are called tumors. Examples include keratinous cysts, small lipomas, fibromas, some lymphomas and other neoplasms.

Vesicle: a vesicle is a circumscribed, elevated lesion containing serous fluid that is less than 5 mm; if it is larger than 5 mm, it is called a bulla or blister. Vesicles or bullae are commonly caused by irritants, allergens, trauma, sunburn, insect bites, or viral infections (e.g. herpes simplex, varicella, herpes zoster). Examples include drug eruptions, pemphigus, dermatitis herpetiformis, erythema multiforme, epidermolysis bullosa, and pemphigoid.

Pustule: a pustule is a superficial, elevated lesion containing pus, usually resulting from a primary infection, secondarily as an infection of vesicles or bullae. The fluid contains an abundance of polymorphonuclear leukocytes, usually in response to infection. Examples include impetigo, acne, folliculitis, furuncles, carbuncles, fungal infections, and pustular psoriasis.

Wheal: a wheal or hive is a transient, elevated lesion caused by localized edema, usually in response to some kind of allergen, or sensitivity to insect bites, medications, or exposure to cold, heat, pressure, or sunlight.

Purpura: purpura is a generalized term referring to areas of extravasated blood, or blood that hemorrhaged from blood vessels into the surrounding tissue. Petechiae are small circumscribed focal of extravasation, whereas ecchymoses are larger confluent areas of extravasation. The term hematoma refers to an area of massive bleeding into the skin and underlying tissues.

Telangiectasia: telangiectasia are dilated superficial blood vessels, often occuring in acne rosacea, in certain systemic diseases such as ataxia telangiectasia and scleroderma, or in long term therapy with topical corticosteroids. In some cases the cause is unknown.” (Berkow 1992)

Secondary skin lesions

Secondary lesions result when primary lesions undergo some kind of change, either in the natural evolution of the condition, or when the lesions are manipulated in some way, such as when the patient scratches the lesion.

The following clinical descriptions of secondary skin lesions are taken from the Merck Manual of Diagnosis (1992):

Scale: a scale is a small, thin flake of keratinized epithelium, most commonly seen in the scaling rashes of psoriasis, seborrheic dermatitis, superficial fungal infections, tinea versicolor, pityriasis rosea, and almost chronic dermatitis of any type.

Crusts: a crust or scab is a solidified hard outer layer formed by the drying of a bodily exudate such as serum, blood, or pus, and occurs in many inflammatory and infectious diseases, as well as in the healing of burns and wounds.

Erosion: erosion is a wearing away or gradual destruction of a focal part of the epidermis, often occurring with herpes virus infection and pemphigus.

Ulcer: an ulcer is a circumscribed crater-like lesion of epidermis and at least a portion of the dermis resulting from necrosis that accompanies inflammatory, infectious or malignant processes. When the ulcer resulst from physical trauma or an acute bacterial infection the cause usually is apparent, but chronic bacterial and fungal infections, peripheral vascular diseases, neuropathies, systemic scleroderma, and tumors can be harder to determine as causal factors.

Excoriation: excoriation is an injury to the epidermis, usually linear or hollowed-out crusted area caused by scratching, rubbing, or picking.

Lichenification: lichenification refers to a thickening of the epidermis seen with an exaggeration or accentuation of normal skin lines, usually due to chronic rubbing or scratching of an area. Atopic dermatitis and lichen simplex chronicus (localized scratch dermatitis) are common causes of lichenification.

Artopy: atrophy is a manifestation of a papery, thin, wrinkled skin, usually occurring in the aged, but also with the long-term use of topical corticosteroids, and is also sometimes seen after burns.

Scars: scars are focal areas of fibrotic tissue that replace normal skin after the destruction of the underlying dermis. Scars are usually caused by burns or wounds. (Berkow 1992)

Classification of skin diseases

Once a skin lesion has been accurately described, it can be placed in one of the following diagnostic categories. From this, the practitioner narrows down the diagnostic possibilities through a process of differential diagnosis, supported by a thorough review of the case history. The primary caveat however is that skin diseases in individuals are quite often highly variable at first presentation, and can change over time. In the case of herpes simplex for example, the initial lesion might present as a series of vesicles on an erythematous base. In certain patients however the lesion may be preceded by pain, itching or tingling, or manifest as a macular erythema or a small group of red papules prior to vesicle formation. As the condition progresses it may present as ulcerations, crusts, or scars in a grouped configuration in the affected area. Thus even in a relatively simple skin condition, there can be substantial changes over time.

An excellent online database of skin disease images can be found at: http://dermatlas.med.jhmi.edu/derm/.

The following are the major classifications of various skin disorders. Please note that there are several methods of classifying skin diseases, and the following is not meant to

be exhaustive.

I. Papulosquamous diseases: characterized by scales, papules, and inflammatory eruptions

1. Psoriasis 2. Lichen planus 3. Pityriasis rosea 4. Syphilis (secondary) 5. Lichen simplex chronicus 6. Atopic eczema 7. Seborrheic dermatitis 8. Stasis dermatitis 9. Nummular dermatitis 10. Tinea 11. Candidiasis 12. Asteatotic eczema 13. Ichthyosis 14. Contact dermatitis 15. Dyshidrotic eczema 16. Neurodermatitis 17. Mycosis fungoides

II. Vesiculobullous diseases : characterized by fluid filled vesicles or bullae on the skin or oral mucosa

1. Dermatitis herpetiformis 2. Pemphigus 3. Pemphigoid 4. Acute contact dermatitis (e.g. “poison ivy”) 5. Bullous impetigo 6. Herpes simplex 7. Herpes zoster-varicella 8. Erythema multiforme 9. Miliaria (“heat rash”)

III. Maculopapular eruptions: characterized by macules or papules or both, with little or no scaling, usually due to viral or immune-mediated causes

1. Most drug eruptions (reactions to medication) 2. Most viral rashes except herpes viruses 3. Urticaria 4. Erythema multiforme

5. Erythema nodosum (blanching nodules or shins) 6. Syphilis (secondary)

IV. Purpuric eruptions: characterized by localized hemorrhage beneath the epidermis, often seen as purplish areas on the skin, usually on the legs

1. Bruises 2. Vasculitis (usually palpable) 3. Schamberg's disease (usually non-palpable) 4. Meningococcemia, gonococcemia

V. Pustular eruptions: characterized by the appearance of a pustular rash

1. Bacterial folliculitis 2. Acne 3. Furunculosis 4. Candidiasis 5. Herpes simplex 6. Shingles

VI. Tumors: neoplasm

1. Basal cell carcinoma 2. Squamous cell carcinoma 3. Malignant melanoma 4. Dermatofibroma 5. Seborrheic keratosis 6. Cherry angioma 7. Hemangioma 8. Melanocytic nevus 9. Nevus sebaceus 10. Acrochordon (skin tag) 11. Neurofibroma 12. Actinic keratosis 13. Bowen's disease

VII. Diaper dermatitis: caused by overhydration of the skin, chaffing, prolonged contact with urine and feces, and irritants such as soap

1. Candida 2. Irritant dermatitis 3. Tinea cruris 4. Psoriasis 5. Seborrheic dermatitis

Part Four: Etiology, Pathology and Treatment of Skin Disorders

From a diagnostic perspective medical dermatology is a highly complex and detailed subject, with many different skin diseases separated into an ever-increasing number of diagnostic sub-classifications. It is beyond the scope of this course to cover them all. Most patients that come into a Clinical Herbalist already have a diagnosis.

We are going to present a few examples of major skin diseases here that are most commonly seen in clinical practice. These conditions can be used as a model to treat other skin diseases.

Despite the diagnostic complexity of skin diseases in modern medicine, it is striking to note the relative lack of sophistication by which treatments are administered. Locally acting agents are the mainstay of modern dermatology, and take the form of cleansing agents (e.g. water, detergents), protectants (e.g. talcum powder, zinc oxide, petroleum), antimicrobials (e.g. antibiotics, antifungals, antiprotozoals), analgesics and anaesthetics (e.g. camphor, lidocaine) and anti-inflammatories (e.g. corticosteroids). Systemic treatments are also implemented on occasion, including system antimicrobials, system corticosteroids, antihistamines and PUVA (psoralen and high intensity ultraviolet A).

In contrast to the rather limited choices of modern dermatology, herbal medicine has much to offer the patient suffering from skin conditions, not only for the diversity of treatments available, but also the relative safety and

efficacy of many traditional therapies, both external and internal.

Acne Acne is an erythematous, irritating skin rash that primarily affects young adults, but can occur at all ages. It typically appears in the sebum-producing areas of the body including the face, chest, and back, and less often on the neck and upper arms.

Most people that have experienced acne can attest to the negative effect that this condition can have upon the psyche. The most common time for acne is in emotional vulnerable stage of adolescents, who are just becoming aware of their social image and physical appearance. This can also be true in adults, who may feel burdened by what is generally thought of as a disease of teenagers. Left untreated, severe acne can lead to disfiguring scars, which can further compound the issue of self-image.

Acne is often associated with uncleanliness, particularly with the formation of “blackheads,” which may appear to be “dirt” trapped inside the pores. In actual fact however, excessive cleanliness and extraction of blackheads (especially with non-sterile implements) may worsen the condition by promoting disturbances in the delicate ecology that forms on the skin.

There are several factors that contribute synergistically to the development of acne. The primary mechanism is attributed to the abnormal flaking and hyperkeratinization of cells within a hair follicle leading to the formation of a plug, which can enlarge and even rupture the hair follicle. Once a ruptured hair follicle spills its contents of oil and debris into the skin it leads to swelling and localized inflammation. Commensal bacteria that live on the skin, and in particular a strain of bacteria called the Propioni bacterium, secrete enzymes that dissolve the sebum. The formation of the plug is enhanced by the activity of the androgens, the secretion of which peaks during adolescence and promotes the enlargement of and increases the activity within the sebaceous glands, providing more nutrients for the bacteria. Although the androgens are secreted in much larger volumes in males, they are also present in females, although the effect is to some extent countered by the

estrogens. Thus young women will often notice that their acne worsens premenstrually as the levels of estrogen drop off to promote menstruation. (Harper 2005; Berkow 1992)

Although not all hairs are immediately visible on the body, hair follicles exist on virtually every surface of the body except for the palms of the hands and soles of the feet. Within the follicle the hair shaft extends upwards from the dermis and exits through a pore. Laying just below the epidermis a sebaceous gland enters the hair follicle where it releases sebum into the follicle at a relatively constant rate to protect the skin surrounding the pore and prevent the hair from drying out and becoming brittle.

There are two major types of acne lesions: non-inflammatory and inflammatory. Non- inflammatory acne lesions include “blackheads” (open comedones) and “whitehead” (closed comedones). Blackheads are open comedones containing oxidized sebum, which has the characteristic black color. In contrast, a closed comedones or whitehead is not exposed to oxygen and thus does not turn black, but appears a tiny, sometimes pinkish bump on the skin. When open and closed comedones manifest with papules and pustules this is referred to as papulopustular acne, which is a form of inflammatory acne. Papules are closed comedones that have become red, swollen, and inflamed (i.e. “blemishes”). Pustules are closed comedones that have become inflamed and begin to rupture into the skin forming pustules heads of various sizes (i.e. “pimples,” “zits”). The severest form of acne is nodular acne, representing large, tender, swollen acne lesions that have become intensely inflamed and rupture under the skin. If left untreated nodular acne can produce deep scarring. (Harper 2005; Berkow 1992)

Medical treatment For mild to moderate acne most doctors will recommend simple hygienic measures including water, soap, and antiseptics such as benzoyl peroxide. More severe forms of acne are often treated both topically and systemically by antibiotics, retinoids, and in young women, birth control pills.

Holistic treatment Holistic measures to control acne are somewhat different than conventional methods. In particular, greater attention is directed to maintaining the normal ecology of the skin, and thus measures such as soap and antiseptics are avoided because they tend to disturb this delicate ecology by stripping oils away from the skin, thus encouraging even greater sebum production. Instead, measures are taken to limit sebum production by the usage of agents that “tone” the skin. Among the best agents for this purpose is cold water, which can be applied in liberal volumes splashed over the face 2-3 times daily to promote local vasoconstriction. This can be used in association with mild facial scrubs, once or twice daily, prepared with botanicals that combine a gentle astringent activity with a demulcent effect, toning the skin while relieving inflammation:

Exfoliation powder 100 g Adzuki beans 40 g Yellow Pond Lily root 20 g Oat groats

Grind together to a moderately fine powder. Apply to moistened skin and scrub away. Rinse face well with cool water and pat face dry with a clean towel.

Teenage acne represents a period of reproductive excess, and often, an accompanying burden upon the liver whose job it is to deactivate and eliminate these circulating hormones. While attempting to down-regulate hormonal secretion is probably unwise, herbalists can support the deactivation of these hormones by enhancing liver catabolism. Used in conjunction with alteratives such as Arctium, Alfalfa, Tribulus, Angelica sinensis and Echinacea to pull toxins away from the skin, cholagogues such as Taraxacum radix, Berberis, Raphanus and Larrea can be safely used along with gentle aperients such as Rumex,

Rhamnus, and the Ayurvedic formula Triphala to promote the elimination of these compounds. Botanicals that have an amphoteric activity on neuroendocrinal function can also be helpful including Fucus and Eleuthrococcus. In females, botanicals that inhibit androgenization such as Serenoa can be helpful, as well as pro-estrogenic botanicals such as Paeonia and Vitex along with weak estrogenic botanicals such as Angelica sinensis, Cimicifuga and Aletris to help regulate the menstrual cycle.

Although most medical doctors believe that there is no physiological connection between diet and acne, these assumptions are based on suspect data that is more than 30 years old. Research has demonstrated a link between a high glycemic diet and acne vulgaris (Cordain 2003). In a study examining the prevalence of acne vulgaris in non- industrialized societies of the Kitavan Islanders of Papua New Guinea and the Aché hunter-gatherers of Paraguay, Cordain et al found that the prevalence of acne in these Suggested Acne Program societies is virtually non-existent, compared with a nearly

Start with a 12 day D-Tox, acne universal incidence in the West, afflicting 79% to 95% of often gets worse before it gets the adolescent population, and 40% to 54% of adults above better during the cleansing the age of 25 (2003). phase. In addition to being much higher in omega-3 fatty acids, Breakfast BEVC, FemaHerb (three tablets), Essential Fatty the diets consumed by the Kitavans and Aché also include Acids (two capsules), Traumeel increased quantities of plant-derived antioxidant vitamins, (1 tab under tongue). minerals, and phytochemicals that support antioxidant Morning Snack Vitamin C pathways. Research demonstrates that omega-3 fatty acids (500 mg). can increase insulin-like growth factor binding protein in Afternoon Snack Vitamin C (500 mg). animals and decrease insulin-like growth factor-1 in Supper Same supplements as healthy humans (Li et al 1999; Bhathena et al 1991). Thus a breakfast. diet high in omega-3 fatty acids could be involved in the . prevention of the hyperkeratinization of sebaceous follicles that leads to acne.

Furthermore, the involvement of the pro-inflammatory leukotriene B-4 (LTB-4) in the pathogenesis of acne has recently been described, and the administration of a novel LTB-4 blocker has been shown promote to a 70% reduction in inflammatory acne lesions (Zouboulis 2001). The anti- inflammatory activities of omega-3 fatty acids, including the inhibition of LTB-4 is well known. Thus a diet rich in omega-3 fatty acids may have a synergistic effect with a diet that reduces the overall glycemic load.

Although it is a poorly researched area, many of the so- called “junk-foods” that are often consumed by adolescents can be seen to worsen acne, and promote the formation and retention of toxins in the blood that induce immunological responses and burden the liver. Such diets also place stress upon the neuroendocrinal system by depriving the body of essential nutrients. Dietary measures to control acne include an avoidance of all junk foods (e.g. chocolate, candy, soda pop), a reduction in refined carbohydrates (e.g. sugar, bread, pasta), fried foods (e.g. french fries), and excessively oily foods (e.g. cheese, pizza). In particular, dairy is problematic, which, despite the fact that it has a low glycemic index, enhances insulin secretion, and in the study by Cordain et al, was notably absent from the Kitavans and Aché diets.

As inferred from the above, the fatty acid content of the diet is particularly important, to prevent the hyperkeratinization and inflammation that is characteristic of the lesions of acne. Omega-3 fatty acids found in fish oils, grass-fed animal products and leafy green vegetables appear to play an important role in regulating proper sebum secretion and decreasing inflammation.

Overall, foods that should be emphasized in the diet include fresh vegetables and fruits, high quality proteins and whole grains. Important supplements include vitamins A, B, C, E, magnesium, and zinc, to promote healing and support antioxidant mechanisms in the liver (see The Inner Alchemist: Hepatobiliary Function and Botanical Medicine).

To correct the underlying ecology of the gut synbiotics should also be implemented, particularly in situations where antibiotics and/or oral contraceptives have been used to control the condition. In such cases attention should be directed to the possibility of secondary candidiasis, and the use of antifungal remedies such as Tabebuia, Berberis and Echinacea, as well as homeopathic Candida nosodes.

Rosacea Rosacea is a chronic inflammatory problem that usually starts in middle age (or later). Women are affected three times more often than men. It is characterized by telangiectasia, erythema, papules and pustules most commonly in the central area of face, but can occur in other areas. Occasionally rosacea can be found on the extremities. Tissue hypertrophy can be seen, especially on the nose (rhinophyma).

The medical cause is unknown, but is more common in people with a fair complexion. Rosacea appears similar to acne without comedones, with granuloma of skin and cutaneous LE.

Medical treatment The mainstay of the medical treatment is oral broad- spectrum antibiotics, even though it has limited success and known side effects. The most commonly used antibiotic is tetracycline, starting with 250 mg tid, reducing to once every day or every other day. Topical corticosteroid have been found to be ineffective, fluorinated corticosteroids aggravate rosacea. Rhinophyma often requires surgical correction.

Holistic treatment Western Clinical Herbalist can have limited success with rosacea. The are several things that have been shown to aggravate rosacea including: alcoholism, menopausal flushing, hot liquids, spicy foods, exposure to sunlight, extreme temperature or humidity, make-up, local infection, B-vitamin deficiencies and gastrointestinal disorders. In general, the oil metabolic pathways in the body are disturbed.

Start a program with a 12 day D-Tox Diet or Cleansing Diet (Lesson one: Fire within: Digestion). Maintenance diet should be high in raw vegetables and organic grains. Avoid fats (especially saturated), alcohol, caffeine, cheese, chocolate, cocoa, dairy products, salt, sugars and excessively spice food. Avoid drinking extremely hot liquids (drink tepid liquids). Investigate allergies, and avoid those foods that cause problems. Avoid hot water when washing and bathing, sauna, steam baths, or hot tubs. Keep make-up to a minimum, using only natural, water based

products.

Research has shown that Rosacea patients have very low hydrochloric acid in their stomachs, affecting other digestive enzymes. Rosacea patients should take 1 - 3 capsules of digestive enzymes (containing HCl) with each meal, depending on size of the meal.

Often Rosacea suffers have a high level of Helicobacter pylori (considered responsible for ulcers). Use Goldenseal, Coptis and/or Garlic, along with the digestive enzymes to lower H. pylori.

Since much of the problem is directly related to oil metabolism, be very cautious of not consuming transfatty acids, while including plenty essential fatty acids (as found in fish and krill oil).

Suggested Program

Breakfast: Essential Fatty Acids (2,000 mg, twice daily), B- complex (1 tablet), Digest (1-3 capsules), Goldenseal or Coptis (500 mg), Cleansing Formula (2 capsules), BEVC(2 tablets), Garlic (1 capsule). Snack: Nettle or Dandelion Tea, Vitamin C (1,000 mg). Lunch: Digest (1-3 capsules), BEVC (2 tablets), Essential Fatty acids (2,000 mg). Snack: Nettle or Dandelion Tea, Vitamin C (1,000 mg). Supper: Essential Fatty Acids (2,000 mg, twice daily), B complex (1 tablet), Digest (1 -3 capsules), Goldenseal or Coptis (500 mg), Cleansing Formula (2 capsules), BEVC (2 tablets), Garlic (1 capsule).

Atopic dermatitis

Atopic dermatitis is a chronic, pruritic, relapsing skin disorder that is thought to have an immunologic basis, often with a personal or family history of atopic conditions such as asthma or hayfever. The etiology however is not established, and has been linked to a number of factors including nutrient deficiencies and dietary allergens. (Berkow 1992; Spagnola 2005)

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 responses 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.

As well, omega-3 fatty acid specifically promotes 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 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 in atopic dermatitis is the role of food allergens and food intolerances. 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, sugar, food additives, egg whites, soy, fish, shellfish and peanuts are Treatment for Atopic often accompanied by significant improvements (see The Dermatitis for children under 10 years old Fire Within: Digestive function and Botanical Medicine). Often a topical application of GLA (found in Black Atopic dermatitis can begin during infancy (i.e. ‘infantile Currant, Borage or eczema’), and can be relatively severe, with red, weeping, Evening Primrose Oil) can completely resolve and crusting lesions over the entire body, particularly the condition within a few face and scalp. In children the manifestations are typically weeks. less acute, more chronic lesions characterized by erythema and lichenification in typical areas such as inside the elbow Chamomile used as a wash or knee. In many people the condition goes into remission or a cream/ointment can also be useful. during puberty or adulthood, sometimes with periodic exacerbations. These applications rarely work in adolescent or Food allergies, especially dairy or flour can often be adults. associated with this condition. In many cases there is a related 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 cases or cases that are not responding to treatment, systemic corticoids may be used, and if the condition is non-responsive to steroids, immuno- suppressives such as cyclosporine are used.

Topical and systemic antipruritics (anti-itch) are another important component of medical therapy, such as

pramoxine (Gold Bond), which blocks nerve conduction and impulses by inhibiting depolarization of neurons, and doxepin (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, which includes promoting liver anabolism, peripheral vasodilation, and skin and neuroendocrinal trophorestoration. Eczema Modifications are made to the diet on the basis that many Galium aparine 1 prt of the foods commonly consumed in the modern diet are Urtica dioica 1 prt inherently antigenic (see The Fire Within: Digestive Trifolium prat 1 prt Function and Botanical Medicine). Up to 5 ml TID also good to drink Galium or Initial herbal therapy consists of a mild eliminatory Urtica tea program, enhancing detoxification through the use of alteratives (e.g. Arctium, Trifolium, Galium, Urtica), cholagogues (e.g. Rumex, Berberis, Raphanus, Curcuma), aperients (e.g. Rhamnus, Rheum, Operculina, Triphala) and diuretics (e.g. Chimaphila, Barosma, Petroselinum, Tribulus), along with circulatory stimulants that direct the activity of these herbs to the periphery (e.g. Zanthoxylum, Zingiber, Capsicum, Piper longum). This approach can be Suggested Program followed or used concurrently with botanicals that support neuroendocrinal function and down-regulate sympathetic Start with 12 day D-tox: stress (e.g. Glycyrrhiza, Turnera, Avena, Ganoderma, Essential Fatty acids (2 – 3,000 mg bid) Withania, Scutellaria etc.), as well as botanicals that have a Psorinoheel (8 – 10 drop tid) vulnerary activity (e.g. Symphytum, Calendula, Plantago, Schwef heel (8 – 10 drop tid) Centella and Stellaria). Trophorestorative nutrients Might apply Calendula including vitamins A, B, C and E are important, as well as ointment. antioxidants (e.g. grape seed extract, MSM, shilajitu), and

Also consider Candida. 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 Curcuma, 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 Symphytum, Calendula, Plantago, Hypericum, Centella and Stellaria.

For weeping, oozing sores a cream prepared with gentle astringents such as Quercus, Hamamelis and Juglans nigra (3-20% v/v) is applied topically.

Secondary bacterial infection can be treated with antibacterial herbs such as Hydrastis, Azadirachta, and Echinacea, in conjunction with the vulneraries stated above.

Psoriasis

Psoriasis is chronic skin disease characterized by persistent epidermal hyperplasia. Classically, the patient will present with sharply demarcated, dry, scaling papules and plaques of various sizes, with an edematous, inflamed base, usually on the dorsal surfaces of the trunk and extremities. It can vary from scaly lesions only found on the elbows to a wide- spread skin disorder associated with arthritis (psoriatic arthritis). (Berkow 1992; Park 2005)

The cause of psoriasis is idiopathic, but is frequently familial and has a world-wide distribution. In some patients the first occurrence of the lesions appear with local trauma, sunburn, or after a viral infection. In others the cause appears to be iatrogenic, associated with drugs such as corticosteroids, antimalarial drugs. lithium, aspirin and beta-blockers.

Similar to atopic dermatitis, psoriasis has a basis in nervous function, and can be brought on during periods of acute stress – researchers have even isolated increased concentrations of neurotransmitters in psoriatic plaques.

Autoimmunity is another potential cause of psoriasis, with the lesions being associated with the increased activity of T cells in underlying skin. Experimental models have shown that psoriasis can be induced by stimulation with

streptococcal superantigen, which cross-reacts with dermal collagen, increasing T cell activity. (Berkow 1992; Park 2005)

The onset of psoriasis is typically gradual, and the course of the disease is marked by chronic remissions and acute exacerbations that can vary in frequency and duration. Regions where psoriasis is frequently found include the scalp, the extremities (elbows and knees), sacrum, buttocks and penis, as well as the nails, eyebrows, armpits, umbilicus, and anus. During remission the lesions heal without scarring and hair growth is normal. Nail involvement is frequent and often resembles a fungal infection.

Medical treatment Medical treatment for psoriasis is essentially very similar as that of atopic dermatitis, with topical corticosteroids being the mainstay of treatment. Topical retinoids such as tazarotene is applied as an aqueous gel to modulate the differentiation and proliferation of epithelial tissue, and is thought to have an anti-inflammatory and immune- modulatory activity.

Vitamin D3 analogs such as calcipotriene are a new class of topical drugs that are used in patients with resistant lesions, but are more expensive than steroids.

Other drugs include immunosuppressive agents such as methotrexate and cyclosporine, but carry with them a significant risk of deleterious side effects.

Another therapy that is sometimes used is psoralen ultraviolet A light therapy (PUVA), which may produce remissions lasting several months, but may increase the incidence of ultraviolet-induced skin cancer. The concomitant use of oral retinoids with PUVA has been shown to decrease the dose of ultraviolet light needed to induce remission.

Holistic treatment In holistic circles there are a variety of perspectives on the cause and treatment of psoriasis. In Western herbal medicine psoriasis is caused by the usual suspects:

improper digestion, an increased toxin and immunological burden, and hepatic congestion. At the root of these causes is intestinal permeability syndrome, and thus measures are undertaken to remove dietary items that damage the gut wall, restore integrity to the intestinal mucosa, promote a healthy bowel ecology, and remove the toxic burden through promoting alterative and eliminatory changes (see The Fire Within: Digestive Function and Botanical Medicine, The Inner Alchemist: Hepatobiliary Function and Botanical Medicine, and Herbal Immunity: Nonspecific Resistance, Immunity and Botanical Medicine).

In Ayurvedic medicine the cause of psoriasis relates to the presence of ama trapped in the skin and failure of the blood to metabolize and remove it, whereas in Chinese medicine psoriasis relates to pathogenic factors that include Blood stasis, Dryness, or Heat and Dampness.

At its root psoriasis appears to be related to a localized, dysfunctional immune response in the skin that induces cellular proliferation. From a herbal perspective the cause of this is some toxin or antigen-antibody complex, or some aspect that causes a derangement in immune function.

In Ayurvedic medicine there is strong link between the complexion and the archetypal nature of the sun: in health the skin is said to display a natural luminescence, just as the sun radiates heat. It is interesting how UV light can actually be used to put psoriasis into remission when we consider this connection. Traditional PUVA therapy consists of using a psoralen (e.g. methoxsalen) in conjunction with UV-A light. Psoralens are also found is the plant kingdom, most notably in Ammi vishnaga and Psoralea coryfolia, and have been used for thousand of years to treat psoriasis in conjunction with sun exposure.

In his book The One Earth Herbal Sourcebook (2001) author Alan Tillotson indicates that the Indian herb Katuka (Picrorrhiza kurroa) strengthens the effect of psoralens, and has obtained clinical results using Katuka in combination with Psoralea (4:1 extracts, 2 g twice daily), in conjunction with exposure to sunlight for a minimum of 20 minutes daily. Tillotson notes that the best results occur in conjunction with alterative and eliminative therapies, outlined under atopic dermatitis, following treatment to

prevent recurrence. Additional therapies outlined under atopic dermatitis to promote healing, relieve pruritis should also be included.

At Wild Rose Clinic we use a program very similar to atopic dermatitis list above. We also pay close attention to bowel cleaning and ecology. It is very common to have Candida or other organisms as co-factors. Special attention is paid to the immune system, with Ganoderma often being used.

References

Bensky, Dan and Andrew Gale. 1993. Chinese Herbal Medicine: Materia Medica. Rev. ed. Seattle, WA: Eastland Press Berkow, Robert ed. et al. 1992. The Merck Manual of Diagnosis and Therapy. 17th ed. Rahway, NJ: Merck and Co. Bhathena SJ, Berlin E, Judd JT, et al. 1991. Effects of omega 3 fatty acids and vitamin E on hormones involved in carbohydrate and lipid metabolism in men. Am J Clin Nutr. 54:684-688. Cordain, L. 2003. Omega-3 Fatty Acids and Acne—Reply. Arch Dermatol. 139:942-943. Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. 2002. Acne vulgaris: a disease of western civilization. Arch Dermatol. 138:1584-1590 Fratkin, Jake. 1986. Chinese Patent Formulas: A Practical Guide. Boulder, CO: Shya Publications Harper, Julie. 2005. Acne Vulgaris. Available from: http://www.emedicine.com/derm/topic2.htm Li Y, Seifert MF, Ney DM, et al. 1999. Dietary conjugated linoleic acids alter serum IGF-1 and IGF binding protein concentrations and reduce bone formation in rats fed (n-6) or (n-3) fatty acids. J Bone Miner Res. 14:1153-116 Mills, Simon and Kerry Bone. 2000. Principles and practice of Phytotherapy. London: Churchill- Livingstone Moore, Michael. 2002. Herbal Energetics in Clinical Practice. Self-published. Available online from: http://www.swsbm.com Moore, Michael. 1991. Herbal Repertory in Clinical Practice: A manual of differential therapeutics for the health care professional 3rd ed. Self-published. Available online from: http://www.swsbm.com Park, Randy. 2005. Psoriasis. Available from: http://www.emedicine.com/emerg/topic489.htm Pizzorno, Joseph and Michael Murray, eds. 1999. Textbook of Natural Medicine. 2nd ed. Vol. 1-2. London: Churchill Livingstone. Rubin, E. ed. 2001. Essential Pathology. 3rd ed. Philadelphia: J.B. Lippinocott. Spagnola, Caroline et al. 2005. Atopic Dermatitis. Available from: http://www.emedicine.com/ped/topic2567.htm Tillotson, Alan. 2001. The One Earth Herbal Sourcebook. New York: Twin Streams (Kensington) Tortora, G. and S. Grabowski. 2003. Principles of Anatomy and Physiology. 10th ed. New York: Harper- Collins. Weiss, Rudolf. 1988. Herbal Medicine. Trans. By A.R. Meuss. Beaconsfield, England: Beaconsfield Publishers Zouboulis CC. 2001. Is acne vulgaris a genuine inflammatory disease? Dermatology. 203:277-279

Appendix I

Incompatible foods from an Ayurvedic perspective

The following incompatibles are among many others described by the Charaka samhita as being incompatible (Sutrasthana 26, 81-85). Those described herein are the most likely to be encountered.

1. fish and milk 2. meat and honey 3. meat and sesame seed 4. meat and sugar 5. meat and milk 6. meat and masa (Phaseolus radiatus) 7. meat and radish 8. meat and lotus stalks 9. meat and germinated grains 10. milk and radish 11. milk and garlic 12. milk and Krishnagandha (Moringa oleifera) 13. milk and Arjaka (Ocimum gratissimum) 14. milk and Tulasi (Ocimum sanctum) 15. milk and hing (Ferula spp.) 16. milk with sour or acidic foods 17. honey and ghee in equal quantities 18. honey and Pushkara (Nelumbo nucifera) 19. hot water and honey 20. hot water and Bhallataka (Semecarpus anacardium)