Complementary and Alternative Medicine at a Glance
- Complementary medicine is a holistic approach to diagnosis and treatment.
- Many dermatologic therapies developed in ways similar to the complementary approach and were subsequently scientifically validated.
- Attention to the environment and its impact on the patient is a fundamental principle of complementary dermatology. This means our world dermatology organizations have an obligation to speak out about what is harming the skin, health, as it is related.
- Herbal therapeutics, supplements, diet, and digestive system aid are four of the primary interventions used in holistic dermatology.
Complementary and alternative medicine (CAM) in dermatology encompasses a wide variety of methods of diagnosis and treatment that either supplement or substitute for conventional dermatologic practice. It is also referred to as holistic dermatology because it considers and addresses the entirety of the individual, including the physical, mental, emotional, and spiritual aspects of the individual's life, as appropriate. Holistic dermatology draws on an expanded knowledge base that includes CAM, conventional practice, and the latest research findings. Its diagnostic and therapeutic choices are made by combining these three knowledge bases, in what might also be termed integrative dermatology.
The alternative healthcare systems considered by holistic dermatology may include time-honored practices such as ancient traditional Chinese medicine, Ayurvedic medicine, American folk medicine, homeopathy along with more recently developed techniques from chiropractic, energetic medicine, functional medicine, and psychosomatic modalities. Furthermore, holistic dermatology includes any other technique that works or makes sense based on science or observation.
Increasingly, patients are using CAM methods in addition to conventional dermatological treatment as cosmeceutical, nutraceutical, and even pharmacological manufacturers more routinely offer these products. CAM practitioners and dermatologists are being called upon to respond to their patients’ expectations, preferences and demands for therapeutic modalities and treatments that avoid or minimize use of prescription drugs, and are safe, natural, and effective.
Alternative medicine often embraces treatment that not only presages but also may ultimately be incorporated into conventional practice. Good CAM practice is rooted in basic science, clinical experience and good medicine, but it often lacks the sanctioned level of proof we have come to demand for scientific, allopathic dermatology. Further, CAM practices arise and are developed differently from conventional practices. For example, when a growing body of anecdotal experience is supported by the understanding of underlying mechanisms of pathology, particular CAM approaches to illness are employed, even before the methods are validated in the usual ways. Many of these methods are difficult to study or assess using conventional research methods because they relate to the individual rather than to the disease or condition itself.
Many CAM methods and practices have slowly been incorporated into more conventional practice and some have gained widespread acceptance and use. Examples include the increasing use of probiotics, which had its tentative beginnings in the 1980s, to counter Candida overgrowth in the gut, which was later shown to enhance barrier function in the intestines and skin. The CAM use of essential fatty acids (EFA) as anti-inflammatory agents preceded the growing literature on this subject.
CAM practice also identified trans-saturated fats as disrupters of cellular functioning, inhibiting the δ-6-desaturase and thus the production of anti-inflammatory prostaglandins. This tenet of CAM medicine was set forth by Horrobin and others in the 1980s, decades before products containing transfats were removed from the shelves and castigated as deleterious for health.1,2 Similarly, kitchen herbalists and small companies were producing herbal skin applications long before the current popularity of cosmeceuticals. And while historically CAM practices have gradually been adopted by mainstream practitioners, in dermatology, the pace of adoption has quickened in recent years. Perhaps most telling is that much of the herbal pharmacopoeia of CAM dermatology referenced in the last edition of this text is now described in the dermatologic literature or is available in products designed for the skin.
Eclectic practice and off-label use of pharmaceutical drugs has always been a part of dermatology, perhaps more so than in medicine in general. These practices provide novel and often effective approaches to disorders of uncertain etiology by incorporating methods from other spheres or from observed benefit. Many of the commonly used pharmacological agents used in conventional allopathic medicine are derived from herbal medicine.3 The American “herbal” tradition dates to the Eclectics, a school of physicians who, during the nineteenth and early twentieth century codified the use of Western herbs according to specific indications.4 Today a wide variety of herbs is used, and the methods of selecting specific herb combinations also originate in other traditions. For example, psoralens have been used in China and India for repigmentation of the skin for more than 4,000 years. Other herbs used in treating the skin include mayapple (podophyllin) for condyloma, horse chestnut for leg veins, bloodroot (sanguinaria) for skin tumors, and oatmeal (Avena sativa) to soothe rough, itchy, or inflamed skin.3
In addition to specific herbal remedies, some of the philosophical tenets of herbal medicine have been incorporated as key concepts in dermatology. For example, the principle of using a crude preparation as opposed to a purified single ingredient as tends to be used in a pharmaceutical product, was one of Sulzberger's observations regarding the use of tar.5 It was the crude tar product from the distillery and not its purified derivative that had activity in treating psoriasis. In fact, variation in batch efficacy was assumed to be an indication of the heterogeneous nature of the preparation.
A virtual explosion in the availability of herbs in cosmeceuticals, herbal supplements, and new pharmaceuticals has occurred during the past 15 years. This growth has been accompanied by a substantial increase in peer-reviewed publications seeking to clarify the mechanism of action of herbs and their components and case studies detailing knowledge inferred from their traditional use. Each herb has a number of different activities and actions, which depend on growth conditions, the extent to which they have been challenged to fend off pathogens and predators, method of extraction, and the culture that utilized the herb or herbal preparation.
One of the advantages of knowing the traditional uses of herbs and their rich history of folk use is the ability to more fully appreciate their spectrums of action. For example, oats, A. sativa, are well known for their soothing anti-inflammatory effects on the skin as a topical soak. The milky white sap from green oats is known for its calming properties as a relaxant to the nervous system. In the context of its use as a folk and home remedy, it is easier and intuitively correct to seek out oat extracts for their calming effects on the nervous tissue in the skin, i.e., soothing and anti-pruritic actions as well.
Antioxidants prevent damage from both exogenous and endogenous free radicals. Ultraviolet radiation from the sun is a major source of free radical damage to the skin, but is beneficial for the production of vitamin D. A symphony of antioxidants prevents excessive damage to either the somatic tissues or DNA of the cells. Plants also must develop their own complex of antioxidants in order to withstand excessive damage from the sun. A young sprout or a plant placed prematurely in full sun will wither and die. It is the complex of antioxidants and light absorbing pigments that plants develop which function to protect them from this damage. Therefore, some argue that eating whole plants, with their functional spectrum of antioxidants, is more protective than isolating the most active fraction, such as β-carotene, and administering it alone.
Nutritional supplementation can supply external antioxidants, or support the generation of endogenous antioxidants. Carotenoids and polyphenols (bioflavonoid) are two major classes of plant-derived antioxidants. Bioflavonoids are especially protective of the capillaries and blood vessels. Oxidative damage and glycation damage induce metalloprotease activity, which destroys the integrity of collagen and elastic tissue in both the skin and the vasculature, and antioxidant protection may slow this process.
The hallmark of CAM is a search for the elements in the causal chain of functional disturbances that lead to a skin disorder. For inflammatory disorders, an attempt is made to identify exposures, which could stimulate and/or disturb immune responses with secondary targeting of skin structures. CAM focuses on correcting probable underlying causes, often with treatments that are not proven in the traditional scientific method. The patient not only assumes the responsibility of making the necessary lifestyle changes but also the risk of using protocols that are neither conventional nor necessarily well researched.
Individual specificity is key to CAM dermatology. Long before knowledge of specific pathogens and genetic polymorphisms, other systems of healing such as Ayurvedic medicine developed classification and treatment paradigms that are still used today, and extend well beyond diagnosis. The long-awaited studies and meta-analyses of CAM in dermatologic disorders such as psoriasis6 will continue to be of very limited usefulness because they persist in classifying patients solely by disease and fail to choose herbs and supplements for time-tested indications in traditional systems, or based on CAM or individual-specific disease mechanism parameters. Appreciation of these distinctions will lead to the design of research studies that truly indicate how to integrate CAM into dermatology as well as how to accurately evaluate the efficacy of CAM practices.
Early Application of Medical Knowledge
The application of medical, scientific, and folk information before it was either proven by double blind studies, incorporated by the majority of physicians as standard of practice, or justified as evidence-based medicine is part of the normal process of therapeutic innovation in dermatology. Advice to stop smoking would have been scientifically premature until a decade ago or so, but many physicians were bold enough to offer that advice to patients years before the dangers of smoking were definitively proven. An eclectic approach to treatment has historically been a mainstay in dermatology. Application of immune therapies, conformational chemical analysis, energy medicine, most food allergy testing, herbal and supplement therapies might all be considered premature if assessed using strict requirements for double blind proven or even evidence-based medical practice. When, however, these methods offer help where there has been none before, and their margin of safety is far greater than that offered by pharmacological interventions, it would seem quite sensible to consider the use of these “alternatives,” even before they are proven to work. The opportunity exists to integrate these alternative treatments into a comprehensive approach that offers a level of patient-specific safety and efficacy beyond what either CAM or conventional therapy alone can offer. A health system that promotes rather than forbids the flexibility necessary for this integrated care is crucial for the best health of the skin of our species.
Cross-Reaction and Molecular Mimicry
In the CAM approach to dermatology, the environment is considered to play a fundamental diagnostic and therapeutic role. Cross-reactions with foods, chemicals, and infectious agents may be key precipitants or contributors to inflammation which itself may play a role in a range of dermatologic conditions. A mainstay of the CAM approach is to search for the inciting cause of an inflammatory response and once it is identified, to correct the ongoing memory response using natural means. Eliminating foods that exacerbate eczema, or enhancing food breakdown into smaller, less antigenic fragments by supplementing with digestive enzymes, is one example of how CAM acts to remove molecular mimics that stimulate skin inflammation.7
There is individual specificity in antigen recognition,8
exposure history, and the type of tissue response to the resulting inflammatory cascade. It is therefore critical to look for the precipitating stimuli of disease onset for each individual. This concept is widely accepted for contact dermatitis but has not yet been adopted for eczema or psoriasis. At the same time, it is critical to consider the existence of factors that either neutralize or exacerbate the response to suspected or confirmed precipitating stimuli. An exhaustively detailed history is essential to understanding why a patient reacts at certain times and not others.
Just as β-hemolytic Streptococcus
can precipitate guttate psoriasis, molecular mimicry by microorganisms is associated with onset of autoimmune conditions. A corollary possibility that should be considered is that many inflammatory and autoimmune conditions of the skin involve cross-reactive initiation to food antigens, microbes, chemicals or other altered forms of self-antigens. This entire mechanism has been well described in celiac disease,9
a condition closely associated with the dermatologic condition, dermatitis herpetiformis.
Autoimmune attack on tissues depends on a number of factors including recognition, molecular mimicry or identity, attack by lymphocytes with receptors that target a similar autoantigen, and propagation of this response by the phenomenon of bystander activation or epitope spreading.10
Normal mechanisms of tolerance and control by regulatory T cells must also fail for this to occur.
Appearance of autoantibodies in the blood, once considered irrelevant in asymptomatic patients, may well be a warning sign to institute changes to prevent the gradual development of clinical autoimmune disease.
Heavy metals and transition metals lead to autoimmunity because they bind to proteins, replace other metals in metalloproteins, and attach to sulfur groups altering molecular configuration. Crucial biotransformation metalloenzymes are inactivated by displacement. All of these actions affect the tertiary structure of proteins, creating neoantigens and altering function.
Of interest to dermatologists is that increased reactivity to heavy metals has been reported in lupus erythematosis, oral lichen planus, oral burning and itching, eczema, and psoriasis, and Sjögren syndrome.11,12
Urticaria, eczema and other systemic conditions have been found to improve after removal of dental fillings and other treatment to facilitate removal of mercury from the body.8
Drug levels may be affected by foods or medications influencing specific P450
Chemicals targeted by the liver for removal are first chemically converted by P450
isoenzymes in phase I to make them either more soluble or more chemically reactive for coupling to molecules in phase II for transport out via renal excretion. With insufficient transporters, these hyper-reactive drug metabolites, made more chemically reactive by the phase I liver P450
enzymes, may combine with molecules in skin tissue structures to create neoantigens or other molecular informational disturbances. Understanding how insufficient or incomplete biotransformation of accumulated toxic substances could trigger a skin reaction enables one to take a focused history, which includes not only the toxic substances, but also the change in hepatic ability to rid the body of molecular triggers.
Oral ingestion is one of the largest sources of foreign material entering the body. It has been established that large molecules, including horseradish peroxidase with a molecular weight over 1,000,000 daltons can be absorbed intact from the gut.14
Drugs are well known causes of skin eruptions.15
Foods have a variety of effects on skin disorders beyond a role as allergens.16
They can serve as informational molecules to incite eruption, direct or indirect hormonal aggravators, gut permeability modifiers, or influence the ecology of the gut flora. Certain nutrients can overcome the liver's capacity to biotransform harmful antigens and toxic intermediates or aid in hepatic biotransformation. Foods can also have a wide variety of effects partially overlapping those of herbs and pharmaceuticals. Dietary effects on gene expression and individual specific food interaction are now known as neutragenomics.17
Dietary treatment of acne was much more prevalent before the advent of antibiotics. In recent years, food triggers for acne had fallen out of favor and diet was widely assumed to be irrelevant. Recently, however, milk has once again been found to have an etiologic role in this disorder.18
“Food Allergy” Determination and Elimination
In addition to classic immunoglobulin E-mediated allergic response, the term food allergy also includes other types of allergy such as immune complex, delayed, and Toll-like receptor activation. There is also nonallergic sensitivity. Food allergies develop to the many common foods such as wheat, milk, soy, yeast, and corn. Some believe that a hallmark of food allergy is food craving with repetitive eating of the same food each day.19 A 5-day elimination and rechallenge on the sixth day is an effective way to determine if the food under consideration is the cause of the symptoms of concern.
Other symptoms beyond the skin could include digestive upset, nasal stuffiness, fatigue after eating, or even “brain fog.” Brain fog is a popular term for a sense of mental confusion, sluggishness, and slowness that may sometimes include a feeling of unreality or disorientation. Small peptides from casein digestion known as caseomorphins, which can also derive from gluten, rice, bovine albumin, and even spinach, have psychoactive properties.20 Treatment involves elimination, substitution with other foods, and food rotation. Enhancing digestion with digestive enzymes and adding metabolites to enhance the gut permeability barrier (and reduce the impact of leaky gut) helps to prevent sensitization to disease inducing cross-reactive antigens.21,22
Diagnosing food allergy is best initiated by a careful history of the specific foods that preceded a reaction; these include foods consumed a few hours or even few days prior to the reaction. A food and reaction diary helps to reinforce memory and document instances of food consumption and reactions. Elimination and challenge is the gold standard for identifying food allergens. Intradermal testing can be helpful, and is far more useful than scratch tests because the latter detect IgE or immediate allergy only.
Abnormal gut flora, including overgrowth of Candida
sp., parasites, and pathogens can lead to inflammation, which compromises the gut barrier and can lead to “leaky gut.” Numerous studies from Scandinavia establish the importance of probiotic supplementation for reducing by half the incidence of atopy in infants.23,24
Studies on treatment of atopy with probiotics have such mixed results that various summaries and meta-analyses conclude probiotics are of little benefit in the prevention of atopy. Most of these studies are carried out with no insight into the model of Candida
discussed here, so they do not begin to address the synergistic factors necessary to shift gut flora to reduce leaky gut, and cross-reactive attack of Malassezia
in the hair follicles. Furthermore, different strains are used, different prebiotics and fiber loads, or lack of them, to support growth.
EFAs play an essential role in skin health. EFAs are the precursors of the eicosanoids produced when phospholipase cleaves a lipid fragment, arachidonate, from the cell membrane. Arachidonate, a common pathway byproduct from most foods, leads, via cyclooxygenase, to production of the proinflammatory prostaglandin E2(PGE2), or via lipoxygenase to production of proinflammatory leukotrienes.25 Specific ω-6 unsaturated EFAs such as γ linolenic acid, found in borage oil, evening primrose oil, and human breast milk, lead to formation of the anti-inflammatory PGE1. ω-3 unsaturated fatty acids such as those found in fish oils contain eicosapentaenoic acid (EPA), which leads to formation of the anti-inflammatory and anticlotting PGE3. Flaxseed oil has an ω-3-EFA known as α-linolenic acid, which requires two carbon chain elongation to become EPA, requiring activity of the δ-6-desaturase enzyme. That enzyme has cofactor requirements of zinc, magnesium, vitamins C, B3 and B6, and low insulin levels. ω-3 EFAs also play a role in formation of the barrier lipid in the brick and mortar structure of the stratum corneum barrier. Partially hydrogenated oils not only lead to proinflammatory PGE2 formation, but also inhibit the δ6-desaturase, which is crucial for formation of anti-inflammatory γ-linolenic acid.
Shifting the balance toward anti-inflammatory EFAs by removing foods with proinflammatory oils and increasing foods and supplements with anti-inflammatory oils (e.g., cod liver oil) is a strategy useful in most conditions involving inflammation and dry skin. It is especially useful in seborrhea and eczema. Rare problems with excessive fish oil include increased bleeding tendency26 and high-birth weight, postmature babies.27
A number of studies have shown the effectiveness of ω-3-EFAs in psoriasis and other inflammatory and autoimmune diseases.28 EFAs also confer powerful protection from UV exposure and have been used to reduce inflammation and promote wound healing in burn victims.29,30
Mental, Emotional, and Spiritual Issues, and the Skin
It has been observed that an extraordinary emotional stress preceded disease onset in 86% of patients with the autoimmune diseases rheumatoid arthritis and SLE.31
Stress has been observed to affect the immune system of the skin at every level.
Repetitive scratching or other subtle manifestations of inflammation should be addressed in a multidisciplinary way. Treatment of chronic skin disorders requires management of the underlying mental, emotional, and spiritual issues, which are often closely related to the pathophysiologic process itself.
There are numerous approaches to this in complementary medicine. An earlier edition of Fitzpatrick mentioned a patient with lupus who was healed by a curandero, a healer who uses Mayan folk medicine techniques.
Tapping deeply into one's belief systems to release major conflicts and traumas is often effective.
Addressing core conflicts that are so painful that skin rashes become more acceptable diversions is beyond the scope of most dermatologists. Along with the drug therapies often employed by practitioners trained in Western allopathic medicine, there are many techniques drawn from culturally diverse spiritual, healing, and folk medicine practices. These methods include spiritual healing techniques, neuromodulation technique, and many others.
Homeopathy pushes the boundaries of the scientific mind because it works by invoking the energy of the substance rather than the substance itself, with greater dilutions having greater potency.32 A key aspect of homeopathy is that substances diluted homeopathically often, but not always, work by counteracting the very symptoms that the undiluted substance produces. For example, Nux vomica is used to counteract nausea, and Coffea, from coffee, is used to induce sleep. Some herbalists also use the information from the provings, the homeopathic repertory, for seeking further insight into the characteristics of herbs.33
Several dermatologic disorders, particularly those that are inflammatory in nature, may benefit from the CAM approach.
Seborrheic dermatitis34 involves inflammation in sebaceous follicular areas of the scalp, eyebrows, and nasolabial folds. All of these regions harbor the yeast Malassezia, which is normal follicular flora. There is evidence that Malassezia is cross-reactive with Candida albicans,35 and it is postulated here that a cross-reactive attack against antigenic epitopes on the Candida and other yeasts and molds becomes directed against the Malassezia organisms in the follicle, causing the inflammation that incites the erythema and desquamative changes characteristic of seborrhea.
An altered pattern of EFAs in infantile seborrheic dermatitis implicates impaired function of the δ-6-desaturase.36 Some of the B vitamins previously reported as helpful in seborrhea may function as cofactors for this enzyme.37–39 The tendency toward inflammation is exacerbated by a predominance of arachidonic acid precursors in the cell membranes derived from dietary sources. Treatment by substituting EPA-rich fish oil in the diet and removing partially hydrogenated and saturated oils can reduce this inflammatory state by favoring the generation of anti-inflammatory PGE3.40–42 Flaxseed oil is another ω-3-fatty acid and PGE3 precursor, but the active ω-3-EFA in it, α-linolenic acid, requires chain elongation to be converted to EPA, and this process is not uniform among individuals.43
Atopic dermatitis is an inflammatory disorder of the skin linked to asthma and hay fever. In the past, dermatologists observed cases in which food was considered a trigger, but were generally puzzled that there did not seem to be a specific food that caused the eczema. One challenge was that eczema could be aggravated by one food, and then after diet change, would be exacerbated by the newly substituted food.
One theory articulated by practitioners of CAM relates to what is known as leaky gut.44 Disruption of the gut barrier can result from inflammation of the intestinal lining. This inflammation may be caused or precipitated by parasites, Candida overgrowth, food sensitivity, foods containing lectins that punch holes in cell membranes, or pathogenic microorganisms. In addition, nonsteroidal anti-inflammatory drugs are irritating to the gut lining, as are alcohol and aspirin. Any food introduced repeatedly into such an environment can lead to sensitization to that food. In these cases, it is believed that the uncontrolled atopic becomes sensitive to whatever he/she eats repeatedly to avoid that which caused trouble initially. For example, the milk-allergic infant switched to soy protein soon becomes “allergic” to soy. Inflammation in the gut wall stimulated by soy causes allergy to whichever nutrient is next exposed to the gut immune system. This “vicious cycle” could account for the name atopic, which was used to describe the changeable nature of the factors initiating the dermatitis.
Treatment consists of removing abnormal microbes and restoring normal flora, removing irritants, eliminating exacerbating foods, enhancing enzymatic breakdown of foods (digestion), coating the gut with mucilaginous herbs, and providing the nutrients needed to support an intact gut barrier.
Proper colonization of the gut with Lactobacillus acidophilus and similar strains has a protective effect against atopy.45 A corollary of this observation is that repeated use of antibiotics favors overgrowth of C. albicans, and simple starches and sugars support Candida growth. It is presumed that consumption of large amounts of yeast, mold, and their byproducts, such as bread, beer, wine, and cheese, could both induce high-dose antigen tolerance to intestinal Candida, and perhaps even sensitize to other antigenic determinants. High-dose tolerance is a lack of immunoreactivity to specific antigenic determinants or substances due to the presence of large quantities of these determinants in the system. Treatment consists of removing the dietary factors that favor Candida and then treating with herbal or other natural remedies to reduce the yeast population. Artemisia annua and short-chain fatty acids such as undecylenic or caprylic acid are a few such treatments. Next, probiotics may be added to prevent Candida from overtaking gut flora.
Only when these measures have been taken should pharmaceuticals be used in a progressive fashion. Otherwise, there is the risk of selecting for resistant strains. Nystatin may be considered, followed by ketoconazole and fluconazole. Nystatin should be slowly increased in dosage from 500,000 units/day in divided doses to 6 million units, over 10–12 days. Highly yeast-sensitive individuals absorb cell content material through an already leaky gut wall and are known to develop exacerbation of previous symptoms and sometimes fever, with a Herxheimer-like reaction. All of these drugs have more potential effectiveness when the environment is changed by dietary restrictions on sugars, simple carbohydrates, and foods high in or derived from yeast.
Anti-inflammatory EFAs, such as EPA from fish oils, appear to help some atopics.46 Hempseed oil, rich in ω-3- and –6-EFAs, improved the serum fatty acids, and the condition of atopics, in a study conducted in Finland.47 There has been a consistent increase in the number of studies showing that γ-linolenic acid from borage or evening primrose oil48 effectively resolves various aspects of atopic dermatitis, and there is clear indication that it is beneficial for some patients with eczema. The results of a small study performed in Germany showed that GLA supplementation from EPO reduced total IgE in the first year of life, but did not prevent atopic dermatitis. Another study found decreased GLA levels in children with eczema and elevated IgE levels and others with atopy, but not in eczema patients with normal IgE levels.49 Meta-analyses to the contrary50 are likely contaminated by issues discussed under EFAs, above, and should not dissuade physicians or patients from a proper trial of EFAs in atopic patients, once oxidative stress has been calmed down. Furthermore, a balance of anti-inflammatory EFAs is likely most effective for allergic individuals. It should be remembered that the industrialization of our food supply over the past half-century, including partial hydrogenization of nearly all food products that required shelf life, hardening oils for convenience in food, importing southern oils where unsaturated northern oils were local, and farm feeding grains to fish, poultry, and livestock that previously consumed local cold grown plants naturally rich in unsaturated fatty acids, all have served to dramatically reduce the proportion of anti-inflammatory EFAs in our diets and thus cell membranes. Some of the increase in atopy, inflammatory, and autoimmune disorders we are now seeing may be in response to the “hair trigger” this shift is placing on the prostenoid aspect of the immune response.
There has been scant attention paid to primary prevention of atopic dermatitis. Although conventional wisdom has held that breastfeeding is associated with reduced incidence of atopic dermatitis in children, recent research questions this, especially when the mother herself is allergic. In fact, it seems likely that dietary allergens present in breast milk of these allergic mothers may actually trigger or contribute to the development of atopic dermatitis in offspring. For this reason, it may be prudent to suggest that mothers of infants at risk for atopic dermatitis avoid dietary allergens. There also is some evidence of benefit from the use of probiotics and supplementation with EFAs.51
Before the availability of tetracycline, diet change was a mainstay in acne treatment. With the advent of antibiotics for acne, many dermatologists argued that the stress produced by restricting favorite foods was itself acne causing, and consensus evolved to minimize the role of diet in acne. This view was supported by seminal papers that demonstrated that common agents such as chocolate did not cause acne.52 More recent data do reveal a relationship between milk consumption, both full-fat and especially nonfat, and acne in teenage girls53 and boys54,55 Darby and others posit that hormones normally present in milk as well as added to enhance milk production may be responsible for this effect. This includes progesterone-related hormones and 5-α-pregnanedione, which is converted directly into dihyrotestosterone.56 Milk protein allergy causing an inflammatory response that blocks the infundibular apparatus also may contribute.44 It now appears that diet may influence a number of mechanisms related to acne development.57
Bovine milk production by postpartum cows contains placenta-derived progesterone and dihydrotestosterone precursors. Other hormones in addition to steroids in milk also may stimulate acne. The most frequently implicated substance is IGF-1 (insulin-like growth factor), which also increases during the teenage years as a result of growth hormone. IGF-1 is present in organic milk and increased in milk from cows treated with bovine growth hormone. IGF-1 increases lipogenesis in sebocytes.58 It stimulates 5-α-reductase and androgen synthesis. It has also been shown that excess carbohydrate consumption increases insulin, which increases IGF-1, which in turn worsens acne.59 IGF-1 and dihydrotestosterone levels in women both correlate with acne.60
Melnik has elegantly suggested the role of deficiency or displacement of nuclear transcription factor Fox01 from suppressing the androgen receptor and the promoter of PPAR-γ as the key initiator of the activation of the genes for sebocyte proliferation, sebum synthesis, and inflammatory cytokines.61 He observes that retinoids increase Fox01, and that all known acne-inducing factors work by decreasing it.
Milk elimination and reduced carbohydrate ingestion can produce a substantial improvement in some acne patients, as does reduction of proinflammatory fats from fried and partially hydrogenated sources. In women with perimenstrual flaring, reduction of dietary estrogens, and pseudoestrogens may be helpful.
The holistic perspective posits that the initiator of the inflammatory process that leads to acne is derived from antigens and informational molecules derived from an improper diet and environment, and that the mechanism of inflammation, so elegantly described in the classic and emergent literature, is a key precipitating step in that cascade.
Recent evidence indicates that inflammation in the pilosebaceous unit may precede the follicular plugging and Corynebacterium acnes proliferation,62,63 and that the predominant presence of CD+ memory/effector cells suggests a specific antigenic T-cell inflammatory, rather than nonspecific, immune response. Timed immunofluorescent studies reveal a type IV delayed hypersensitivity response, and, therefore, point to a soluble antigen stimulus initiating the acne lesion.64 A primary response to antigen in a structure that concentrates antigenic material from the blood, which ultimately comes predominantly from the digestive tract, makes acne an inflammatory disorder that should respond to the alteration of gut-derived antigens described in this chapter.
There is evidence from animal studies that carbon-14-radiolabeled α-linolenic acid, dietary ω-3-EFA found in flaxseed, is preferentially found in the coat of guinea pigs, suggesting sebaceous excretion of this dietary lipid.65 There is reason to believe that all of the lipids, and indeed all of the other molecular moieties that are secreted or synthesized into secretions in the pilosebaceous unit, are derived either from diet, body stores, microbial metabolites, or topical absorption. The infundibular apparatus concentrates and excretes both water-soluble wastes in the sweat, and lipid and proteinaceous material in the sebum. Medications, such as ketoconazole, have been found in sebum.66
Hidradenitis suppuritiva (HS) may respond to treatment that enhances digestive function, gut barrier function, and elimination of reaction to allergenic foods. HS is increasingly being recognized as a disorder of immune function, at least in the local tissues.