but are unlikely to be able to determine and treat the underlying causal factors for each individual patient. The success of Biologics in treating psoriasis and atopic dermatitis is based on understanding the mechanistic fine points of the immune responses causing those skin conditions.
The second is an integrative approach that identifies a probable concert of etiologic factors that lead to attack of cross-reactive epitopes in the target areas such as the follicle structure in this disorder. Likely antigens would come from diet, the gut, the microbiome, and the environment, fostered by inability to prevent their leakage across the gut barrier into the lymphatics and circulation, compounded by immune dysregulation and a host of other functional organ deficiencies.
By trying to identify and alter the individual’s likely causative factors, I have had success in treating AA patients and in those with a variety of other inflammatory and autoimmune skin diseases.7,8 For over 3 decades, I helped a portion of those with immune mediated skin disorders that did not respond to the treatment of multiple dermatologists or alternative health practitioners. I have treated AA and inflammatory skin disorders, in part by extending beyond probiotics by using diet, and supplements to reduce the population of yeast in the gut microbiome.9 That intralesional Candida extract has also been shown to reverse AA and may indicate a dose-related specific immune informational relationship of that organism to AA pathogenesis.10,11
Literature supports the concept that T-cell immune attack of the follicle is a key mechanism in the loss of hair in AA.12 Based on my past research on the genetic specificity of human lymphocyte cellular immune cross reactivity,13-16 I search for potential antigens from the gut, microbiome, or environment, and attempt to greatly limit their exposure by a series of enhancements of normal flora and organ-processing supports. Often, these individuals have signs of IBS or leaky gut such as bloating, gas, fatigue, or pain after eating, which typically clears on treatment of the digestive system before the skin condition improves. It is crucial to remove causes of leakage across the intestinal barrier into the lymphatics and blood stream.17
This involves removing foods containing gluten, and foods that favor pro-inflammatory organisms, such as Candida albicans,18 that both promotes gut barrier disruption and also has been shown to cross-react with a number of different human organs,19 as well as with Malassezia yeast common to the follicular apparatus. Identifying and reducing exposure to gluten and causes of Candida overgrowth are essential to controlling leakage of antigens across the gut border to stimulate immune attack of targets in the skin and elsewhere. Other proinflammatory organisms invading the small intestines in SIBO, and drugs that either facilitate excessive leakage across the intestinal barrier, and food or microbial antigens that potentially stimulate cross-reactive attack against the hair follicle,20 are also removed or remedied. The medical literature clearly documents concepts of inflammation in autoimmune disease, and crossreactivity leading to inflammation. Preceding conditions such as severe stress and bacterial infections such as Lyme disease, and viral infections including EBV, CMV, and Covid are considered to predispose by dysregulating the immune system.
The basic concept is that specific epitopes from the gut enter the lymphatics or circulation and stimulate cross-reactive attack of similar specific epitopes in the inflamed structure, such as the follicular apparatus in AA.21,22 This thinking is appearing more in the medical literature, supported by basic immunologic studies. Additional genetic, predisposition, and exposure variables determine what specific tissues and organs are attacked and the nature of the response, and therefore, what inflammatory disease presents itself. An example would be the tendency for reactive hyperproliferation of epidermal cells in psoriasis. Although specific auto-antibodies may be present as markers, reactive T cells are most likely key to the immunopathology in most of these diseases.23 Their targets may have complex specificity related tissue and HLA antigens, tissue antigens, structural tissue peptide sequences, conformational changes, and chemical or additional microbial modifications. That would account for different “triggers” in different individuals with the same disease.
Probable determination of some of these triggers can be made from a careful sequential history of events preceding onset or aggravation of an inflammatory skin disorder. Lab testing or trial of diet therapy often confirms etiologic factors. Support for the time and complexity of medical practice seeking treatment of etiology is typically not covered by insurance, which favors pharmaceutical solutions. Funding for studies done to modify individual-specific causes would help improve their precise application, and help understand the mechanisms involved. The cost of newer drugs would help determine the value added by a holistic approach that increases the efficacy of those drugs to the patient. By reducing the causal factors, the efficacy of pharmacologic agents could be enhanced.
The proposed CORE index being created, and other dermatologic evaluative guidelines, would be more able to predict factors relating to cause and successful treatment if the methodology of searching for and treating underlying causes that I have described would be included in a section of the domains to be evaluated. It would not take long to see whether these were relevant factors to the etiology of inflammatory disorders such as AA, and thus worth moving to the core section. Phenotypic variables and repeated sequential exposure-disease aggravation episodes raise the probability for a cause-and-effect relationship.
The second is an integrative approach that identifies a probable concert of etiologic factors that lead to attack of cross-reactive epitopes in the target areas such as the follicle structure in this disorder. Likely antigens would come from diet, the gut, the microbiome, and the environment, fostered by inability to prevent their leakage across the gut barrier into the lymphatics and circulation, compounded by immune dysregulation and a host of other functional organ deficiencies.
By trying to identify and alter the individual’s likely causative factors, I have had success in treating AA patients and in those with a variety of other inflammatory and autoimmune skin diseases.7,8 For over 3 decades, I helped a portion of those with immune mediated skin disorders that did not respond to the treatment of multiple dermatologists or alternative health practitioners. I have treated AA and inflammatory skin disorders, in part by extending beyond probiotics by using diet, and supplements to reduce the population of yeast in the gut microbiome.9 That intralesional Candida extract has also been shown to reverse AA and may indicate a dose-related specific immune informational relationship of that organism to AA pathogenesis.10,11
Literature supports the concept that T-cell immune attack of the follicle is a key mechanism in the loss of hair in AA.12 Based on my past research on the genetic specificity of human lymphocyte cellular immune cross reactivity,13-16 I search for potential antigens from the gut, microbiome, or environment, and attempt to greatly limit their exposure by a series of enhancements of normal flora and organ-processing supports. Often, these individuals have signs of IBS or leaky gut such as bloating, gas, fatigue, or pain after eating, which typically clears on treatment of the digestive system before the skin condition improves. It is crucial to remove causes of leakage across the intestinal barrier into the lymphatics and blood stream.17
This involves removing foods containing gluten, and foods that favor pro-inflammatory organisms, such as Candida albicans,18 that both promotes gut barrier disruption and also has been shown to cross-react with a number of different human organs,19 as well as with Malassezia yeast common to the follicular apparatus. Identifying and reducing exposure to gluten and causes of Candida overgrowth are essential to controlling leakage of antigens across the gut border to stimulate immune attack of targets in the skin and elsewhere. Other proinflammatory organisms invading the small intestines in SIBO, and drugs that either facilitate excessive leakage across the intestinal barrier, and food or microbial antigens that potentially stimulate cross-reactive attack against the hair follicle,20 are also removed or remedied. The medical literature clearly documents concepts of inflammation in autoimmune disease, and crossreactivity leading to inflammation. Preceding conditions such as severe stress and bacterial infections such as Lyme disease, and viral infections including EBV, CMV, and Covid are considered to predispose by dysregulating the immune system.
The basic concept is that specific epitopes from the gut enter the lymphatics or circulation and stimulate cross-reactive attack of similar specific epitopes in the inflamed structure, such as the follicular apparatus in AA.21,22 This thinking is appearing more in the medical literature, supported by basic immunologic studies. Additional genetic, predisposition, and exposure variables determine what specific tissues and organs are attacked and the nature of the response, and therefore, what inflammatory disease presents itself. An example would be the tendency for reactive hyperproliferation of epidermal cells in psoriasis. Although specific auto-antibodies may be present as markers, reactive T cells are most likely key to the immunopathology in most of these diseases.23 Their targets may have complex specificity related tissue and HLA antigens, tissue antigens, structural tissue peptide sequences, conformational changes, and chemical or additional microbial modifications. That would account for different “triggers” in different individuals with the same disease.
Probable determination of some of these triggers can be made from a careful sequential history of events preceding onset or aggravation of an inflammatory skin disorder. Lab testing or trial of diet therapy often confirms etiologic factors. Support for the time and complexity of medical practice seeking treatment of etiology is typically not covered by insurance, which favors pharmaceutical solutions. Funding for studies done to modify individual-specific causes would help improve their precise application, and help understand the mechanisms involved. The cost of newer drugs would help determine the value added by a holistic approach that increases the efficacy of those drugs to the patient. By reducing the causal factors, the efficacy of pharmacologic agents could be enhanced.
The proposed CORE index being created, and other dermatologic evaluative guidelines, would be more able to predict factors relating to cause and successful treatment if the methodology of searching for and treating underlying causes that I have described would be included in a section of the domains to be evaluated. It would not take long to see whether these were relevant factors to the etiology of inflammatory disorders such as AA, and thus worth moving to the core section. Phenotypic variables and repeated sequential exposure-disease aggravation episodes raise the probability for a cause-and-effect relationship.
