Treating Alopecia Areata
Currently there are NO effective medical treatments for Alopecia Areata.
However, despite their poor track records, a small number of treatments remain the standard protocol followed by the medical establishment – even on very young children. Unfortunately, as with many pharmaceutical treatments, the question of safety and long terms effect is still unanswered.Is there something else that can be done to effectively and safely combat Alopecia Areata? Read on and decide for yourself.
For some, the mere suggestion that diet could be used to treat anything somehow seems to cross the line of reason…conjuring up images of unicorns and fairy dust. It’s a preposterous notion that they categorically reject. To them, if it doesn’t come in the form of a prescription pill bottle, an injection, or a scalpel, it’s on par with talking about Bigfoot or the Loch Ness Monster.
One girl I spoke with recently about the potential of nutritional intervention cut me off and then flatly stated that she simply didn’t believe in ‘home remedies.’ Now, this was a very smart girl. She was extremely knowledgeable and well-versed in the medical details and technical language of her many health problems and treatment scenarios. But for her, like some people, if the information didn’t come wrapped in a white lab coat, it was a ‘home remedy.’
Despite longstanding experience and new reports that emerge regularly supporting the curative power of nutrition, some people just refuse to buy in.
I suppose that treating diseases like Beriberi, or B1 (thiamine) deficiency, which causes weight loss, body pain and weakness, brain damage, heart failure and death; Pellagra, or B3 (Niacin) deficiency, which causes diarrhea, dermatitis, dementia and death; Biotin (B7) deficiency, especially in pregnant women, which can cause rashes, baldness, anemia, dermatitis and fungal infections; Scurvy, or vitamin C deficiency; Rickets from lack of calcium, vitamin D, or sunlight; Arboflavinosis; Hypcobalaminenia….just to name some at the top of the list, by supplementing with one particular vitamin or food would fall under the category of ‘home remedy’ then.
Interestingly, while you could throw prescription drugs and creams at the symptoms of these diseases all day long, drugs would do nothing to treat and heal the underlying cause.
Still, despite this almost militant subgroup of absolutists, the debate still rages amid the majority of us; discussion and speculation swirl endlessly about diet as a possible treatment for many things… including Alopecia Areata, Totalis and Universalis.
Have we resorted to this ‘outside-the-box’ searching merely because we feel that science and medicine have abandoned us on a dark and desolate stretch with no place to turn?
If that is the case, in part, it’s understandable. The TRUTH is that our ‘experts’ can’t really tell us much. They can’t tell us WHY a person is at risk for AA. They don’t know WHAT triggers it. They can’t PREDICT the duration or severity of the disease. And perhaps worst of all, they don’t have any effective means to TREAT us. See my previous article summarizing what we REALLY know about AA: http://globalalopeciamission.org/why-more-research-for-alopecia-areata/
So is desperation why we are looking elsewhere for answers? Are we gazing across the rainbow trying to imagine that a little magical ‘pot-o-gold’ waits somewhere on the other side?
Or is there something more to this diet talk? Is there some good reason to believe that diet might in fact play a role in delivering our bodies from its autoimmune prison?…even over and above the miraculous AA ‘cure’ stories that emerge from time to time that are chalked up to diet and nutrition.
Better yet, is there some sound logical, scientific basis for making a case that diet and nutrition might be used to reverse Alopecia Areata?
Well, I firmly believe there are very real and specific reasons why nutritional therapy can be central to treating AA….not only based on my proof positive experience in reversing longstanding Alopecia Universalis and my ability to control its expression…but also because unrelated scientific research has been leaving us clues for some time. This is an area of research that simply cannot be left off the table in any real results-driven AA research strategy. It requires serious scientific scrutiny alongside the other topics!
Now there are two primary problems that exist when attempting to introduce new evidence or a new stream of thinking in science and medicine, particularly if this new thinking represents an ‘unconventional’ direction or when, in general, the disease research does not have an adequate source of independent funding.
The first is that most research is profit driven…period. Patents and drugs are the real goal. So money is invested in those avenues which are most promising for drug development and money-making. That investment is made by those that stand to make money. If return on investment is not the likely outcome, then even the best evidence will get minimal attention and research dollars….exponentially so, if it’s not a life-threatening disease.
Second, is that research labs are generally discipline-specific. For instance, a genetics lab researches genetic topics; their labs are full of geneticists and special genetic equipment which has been funded by genetic grant money; so no matter where the evidence points, their focus will remain on genetics. They can’t just decide to chase a promising finding if it falls outside their field of expertise. Even worse is when overall resources available for research are small and have been concentrated in one narrow area. This is a particularly acute problem in AA because genetic research and drug development have been the greatest focus by AA’s largest advocate for some time….with the intention of producing drugs.
Since examining the role of nutritional in AA – no matter how promising – is unlikely to yield a new patented drug, you can be sure there will be no concerted push to bring it into any lab, unless that lab is independently funded. This lack of impartial funding effectively thwarts pursuing promising lines of research.
And therein lays the biggest argument for a NEW and INDEPENDENT research initiative in the battle against AA: too many of our eggs are trapped in one basket and we need to get them out. The need for a collaborative research program that looks at the complete AA picture and is not limited to a single scientific discipline is urgently necessary. One that incorporates the best of what we currently know, but that is willing to look in whatever direction offers the most promise to the men, women and children with AA, disregarding patents and profits, and instead seeking the quickest route to an effective treatment and cure.
In part one of my series, Researching Nutrition 1 – All Great Truths Begin as Blasphemies, I posed the question: “is there some sound logical, scientific basis for making a case that diet and nutrition might be used to reverse Alopecia Areata?”My answer to this question is unequivocally ‘YES’. There is a very sound basis for making that claim. The reason? Because it is DIET that may be the very thing that can most directly impact the root cause of Alopecia Areata in the first place.Let me offer some food for thought. (Pun intended.)First, there is very good research (although not AA specific) that suggests that the likely point of origin, or etiology, of Alopecia Areata, Totalis, and Universalis in predisposed individuals lies within the human gut and is caused by the microbiota (microflora), or gut flora, that populate and thrive there. From Multiple Sclerosis (MS) to Irritable Bowel Syndrome (IBS), evidence of gut flora involvement in autoimmune disease pathology continues to increase. The traditional view that the immune system regulates the microbes within the gut is evolving based on new evidence to one that recognizes that, in certain cases at least, it is the microbes that in fact control the immune response.It is within this complex microbiome of the human intestinal tract that microflora balance becomes unstable triggering a cascading inflammatory immune response that directs attack of the hair follicles.Research indicates that gut flora have a mutualistic, or helpful, relationship with the human body, in that they provide many useful functions such as ‘fermenting unused energy substrates, training the immune system, preventing growth of harmful, pathogenic bacteria, regulating the development of the gut, producing vitamins for the host (such as biotin and vitamin K), and producing hormones to direct the host to store fats. However, under certain conditions, some species are thought to be capable of causing disease…’ Furthermore, recent discovery that specific microbiota direct differentiation of Th17 cells in the mucosa of the small intestine is of particular interest because of their key role in the inflammatory process and their potential role in the development multiple sclerosis, psoriasis, juvenile diabetes, rheumatoid arthritis, Crohn’s disease, and others?There are several inhabitants of the gut that have been most notably advanced as suspect candidates in other autoimmune diseases and are worth pointing out. Some are considered ‘good’, while other are referred to as ‘bad’, but each are routine inhabitants of the gut and the distinction between good and bad is generally based on overcolonization or location. The most notable are: Helicobacter pylori (H. pylori), Clostridium difficile (C. diff), and Candida albicans.Disruption of the gut’s ecobiology can occur through any physiologically traumatic event, including exposure to sickness and disease (including vaccinations). Some noteworthy viral antagonists that have come under scrutiny are Cytomegalovirus (HCMV) and Chlamydia Pneumoniae (Cpn).Similarly, antibiotic or drug use, environmental toxins (including those ingested as processed and chemical additives in food), and poor diet composition have been shown as factors in destabilizing the microbiota of the gut.
For instance, recent research at the University of Chicago found that “concentrated milk fats, which are abundant in processed and confectionery foods, alter the composition of bacteria in the intestines. These changes can disrupt the delicate truce between the immune system and the complex but largely beneficial mix of bacteria in the intestines. The emergence of harmful bacterial strains in this setting can unleash an unregulated tissue-damaging immune response that can be difficult to switch off.”Stress, while not likely a root cause, may be an exacerbating or compound factor because of its impact on the gut. The release of hypothalamic Corticotropin-releasing factor (CRF) (which is an essential mediator of the endocrine system) in response to stress, is known to directly disrupt the stasis of the microbiome of the gut. Hormonal changes, through the same mechanism, may be a contributing factor as well.In the very young, and especially children born by cesarean section or non-breast fed children, the pathology of AA could be accelerated because of the slower maturity of the gut microbiome and lower transferred immunity when confronted with triggering events. ‘Community DNA sequencing of intestinal flora comparing healthy and autoimmune children showed that autoimmune children had relatively unstable gut biomes with significantly decreased levels of species diversity..’Permeation of the mucosal barrier of the gut (gut barrier) by microbiota is recognized by the body as an infectious event and results in widespread immune system response…potentially inducing ULBP3 gene up-regulation which has been directly implicated in AA pathogenesis in AA predisposed individuals. NKG2D ligands recognize the up-regulation (‘switching on’) of ULBP3 upon cellular stress exposure including viral or bacterial infection or tumor transformation.Environmental stressors are known to trigger alterations in the epigenetic regulation of gene activity, like in the case of ULBP3 up-regulation in AA. Epigenetic modifications refer to the process whereby non-genetic factors cause genes to behave or express themselves differently even though there is no change to the underlying DNA. These changes may be short-lived or last for multiple generations. Epigenetic factors through DNA methylation have recently been identified as part of the AA pathogenesis.
Previously this had been observed in other autoimmune diseases, including lupus erthematosus, psoriasis and vitiligo. ULBP3 up-regulation and the resulting NKG2D activity target the hair follicle for attack by T cells, forcing normally healthy anagen (growth) follicle into a telegen (resting) dormancy.So then, perhaps the most critical necessity in reigning in runaway and aberrant microflora and re-establishing gut equilibrium is DIET. Diet has the power to quickly and powerfully regulate the microbiome and either depress or fortify the body’s ability to eliminate or fight disease on many levels, acting as both a corrective and preventative strategy against AA.Recently a 2011 study stated conclusively that: “Diet strongly affects human health, partly by modulating gut microbiomecomposition…”Furthermore, it went on to make the incredible finding that “a controlled-feeding study of 10 subjects showed that microbiome composition changed detectably within 24 hours of initiating [diet changes]…“If this disease process is mediated by the development of aberrant intestinal microbiota and microbiome breakdown in response to physiological stress, then controlling or eliminating the offending microbiota and restoring integrity to the gut would eliminate the AA trigger.Furthermore, specific dietary composition can be used to enhance overall cellular health, immune activity and aid in the repair of cellular damage corresponding to AA activity.My own personal experience of recovery from Alopecia Universalis in less than 2 months after nearly two decades with AU makes an incredibly strong case for this approach to reversing and controlling AA, when you consider::
- my initial rapid recovery from AU was centered around reestablishing the equilibrium of the gut microbiome;
- my ability to intentionally cause AA relapse and regrowth is directly controlled by modifying my nutritional therapy;
- my ability to duplicate similar reactions in others is based on the same principles.
While this is an area of research that is slowly beginning to move forward, I suggest that it might possibly hold the greatest prospect of a successful treatment strategy for AA in the short term and needs to be elevated to a priority position quickly.In part three, we’ll take a look at the specifics of my own treatment strategy and examine how and why it might be effective.
For the final part of this series: Researching Nutrition – All Great Truths Begin as Blasphemies, we will examine my specific experience and treatment regimen and look at why I believe it did work for me and also how it may work for those with alopecia areata and its various manifestations, generally.Because of the unexpected length of this final part, I have elected to break it into two more readable pieces: this part, which is something of a preface, and then the second portion, which goes into detail on the subject. The second half will be posted immediately afterward.So then, I will preface this discussion of my recovery from Alopecia Universalis with the plain statement that I DO NOT think my therapy represents a cure. It is a treatment. A cure in its proper definition implies that the underlying defect has been corrected or the dysfunction eliminated. My therapy is an ongoing process that must be continued and therefore not a cure. In fact, I still have Alopecia Areata. The underlying predisposition of my body to express AA is still primed and ready to jump into action if I discontinue my therapy. While it will take weeks to emerge, I will relapse…first with slowed rate of growth, then with a change of hair texture, and then finally with patches of follicles moving into the dormancy (telegen) phase. Whiskers, which have a naturally accelerated growth rate, have proved to be an exceptional means of measuring this process.I have forced relapse on several occasions – fighting back considerable anxiety, I will admit – in order to research and document the mechanics of my disease. More importantly, I have done this to definitively and conclusively rule out ‘random regrowth’ as the mechanism responsible for my recovery.My regrowth is not random. I did not recover from Alopecia Universalis after almost 20 years due to random regrowth.
My disease is controlled through the process that I employ.
Furthermore, it is controlled at the most base level – perhaps right above the improper genetic coding that marks the predisposition to express AA; before ULBP3 up-regulation and NKG2D ligand activity occur. (Additionally, I recovered from widespread arthritis and photosensitivity that had accompanied my AU, as well). I suspect if measured, we would find that neither ULBP3 up-regulation or NKG2D is in play while I am in a controlled state. For the record, I have offered myself as a test subject to the leading AA researcher in this field of study with the hope that my experience might shed some light on the process to the advantage of the AA community. Perhaps because of my uniquely charming personality, my offer was never accepted.I also would like to make clear that I do not think that my experience represents a concluding moment in the fight against AA. I believe it is an excellent beginning; a new chapter…an opportunity and invitation to each of us in the community and those in the science fields to see that we are ignoring critical avenues of research and treatment possibilities right now. I believe that once we bring the proper spectrum of science to collaboratively bear on this disease we will see incredible and rapid progress. And shouldn’t that be the goal? Isn’t it time to stand up together and make this happen.
As stated in my previous article, the treatment under discussion here – the one that I used to successfully reverse my Alopecia Universalis after nearly two decades – is in many ways only a beginning.Yes, while it undoubtedly offers potential and promise as a highly safe and effective treatment strategy for all degrees of AA right now, it also asks us to re-examine our current understanding of the pathogenesis of AA. It also clearly exposes the limitations of current AA research and begs us to insist on a new and comprehensive strategy for future research….Once again, this is the vision of Global Alopecia Mission: a comprehensive, sequential AA-only research agenda carried out by a multi-discipline collaboration of all relevant sciences, including much deeper examination of the microbiology and nutritional relationships of autoimmune Alopecia Areata.Simply put, hair loss in Alopecia Areata occurs when the hair follicle is exposed to an inflammatory process through an undesired immune system response. AA is an ‘organ-specific’ or ‘organ-restricted’ autoimmune disease characterized by the immune privilege collapse of the hair follicle, wherein an as of yet unidentified ‘trigger’ in predisposed persons sets in motion a T-cell mediated process which arrests the normal growth (anagen) phase of the follicle.
In the strictest sense the hair follicle IS still healthy and capable of producing hair. The area of the follicle that contains epithelial stem cells is not affected. Therefore, the functional and structural integrity of the follicle is undamaged. The mechanical ability and innate ‘desire’ of the follicle to produce hair remains, witnessed by the intermittent appearance of un-pigmented, immature, vellus hairs that often appear even for those with complete AU.The process of AA, as with other autoimmune disorders, is an exceedingly complex series of interrelated reactions. However, for clarity, we will oversimplify the disease process into three general categories. In order to reverse AA, at least one these points require successfully remediation:1) Susceptibility - the genetic variation that causes the predisposition or susceptibility and permits the AA event to occur in the first place;2) Trigger - the triggering event or stimuli (either a one-time occurrence or an ongoing process or pathogen), which when coupled with innate susceptibility, stimulates the onset of the immune response;3) Immune Response - the resulting immune response itself, anywhere along the process from the signaling point to the resulting inflammatory event at the hair follicle.All current medical treatments – in one form or another – including the most recently heralded research findings, are focused on the third category. The goal being to pharmaceutically target mechanisms involved along the immune response chain to disrupt the resulting inflammatory end process. In other words, to develop a drug that will break the chain of events somewhere leading up to T-cell activity at the hair follicle. Such a drug therapy – far downstream in the disease process – would require routine use because neither susceptibility nor trigger is addressed.This would make great commercial sense from a pharmaceutical profit standpoint because AA patients would become indefinitely reliant on such a drug. And as a pharmaceutical friend of mine once told me, “the real success of a drug is measured by refills.”Such a drug would likely become the standard pitch for any AA patient that presented even the tiniest patch of AA – not just as a curative, but also as a precautionary or preventative measure, whether or not it was in fact necessary.Unfortunately, all drugs have side effects. For every action, there is a reaction. Trying to unnaturally force or trick the body against its natural processes without addressing the root cause always has consequences.In the case of the most notable current focus that we have heard about – based on the ‘leading’ genetic research – of using IL (interleukin) blocking agents in either infusion or topical form to disrupt the immune process in AA, it’s important to note that blockage of interleukins also blocks their positive protective role in the body, resulting in immunosuppression and potentially opening the door for opportunistic sickness and disease.Our greatest goal must always be to ensure that any therapy, drug or otherwise, is safe and effective; and must always aim for the highest goal which is a cure.One possibility with significant promise, theorizes a microbiota origin as the instigating stimuli and attempts to address Alopecia Areata further upstream than current research.
This patent-pending combination therapy method will be, hereinafter, referred to as ‘RLT’.For reference, RLT resulted in complete reversal of my Alopecia Universalis (and related arthritis and photosensitivity) after almost 20 years, with full regrowth of my hair in 43 days. RLT has been further demonstrated to effectively manage expression of my AA ruling out random regrowth as the basis of my recovery.
As a side note, I have made many attempts to share my experience with those in the mainstream of AA research. Though some have labeled these mainstream players the ‘critical ear and voice of the alopecia areata research community’, their ear apparently is not tuned to the sound of any uniquely documented instances of recovery outside their particular concentration because I never received any responses.
I consider that a very sad statement for the AA community, as should anyone who is concerned about genuine progress toward a treatment and cure.Particularly when I believe that most who are familiar with AA understand that my ability to reverse and then control my AU is an unprecedented development. I have yet to see an equivalent documented experience…period. And there is absolutely no similar experience of complete reversal in only 43 days.So then, what is it that enabled me to reverse my longstanding AU and subsequently allows me to control its expression?Assuming that microbiome dysfunction lies at the root of AA, RLT provides a comprehensive treatment strategy which addresses both the trigger and corresponding immune response to halt, counter and reverse the disease progression of AA. While the course of each case of AA cannot be predicted, statistically Alopecia Areata follows a progressive prognosis curve, moving from limited patchy AA to potential hair loss over the entire body in Alopecia Universalis. Based on the underlying premise of microbiome dysfunction as the instigating factor in AA pathogenesis, RLT should be a beneficial treatment option for anyone affected by AA. Efficacy data is undetermined due to the need for further sampling, but speed and degree of positive patient response to RLT would likely vary from person to person as with any treatment. I can be contacted via email at firstname.lastname@example.org.