Researching Nutrition 2 – All Great Truths Begin as Blasphemies
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 confectionary 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 microbiome composition…”
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.
A big note of thanks to Lana Becker and Jayne Waddell for the incredible contributions and feedback they so enthusiastically share as we continue to examine the mechanisms at work in Alopecia Areata and search for answers.