Besides being skin diseases, what do psoriasis, rosacea, eczema and a number of other skin conditions have in common? This is a somewhat complex topic, but stick with me if you desire improved skin health.
While traditionally viewed as conditions of just the skin, they are actually systemic diseases, i.e., conditions with body-wide involvement but most visible on the skin. For example, people with rosacea or psoriasis are much more likely to also develop inflammatory bowel diseases like ulcerative colitis, be obese, have genitourinary complaints, and have irritable bowel syndrome. It therefore helps to think of skin as a reflection of internal health: metabolic health, insulin resistance, inflammation. Skin is, in particular, a reflection of gastrointestinal (GI) health, specifically the health of the intestinal microbiome and the intestinal lining, i.e., the gut “talks” to the skin and other organs. If this association is true in various skin diseases, is it also true for skin health outside of disease, i.e., features such as skin color, moisture, firmness, protection from sun damage, presence or absence of wrinkles? I am going to argue that management of your GI microbiome and thereby the gut-skin axis is among the most important strategies you can adopt for skin health, whether or not you have a skin condition.
Ongoing efforts to characterize the microbiome of skin in people with skin conditions indeed document changes: reductions in some species (e.g., Staphylococcus epidermidis, Cutibacterium acnes), over-proliferation of others (e.g., Staphylococcus aureus). But if the skin microbiome were the cause, these conditions should be contagious if someone contacts the skin of a person with, say, psoriasis, and thereby acquires the microbes from the lesions. It could also mean that skin microbiome transplantation, much like fecal transplantation, could be curative. But these conditions are not contagious, even if you were to experience prolonged contact, and it is highly unlikely that skin microbiome transplantation would reverse all the phenomena associated with skin disease. In other words, exposure to the disrupted microbiome of a psoriatic lesion is insufficient to contract the disease, and normalization of the skin microbiome is also likely insufficient to reverse abnormalities in the skin and other organs. And it’s unlikely such shifts in skin microbiome would be responsible for, say, triggering arthritis (e.g, psoriatic arthritis), ulcerative colitis, or obesity. It is much more likely that changes in the skin microbiome are a consequence, not a cause.
Let’s consider the GI tract as a determinant of skin status. How does the GI tract communicate with the skin? One important way is when the integrity of the intestinal barrier—the barrier to microbes, microbial byproducts, and food digestate—is compromised. A number of factors can disrupt the intestinal barrier, both the mucus barrier and intestinal cellular barrier:
- Overgrowth of unhealthy microbes, especially if they colonize the small intestine where there is a thinner and more fragile single-layer mucus barrier (unlike the thicker two-layer mucus barrier of the colon that is thereby less penetrable)
- Emulsifying agents in common foods such as ice cream
- “Supplements” with emulsifying properties such as N-acetyl cysteine that people unknowingly take for various purposes, a potent disrupter of intestinal mucus
- Polyethylene glycol in the common bowel prep Miralax that disrupts the mucus barrier for several days after consumption (and worse if taken chronically for constipation)
- Chlorinated drinking water
- The gliadin protein of wheat and related proteins in other grains—as reflected by increased levels of the zonulin protein in the bloodstream, the protein that mediates the intestinal barrier
An impaired intestinal barrier is therefore more penetrable to intestinal contents.
I’ve discussed this issue of small intestinal bacterial overgrowth, or SIBO, in several blog posts. In a nutshell, exposure to antibiotics and other factors has resulted in the loss of beneficial species, allowing pathogenic bacterial species to proliferate in the colon. In many people (1 in 2 Americans, by my estimate), these unhealthy microbes also ascend into the 24-feet of small intestine. This adds up to 30-feet of GI tract populated by trillions of mostly unhealthy microbes. These creatures live for only a few hours, then die. This means that trillions of microbes live and die constantly, releasing their components into the intestinal lumen (interior). In particular, the lipopolysaccharide (LPS) endotoxin of species such as E. coli, Klebsiella, Campylobacter and other so-called Gram-negative species breach the small intestinal barrier and gain entry into the bloodstream: endotoxemia. High levels of LPS endotoxin in the bloodstream can then have effects on the various organs of the body. In the bloodstream, it triggers insulin resistance. In the liver, it contributes to fatty liver. In the skin, it triggers an inflammatory cascade that results in skin rashes. To make matters worse, people with skin rashes also tend to lack beneficial intestinal species such as Akkermansia, Faecalibacterium, and Ruminococcus, all vigorous producers of the protective fatty acid, butyrate, a major determinant of both intestinal and metabolic health. In the absence of an overt skin disease, endotoxemia still causes increased skin inflammation, redness, and accelerates the loss of dermal collagen. Preliminary evidence suggests that the low-grade endotoxemia associated with SIBO increases the activity of inflammatory skin enzymes such as matrix metalloproteinase that degrade collagen, thereby accelerating skin aging.
To illustrate further, let’s consider psoriasis, a form of rash that plagues 100 million people worldwide (according to the World Health Organization). The more overweight a person is, the greater the likelihood they develop psoriasis; losing weight is associated with increased likelihood of remission of psoriasis, all suggesting that the skin or skin microbiome alone are not the active factors. People with psoriasis or psoriatic arthritis are also much more prone to developing inflammatory bowel diseases, Crohn’s disease and ulcerative colitis, also both largely due to disruptions of bowel flora composition. Even without overtly developing these diseases, people with psoriasis have intestinal inflammation seen at biopsy. In other words, with psoriasis, intestinal inflammation and dysbiosis are major components of the disease and likely a driving force in developing the skin inflammation of psoriasis.
If this is true, i.e., that skin rashes such as psoriasis and rosacea are triggered by disruptions of the GI microbiome, then probiotics might be expected to exert positive effects. While the optimal mix of probiotic species has not yet been determined, several bacterial species have demonstrated beneficial effects, sometimes dramatic, on skin rashes. These species include Leuconostoc mesenteroides (obtainable from fermented foods such as kimchi and sauerkraut), Lactobacillus pentosus GNML-77, Lactobacillus paracasei CNCM-I and NCC2461, Bifidobacteria infantis 35624. In one study in 90 people with psoriasis, 66.7% of participants experienced 75% or greater reduction in rash severity with administration of a mix of Bifidobacterium longum CECT 7347, B. lactis CECT 8145 and Lactobacillus rhamnosus CECT 8361, one billion CFUs per day.
Topical skin products are, of course, extremely popular. Moisturizers, concealers, and other products that are applied topically do not improve skin health, any more than polishing your car makes it run better. While there may be nothing wrong with such topical products, they do not address the underlying factors that lead to skin issues such as loss of dermal collagen and hyaluronic acid, loss of moisture, increased inflammation, increased susceptibility to sun damage, glycation of collagen that makes it brittle, increased wrinkles and skin aging, or the emergence of skin diseases. No topical product addresses these intrinsic, mostly dermal, phenomena.
One major disruption of the GI microbiomes of modern people that is associated with deteriorating skin health is loss of the keystone species, Lactobacillus reuteri, the species that many of us proliferate to high counts by making L. reuteri yogurt using prolonged fermentation and prebiotic fiber fertilization. Among the potential means by which L. reuteri may effect beneficial changes in skin health include:
- Upper GI colonization—this is where SIBO occurs, of course
- Bacteriocin production—L. reuteri is among the microbes that produce potent bacteriocins, natural antibiotics effective against numerous pathogenic species, including those that overpopulate in SIBO
- Oxytocin provocation—This has been demonstrated in studies with mice, not yet corroborated in humans (although we are currently conducting a human clinical trial to examine this question). I do, however, suspect that oxytocin provocation is a real phenomenon in humans, given the emotional and social effects many of us experience with consumption of L. reuteri yogurt: increased sociability, reduced social anxiety, increased libido. In experimental models, L. reuteri and thereby oxytocin increases dermal collagen and dermal thickness and accelerates healing of skin wounds, suggesting a major role in skin health.
In summary, whether your interests are obtaining relief from skin rashes such as eczema or psoriasis, or just enjoying smoother, healthier, more youthful skin, your efforts should not stop at applying topical preparations or taking a drug that blocks some step in an inflammatory pathway. Your efforts should also include addressing the GI microbiome by looking for SIBO and addressing it, consuming nutrients that boost species such as Akkermansia and Faecalibacterium for their butyrate-producing capacity, and restoration of lost microbes that play big roles in skin health such as L. reuteri. If you desire a detailed blueprint for how to achieve such effects, see the many other posts in this blog, my Super Gut book, or the many discussions we have in my DrDavisInfiniteHealth.com website.