May 30, 2021

Part 3: The Role of Botanicals in Supporting Microbial Balance and Systemic Health

Part 1 and 2 Review

Part 1 of this series discussed the importance of short-chain fatty acids (SCFAs) in regulating intestinal inflammation and epithelial barrier function. SCFAs also decrease pro-inflammatory cytokines (IL-3, IL-6, tumor necrosis factor-α), and reduce NF-κβ. Additionally, lipopolysaccharides (LPS) found throughout the cell wall of gram-negative bacteria cause damage to epithelial cells and tight junctions. This begins the cascade of inflammation by binding to TLR4 and activating NF-κβ and inflammatory cytokines (1).

Part 2 discussed diseases associated with gut dysbiosis, decreased diversity of beneficial gut microbes, and LPS translocation. From a clinical standpoint, we addressed adding microbiome and LPS-based inflammation to the differential diagnosis for a patient presenting with chronic fatigue, aching joints, and dementia.

Now that we understand the role of the microbiome and its ability to predispose towards good health or systemic illness, let’s apply this information in our clinical practices.

Botanicals and the Gut Microbiome

Botanicals have long been used for a variety of health reasons, and a review of the literature by Feng et al. found, “Herbal medicines are an important resource provider for production of SCFAs and have been demonstrated to be able to modulate gut microbiota composition and regulate SCFAs production” (1). The way that botanicals accomplish this is by providing nutrients to the gut microbiota that secrete enzymes to metabolize carbohydrates into SCFAs (1). SCFAs help maintain epithelial integrity in the gastrointestinal (GI) tract. They prevent gram-negative bacteria (including LPS) from passing through and entering the bloodstream, blocking inflammatory systemic disease.

Botanicals and the Oral Microbiome

Not only are botanicals effective in the gut microbiome, but also in the oral microbiome. A biocidal formula containing 17 herbs and essential oils was used by John Rothchild, DDS, in a dental pilot study. Dr. Rothchild used phase-contrast microscopy and examined nine participants that exhibited elevations in pathogenic microorganisms (gram-negative rods and spirochetes) in gingival crevicular fluid derived from the periodontal tissues.

Seven out of nine participants had a significant reduction or elimination of pathogens when using Biocidin® formula for one month (2).

Botanicals and Biofilms

Hashioka et al. showed that periodontal gram-negative bacteria like Porphyromonas gingivalis and its component LPS are found in the periodontal pocket (3). These harmful bacteria form biofilms and enter the pocket epithelium where they gain access to systemic circulation and release pro-inflammatory cytokines (3). Incredibly, botanicals have the power to break down biofilms, thus decreasing the likelihood of chronic oral microbial dysbiosis. A pilot study done by Binghamton University looked at Pseudomonas aeruginosa (P. aeruginosa) and Escherichia coli (E. coli) biofilms and exposed them to a 50% concentration of Biocidin®(4). At 24 hours, most of the biofilms were eradicated in both species (see diagram). Of note is both of these species are gram negative.

Endotoxemia and Spore Probiotics

Endotoxemia is the presence of endotoxins, like LPS, in the blood. A study done by McFarlin et al. set out to find out if spore-based probiotics would help decrease post-prandial endotoxemia. This was of consideration because the presence of endotoxins in the blood “may be a hallmark sign of intestinal permeability and ‘leaky gut’” (5). The researchers found, “Oral supplementation with a viable, spore-based probiotic was associated with a significant reduction in post-prandial endotoxin and triglycerides... It is reasonable to speculate that the spore-based probiotic supplement may have exerted its effect by altering the gut microbial profile, altering intestinal permeability, or a combination of the two effects” (5). A sporebased probiotic is another useful tool to help support a patient with leaky gut and decreased diversity in their gut microbiome.

Final Thoughts

I want to leave you with some final thoughts and ask what wellness care looks like in your office. After this three-part series discussing LPS and associated systemic conditions, we have determined ways to identify LPS as the root cause of disease. But what if you could catch gut dysbiosis or increase microbial diversity before LPS became systemic, causing severe symptoms? Several labs use testing to analyze the gut microbiome. Annual testing is a great tool to assess gut microbiome balance. It may also help identify harmful microbes and their metabolites. Even if the bacteria are not yet causing symptoms, a botanical cleanse could help to decrease the harmful bacteria and increase the beneficial and keystone species. Eating a diet high in fiber to help support SCFA production would also benefit the health of the gut epithelium and reduce system-wide inflammation. Botanical formulations and probiotics are useful tools to support patients with whole-body health. For further information about Biocidin products, please visit biocidin.com or reach out to our clinical consultants at care@biocidin.com.

REFERENCES

Feng W, Ao H and Peng C (2018) Gut Microbiota, Short-Chain Fatty Acids, and Herbal Medicines. Front. Pharmacol. 9:1354. doi: 10.3389/fphar.2018.01354.
Rothchild, John. Personal interview. 25 February 2021.
Hashioka, Sadayuki et al. “The Possible Causal Link of Periodontitis to Neuropsychiatric Disorders: More Than Psychosocial Mechanisms.” International Journal of Molecular Sciences, vol. 20,15 3723. 30 Jul. 2019, doi:10.3390/ijms20153723.
Marques, C. (2013). Preliminary Report on Activity of Biocidin against Multiple Species of Biofilms (Rep.). Binghamton University Biological Sciences Dept.
McFarlin BK, Henning AL, Bowman EM, Gary MA, Carbajal KM. Oral spore-based probiotic supplementation was associated with reduced incidence of post-prandial dietary endotoxin, triglycerides, and disease risk biomarkers. World J Gastrointest Pathophysiol 2017; 8(3): 117- 126, doi: 10.4291/wjgp.v8.i3.117.