Intro

A recent paper discussed the possible benefits of consuming fibrous rich diets and how the short chain fatty acids (SCFAs) associated with these diets can improve the health of your gut microbiota. The SCFAs are acetate, propionate, and butyrate.

The paper presents 7 major points of interest.

The 7 Arguments

1. Competitive Exclusion – high-fiber nutrition expands commensal bacteria (good bacteria), limiting pathogenic bacteria’s access to the gut epithelium.

This means that your gut populations compete with each other for territory.

Whereas the consumption of highly processed foods (such as bread – all types, pasta – all types, wheat products, sweets, chips, canned foods, etc) can expand pathogenic bacteria and lead to issues like Candida, IBD, IBS, auto-immunity conditions, and others, consuming diets rich in fiber and eliminating processed foods would promote the expansion of good bacteria.

I usually get my SCFAs and fiber from kale, leafy greens, brocolli, dark chocolate, the cabbage family, butter, and others.

2. SCFA-induced promotion of mucus by gut epithelial cells

This mechanism has the ability to optimize gut membrane function, lower the chances of inflammatory conditions, protect against ulceration, and prevent unwanted chemicals to cross the gut membrane.

3. SCFAs induce the secretion of IgA by B cells

Immunoglobulin A (IgA) plays a key role in maintaining a non-inflammatory relationship between the host and the gut microbiota, as well as microbiota composition. Peterson et al., Ishikawa and Nanjo, and Round and Mazmanian further explore these processes.

4. SCFA-induced promotion of tissue repair and wound healing

The gut is prone to ulceration, physical damage, and parasitic activity. This is also shown in a study where the authors used a single commensal microbe called SFB (segmented filamentous bacteria) to colonize mice microbiota.

This has lead to the production of IL-17 and IL-22, which are responsible for defense against certain microbes and help in managing inflammatory conditions.

SFB also promote the production of anti-inflammatory peptides and help with tissue repair.

5. SCFA-induced T-Reg (T regulatory) cell production

T-Reg cells presumably facilitate immunological tolerance to food antigens. Butyrate is thought to directly influence the number and function of inducible T-Reg cells (Arpaia).

I would assume that a higher number of T-Reg cells may protect my gut and my body when consuming foods that are allergenic to other people, such as legumes for example.

6. SCFA-mediated enhancement of epithelial integrity

In this case, acetate may be (to a certain extent) responsible for the activation of the inflammasome pathway and the production of IL-18 (Interleukin 18).

The IL-18 gene codes for a pro-inflammatory cytokine which enhances the activity of NK (natural killer) and can lead to higher IFN-γ (Interferon Gamma) – which can activate macrophages or other cells.

IL-18 has various implications in conditions such as: Hashimoto’s Thyroiditis, Age-Related Macular Degeneration (AMD), and Alzheimer’s Disease, to name a few.

IL-18 is in its basic core a pro-inflammatory cytokine needed by the body to fight pathogens. One of its crucial responses is with regards to LPS infection (lipopolysaccharides). Too much or too inappropriate IL-18 signaling can lead to auto-immunity and other diseases.

7. Anti-inflammatory effects – Inhibition of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) – looks funky and hieroglyphic, I know! 🙂

If NF-κB is regulated incorrectly, it can be linked to conditions of infections, cancer, auto-immunity, and also synaptic plasticity and memory related problems.

According to the authors, SCFAs reduce inflammatory chemokine output, reduce TNF (tumor necrosis factor), IL-6 and IFN-γ, which are pro-inflammatory markers. Several studies have reported the anti-inflammatory mechanism through NF-κB inhibition.

Omega-3 fatty acids are other metabolites that work in conjunction with SCFAs to fight abnormal inflammation and to promote gut integrity.

Conclusion

SCFAs (butyrate, propionate, and acetate) as well as dietary fiber itself seem to be key players in the equation of microbiota wellbeing by promoting commensal bacteria expansion, by reducing inflammation and by enhancing anti-inflammatory processes.

Consuming foods that are rich in these metabolites can protect you from developing conditions related to poor gut health, auto-immunity, and brain disorders. However, this should not serve as licensing for the consumption of sticks of butter and oil enriched coffee all at once. I think this would deprive the body from other important nutrients, as this is an energy-rich-nutrient-poor protocol.

I personally consume foods similar to Wahl’s approach (many greens, red and white cabbage, kale and brocolli, and sometimes spinach). When I eat salads with my high-fat meals, I usually dress them with olive oil, vinegar (acetate source) and other seasonings.

Sometimes, very rarely I use potato starch (unheated) and psyllium husk in my protein shakes. In my current regime I consume protein shakes hardly ever. I do use butter in a mix with olive oil or in an extremely delicious cream for a keto-friendly raspberry cheesecake.

I think it’s wise to be rational and not fall into extremes like the potato starch movement (when potato starch is the holy grail of nutrition), the oil or butter enriched coffee trend, or eating plain butter just for fun. In my opinion, that’s stupid and irrational. I recommend being reserved and skeptic and always check your information from various good sources before you make a decision.

References:

1. Peterson, D. A., McNulty, N. P., Guruge, J. L., & Gordon, J. I. (2007). IgA response to symbiotic bacteria as a mediator of gut homeostasis. Cell host & microbe, 2(5), 328-339.

2. Ishikawa, T., & Nanjo, F. (2009). Dietary cycloinulooligosaccharides enhance intestinal immunoglobulin A production in mice. Bioscience, biotechnology, and biochemistry, 73(3), 677-682.

3. Round, J. L., & Mazmanian, S. K. (2009). The gut microbiota shapes intestinal immune responses during health and disease. Nature Reviews Immunology, 9(5), 313-323.

4. Thorburn, A. N., Macia, L., & Mackay, C. R. (2014). Diet, metabolites, and “western-lifestyle” inflammatory diseases. Immunity, 40(6), 833-842.

5. Arpaia, N., & Rudensky, A. Y. (2014). Microbial metabolites control gut inflammatory responses. Proceedings of the National Academy of Sciences, 111(6), 2058-2059.

6. den Besten, G., van Eunen, K., Groen, A. K., Venema, K., Reijngoud, D. J., & Bakker, B. M. (2013). The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. Journal of lipid research, 54(9), 2325-2340.

7. Dietary Fiber – What is?

8. Park, J., Kim, M., Kang, S. G., Jannasch, A. H., Cooper, B., Patterson, J., & Kim, C. H. (2014). Short-chain fatty acids induce both effector and regulatory T cells by suppression of histone deacetylases and regulation of the mTOR–S6K pathway. Mucosal immunology.

9. IL-18 – Interleukin 18

10. NFKB – Signaling Pathway – Cell Signal

Photos: here and here