Butyrate’s role in ameliorating neurological decline

Maguire G Justin, July 2023

Intellectual capacity can be hacked! Lazar S et al ( 2020) [1] disproved Arthur Jensen’s claim that compensatory education has little impact on boosting intelligence [2] through a 296 participant RCT (randomized control trial), illustrating that prolonged intensive training in creative problem solving can in fact increase IQ!

Essentially, we all have the potential to become smarter and perform better in an ever-evolving cognitively demanding world. As with any possible education our state is imperative to consider, in short, if we choose to augment our intellect through creative problem-solving exercise, we need to ensure our neurochemistry is optimally aligned to allow the least path of resistance toward cognitive enhancement.

Pritchard, C and Rosenorn-Lanng, E provided statistically relevant findings of increased neurological deaths occurring among individuals between 55-74 years of age [3]. Neurological enhancement and rates of decline are interlinked to neurochemical factors stemming from immunological peripheral and subsequent central neurological alterations. Thus, when we strive toward improving our cognition consideration of both internal and external environmental disruptors needs to be included. In doing so we not only gain smarts but offset the chance of neurological decline!

Through holistic consideration, this article provides insight into factors stemming from peripheral metabolism which may positively influence one’s opportunity to succeed with an elevated IQ whilst also offsetting the likelihood of neurodegenerative disease. 

Cenit, CM. et al (2017) demonstrated statistically significant relevance (p<0.05) between the health of our gut and brain or gut-brain axis[4]. Immunological reactions set off through bacterial translocation can influence key factors within neurotransmitter production, metabolism and regulation, including factors such as:

• Methylation
• Acetylation
• Non-coding RNA

All which impact histone tails and the respective ability to produce not only signals for our nervous system to use but also nootropic factors, which enable neurogenesis and recovery from injury.

SCFA (Short chain fatty acids) are by-products developed through fermentation of fiber by specific bacteria in our microbiome. Namely, we have three major types of SCFA: acetate, propionate and butyrate [5], each of which has its unique role in regulating not only metabolism but also neurological activity through free fatty acid receptor binding [6]. Interestingly the integrity of our gut lining is intimately correlated to the quantity of either butyrate (which seals tight junctions) or propionate (which opens tight junctions), thus efforts to regulate butyrate production plays an intimate role within inflammatory outcomes associated with leaky gut.

When our guts become ‘leaky’ a host of immunological processes are fired, resulting in the possible outcome of depleted CNS (central nervous system) serotonin, increased splenic 5HT (5-hydroxytryptophan) and elevated neurotoxic compounds such as quinolinic acid and dopamine quinone[7]. Fortunately, through a focus on improving butyrate formation and even supplementation, our brains have a chance to offset an immunological demand that may often lead to neurodegenerative and cognitive disorders.

Through meta-analysis Skonieczna-Zydecka, K et al (2020) recorded that butyrate supplementation can even assist in restoring dopamine turnover in animals exposed to cocaine and other amphetamine based drugs[8]. Notably, Butyrate stimulates TGFbeta which inhibits histone de-acetylation, leading into increased acetylation of histones in FOXP3, providing us with an increase of BDNF (brain derived nootropic factor) and NGF (nerve growth factor) and inevitably modulating CNS immunity. Butyrate also inhibits synucleic-induced DNA damage and thus improves availability of dopamine, which is often associated to be compromised in those with ADHD (attention-deficit-hyperactivity- disorder)[9]. Overall Butyrate has the ability to prevent neurological ageing, increase focus and decrease the likelihood of monoamine related depression.

Specific species of bacteria have been identified to increase butyrate formation[10]. Find out more about how specific probiotic species may have a neuroendocrine benefit in your nutritional efforts through this link (Sonja please give online url access to the document I wrote in the topic).

In a modern world full of growing environmental toxicity, focus on our internal and external environmental terrain needs to be considered if we aim toward improving cognitive function and importantly offsetting an ever growing neurological death statistic. Through the holistic perspective of whole systems physiological impact on biochemical and correlated neurochemical alteration can be treated, supported and optimized. Medication has its place, yet before throwing chemicals at a problem there may be alternative solution sourced via healing an internal paradigm of microbiome health. Those struggling with cognition are welcome to review our free systems biology app, in which clear systems contributory indication toward faulty thinking can be identified.

https://autonomic-coaching.web.app/tabs/home

[1] Lazar, S. Jihyun, L. Nov 2020. We can boost IQ: revisiting Kvashchev’s experiment’. Available at: https://pubmed.ncbi.nlm.nih.gov/33256082/#:~:text=We%20concluded%20that%20prolonged%20intensive,%2Dsolving%3B%20intelligence%3B%20training.

[2] Jensen A. 1969. “How much can we boost IQ and scholastic achievement,” in environment, heredity, and intelligence. Available at: https://doi.org/10.17763/haer.39.1.l3u15956627424k7

[3] Pritchard, C and Rosenorn-Lanng, E. Jul 2015. Neurological deaths of American adults (55-74) and the over 75’s by sex compared with 20 western countries 1989-2010: cause for concern. Available at: https://pubmed.ncbi.nlm.nih.gov/26290774/

[4] Cenit, C M. et al. Aug 2017. Influence of gut microbiota on neuropsychiatric disorders’. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5558112/

[5] Silva, P Y. et al. Jan 2020. The role of short chain fatty acids from gut microbiota in gut-brain communication. Available at: https://www.frontiersin.org/articles/10.3389/fendo.2020.00025/full#:~:text=The%20SCFAs%20acetate%2C%20propionate%2C%20and,and%20resistant%20starch%20(22).

[6] Rogers, BG. Et al. 2016. From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways. Available at: https://pubmed.ncbi.nlm.nih.gov/27090305/

[7] Liu, T R. 2017. The microbiome as a novel paradigm in studying stress and mental health. Available at: https://pubmed.ncbi.nlm.nih.gov/29016169/

[8] Skonieczna-Zydecka, K. et al. Gut Biofactory-neurocompetent metabolites within the gastrointestinal tract. A scoping review. Available at: https://pubmed.ncbi.nlm.nih.gov/33139656/

[9] Blum, K. et al. Oct 2008. Attention-deficit-hyperactivity disorder and reward deficiency syndrome. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626918/pdf/NDT-4-893.pdf

[10] konieczna-Zydecka, K. et al. Gut Biofactory-neurocompetent metabolites within the gastrointestinal tract. A scoping review. Available at: https://pubmed.ncbi.nlm.nih.gov/33139656/