Regeneration of tissues in your body following an injury is a normal part of life. When you injure a tissue of your body there are stages of repair that your body goes through to create new cells and replace the injured tissues. When your body is in a healthy balance, this state of repair and reconstruction is limited to a defined period. When your body is in a state of imbalance and chronic inflammation, this state of repair and stress on your body continues and can cause your tissues to lose their function.
Fibrosis is defined as ‘a complex pathological process that results from excessive deposition of extracellular matrix (ECM) components in response to tissue injury. It is the final pathological outcome of most chronic inflammatory diseases and a major contributor to organ malfunction and failure [1 and 2].
If fibrosis occurs to your organs, this can lead to the organ not able being able to function and eventually die. In developed nations, fibrosis of tissue is responsible for forty five percent of deaths. New research provides insight to the role of your gut microbiome in promoting or inhibiting fibrosis in your body.
When you have a healthy gut microbiome, the microbes release health promoting factors such as short chain fatty acids. These promote health and optimal function to almost every component of your body including your immune system. When your gut is in a state of imbalance or dysbiosis, these health promoting factors can be limited or completely depleted. In addition, toxic compounds, specifically uremic toxins, can build up.
The effect of this imbalance can cause an imbalance ability of your gut barrier to function optimally, allow toxins and microbes which are not meant flow through the gut barrier to translocate and promote a state of ongoing or chronic inflammation in your body. This can cause damage to the tissues or your body and is one proposed promoter of fibrosis. Commonly known diseases which are the consequence of fibrosis include progressive kidney disease, heart disease, liver cirrhosis and intestinal fibrosis.
Lifestyle habits you can add to your day to promote a healthy gut microbiome with optimal diversity and variety is by including both probiotic and prebiotic foods in your diet. The FAO/WHO definition of a probiotic to be “live microorganisms which when administered in adequate amounts confer a health benefit on the host’’. Aim to include two sources of probiotic rich foods each day.
Examples of probiotic rich foods include:
• Yoghurt
• Sauerkraut
• Sourdough bread
• Miso
• Tempeh
• Kefir
• Kimchi
• Sour pickles
The health promoting microbes in your gut need to be fed to stay alive and well. These come from plant-based foods such as wholegrains, nuts, seeds, legumes, beans, fruits, and vegetables. These foods provide prebiotic fibre which is a type of fibre that is a fuel for the health promoting microbes.
A healthy lifestyle strategy can be to include thirty different plant foods a week. Each plant-based food provides diverse types of prebiotic fibre and supports the health of different health promoting microbes. An example of a diet which promotes optimal gut health is the Mediterranean Diet.
In addition to these strategies, aiming to limit the inclusion of added sugars, trans, and saturated fats. The typical Western Diet is an example of the type of eating style which promotes gut dysbiosis.
Take home message: Your gut microbiome is a powerful conductor to your overall health and longevity. Promote optimal health for life by looking after your gut microbiome, which in turn may help promote the health of all the tissues in your body and prevent chronic inflammatory conditions such as fibrosis.
References:
- Dees, C.; Chakraborty, D.; Distler, J.H.W. Cellular and molecular mechanisms in fibrosis. Exp. Dermatol. 2021, 30, 121–131.
- Wynn, T.A. Cellular and molecular mechanisms of fibrosis. J. Pathol. 2008, 214, 199–210.
- Costa CFFA, Sampaio-Maia B, Araujo R, Nascimento DS, Ferreira-Gomes J, Pestana M, Azevedo MJ, Alencastre IS. Gut Microbiome and Organ Fibrosis. Nutrients. 2022; 14(2):352. https://doi.org/10.3390/nu14020352
