You, Your Diet and Your Microbiome
The relationship between our health, our dietary choices, and our gut microbiome is a fascinating research topic. We are only starting to understand the deep connection between the microbiome and our health. Read on for an overview of what the current scientific literature is beginning to unfold about this symbiotic relationship.
What is the microbiome?
Up to 70% of the cells in our body are non-human and consist of microorganisms such as bacteria (but also viruses, fungi, and protozoa). These microorganisms reside in the skin, the respiratory tract, and the gut. All these cells are referred to as the microbiota. Their relative genetic material is called the microbiome (1). Altogether, the genetic material of the microbiome encodes for a staggering 3.3 million genes. In contrast, the human genome encodes approximately 22,000 genes (2). This equates to about 150 bacterial genes for every human gene!
The relationship between our microbiome and us
We are only starting to understand the deep connection between the microbiome and our health. Throughout human evolution, we have cooperated with microorganisms, borrowing their genes as evolutionary shortcuts to acquire new capabilities (3).
In the large intestine, microorganisms synthesise a multitude of metabolites impacting our metabolism, and influencing how nutrients are stored and processed by the liver and muscle cells. For example, these molecules can determine whether glucose should be stored as fat or glycogen and affect the response to insulin (4). These are only some interesting facts about the microbiota, and as scientific research advances, we are starting to understand more about it.
How do the bacteria in our gut communicate with the brain?
Our gut bacteria communicate with the brain through neural, endocrine, and immune signalling mechanisms. The brain uses the autonomic nervous system to regulate gut movements, secretions, permeability, and hormone secretions; these can directly affect the microbiome and its gene expression (5). This bidirectional system is known as the gut-brain axis. Changes in the brain-gut-microbiome communication appear to be involved in the pathophysiology of conditions such as irritable bowel syndrome (6). Bacterial compounds can even regulate appetite and weight and influence hormones and neurotransmitters, thus controlling our mood, energy levels and behaviour (7, 8).
How our dietary choices can positively impact our microbiome
The food we eat not only nourishes our bodies but also feeds the gut microbiota. Our diet plays a crucial role in determining the types of microorganisms that thrive within our gut, thus impacting our metabolism and physiology (9). Many factors can impact the unique composition of an individual’s gut bacteria. These factors include the mode of birth delivery, feeding practices during infancy, geographical location, medications, stress, and ageing (10).
Research shows that nutrition appears to be one of the most important factors impacting the composition of our microbiome (9). Long-term dietary changes, particularly the consumption of fibre from fruits, vegetables, and grains, have been linked to an increased prevalence of microbes associated with a healthy gut (11, 12). These health-promoting bacteria can ferment dietary fibre into short-chain fatty acids (SCFA) (13). This fermentation process leads to a decrease in colon pH (14). The lowered pH inhibits the growth of acid-sensitive and harmful bacteria and promotes the growth of beneficial types of bacteria such as Firmicutes (14). Ongoing research on SCFA is exploring their health effects, including their ability to modulate inflammation, maintain normal blood glucose and cholesterol levels and stimulate immune cell activity (15, 16). They play a crucial role in gut health as they provide energy for enteric bacteria and help prevent excessive cell growth, promoting apoptosis and cell differentiation and might help prevent colon cancer (17-19). SCFAs can also directly impact metabolism, regulating factors like body weight and diabetes through epigenetic mechanisms (18).
The composition of intestinal bacteria varies significantly across populations. A comparative study considering children from a rural Western African village and Western Europe revealed substantial differences in the composition of their microbiota (20). The diet from the Western African village was mostly vegetarian and based on whole grains such as sorghum and millet while the diet of the European children was rich in fats, free sugars and animal protein and low in dietary fibre.
The microbiota of the African children was high in Bacteroidetes and low in Firmicutes. Moreover, the African children’s microbiota was abundant in bacteria specialised in breaking down cellulose and xylan (two types of dietary fibre). Additionally, in the African children, the presence of Enterobacteriaceae such as Shigella and Escherichia (i.e. two potentially pathogenic groups of bacteria) was considerably lower. This observation has led to the hypothesis that the gut microbiota of African children coevolved in response to Western African diets high in polysaccharides and dietary fibre. This particular type of microbiota maximises energy production from dietary fibre, and it might provide protection against inflammation and non-infectious intestinal diseases (20).
Dietary fibre, microbiome and inflammation
The metabolites produced by gut microbiota enter the bloodstream through absorption and enterohepatic circulation and can influence various aspects of the host’s metabolism and physiology (21). These metabolites may have a role in the prevention or promotion of inflammation, act as antioxidants, regulate the blood-intestinal barrier function, and contribute to the production of vitamins and energy sources. Water-soluble vitamins produced by intestinal bacteria can also impact infection outcomes (22). A recent study led by Dr Wagenaar from PAN Netherlands investigated the link between the microbiome, dietary change and chronic inflammatory conditions (23). The study demonstrated that dietary interventions aimed at increasing the consumption of dietary fibre had a positive impact on the diversity of the microbiome, leading to improvements in disease-specific outcomes and a reduction in pathogenic bacteria (23). Notably, the review showed more beneficial and pronounced outcomes in patients with type 2 diabetes, which is one of the most prevalent non-communicable diseases affecting more than 500 million people worldwide (24).
However, a more recent trial showed that in people with poor microbiome diversity, a sudden increase in dietary fibre increased SCFA but also inflammatory markers (25). The study also involved another arm which involved the administration of fermented foods such as yoghurt, kombucha and kimchi. In this group, the inflammation markers decreased while the microbiome diversity increased. The study results suggested that a gradual increase in both dietary fibre and fermented foods might be an ideal strategy to slowly improve microbiome diversity, reduce inflammation and increase the production of health-promoting metabolites such as SCFA (25).
Plant-based diets, omnivore diets and their effects on the microbiome
Research suggests that following a plant-based diet can have a notable impact on the diversity of the gut microbiota. Several studies have found that individuals following plant-based dietary patterns tend to exhibit greater microbial diversity and more beneficial microbiome composition. For example, they have a higher richness of Bifidobacteria, Lactobacillus, Prevotella, Eubacterium and Roseburia compared to those following Western diets high in meat (11, 26). As discussed above, fibre-degrading bacteria produce beneficial metabolites, such as SCFAs, which have various health benefits (16, 18, 19).
Animal-based foods can provide specific nutrients that may be involved in cardiovascular health. For example, certain animal-based foods contain choline and carnitine, which can be metabolised by specific bacteria into compounds like trimethylamine N-oxide (TMAO). TMAO has been linked with adverse cardiovascular outcomes (27, 28). However, it is not clear yet if TMAO is a mediator or a bystander in the disease process and more research is needed in this area (29).
Regardless of whether one follows a plant-based or omnivorous diet, what matters most for promoting a healthy microbiota is consuming a diet high in vegetables, whole grains, legumes, fruit and nuts. These foods are high in dietary fibre which is the favourite food of our microbiome! The Mediterranean diet is a good example of a healthy plant-based dietary pattern.
Additional Information:
-
Valdes AM, Walter J, Segal E, Spector TD. Role of the gut microbiota in nutrition and health. The BMJ. 2018 Jun 13;361:k2179.
International Human Genome Sequencing Consortium. Finishing the euchromatic sequence of the human genome. Nature. 2004 Oct 21;431(7011):931–45.
Bäckhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Host-Bacterial Mutualism in the Human Intestine. Science. 2005 Mar 25;307(5717):1915–20.
Wu J, Wang K, Wang X, Pang Y, Jiang C. The role of the gut microbiome and its metabolites in metabolic diseases. Protein Cell. 2021 May;12(5):360–73.
Martin CR, Osadchiy V, Kalani A, Mayer EA. The Brain-Gut-Microbiome Axis. Cell Mol Gastroenterol Hepatol. 2018 Apr 12;6(2):133–48.
Labus JS, Hollister EB, Jacobs J, Kirbach K, Oezguen N, Gupta A, et al. Differences in gut microbial composition correlate with regional brain volumes in irritable bowel syndrome. Microbiome. 2017 May 1;5(1):49.
van de Wouw M, Schellekens H, Dinan TG, Cryan JF. Microbiota-Gut-Brain Axis: Modulator of Host Metabolism and Appetite. J Nutr. 2017 May;147(5):727–45.
Sasso JM, Ammar RM, Tenchov R, Lemmel S, Kelber O, Grieswelle M, et al. Gut Microbiome–Brain Alliance: A Landscape View into Mental and Gastrointestinal Health and Disorders. ACS Chem Neurosci. 2023 May 8;14(10):1717–63.
Rothschild D, Weissbrod O, Barkan E, Kurilshikov A, Korem T, Zeevi D, et al. Environment dominates over host genetics in shaping human gut microbiota. Nature. 2018 Mar;555(7695):210–5.
Jardon KM, Canfora EE, Goossens GH, Blaak EE. Dietary macronutrients and the gut microbiome: a precision nutrition approach to improve cardiometabolic health. Gut. 2022 Jun 1;71(6):1214–26.
De Filippis F, Pellegrini N, Vannini L, Jeffery IB, La Storia A, Laghi L, et al. High-level adherence to a Mediterranean diet beneficially impacts the gut microbiota and associated metabolome. Gut. 2016 Nov;65(11):1812–21.
Sonnenburg ED, Smits SA, Tikhonov M, Higginbottom SK, Wingreen NS, Sonnenburg JL. Diet-induced extinctions in the gut microbiota compound over generations. Nature. 2016 Jan 14;529(7585):212–5.
Kang J, Yin S, Liu J, Li C, Wang N, Sun J, et al. Fermentation models of dietary fibre in vitro and in vivo – A review. Food Hydrocoll. 2022 Oct 1;131:107685.
Holscher HD. Dietary fiber and prebiotics and the gastrointestinal microbiota. Gut Microbes. 2017 Mar 4;8(2):172–84.
He J, Zhang P, Shen L, Niu L, Tan Y, Chen L, et al. Short-Chain Fatty Acids and Their Association with Signalling Pathways in Inflammation, Glucose and Lipid Metabolism. Int J Mol Sci. 2020 Sep 2;21(17):6356.
Corrêa-Oliveira R, Fachi JL, Vieira A, Sato FT, Vinolo MAR. Regulation of immune cell function by short-chain fatty acids. Clin Transl Immunol. 2016 Apr 22;5(4):e73.
Hinnebusch BF, Meng S, Wu JT, Archer SY, Hodin RA. The effects of short-chain fatty acids on human colon cancer cell phenotype are associated with histone hyperacetylation. J Nutr. 2002 May;132(5):1012–7.
Remely M, Aumueller E, Merold C, Dworzak S, Hippe B, Zanner J, et al. Effects of short chain fatty acid producing bacteria on epigenetic regulation of FFAR3 in type 2 diabetes and obesity. Gene. 2014 Mar 1;537(1):85–92.
Mirzaei R, Afaghi A, Babakhani S, Sohrabi MR, Hosseini-Fard SR, Babolhavaeji K, et al. Role of microbiota-derived short-chain fatty acids in cancer development and prevention. Biomed Pharmacother. 2021 Jul 1;139:111619.
De Filippo C, Cavalieri D, Di Paola M, Ramazzotti M, Poullet JB, Massart S, et al. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14691–6.
Bäckhed F, Fraser CM, Ringel Y, Sanders ME, Sartor RB, Sherman PM, et al. Defining a healthy human gut microbiome: current concepts, future directions, and clinical applications. Cell Host Microbe. 2012 Nov 15;12(5):611–22.
Cordonnier C, Le Bihan G, Emond-Rheault JG, Garrivier A, Harel J, Jubelin G. Vitamin B12 Uptake by the Gut Commensal Bacteria Bacteroides thetaiotaomicron Limits the Production of Shiga Toxin by Enterohemorrhagic Escherichia coli. Toxins. 2016 Jan 5;8(1):14.
Wagenaar CA, van de Put M, Bisschops M, Walrabenstein W, de Jonge CS, Herrema H, et al. The Effect of Dietary Interventions on Chronic Inflammatory Diseases in Relation to the Microbiome: A Systematic Review. Nutrients. 2021 Sep 15;13(9):3208.
IDF Diabetes Atlas 2021 | IDF Diabetes Atlas [Internet]. [cited 2023 Mar 6]. Available from: https://diabetesatlas.org/atlas/tenth-edition/
Wastyk HC, Fragiadakis GK, Perelman D, Dahan D, Merrill BD, Yu FB, et al. Gut-microbiota-targeted diets modulate human immune status. Cell. 2021 Aug 5;184(16):4137-4153.e14.
Tomova A, Bukovsky I, Rembert E, Yonas W, Alwarith J, Barnard ND, et al. The Effects of Vegetarian and Vegan Diets on Gut Microbiota. Front Nutr [Internet]. 2019 [cited 2023 Mar 16];6. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478664/
Fretts AM, Hazen SL, Jensen P, Budoff M, Sitlani CM, Wang M, et al. Association of Trimethylamine N-Oxide and Metabolites With Mortality in Older Adults. JAMA Netw Open. 2022 May 20;5(5):e2213242.
Yang S, Li X, Yang F, Zhao R, Pan X, Liang J, et al. Gut Microbiota-Dependent Marker TMAO in Promoting Cardiovascular Disease: Inflammation Mechanism, Clinical Prognostic, and Potential as a Therapeutic Target. Front Pharmacol [Internet]. 2019 [cited 2023 Mar 6];10. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877687/
Velasquez MT, Ramezani A, Manal A, Raj DS. Trimethylamine N-Oxide: The Good, the Bad and the Unknown. Toxins. 2016 Nov 8;8(11):326.
