What does it mean to have a ‘healthy gut?’

Healthy gut

Can you improve the health of your gut?

The phrase ‘healthy gut’ is used a lot in the health space at the moment. But what does this actually mean? And can you improve the health of your gut? I will address these questions in the following article.

First of all, let’s define some terminology. The gut refers to the human gastrointestinal tract or GI tract. This is composed of the stomach, the small intestines and the large intestines or colon.

You may have heard the term ‘gut microbiome’ when gut health is being discussed. The human GI tract is home to 1013-1014 microorganisms or microbes (that is between 100 000 000 000 000 – 1000 000 000 000 000). In fact there are over 10 times more bacterial cells in your gut than there are your own cells making up your body. The community of microbes living in your gut is referred to as the gut microbiota. The gut microbiota is mostly made up of bacteria, but viruses and fungi are also present. The total genome content of these microbes, meaning all of the genes carried by all of these microorganisms, is referred to as the gut microbiome. Thanks to advances in the ability to sequence DNA, scientists are now starting to understand just how important this complex community of microbes is to human health and disease.

Health benefits provided by the gut microbiota

The health benefits provided by the gut microbiota include preventing disease causing bacteria, breaking down toxic compounds, shaping the immune system (1), providing nutrients, the synthesis of vitamins, particularly vitamin B and K (2) and the production of important metabolites. Metabolites are the intermediates or end products of metabolism. The metabolites produced by the microbes in the gut make up one third of all the metabolites found in the human blood and these compounds have some very important functions. Short-chain fatty acids are the main metabolic end products produced by the gut microbiota.

What are short-chain fatty acids (SCFAs)?

The main end products produced from the fermentation of undigested carbohydrates by the microbes of the colon are the short-chain fatty acids (SCFAs) acetate, propionate and butyrate (3). Fermentation is a metabolic process that converts sugars to acids, gases or alcohol that often occurs when oxygen is lacking, known as an anaerobic environment.

One of the health effects of SCFAs in the human gut is lowering the pH making a more acidic environment. This stops the growth of disease causing bacteria and increases the absorption of some nutrients (3).

Another important function of SCFAs is maintaining the gut barrier function. Don’t worry – I will explain what this means. The gut barrier is a layer of cells lining the inside of the GI tract. This layer of cells, referred to as the intestinal epithelial cells, has two jobs: controlling the absorption of nutrients, electrolytes and water from the inside of the gut into the blood stream and preventing harmful substances, such as disease causing bacteria and toxins, entering the blood stream. The mucus produced by this layer of cells also helps maintain this barrier (4). SCFAs play a role in gut barrier function by providing a fuel source for the intestinal epithelial cells thereby increasing mucus production.

The cells of our colon, known as colonocytes, also use the SCFA butyrate as an energy source (5). The SCFAs that are not used by the colonocytes travel to the liver and will be used in gluconeogenesis (a metabolic pathway that produces glucose from non-carbohydrate substances) and lipid (fat) synthesis. So SCFAs provide an energy source for the human host.

SCFAs can even act as signalling molecules in the gut where they can influence appetite by changing the production of particular hormones. A study in 2003 showed that SCFAs can activate free fatty acid receptor (FFAR) 2 and 3 (6). These receptors are found on cells in the colon that secrete the appetite suppressing hormones peptide tyrosine tyrosine (PYY) and glucagon-like peptide (GLP)-1. Studies in rabbits and rats have shown that SFCAs increase the production of PYY and GLP-1 (7, 8). A recent study using human volunteers showed that the SCFA propionate, when delivered to the colon, increased the release of PYY and GLP-1 and prevented weight gain over a 24-week period (9). While there is still a lot more research needed in this area, these results suggest that the right combination of gut bacteria producing the right amounts of SCFAs could prevent obesity.

Diseases/conditions associated with disruptions to the gut microbiota

A major change in the gut microbial community is known as dysbiosis. Dysbiosis has been linked to a number of diseases and conditions in humans including the following:

Obesity and metabolic disorder

Obesity and the associated metabolic diseases, such as type 2 diabetes, were thought to be a result of a combination of genetics and life-style factors. It now seems that the gut microbiota is also playing a role. Studies in mice have shown evidence that the gut microbiota can influence obesity. Transfer of the microbiota from obese mice to mice with no microbiota caused weight gain and insulin resistance. This did not happen when the microbiota from lean mice were transferred to mice with no microbiota (10).

Inflammatory bowel disease and Irritable bowel syndrome

Major changes in the composition and the diversity of the gut microbiota have been found in patients with inflammatory bowel diseases (11). Currently it is thought that low levels of SCFAs, particularly butyrate, are causing the inflammation that is associated with inflammatory bowel disease (12).

Problems with the composition of the gut microbiota have also been found in patients with irritable bowel syndrome (IBS). IBS is different from inflammatory bowel disease as in this disorder there is no inflammation of the lining of the intestines and the symptoms are abdominal pain, diarrhea and/or constipation. Again it is thought that low levels of butyrate are involved, as well as increases in the gas hydrogen sulfide in the gut (13).

Mood and neurological disorders

Would you believe that the microbes in your gut can change your mood and your brain function? Dysbiosis has been linked to a range of mental illnesses including autism (14), stress (15), anxiety (16) and depression (17). How is this possible? The gut microbiota are able to influence the enteric nervous system (ENS) (18). The ENS is basically the brain of the gut and controls intestinal motility and sends signals to the central nervous system (CNS). The communication that occurs between the gut microbiota, the ENS and the CNS is referred to as the microbiota-gut-brain-axis.

One way that the gut microbiota can influence the ENS is through the production of neurotransmitters. Studies in mice have shown that bacteria found in the gut can affect the metabolism of tryptophan (19), an amino acid which is required for the synthesis of the neurotransmitter serotonin. Certain bacteria from the gut of mice and humans are even able to directly make serotonin (20). Serotonin has many effects in the body, including regulating mood, perception, fear, anger and appetite, so this suggests that our gut microbiota can directly influence our behaviour in a major way!

Also, chronic stress can disrupt the intestinal barrier. This disruption is known as ‘leaky gut’. When leaky gut occurs, parts of the outer protective layer of the bacterial cell, known as the cell wall, can leak into the blood stream and cause inflammatory responses. A study from 2012 showed that the leaking of bacterial cell wall components into the blood stream may play a role in causing chronic depression in people (21).

But it is not clear whether changes in the gut microbiota can cause neurological disorders OR if neurological disorders cause changes in the gut microbiota.

What makes up a healthy gut microbiota?

The human gut contains over 1 000 different bacterial species (22). It is not yet known which combinations of microbes make up the ideal ‘healthy gut’. However, high levels of diversity are thought to be important for a healthy, well-functioning gut microbial community (23) and several diseases of the human GI tract are associated with a reduction in microbial and genetic diversity (24). A diverse gut microbiota is necessary to ensure that we extract all of the nutrients out of our diet. Humans only produce less than 20 enzymes for the digestion of complex carbohydrates. Therefore, we rely on the microbiota in the digestive tract to break down the complex carbohydrate structures found in fruits and vegetables (25).

Interestingly, major differences in the gut microbiome between Westerners and members of hunter-gatherer tribes have been observed. For example, the gut microbiota from the Hadza hunter-gatherer tribe from Tanzania is more diverse compared to urban living adults from Italy (26). The Hadza are one of the last remaining hunting-gathering communities in the world and live on a diet of wild foods including meat, honey, baobab (a fruit high in dietary fibre, vitamin C and polyphenols found in sub-Saharan Africa (27)), berries and tubers. One study has shown that a loss of diversity in the gut microbiota can result from a low fibre diet, such as a typical Western diet (28). The decrease in gut microbial diversity resulting from a typical Western diet could be a reason for the high rates of obesity and metabolic disorder in today’s population.

How can you maintain a healthy gut microbiota?

A number of factors can affect your gut microbiota including antibiotics, inflammation, ageing, GI tract motility and even the way you are born. However, it appears that diet has the greatest influence on the composition of the gut microbiota. So what can you include in your diet to promote a healthy gut microbiota?

One thing that stands out from the studies on diet and the gut microbiota is the influence of dietary fibre. Dietary fibre, particularly fibre that is classified as a prebiotic (29), appears to be important in maintaining a healthy and diverse gut microbiota (30). Prebiotics are defined as a selectively fermented ingredient that results in specific changes in the composition and/or activity of the gastrointestinal microbiota, thus conferring benefit(s) upon host health.

Finally, there is a method that is receiving attention at the moment that may gross you out, but is interesting. I am talking about feacal microbiota transplantation (FMT). Basically this means implanting the poop from a healthy person into the stomach, small intestine or large intestine of a sick person. FMT has been used successfully to treat infections with Clostridium difficile, which you may have heard referred to as C. diff. C. diff. is a nasty species of bacteria that causes severe diarrhea (31).

In the future, once we know more about what makes up the ideal healthy gut microbiota, ‘cocktails’ of beneficial bacteria may be a common method of treatment for a number of diseases and health conditions. But until then eating a diet rich in dietary fibre can help maintain a healthy gut.

  1. Ivanov, II, et al. (2008) Specific microbiota direct the differentiation of IL-17-producing T-helper cells in the mucosa of the small intestine. Cell host & microbe 4(4):337-349.
  2. Hill MJ (1997) Intestinal flora and endogenous vitamin synthesis. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation 6 Suppl 1:S43-45.
  3. Macfarlane GT & Macfarlane S (2012) Bacteria, colonic fermentation, and gastrointestinal health. Journal of AOAC International 95(1):50-60.
  4. Groschwitz KR & Hogan SP (2009) Intestinal barrier function: molecular regulation and disease pathogenesis. The Journal of allergy and clinical immunology 124(1):3-20; quiz 21-22.
  5. Pryde SE, Duncan SH, Hold GL, Stewart CS, & Flint HJ (2002) The microbiology of butyrate formation in the human colon. FEMS microbiology letters 217(2):133-139.
  6. Brown AJ, et al. (2003) The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. The Journal of biological chemistry 278(13):11312-11319.
  7. Psichas A, et al. (2015) The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. International journal of obesity 39(3):424-429.
  8. Longo WE, et al. (1991) Short-chain fatty acid release of peptide YY in the isolated rabbit distal colon. Scandinavian journal of gastroenterology 26(4):442-448.
  9. Chambers ES, et al. (2015) Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut 64(11):1744-1754.
  10. Turnbaugh PJ, et al. (2006) An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444(7122):1027-1031.
  11. Damman CJ, Miller SI, Surawicz CM, & Zisman TL (2012) The microbiome and inflammatory bowel disease: is there a therapeutic role for fecal microbiota transplantation? The American journal of gastroenterology 107(10):1452-1459.
  12. Tedelind S, Westberg F, Kjerrulf M, & Vidal A (2007) Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: a study with relevance to inflammatory bowel disease. World journal of gastroenterology 13(20):2826-2832.
  13. Matsunami M, et al. (2009) Luminal hydrogen sulfide plays a pronociceptive role in mouse colon. Gut 58(6):751-761.
  14. Kang DW, et al. (2013) Reduced incidence of Prevotella and other fermenters in intestinal microflora of autistic children. PloS one 8(7):e68322.
  15. Bailey MT, et al. (2011) Exposure to a social stressor alters the structure of the intestinal microbiota: implications for stressor-induced immunomodulation. Brain, behavior, and immunity 25(3):397-407.
  16. Bercik P, et al. (2010) Chronic gastrointestinal inflammation induces anxiety-like behavior and alters central nervous system biochemistry in mice. Gastroenterology 139(6):2102-2112 e2101.
  17. Jiang H, et al. (2015) Altered fecal microbiota composition in patients with major depressive disorder. Brain, behavior, and immunity 48:186-194.
  18. Hyland NP & Cryan JF (2016) Microbe-host interactions: Influence of the gut microbiota on the enteric nervous system. Developmental biology.
  19. Wikoff WR, et al. (2009) Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proceedings of the National Academy of Sciences of the United States of America 106(10):3698-3703.
  20. Yano JM, et al. (2015) Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell 161(2):264-276.
  21. Maes M, Kubera M, Leunis JC, & Berk M (2012) Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut. Journal of affective disorders 141(1):55-62.
  22. Rajilic-Stojanovic M & de Vos WM (2014) The first 1000 cultured species of the human gastrointestinal microbiota. FEMS microbiology reviews 38(5):996-1047.
  23. Costello EK, Stagaman K, Dethlefsen L, Bohannan BJ, & Relman DA (2012) The application of ecological theory toward an understanding of the human microbiome. Science 336(6086):1255-1262.
  24. Walker AW & Lawley TD (2013) Therapeutic modulation of intestinal dysbiosis. Pharmacol Res 69(1):75-86.
  25. Cantarel BL, Lombard V, & Henrissat B (2012) Complex carbohydrate utilization by the healthy human microbiome. PloS one 7(6):e28742.
  26. Schnorr SL, et al. (2014) Gut microbiome of the Hadza hunter-gatherers. Nature communications 5:3654.
  27. Coe SA, Clegg M, Armengol M, & Ryan L (2013) The polyphenol-rich baobab fruit (Adansonia digitata L.) reduces starch digestion and glycemic response in humans. Nutrition research 33(11):888-896.
  28. Sonnenburg ED, et al. (2016) Diet-induced extinctions in the gut microbiota compound over generations. Nature 529(7585):212-215.
  29. Gibson GR & Glenn R (2010) Dietary prebiotics: current status and new definition. Food Sci Technol Bull Funct Foods 7:1-19.
  30. Simpson HL & Campbell BJ (2015) Review article: dietary fibre-microbiota interactions. Alimentary pharmacology & therapeutics 42(2):158-179.
  31. Borgia G, Maraolo AE, Foggia M, Buonomo AR, & Gentile I (2015) Fecal microbiota transplantation for Clostridium difficile infection: back to the future. Expert opinion on biological therapy 15(7):1001-1014.

Image Copyright: http://www.123rf.com/profile_rangizzz’>rangizzz / 123RF Stock Photo

10 thoughts on “What does it mean to have a ‘healthy gut?’

      • My dry sense of humor! I completely agree with your findings. I did research ‘healthy eating’ one summer about 10 years ago. From everything I read I concluded that the source for most good and bad health pointed to the gut. I’m glad people are taking it seriously.

        Like

  1. Pingback: What does it mean to have a ‘healthy gut?’ | I can’t believe that’s healthy | Advanced Mediterranean Diet

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s