Fibre and Gut Microbiome
Fibre is the indigestible carbohydrate portion of food that is derived from plants. Fibre may be considered either soluble or insoluble, both of which have different effects on the digestive system.
Soluble fibre dissolves in water and is readily fermented by bacteria in the colon, producing short-chain fatty acids and gases. 90% of the short chain fatty acids produced are either acetate, proprionate or butyrate.The short chain fatty acids are then metabolised by colonocytes which line the colon, producing ketones.
It is commonly believed that this supply of energy to the colonocytes may be of therapeutic benefit in the management of inflammatory bowel disease, however this view is not strongly supported by evidence. Further, the bacterial production of gases from fermentation of fibre can lead to bloating, abdominal pain and reflux.
The production of short-chain fatty acids from bacterial fermentation of fibre permits harvesting of energy which would otherwise be inaccessible. This is thought to contribute up to 5% of total energy derived in Western diets. The ability of soluble fibre to nourish bacteria also gives rise to its classification as a prebiotic, giving rise to the proliferation of certain bacterial species. In contrast to soluble fibre, insoluble fibre is relatively resistant to fermentation by colonic bacteria and provides bulk to faeces.
While fibre is widely regarded as an effective means to prevent and treat constipation, there is a paucity of experimental data to support this. At the time of writing, there were no published randomised controlled trials on the effects of fibre on the symptoms of constipation. While insoluble fibre adds bulk to stool and decreases colonic transit time, it does not increase stool moisture content.
One 2012 experimental study on subjects with idiopathic constipation found that complete elimination of dietary fibre led to statistically significant reductions in constipation, bowel strain, bloating and anal bleeding. Further, several studies have found increased symptoms of constipation with higher intakes of insoluble fibre. These findings bring into question the current paradigm of recommending fibre for treatment of constipation, with a clear need for further research.
Other proposed benefits of fibre include reduced all-cause mortality, improved blood sugar control and reduced risk of colorectal cancer. Despite the widespread acceptance of these claims, not all are supported by empirical evidence. High fibre diets have been demonstrated in several observational studies to be associated with reduced risk of cardiovascular disease and all-cause mortality. This however, is not a universal finding with regards to all sources of fibre, as fruit-associated fibre intake does not lead to a reduction in all-cause mortality. This again highlights the limitations of epidemiological research.
|Box. Gut microbiome
The gut microbiota refers to the trillions of microbes (bacteria, fungi and viruses) that reside in our gastrointestinal tract. Healthy adult humans each typically harbour more than 2000 species of bacteria, mainly members of four phyla (Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria) (Thursby 2017). There is considerable variation in composition of gut bacteria between individuals. While some consider microbial diversity a sign of healthy gut function (Mosca 2016), this has not yet been conclusively demonstrated. Dietary fibre, for example, has been shown to reduce microbial diversity (Zhao 2018), with the significance of this finding uncertain.
In humans, the proximal colon is the site of highest bacterial numbers due to substrate availability (Macfarlane 1992, Rowland 2018). Gut microbiota can utilise non-digested food components such as fibre, protein and peptides to produce short chain fatty acids (SCFAs). 90% of the short chain fatty acids produced are either acetate, proprionate or butyrate. Fibre fermentation produces most SCFAs in diets containing plant foods, while amino acid fermentation is quantitatively more important in animal food based diets (Evelien 2015, David 2014).
Butyrate, a short chain fatty acid, is one of the few substrates able to provide energy to colonocytes, the others being glutamine and ketone bodies (Ardawi 1985). Following absorption, colonocytes oxidise butyrate to ketone bodies for energy. SCFAs may supply some 60% to 70% of the energy needs of isolated colonocytes (Besten 2013). The production of SCFAs allows the salvage of energy mainly from carbon sources as dietary fibre that is not digested in the small intestine. It has been estimated that SCFAs can contribute to about 5–15% of the total caloric requirements of humans (Hamer 2007).
Alterations in the gut microbiota have been associated with a growing number of disease states, such as cardiovascular disease, obesity, type 2 diabetes, irritable bowel disease and inflammatory bowel and skin disease. However, with the exception of Clostridium difficile infection, the role of these microbiota alterations in the pathogenesis of disease is still poorly understood.
Clostridium difficile infection is a symptomatic infection of the colon with symptoms including watery diarrhoea, fever, nausea, and abdominal pain. Around the year 2000, a previously rare ribotype of Clostridium difficile causing severe and often fatal infections became more common. This has been associated with dietary trehalose, a manufactured sugar used to lower the freezing point of foods like ice cream. Two epidemic ribotypes of clostridium difficile have been shown to uniquely metabolise trehalose leading to their proliferation, with the introduction of trehalose as a food additive into the diet occurring shortly before the emergence of these two epidemic lineages (Collins 2018). This demonstrates the ability of diet to influence the gut microbiota. Faecal microbiota transplant has also been shown to be effective in treating Clostridium difficile infection (van Beurden 2017).
Most human studies to date are observational, which are unable to demonstrate causality. The limitations of observational research in making conclusions regarding the health impacts of the microbiota can be seen with the association of certain microbiota with impaired metabolic health. Diets correlating with certain microbiota growth patterns and increased risk of type 2 diabetes have also been associated with reduced fasting glucose and HbA1c levels (Korem 2015). It is perhaps more likely that dietary changes lead to reduced metabolic risk, and alterations in the microbiota are merely a surrogate marker. While numerous health states including obesity, type 2 diabetes and fatty liver disease (NAFLD/NASH) have been linked to altered gut microbiota, causality has not yet been proven (Aydin 2018).
The Bacteroidetes and the Firmicutes phyla are the most plentiful of bacteria in the human gut (Zhang 2016). The relative proportion of Firmicutes has been shown to be higher in obese persons, reducing with weight loss (Ley 2006). While this association has been demonstrated, mechanistic understanding is still relatively limited. The gut microbiome was famously associated with obesity in a study in which microbiota from lean and obese mice, were transplanted into germ free mice. It was found that the microbiota from obese mice produced a greater energy harvest through bacterial production of short chain fatty acids from indigestible carbohydrate (Turnbaugh 2006).
While interesting, this study has limitations in translating findings to humans. Existing microbe colonies are likely to limit the establishment of introduced microbes (Kristensen 2016, Walter 2018). Further, given that ketones have been shown to have an appetite suppressant effect (Stubbs 2018, Gibson 2015), ketone production resulting from metabolism of short chain fatty acids may lead to reduced food intake compensating for increased energy harvest.
Prebiotics are non-digestible food components, usually but not always carbohydrates such as fibre, able to selectively nourish specific bacteria (Gibson 2017). Prebiotics have been demonstrated to lead to alterations in the microbiota and enhance the production of short chain fatty acids (Scheid 2013). Production of short chain fatty acids are thought by many to provide health benefits, especially in the management of inflammatory bowel disease, however the evidence for this is limited (Seksik 2008).
In addition to fibre, other non-digestible food components include what are known as FODMAPs, which comprise short chain carbohydrates and sugar alcohols. Due to poor absorption in the small intestine, FODMAPs transit to the distal small intestine and large bowel. Here they are osmotically active, attracting fluid and contributing to loose stool. FODMAPs may also be fermented by gut bacteria leading to gas production including hydrogen and methane causing bloating. Dietary restriction of FODMAPs has been shown to be effective in the management of irritable bowel syndrome (Whelan 2018), though the implications of the resultant microbiota change have not been established.
High-intensity sweeteners are commonly used as sugar alternatives, being many times sweeter than sugar with minimal calories. Despite being “generally recognised as safe” by regulatory agencies, some animal studies have shown that these sugar substitutes may have negative effects on the gut microbiota (Nettleton 2016). Sucralose, aspartame, and saccharin have been shown to disrupt the balance and diversity of gut microbiota(Nettleton 2016). Sugar alcohols which are commonly used as artificial sweeteners are also FODMAPs and have been associated with osmotic diarrhoea in addition to their effects on the microbiota (Mäkinen 2016).
Certain emulsifiers commonly found in processed foods can also affect the gut (Chassaing 2015). One study found that mice fed two common emulsifiers, carboxymethylcellulose and polysorbate-80, led to changes in gut microbiota which appeared to contribute to inflammation (Chassaing 2015).
The effect of antibiotics on gut microbiota is well documented showing a long term reduction
in bacterial diversity after use of antibiotics. Significant antibiotic use around the world is for agriculture, with low doses routinely given to livestock to increase growth (Blaser 2016). While several observational studies suggest that antibiotic use in humans may contribute to obesity, interventional studies have shown variable results, and further research is needed (Reijnders 2016).