We’ve all heard it countless times before: eat your 5 a day, swap the whites for the browns, fill your cupboards with whole-grains and, whilst we’ve at it, why not swap the crisps for a handful of nuts? But, despite the relentless tips put out in the media or splurged all over your newsfeed, less than 10% of the UK adult population reached the recommended 30 g/day fibre intake in 20161. Considering that not getting adequate amounts of fibre increases overall mortality by a whopping 20-30%, I would say this is a pretty big deal. Study after study have highlighted the role high fibre diets have in preventing cardiovascular disease, stroke, coronary heart disease, Type II diabetes and colorectal cancer2. Fibre is unquestionably a key component of a healthy human diet and low fibre intake observed nationwide could be potentially contributing to the massive metabolic disease crisis.
But how does this fabulous fibrous lifeline work?
Fibres feed our friend – the gut microbiota
Each and every one of us has a massive biodiverse ecosystem thriving in our intestines – the gut microbiota. To put the diversity and expanse of the gut microbiota into some context; each human has approximately 23 thousand genes, whereas the typical gut microbiota found in just one human being contains a whopping 3 million genes.
Of course, these genes are not without effect, and contribute to our health enormously – in particular, our metabolism, physical fitness and energy levels. Discrepancies in the gut microbiota profile have been correlated with many disease states, including mental health, neurodegenerative disorders, inflammatory disorders and obesity3.
Fibre is made up of complex rope-like structures that are bound together in a meshwork. Our lowly human digestive system is unable to break down this highly-resistant structure alone using traditional enzymes that are produced endogenously in humans. Instead, we need to call upon the help of the gut microbiota to provide the machinery needed to digest fibre-rich foods. As a by-product of these break-down reactions, small metabolites known as short chain fatty acids (SCFAs) are produced. These SCFAs consist of acetate, propionate and butyrate, all of which have a range of actions that positively impact physiology. The desirable action of SCFAs is highly dependent on the complex interplay between the gut microbiota composition and the diet. A healthy, diverse gut microbiota, which provides you with SCFAs in plentiful supply, needs you to provide it with fibre so it can continue to thrive. If you don’t provide it with the fuel it needs, it will start breaking down the protective mucus layer of your gut, leading to inflammatory diseases such as IBS. You get what you give in this world.
So, SCFAs, what’s the big deal?
The gut is the key sight of SCFA biogenesis, so the neighbouring cells lining the gut have immediate access to this supply. This exposure helps the gut cells weld themselves together more tightly, reducing the “leakiness” of the gut and stopping you absorbing unwanted toxins, inflammatory mediators and even excess nutrition. However, SCFAs also enter the blood circulation, spreading them throughout the perimeters of the body and allowing them to impart a whole magnitude of benefits.
How do SCFAs benefit your body?
Number 1: SCFAs actually change which genes are expressed
Although each and every cell in your body, excluding gonad (sex) cells, contain exactly the same genetic code, they appear different and perform divergent and specialised functions. This is only possible because each cell type can “choose” which genes to express and which to silence. However, this is not a static process, and fluctuations in the signals from the surrounding environment can alter the expression levels of genes- this is known as epigenetics. One of the mechanisms by which this happens is by proteins named HDACs. They remove small carbon based groups (acetyl groups) from the histone proteins associated with DNA. The DNA in our cells is coiled, folded and tied up with histone proteins in a complex mesh, but adding or taking away acetyl groups gives an element of control of how tightly associated the strands are, and subsequently affect the likelihood of whether the gene will be switched on or off.
It has been shown that butyrate, and, to an extent, propionate, can enter cells and inhibit HDACs, stopping them from removing the acetyl groups. This ultimately changes expression of many genes, some of which are key to governing metabolism. For example, in the colon butyrate alters the expression of genes involves in transport of fats, fatty acid metabolism, energy metabolism and proteins involved oxidative stress, a condition often associated with inflammation and metabolic disease2. Additionally, butyrate increases the expression of a gene known as pyy, which codes for a peptide hormone secreted by the gut in response to a meal. PYY enters the circulation and can also modulate signals to the brain via the vagal nerve, promoting satiety and inhibiting appetite4.
Number 2: SCFAs can act as messengers, producing many signal responses
In addition to direct modulation of gene expression, SCFAs are actually able to signal via other mechanisms. Proteins; FFAR2 and FFAR3; on the surface of certain cells are receptive to SCFAs, and elicit signalling cascades when associating with them. In gut endocrine cells, these signalling cascades lead to the release of PYY, GLP-1 and other satiating gut hormones that act in key brain areas to inhibit appetite4,5. These hormones also slow the gut motility, allowing the feeling of fullness to be prolonged. FFAR3 is expressed throughout your sympathetic nervous system – the one which governs the “fight or flight” response requiring a high metabolic output (preparing your body to run from a lion or fight with a bear) – and thus, acts to balance energy expenditure and increase insulin sensitivity6. FFAR2 is expressed in adipose tissue, and, when activated, encourages the usage of fat instead of glucose as the fuel to power your body6. These effects promote a lean phenotype and protect against diabetes.
So where can you find this fibre-rich goodness?
Although “carbs” have been bad-mouthed relentlessly in society, fibre is a form of carbohydrate. Bread, pasta, rice and chips are the typical foods you may think of immediately when considering carbs. However, carbs are also found in fruits, nuts and vegetables. Even the wood making up tree trunks is predominantly cellulose – a carb. Next time you hear someone stating grandly they are “cutting out carbs” it may be useful to inform them that includes broccoli, celery and basically any type of vegetable or salad. However, be wary, many highly-processed foods claim to be rich in fibre, but are also very high in refined sugars and have had many beneficial components of the original grain stripped away. To get the recommended amount of fibre a day, you would have to eat 13 pieces of Hovis’s “wholemeal” brown bread – maybe not such a wise idea. On the other hand, getting your 5 a day is a healthier (and more pleasant) method of ensuring you hit your fibre targets. Really, you should aim to consume the natural whole grains, vegetables, nuts and fruits we evolved as a species to survive as this also provides you with many essential vitamins, minerals, antioxidants and polyphenols.
1. Roberts, Caireen, et al. “National Diet and Nutrition Survey: results from years 7 and 8 (combined) of the Rolling Programme (2014/2015–2015/2016).” (2018).
2. Reynolds, Andrew, et al. “Carbohydrate quality and human health: a series of systematic reviews and meta-analyses.” The Lancet 393.10170 (2019): 434-445.
3. Anderson, James W., Belinda M. Smith, and Nancy J. Gustafson. “Health benefits and practical aspects of high-fiber diets.” The American journal of clinical nutrition 59.5 (1994): 1242S-1247S.
4.. Shreiner, Andrew B., John Y. Kao, and Vincent B. Young. “The gut microbiome in health and in disease.” Current opinion in gastroenterology 31.1 (2015): 69.
5.. Larraufie, Pierre, et al. “SCFAs strongly stimulate PYY production in human enteroendocrine cells.” Scientific reports 8.1 (2018): 74.
6.. Tolhurst, Gwen, et al. “Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein–coupled receptor FFAR2.” Diabetes 61.2 (2012): 364-371.
7. Kimura, Ikuo, et al. “Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 (GPR41).” Proceedings of the national academy of sciences 108.19 (2011): 8030-8035.
8.. Ge, Hongfei, et al. “Activation of G protein-coupled receptor 43 in adipocytes leads to inhibition of lipolysis and suppression of plasma free fatty acids.” Endocrinology 149.9 (2008): 4519-4526.