Train Loco Nation! Today we have a fantastic guest post by our friend Danny Lennon on “Gut Bacteria.” He talks about what you should know about it, what the research says, and some great take home action steps.
If you don’t know who Danny is, then after this article we highly, highly recommend you to subscribe to his amazing podcast Sigma Nutrition. We have been long time listeners and we have learned a ton from his podcast.
Without further ado, let’s learn about gut bacteria
– Chris and Eric
The human body contains ten times more bacterial cells than it does human cells. And within the bacteria of our gut, there are 3.3 million unique genes. That’s 150 times more than that of the human genome [1]. No wonder researchers have affectionately referred to the gut microbiome as “the second genome”.
Unsurprisingly then, our gut microbiota exert an influence on numerous bodily systems. The bacterial composition can affect intestinal permeability in the gut itself. The more permeable our intestinal wall, the poorer we are at regulating what gets from the environment outside into our circulation [4].
But this stretches far beyond just the health of the gut. Those microbes in our gut influence our immune function (remember the gut makes up a huge part of your immune system), as well as our endocrine system. So it’s little wonder that many areas of research have begun connecting chronic health issues with a disturbed microbiota [2].
We see connections being made with psychiatric disorders [3], obesity [5], cardiovascular disease [6], intestinal disorders [11], among many others.
So clearly the microbiome influences health. That’s not in question. The question we do need to ask though is; can the gut microbiome be adequately manipulated via diet/supplementation in order to elicit actual real world benefits?
Before we answer, some important background context is required.
What Is The Gut Microbiome?
The gut microbiome is essentially the collection of a large number of different species of bacteria that inhabit our gut. Some bacteria are beneficial to us (symbiotic), some are detrimental (pathogenic) and some are neutral (commensal) [12].
When we get a shift in composition to a microbiome where there is an imbalance, with too many pathogenic bacteria present, many negative health effects can result. This imbalance is referred to as dysbiosis.
While research has been able to point to certain classes and species of bacteria as being either beneficial or pathogenic, we are still a long way from understanding what the “optimal” composition of the gut microbiota is. In fact, it’s likely that there is no one true “optimal” composition.
Why? Because the gut microbiome is dynamic, not static. It is constantly changing based on what we come in contact with, both via diet and our environment.
However, whilst we can’t yet definitively say “this is what a healthy microbiome looks like”, we do have some clear markers of a healthy microbiome. One of the most well-supported is the presence of a high degree of bacterial diversity. It seems the more diverse our microbiome is, in terms of bacterial species present; with no one type being overly dominant, the better.
In research we generally see leaner people have more bacterial diversity in the gut than overweight and obese folks [7]. We also see a link between poor bacterial diversity and type 2 diabetes incidence. Specifically, a number of research groups have independently found a decrease of beneficial butyrate-producing bacteria in the gut microbiota of patients with type 2 diabetes compared with healthy people [13, 14].
What Factors Influence Microbiota Composition?
Things start to get pretty complicated when we start to examine the potential variables that can influence our gut microbiota. Interestingly, when the microbiota of a Hadza hunter-gatherer tribe was compared to that of urban-dwelling Italians, the Hadza had much more diverse microbiota compositions [8].
A detailed analysis of the exact reasons why is beyond the scope of this article and so for the sake of simplicity I will instead offer a brief list of the main contributors:
- Exposure to Bacteria at Birth – The gut is sterile in utero. Newborns will first come into contact with Prevotella bacteria from the birth canal/vagina, inoculating their gut with lots of bacteria (their guts are sterile in utero). Children who are born via Caesarean section do not get the early bacterial exposure that those born vaginally do.
- Over-sanitation – Bacterial exposure is important for the development of our immune system. Higher sanitation standards mean we have less exposure to microbes (particularly in the critical childhood stage of immune development) [21].
- Antibiotic Use –Antibiotics are not highly-selective; in addition to wiping out an infection they can equally cause a dwindling bacterial species in our guts. The over-zealous and indiscriminate use of antibiotics by many people in the modern world has led to problems for our microbiota.
- Stress – [19]
- Alcohol [20]
- Diet – see section below
So while I acknowledge all of these different factors play a significant role, the remainder of this article will focus only on one; diet.
Influence of Diet on Gut Microbiota
Diets with high intakes of highly-processed foods (i.e. low in fibre, high in refined carbohydrates and high in fat) are associated with dysbiosis and lack of diversity. It has been shown, most commonly in animal studies, that negative shifts in microbiota composition have occurred in response to various dietary changes; high-fat diets [16], refined carbohydrates [17] and omega-6 fatty acids [15].
There are numerous studies showing that low fiber intakes, especially fermentable or prebiotic fiber, can lead to decreased bacterial diversity or a dwindling in numbers of beneficial bacteria [18]. In fact, just a few days ago a new paper was published in the eminent journal Nature, in which researchers found that a low-fibre diet caused half of the bacterial species in the guts of mice to dwindle by almost 75%! [22]
To clarify before we move on, prebiotics are what gut bacteria “feed on” (not to be confused with probiotics which are the actual bacteria that we introduce to the gut).
Let’s examine the chain of events that occurs when we consume a food containing fermentable fibre:
- The fiber resists digestion in the small intestine, where digestion usually takes place, and makes its way down into the large intestine. Now that it’s in the large intestine it can begin to ferment or be broken down by certain bacteria in the gut.
- These bacteria break those fermentable fibers into smaller carbohydrate molecules, and these in turn can be “fed on” by other neighbouring bacteria. So these bacteria can flourish and thrive, thus promoting a healthy microbiome with a diverse make-up of beneficial bacteria.
- But secondary to that, in the same way that humans consume nutrients and produce waste, these bacteria do the same. The “waste” product of these bacteria is some type of a short-chain fatty acid (SCFA). Potentially the most important of these in relation to gut health is a SCFA called butyrate.
- Butyrate is the major energy source for the cells of our gut (colonocytes). And via a number of different mechanisms which we won’t get into, it can nourish those gut cells in the mucosal layer of the large intestine. Sufficiently high butyrate levels have been linked with a number of potential long-term health effects (such as colon cancer prevention), as well as having anti-inflammatory effects or increasing insulin sensitivity.
- These SCFA contribute to keeping the pH in the gut low. Whereas pathogenic bacteria prefer a higher pH, closer to a more neutral pH, and so an inadequate amount of SCFA may allow pH to drift upwards, hence providing a more suitable environment for pathogenic bacteria to flourish, and so potentially leading to dysbiosis.
Note there is a clear difference between fermentable and non-fermentable fiber. With non-fermentable fiber we don’t get that interaction with the gut bacteria. It just goes straight through undigested. So the benefit of non-fermentable fiber is strictly down to its ability to increase stool weight and transit time through the gut, i.e. the typical benefit of being “more regular” that the person on the street will think of when they hear the term ‘fibre’. But fermentable/prebiotic fibre can have a myriad of other benefits.
Practical Application: What Can We Do?
Probiotic Supplementation – This could be a topic for a whole other article. But to give the cliff notes, right now it seems that supplementing with probiotics mainly has benefit in an acute manner. In others words, taking a probiotic can lead to decreased localized inflammation as well as introducing some bacteria that can exert positive benefits. However, it seems that in the long-term if probiotic supplementation is stopped then there are no lasting changes to the composition of the microbiome.
Prebiotic Supplementation – Supplementing with prebiotic fiber has been linked with weight loss and improving markers in the obese, potentially via increasing numbers of bifidobacteria [9]. Other research has suggested that oligofructose supplementation has the potential to promote weight loss and improve glucose regulation in overweight adults [10].
Diet – At this point there is an important caveat to insert into the conversation; extreme caution must be taken when taking all this promising, exciting research and attempting to translate it into practical, actionable steps.
As Dr. Michael Ruscio put it on episode 97 of Sigma Nutrition Radio: “It is bad science and bad practice to take an observation in field research and then say ‘now we should make this a treatment for people’”.
The Institute of Medicine recommends a daily fiber intake of 38 grams for men and 25 grams for women. In terms of sources, fibrous veggies are the first port of call for inclusion. And if we’re talking foods with prebiotic/ fermentable fiber, then we have a few different classes:
- Resistant Starch (RS) – go for tubers, roots, green bananas, legumes, lentils, peas, nuts, carrots, rice, maize/grains.
- Oligosaccharides (inulin, FOS, GOS, XOS) – think onion, leek, asparagus, green bananas, legumes, lentils, oats, grains.
- Non-Starch Polysaccharides (NSP): β-Glucan, Pectin, Glucomannan, Gums
Each day try to have a couple of things on that list: fibrous vegetables, oats, beans, peas, lentils, nuts, onions leeks, apples, cooked and cooled potatoes, cooked and cooled parboiled rice, etc.
Take-Home Action Points
- Your gut microbiome is dynamic and changes in response to your diet and environment
- It is important to “feed” your gut microbes by consuming plenty of fermentable/prebiotic fiber in your diet.
- A majority of your diet should generally be composed of whole, nutrient-dense foods.
- Get exposure to beneficial bacteria; eat fermented foods like sauerkraut, get outside & avoid over-sanitization (you don’t need to wash your hands every time you pet the dog!).
- It is still uncertain what gut microbiota composition is “best” or all the effects of different bacterial species.
- Probiotics may have some beneficial acute effects. However, short-term use within the context of a generally poor diet (low-fibre) and lifestyle is not going to elicit any real benefit long-term.
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About Danny:
Site: http://sigmanutrition.com
Podcast: Sigma Nutrition Radio on iTunes/Stitcher
Twitter: @NutritionDanny
Instagram: dannylennon_sigmanutrition
References:
[1] Baoli Zhu , Xin Wang, Lanjuan Li, Protein & Cell, August 2010, Volume 1, Issue 8, pp 718-725 [2] Kelly et al., Front Cell Neurosci. 2015; 9: 392 [3] Dinan & Cryan ,Neurogastroenterol Motil. 2013 Sep;25(9):713-9 [4] Farhadi et al., J Gastroenterol Hepatol., 2003 May;18(5):479-97 [5] DiBaise, Frank & Mathur, Am J Gastroenterol Suppl (2012) 1:22–27 [6] Wilson Tang and Hazen, J Clin Invest. 2014 Oct 1; 124(10): 4204–4211 [7] Turnbaugh, Hamady & Gordon, Nature, Jan 22, 2009; 457(7228): 480-484 [8] Schnorr et al., Nature Communications, 15 April 2014; 5, Article number: 3654 [9] da Solva et al., Nutr Hosp. 2013 Jul-Aug;28(4):1039-48 [10] Parnell & Reimer, Am J Clin Nutr June 2009 vol. 89 no. 6 1751-1759 [11] Carding et al., Microb Ecol Health Dis. 2015; 26: 10.3402/mehd.v26.26191 [12]Lederberg & McCray, Scientist, 2001;15:8 [13] Karlsson et al., Nature, 2013;498:99–103 [14] Qin et al., Nature 2012;490:55–60 [15] de La Serre et al., Am J Physiol Gastrointest Liver Physiol. 2010 Aug; 299(2):G440-8 [16] Zhang et al., ISME J. 2010 Feb; 4(2):232-41 [17] Berg, Kelly & Farraye, Inflamm Bowel Dis. 2013 Jan; 19(1):194-204 [18] Walker et al., BMC Microbiol. 2011 Jan 10; 11():7 [19]Moloney et al., CNS Neurosci Ther. 2015 Dec 10 [20]Engen et al., Alcohol Res. 2015;37(2):223-36 [21] Arrieta et al., Front Immunol. 2014; 5: 427 [22] Sonnenburg et al., Nature, 2016; 529 (7585): 212
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