The Brain-Bug Connection: The Link between Health Conditions and your Gut Bacteria
Our guts house a diverse eco-system of trillions of bacteria, collectively known as ‘microbiotia’. Scientists have nicknamed the gut the ‘second brain’ due to its’ vast array of neural connections.
This second brain is not responsible for your higher-cognitive thinking, rather, takes on a more subconscious, emotional role via communication along the vagus nerve. The familiar phrases ‘gut feeling’, ‘gut instinct’, and ‘butterflies in your stomach’ may be more than common figures of speech—your gut is likely the residence of intuition.
We are more bacteria than we are human, thus, it would be a fair assumption to speculate that these underrated bugs play a crucial role in maintaining our health. We are only just beginning to discover the relevance of our gut bacteria and thus far, science has revealed our microbiome is indeed connected to obesity, mental health, metabolic syndrome, insulin resistance, chronic inflammation, allergies, and immunity.
The process of bacterial colonization
The process of bacterial colonization in the gut begins prenatally through transmission from mother to fetus. According to Boulange et al., (2016) colonization of the human gut continues post birth and is impacted by factors including gestation age, antibiotic use, mode of birth delivery (C-section or natural birth), diet (breast feeding or formula), and hygiene practices. Boulange et al., (2016) state that the environment and diet during an infant’s first three years of life is critical to the acquisition of adult-like gut bacteria and to the inauguration of a bacterial-host working relationship that influences the development of both immunity and neurological health.
Both human and animal studies have illustrated the altered eco-system of the microbiome with regards to obesity.
Firmicutes and Bacteroidetes
In a comparison between lean and obese mice, there was a difference in the ratio of two dominant bacterial types: Firmicutes and Bacteroidetes. A high fat diet increases the concentration of Firmicute bacteria, reducing the endogenous production of an intestinal peptide, known as GLP-2. GLP-2 functions to reduce intestinal permeability, preventing lipopolysaccharides (LPS) from entering the plasma. Thus, when there is a reduction in GLP-2, there is an increase of LPS entering the plasma, leading to an increase in the number of calories and amount of fat being extracted from food (Boulange et al., 2016).
Human trials have shown similar results, demonstrating that the microbiota of lean vs. obese individuals responds differently to calorie content in the diet, resulting in a relative abundance of Firmicutes in obese persons (Boulange et al., 2016).
The link between LPS and chronic inflammation is based on the stealth ability of LPS to infiltrate the circulatory system, and saturate tissues such as the liver or adipose (fat) tissues, creating an immune response. Several pro-inflammatory molecules are recruited due to what the body assumes is a declaration of war, resulting in low-grade inflammation.
It is confirmed that LPS are found in lower concentrations in individuals within a healthy weight range compared to obese individuals (Boulange et al., 2016).
Are we being ‘stabbed in the gut’
Are we being ‘stabbed in the gut’ by external factors, destroying our internal microbiota? Notably, mental health disorders are commonly united by issues such as immune dysfunction and chronic, low-grade inflammation. Sound familiar? Logan et al., (2016) uses the example of depression to highlight the fact that many pro-inflammatory molecules come into the picture and can have pro-inflammatory consequences on the nervous system, interfering with neural transmission. Logan et al., (2016) stated that when lean, healthy mice are the recipients of faecal microbiotia derived from obese mice raised on a high-fat diet, significant behavioural changes are observed. These include anxious behaviour, cognitive difficulities, and repetitious behaviour.
What about the connection to gut bacteria?
In experimental studies, dietary phytochemicals from turmeric, apples, cherries, grapes, plums, and blueberries (citing only a few examples) improved behavioural aspects of stress, anxiety, and depression (Logan et al., 2016).
What about the connection to gut bacteria? These nutritious foods are also rich in fibre. By-products of fibre digestion include the production of short chain fatty acids (SCFA). These short chain fatty acids act as a food source for our gut bacteria, allowing the ‘good’ gut bugs to thrive and flourish.
We are more than just what we eat… we are also what our bacteria are eating!
While life-saving and necessary when used appropriately, Logan et al., (2016) argue that the incidence of antibiotic resistant infections is rising sharply, largely in part due to overuse or misuse. It has been proven that a large range of antibiotics has been shown to transiently or permanently shift the composition of healthy adult microbiomes, usually by depletion of several different types of bacterial strains (Logan et al., 2016). For example, oral amoxicillin exposure caused marked alterations in microbiotia composition that lasted 30 days on average and were observed for more than 2 months (Logan et al., 2016).
Some of the negative repercussions of antibiotics on the composition of gut bacteria include the use of broad spectrum antibiotics. As an alternative, narrow-spectrum antibiotics are being researched and developed in order to curtail the current dilemma of overuse (Logan et al., 2016).
Furthermore, strategies to promote, enhance, or increase the growth of good gut bacteria via the intake of probiotics has become most widely accepted as an appropriate intervention strategy.
According to Logan et al., (2016) probiotics are often seen as an approach to restore or recolonise a dysbiotic (unbalanced) microbiome, also serving as an effective treatment for a range of gastrointestinal diseases including C. difficile infection, antibiotic associated diarrhea, and acute infectious diarrhea.
Bringing it all back to pragmatic advice, it’s time to touch on what you can do to promote the growth of healthy gut flora and support your digestive system:
- Eat probiotic rich foods, such as sauerkraut, kimchi, miso, yogurt or tempeh, 2-3 times per week.
- Consume ¼ teaspoon of bitter herbs before heavy meals to enhance the flow of digestive juices.
- Ensure adequate intake of fruits and vegetables to meet your daily fibre needs. Remember, it is the production of short chain fatty acids via the intake of fibre rich foods that provide health promoting benefits.
- A squeeze of fresh lemon juice on Cruciferous vegetables will reduce the bloating and nose-pinching smells that can fire from the backside after ingestion (gives a whole new meaning to the word backfire!).
- Have a good laugh. Stress decreases stomach acid thus, decreasing the ability of your digestive system to function optimally.
- Remove any possible dietary offenders that may be exacerbating gut inflammation. These may include wheat and dairy.
- Only use antibiotics if necessary. If taking antibiotics, ensure to supplement on high-dose probiotics post antibiotic therapy.
- Spice up your life! Consume plenty of anti-inflammatory foods and spices, including brightly coloured fruits and vegetables, ginger, turmeric, cayenne, black pepper, rosemary, sage, and cinnamon.
- Get adequate sleep. Your digestive organs replenish and rejuvenate themselves when you sleep. Aim for 7-8 hours per night.
- Ensure adequate intake of prebiotic rich foods. Prebiotics feed your probiotics. These foods include (this is not an extensive list): almonds, asparagus, bananas, chicory root, endive, Jerusalem artichokes, dandelion greens, jicama, kiwi, leeks, oats, legumes, mushrooms, onions.
- Eat less refined sugar. Refined sugar promotes inflammation and may feed more of the ‘bad’ bacteria, disrupting the delicate microbiota balance.
BA, MPH (Nutrition),
Naturopath, Nutritionist, Herbalist
Boulange C, Luisa Neves A, Chilloux J, Nicholson J, Dumas M. Impact of the gut microbiota on inflammation, obesity, and metabolic disease. Genome Medicine. (2016) 8:42. Doi: 10.1186/s13073-016-0303-2.
Langdon A, Cook N, Dantas G. The effects of antibiotics on the microbiome throughout the development and alternative approaches for therapeutic modulation. Genome Medicine. (2016) 8:39. Doi: 10.1186/s13073-016-0294-z.
Logan A, Jacka F, Craig J, Prescott S. The microbiome and mental health: looking back, moving forward with lessons from allergic diseases. Clinical Psychopharmacology and Neuroscience. 2016;14(2):131-147. Retrieved from http://dx.doi.org/10.9758/cpn.2016.14.2.131.