The Surprising Impact Your Gut Has on Mental Health

Being aware of our gut health can go a long way to improving our mental health, which will provide us with the opportunity to live a better quality of life.

We think so much about nutrition when it comes to our physical health, such as how many calories or grams of protein we need to consume to gain this much muscle mass or lose this much fat.

With the topic of mental health being talked about more and more, it is important to consider how much our gut plays into the state of our psychological well-being.

We know the importance of the mind-muscle connection in weight training, now it is time to examine the mind-gut connection and the role it plays in our overall health.

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We think so much about nutrition when it comes to our physical health, such as how many calories or grams of protein we need to consume to gain this much muscle mass or lose this much fat.

With the topic of mental health being talked about more and more, it is important to consider how much our gut plays into the state of our psychological well-being.

We know the importance of the mind-muscle connection in weight training, now it is time to examine the mind-gut connection and the role it plays in our overall health.

Gut-Brain Axis

Even though there is an anatomical distance between our gut and our brain, there does exist a bidirectional connection between these two pieces of our body (Ma et al., 2019).

This gut–brain axis is a form of communication that includes neural, hormonal and immunological signaling between our brain and our gut which provides our gut bacteria with the ability to access the brain (Collins, Surette, and Bercik, 2012; Cryan and O'mahony, 2011).

This bidirectional relationship of the gut-brain axis is known as the "gut-brain-connection," where the brain controls gut activity, such as peristalsis (motility), the migrating motor complexes, and immunological and hormonal processes. This gut-brain axis can be disrupted due to antibiotic use, trauma repression, opiate/antidepressant side effects, brain inflammation, aging, or disuse such as eating a poor diet (Tips, 2015).

It has been found that changes in gut-brain interactions are related to gastrointestinal disorders, changes in the stress response, overall behavior, and psychiatric disorders (Dinan and Cryan, 2013).

The Microbiome

This gut-brain connection means that bacteria in our gut play a large role in what we think, do, and feel by communicating directly with the brain (Tips, 2015).

The total gut microbiota, including: bacteria, fungi, viruses, and microscopic protozoa, that make up our gastrointestinal (GI) tract is known as our microbiome (Cox and Weiner, 2018; Ma et al., 2019).

It is estimated that more than 10 trillion cells with a diversity of hundreds to thousands of microbial species are inside each human being, and there are more than one hundred times the amount of genes within the microbiome than in the human genome (Cox and Weiner, 2018).

The stability and diversity of our microbiome can be important for our overall health.

A reduction in microbial diversity or the complete absence of the gut microbiota can affect immune system function and decrease the ability to extract nutrients from our diet, generate vitamins, protect from infectious agents, educate the immune system, maintain gut barrier integrity, and impact metabolic and neurologic development (Cox and Weiner, 2018; Lach et al., 2018).

Changes in early-life microbiota has the potential to effect metabolism, immunity, and neurologic function (Cox and Weiner, 2018). The microbiota can produce neurotransmitters or digestive hormones that in turn change brain function.

Microbiota have been seen to secrete neuroactive metabolites into the circulation, modulate local immune populations that traffic to the central nervous system (CNS), and stimulate the vagus nerve to have an effect on behavior.

The enteric nervous system, within the autonomic nervous system, has both afferent and efferent function. Afferent function refers to the communication from the GI tract to the CNS while efferent function refers to the communication from the CNS to the GI tract (Cox and Weiner, 2018). Since microbiota influence the CNS, it is reasonable to consider its contribution to various neurological disorders (Ma et al., 2019).

Antibiotic use, probiotic treatments, gastrointestinal infection studies, fecal microbiota transplantation, and germ-free studies have been used to study the impact of the microbiota on brain function (Cryan and O'mahony, 2011; Dinan and Cryan, 2013). These studies have shown that microbiota can influence brain chemistry, and thus, behavior (Dinan and Cryan, 2013)

Your Gut and Mental Health

Studies support that intestinal microbiota represent a component input to the brain, influencing behavior on a real-time basis which can support the frequent coexistence of psychiatric illness in patients with irritable bowel syndrome (IBS) and inflammatory bowel diseases. These studies can support that the shifts in the microbiota contribute to the behavioral changes that occur in up to 80 percent of those with IBS, along with the behavioral changes that have been seen to accompany antibiotic therapy (Collins, Surette, and Bercik, 2012).

Depression

Major depression is a stress-related disorder where patients commonly have hypothalamic-pituitary-adrenal (HPA) changes such as increased cortisol levels in blood, increased corticotropin releasing factor (CRF) in the cerebrospinal fluid, and a failure to suppress cortisol (Dinan and Cryan, 2013).

The gut bacteria in our microbiome can influence the HPA, and so it is not very surprising to see a link between microbiota and depression. Sudo et al. (2004) found that germ-free mice have an overactive HPA when under stress. This hyper-response of the HPA was reversed by a specific Bifidobacterium strain that is a predominant bacterium in the gut of an infant. Studies have also shown that the central CRF infusion reduces the relative diversity of our gut bacteria (Dinan and Cryan, 2013).

Antidepressants are known to alter the gut microbiome and reshape the brain biochemistry of those with anxiety and depression. Some studies have shown that antibiotic use has been associated with an increased incidence of anxiety and depression (Lach et al., 2018).

Serotonin is a neurotransmitter related to depression, migraine, and other neuropsychiatric illnesses. Approximately 95 percent of serotonin is found in the GI tract while the remaining five percent is found in the brain.

Almost all serotonin in the blood comes from the GI tract (Kim and Camilleri, 2000).

Yadav et al. (2008) found that serotonin in the gut stunted bone formation through circulation, which was independent of serotonin activity in the brain. It has been found through several studies that clinical depression has been associated with low bone mass. Two cohort studies revealed that the use of selective serotonin reuptake inhibitors, the class of drugs most frequently prescribed for depression, is associated with twice the amount of annual rate of bone loss versus older antidepressants (Rosen, 2009).

Anxiety

Anxiety and depression have been shown to influence chronic gut illnesses such as inflammatory bowel diseases, including Crohn's disease and ulcerative colitis, and IBS by means of the gut–brain axis. Anxiety can impact the integrity of the gut lining and to disrupt gut motility, secretions, and mucin production, thus making changes in microbial composition or activity (Collins, Surette, and Bercik, 2012).

A study of germ-free mice showed the ability of the gut bacteria to influence brain development and anxiety specifically. The response of the HPA to mild amounts of stress is greater in germ-free mice and is normalized in mice with the administration of good bacteria such as Bifidobacterium (Collins, Surette, and Bercik, 2012). Tannock and Savage (1974) noted that stressed mice showed dramatic reductions in good bacteria such as Lactobacillus (Dinan and Cryan, 2013). Dinan and Cryan (2013) saw that the administration of probiotics, specifically Lactobacillus, decreased anxiety on several behavioral measures along with neurotransmitter receptors such as GABA. An additional study saw that good bacteria such as certain Lactobacillus strains prevented diet-induced anxiety-like behavior and improved memory, while Bifidobacterium reversed colitis-induced anxiety in mice through the vagus nerve. Also, a mixture of Lactobacillus and Bifidobacterium strains improved diabetes-induced cognitive change while improving anxiety and depression in rats (Dinan and Cryan, 2013). Greater turnover of anxiety-related neurotransmitters such as dopamine, noradrenaline, and 5-hydroxytryptamine (5‑HT) has been observed in germ-free mice, as well as changes in the levels of proteins that regulate brain development and function (Collins, Surette, and Bercik, 2012).

Aggression

Sylvia et al. (2017) found that treating Siberian hamsters with a broad-spectrum antibiotic decreased aggression. Studies have found that the microbiota can manage hormones such as testosterone, which is involved in aggressive behavior.

(Cox and Weiner, 2018).

Appetite

Even though ghrelin, known as the hunger hormone, is released in the stomach, the role of ghrelin in regulating appetite is primarily conducted centrally through the brainstem. As a result, it is possible that the management role of ghrelin in the CNS can be affected by the gut microbiota through the vagus nerve. It has been seen that germ-free mice have smaller amounts of plasma ghrelin compared to conventional mice. Serum ghrelin levels are negatively correlated with the presence of gut bacteria such as Bifidobacterium and Lactobacillus strains. It has also been seen that chronically elevated ghrelin in plasma can prevent anxiety- and depression-like behavior through ghrelin receptors (Lach et al., 2018).

Probiotics and the Gut-Brain Axis

In an animal study involving mice, it was found that ProBiotic-4, which contains strains of Bifidobacterium and Lactobacillus, improved memory deficits, cerebral neuronal and synaptic injuries, glial activation, and microbiota composition in the feces and brains.

These findings suggest that targeting gut microbiota with probiotics may have a therapeutic effect on the deficits of the gut–brain axis (Yang et al., 2019).

Another study found improvements in brain function and faster task completion times from taking probiotics (Dinan and Cryan, 2013). Furthermore, a different study found that the ingestion of probiotics by human subjects had beneficial psychological effects with a lowering of serum cortisol. The term "psychobiotics" is now used to describe probiotics that positively impact symptoms of depression or anxiety (Dinan and Cryan, 2013).

In addition, it has been found in a rat study that probiotics reduced dopamine, normalized depression-like behavior, and also changed the levels of noradrenaline and CRF in the brain. It has also been found that specific strains of probiotics normalize anxiety-like behavior and brain-derived neurotropic factor (BDNF) expression in the hippocampus of mice with colitis. Pretreatment of mice with the combination of Lactobacillus strains of bacteria prevented stress-induced memory dysfunction and normalized BDNF expression, which is linked to depression and anxiety (Collins, Surette, and Bercik, 2012).

A study that assessed the effect of a combination of Lactobacillus and Bifidobacterium strains on both human subjects and rats showed that these probiotics reduced anxiety in animals and had beneficial psychological effects with a decrease in serum cortisol in humans (Cryan and O'mahony, 2011).

Multiple animal studies have found that administration of Lactobacillus and Bifidobacterium strains decrease depressive-like behaviors. Providing Bifidobacterium strains to mice reduced anxiety levels, however the effect was lost when the vagus nerve was severed, suggesting the importance of the vagus nerve connecting the gut to our brain (Cox and Weiner, 2018). The vagus nerve is involved in the parasympathetic control of the digestive tract (Clark and Kruse, 1990). Studies such as these show the ability of probiotic strains to modulate brain and behavior (Cox and Weiner, 2018; Cryan and O'mahony, 2011).

We can see from this information that how we treat our gut is not just important for reaching our training goals, it is important for our overall well-being.

Being aware of our gut health can go a long way to improving our mental health, which will provide us with the opportunity to live a better quality of life and perform at our best.

References:

Clark, V. L., & Kruse, J. A. (1990). Clinical methods: the history, physical, and laboratory examinations. Jama, 264(21), 2808-2809.

Collins, S. M., Surette, M., & Bercik, P. (2012). The interplay between the intestinal microbiota and the brain. Nature Reviews Microbiology, 10(11), 735.

Cox, L. M., & Weiner, H. L. (2018). Microbiota signaling pathways that influence neurologic disease. Neurotherapeutics, 15(1), 135-145.

Cryan, J. F., & O'mahony, S. M. (2011). The microbiome‐gut‐brain axis: from bowel to behavior. Neurogastroenterology & Motility, 23(3), 187-192.

Dinan, T. G., & Cryan, J. F. (2013). Melancholic microbes: a link between gut microbiota and depression?. Neurogastroenterology & Motility, 25(9), 713-719.

Kim, D. Y., & Camilleri, M. (2000). Serotonin: a mediator of the brain–gut connection. The American journal of gastroenterology, 95(10), 2698.

Lach, G., Schellekens, H., Dinan, T. G., & Cryan, J. F. (2018). Anxiety, depression, and the microbiome: a role for gut peptides. Neurotherapeutics, 15(1), 36-59.

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Sudo, N., Chida, Y., Aiba, Y., Sonoda, J., Oyama, N., Yu, X. N., ... & Koga, Y. (2004). Postnatal microbial colonization programs the hypothalamic–pituitary–adrenal system for stress response in mice. The Journal of physiology, 558(1), 263-275.

Sylvia, K. E., Jewell, C. P., Rendon, N. M., John, E. A. S., & Demas, G. E. (2017). Sex-specific modulation of the gut microbiome and behavior in Siberian hamsters. Brain, behavior, and immunity, 60, 51-62.

Tannock, G. W., & Savage, D. C. (1974). Influences of dietary and environmental stress on microbial populations in the murine gastrointestinal tract. Infection and immunity, 9(3), 591-598.

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Yadav, V. K., Ryu, J. H., Suda, N., Tanaka, K. F., Gingrich, J. A., Schütz, G., ... & Mann, J. J. (2008). Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum. Cell, 135(5), 825-837.

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Topics: MENTAL HEALTH