The popularity of yoga practice has risen sharply in recent years. In 2006, already 2.6 million people in Germany practiced yoga regularly (1). The arguments for yoga are widely spread in the population, for example the energy and immune function are increased and back pain, arthritis and stress are relieved (2). For others, the practice of yoga is an important factor in doing something good for themselves, while for others the discipline and control of the body is more in focus.

But, where does yoga come from?
The yoga tradition originates from India, the religion of Buddhism, and has a philosophical background with original roots reaching back over 2000 to 5000 years. The term “yoga” comes from the word “yui”, which has its origin in Sanskrit, a very ancient Indian language, and means “unite”. Accordingly, yoga refers to the union of body, mind and soul (3).

What exactly does a yoga practice involve?
In western countries the focus is especially on the Asana practice, the postures. The postures can be lying, sitting or standing and should be performed as attentively as possible. All Asanas have associated Sanskrit names and also pictorial names such as the Cobra (Bhujangasana) or the down looking dog (Adho Mukha Svanasana). Further essential elements are the breathing techniques (Pranayama), where the breath is consciously directed (e.g. Kapalabathi, alternative breathing) and the meditation (Dhyana), where the mind is consciously directed, by calming down, insight can be attained and a state of deep relaxation can be achieved.

But, can yoga really have a positive effect on mental and physical health?
In view of the study and literature available, YES! A meta-analysis results that yoga is effective as a complementary treatment for psychiatric disorders such as schizophrenia, depression, anxiety, and posttraumatic stress disorder (4).

Yoga can have a positive influence on the reduction of depression symptoms, the reduction of stress and anxiety, and can lead to an increase in self-love, awareness and life satisfaction (5, 6). On the physiological level, the results can also be found in the reduction of the stress hormone cortisol (7).

In the case of anxiety disorders, relaxation is a central component of yoga practice. Clients lack confidence, courage and stability, so that autogenic training, progressive muscle relaxation and deep relaxation can be beneficial.

In the presence of eating disorders, yoga can make an important contribution to increasing body satisfaction, awareness and receptivity as well as reducing self-objectivity and psychological symptoms (8). Prevention programs with concentration on yoga appear promising, as body satisfaction and social self-concept have been increased and bulimic symptoms reduced.

Conclusion: The integration into the health system for prevention and complementary therapy seems to be reasonable and as Mind Body Therapy, integrated into the treatment concept, positive effects on mental health can be achieved. In addition to body awareness, yoga concentrates on personal awareness and self-love and has an effect on the emotional, mental, cognitive and physical body levels. The yoga classes can be specifically adapted to the needs of the participants and can be set up in a disorder-specific way.

Advantages of yoga as a complementary therapy:
– Lower costs
– At the same time positive effect on the body
– No side effects
– Preventive and therapeutic support
– Less time required
– New contacts

What do you need to consider?
1. Choice of Yoga-Studio (atmosphere, costs, course offers)
2. Yoga teacher (e.g. education of teacher, authentic)
3. Yoga style (discover your preference, adapt to your daily state, examples follow)

– Vinyasa = flowing asanas, activating, breath and asanas in harmony
– Hatha = origin, breathing exercises, meditation, gentle asanas
– Ashtanga = powerful, always constant flowing sequences, condition
– Yin = relaxing, longer lasting asanas, calm, passive
– Acro Yoga = combination of acrobatics and yoga
– Kundalini = spiritual, mantras singing, meditation, energies

REFERENCES

  1. Klatte, R., Pabst, S., Beelmann, A. & Rosendahl, J. S. (2016). The efficacy of body-oriented yoga in mental disorders. Deutsches Arzteblatt international, 113 (20), 359. https://doi.org/10.3238/arztebl.2016.0195.
  2. Cramer, H., Ward, L., Steel, A., Lauche, R., Dobos, G. & Zhang, Y. (2016). Prevalence, Patterns, and Predictors of Yoga Use: Results of a U.S. Nationally Representative Survey. American journal of preventive medicine, 50 (2), 230–235.
  3. Jaquemart, P. & Elkefi, S. (1995). Yoga als Therapie. Lehrbuch für die Arzt und Naturheilpraxis. Augsburg: Weltbild Verlag.
  4. Cabral P, Meyer HB, Ames D. (2011). Effectiveness of yoga therapy as a complementary treatment for major psychiatric disorders: A meta-analysis. Prim Care Companion CNS Disord. 2011;13:pii: PCC10r01068.
  5. Ponte, S. B., Lino, C., Tavares, B., Amaral, B., Bettencourt, A. L., Nunes, T. et al. (2019). Yoga in primary health care. A quasi-experimental study to access the effects on quality of life and psychological distress. Complementary therapies in clinical practice, 34, 1–7. https://doi.org/10.1016/j.ctcp.2018.10.012
  6. Snaith, N., Schultz, T., Proeve, M. & Rasmussen, P. (2018). Mindfulness, self-compassion, anxiety and depression measures in South Australian yoga participants: implications for designing a yoga intervention. Complementary therapies in clinical practice, 32, 92–99. https://doi.org/10.1016/j.ctcp.2018.05.009
  7. Bershadsky, S., Trumpfheller, L., Kimble, H. B., Pipaloff, D. & Yim, I. S. (2014). The effect of prenatal Hatha yoga on affect, cortisol and depressive symptoms. Complementary therapies in clinical practice, 20 (2), 106–113. https://doi.org/10.1016/j.ctcp.2014.01.002
  8. Neumark-Sztainer, D. (2014). Yoga and eating disorders: is there a place for yoga in the prevention and treatment of eating disorders and disordered eating behaviours? Advances in eating disorders (Abingdon, England ), 2 (2), 136 145. https://doi.org/10.1080/21662630.2013.862369

 

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Cigarette smoking may give immediate pleasure but is dangerous for your health. Smoking may be seen as a way to deal with feelings like anxiety and stress and may be viewed as a way of coping with everyday life. Smoking a cigarette may also be used as a reward, and as part of a celebration of big and small victories. But what happens to your mental well-being if you quit smoking?

Smoke cessation is one of the best things, if not the best, you can do for your health! Smoking is ranked as the second leading cause of death by a body called “the Global Burden of Disease 2017 Risk Factor Collaborators”.1 Quitting smoking lowers your risk of cardiovascular diseases and your risk of cancer. 2 But does this come at a price concerning your mental health – how is that impacted by quitting smoking?

A systematic review of 26 studies assessing mental health before and after smoking cessation found that quitting was associated with mental health benefits. 3 Assessment of mental health were made both in the general population and in clinical populations, including persons with physical or psychiatric conditions. In the included studies, the assessment of mental status at least 6 weeks after cessation was compared with the baseline assessment. Smoking cessation was associated with improvements in levels of anxiety, depression, stress and psychological quality of life. The authors point to clinicians to recommend smoking cessation interventions also among smokers with mental health problems.

There are several aides to be used by smoke quitters. These span from brief advice to nicotine replacement therapy. How do you get help for smoking cessation? Talk to your doctor about it! And don’t give up if you fail at a quit attempt! Each attempt will bring you closer to the status “former smoker”.

REFERENCES:

  1. Collaborators GBDRF. Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 2018;392:1923-94.
  2. https://www.who.int/tobacco/quitting/benefits/en/
  3. Taylor G, McNeill A, Girling A, Farley A, Lindson-Hawley N, Aveyard P. Change in mental health after smoking cessation: systematic review and meta-analysis. BMJ 2014;348:g1151. https://www.bmj.com/content/348/bmj.g1151

 

 

 

 

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Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopment disorder characterized by inattention or hyperactivity–impulsivity, or both. It might seem paradoxical, but many studies indicate that individuals with a diagnosis of ADHD suffer from overweight and obesity. Therefore, it is important to understand the underlying mechanism that put individuals with ADHD at risk for obesity.

 Evidence from within-individual study
A systematic review and meta-analysis (1) based on 728,136 individuals from 42 studies, suggested a significant association between ADHD and obesity both in children/adolescents and adults. The pooled prevalence of obesity was increased by about 70% in adults with ADHD and 40% in children with ADHD compared with individuals without ADHD. However, due to the lack of longitudinal and genetically-informative studies, the meta-analysis was unable to explain the exact direction of association and the underlying etiologic mechanisms. There are several potential explanations:

  • ADHD causing obesity: The impulsivity and inattention components of ADHD might lead to disordered eating patterns and poor planning lifestyles, and further caused weight gain.
  • Obesity causing ADHD: Factors associated with obesity, for example dietary intake, might lead to ADHD-like symptoms through the microbiota-gut-brain axis.
  • ADHD and obesity may share etiological factors: ADHD and obesity may share dopaminergic dysfunctions underpinning reward deficiency processing. So the same biological mechanism may lead to both ADHD and obesity. This is difficult to investigate within individuals, but family studies can help to test this hypothesis.

We will further investigate these possibilities in the Eat2beNICE research project by using both perspective cohort study and twin studies.

Evidence from a recent within-family study
Recently, a population-based familial co-aggregation study in Sweden (2) was conducted to explore the role of shared familial risk factors (e.g. genetic variants, family disease history) in the association between ADHD and obesity. They identified 523,237 full siblings born during 1973–2002 for the 472,735 index males in Sweden, and followed them until December 3, 2009. The results suggest that having a sibling with overweight/obesity is a risk factor for ADHD. This makes it likely that biological factors (that are shared between family members) increase the risk for both ADHD and obesity.

Evidence from across-generation study
Given that both ADHD and obesity are highly heritable complex conditions, across-generation studies may also advance the understanding of the link between ADHD and obesity.

A population-based cohort study (3) based on a Swedish nationwide sample of 673,632individuals born during 1992-2004, was performed to explore the association between maternal pre-pregnancy obesity and risk of ADHD in offspring. The sibling-comparison study design was used to test the role of shared familial factors for the potential association. The results suggest that the association between maternal pre-pregnancy obesity and risk of ADHD in offspring might be largely explained by shared familial factors, for example, genetic factors transmitted from mother to child that contribute to both maternal pre-pregnancy obesity and ADHD.

Together, based on previous evidence from various study designs, there is evidence to suggest that the association between ADHD and obesity mainly is caused by shared etiological factors. However, future studies on different population are still needed to further test these findings.

REFERENCES:
1. Cortese S, Moreira-Maia CR, St Fleur D, Morcillo-Penalver C, Rohde LA, Faraone SV. Association Between ADHD and Obesity: A Systematic Review and Meta-Analysis. The American journal of psychiatry. 2016;173(1):34-43.

2. Chen Q, Kuja-Halkola R, Sjolander A, Serlachius E, Cortese S, Faraone SV, et al. Shared familial risk factors between attention-deficit/hyperactivity disorder and overweight/obesity – a population-based familial coaggregation study in Sweden. J Child Psychol Psychiatry. 2017;58(6):711-8.

3. Chen Q, Sjolander A, Langstrom N, Rodriguez A, Serlachius E, D’Onofrio BM, et al. Maternal pre-pregnancy body mass index and offspring attention deficit hyperactivity disorder: a population-based cohort study using a sibling-comparison design. Int J Epidemiol. 2014;43(1):83-90.

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Why 12 genetic markers for ADHD are exciting news for New Brain Nutrition

We are finally here: for the first time, genome-wide significant markers are identified that increase the risk for Attention Deficit / Hyperactivity Disorder (ADHD). This research was conducted by an international consortium of more than 200 experts on genetics and ADHD, and includes several researchers that are also involved in our Eat2beNICE project (the scientific basis of this New Brain Nutrition website). The findings were recently published in the prestigious journal “Nature Genetics” and will greatly advance the field of ADHD genetics research.

Why is this finding so important?

The genetics of ADHD are very complex. While ADHD is highly heritable, there are likely to be thousands of genes that contribute to the disorder. Each variant individually increases the risk by only a tiny fraction. To discover these variants, you therefore need incredibly large samples. Only then can you determine which variants are linked to ADHD. The now published study by Ditte Demontis and her team combined data from many different databases and studies, together including more than 55,000 individuals of whom over 22,000 had an ADHD diagnosis.

We can now be certain that the twelve genetic markers contribute to the risk of developing ADHD. Their influence is however very small, so these markers by themselves can’t tell if someone will have ADHD. What’s interesting for the researchers is that none of these markers were identified before in much smaller genetic studies of ADHD. So this provides many new research questions to further investigate the biological mechanisms of ADHD. For instance, several of the markers point to genes that are involved in brain development and neuronal communication.

Why are our researchers excited about this?

A second important finding from the study is that the genetic variants were not specific to ADHD, but overlapped with risk of lower education, higher risk of obesity, increased BMI, and type-2 diabetes. If genetic variants increase both your risk for mental health problems such as ADHD, and for nutrition-related problems such as obesity and type-2 diabetes, then there could be a shared biological mechanism that ties this all together.

We think that this mechanism is located in the communication between the gut and the brain. A complex combination of genetic and environmental factors influence this brain-gut communication, which leads to differences in behaviour, metabolism and (mental) health.genetic markers for adhd

The microorganisms in your gut play an important role in the interaction between your genes and outside environmental influences (such as stress, illness or your diet). Now that we know which genes are important in ADHD, we can investigate how their functioning is influenced by environmental factors. For instance, gut microorganisms can produce certain metabolites that interact with these genes.

The publication by Ditte Demontis and her co-workers is therefore not only relevant for the field of ADHD genetics, but brings us one step closer to understanding the biological factors that influence our mental health and wellbeing.

Further Reading

Demontis et al. (2018) Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature Genetics. https://www.nature.com/articles/s41588-018-0269-7

The first author of the paper, Ditte Demontis, also wrote a blog about the publication. You can read it here: https://mind-the-gap.live/2018/12/10/the-first-risk-genes-for-adhd-has-been-identified/

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What is inflammation?

Inflammation is the response of the body’s immune system against external factors that can put your health in danger. When this system feels it is attacked by something that may harm your health, it activates some molecules that are called cytokines in order to neutralize or avoid any damage so you can be safe.

Why is inflammation bad? What does it do?

Inflammation isn’t bad by itself, since its purpose is to protect our body. In some cases however, when the duration of this response is extended for too long- I’m talking about years- it can cause harmful effects to your health. Especially, it can affect the brain by active transport of cytokines throughout this organ.

Neuro-inflammation may occur if this process continues past early stages. Neuro-inflammation plays an important role in the development of mental diseases such as attention-deficit/hyperactivity disorder (ADHD), autism, schizophrenia, depression, anxiety, bipolar disorder (BD), and obsessive-compulsive disorder (OCD), where elevated levels of inflammation have been found(1).

What causes inflammation? 

Inflammation can occur by different factors. Some of them could be: pathogens, injuries, chronic stress, and diseases like dermatitis, cystitis or bronchitis to mention a few.

Nutritional factors like overweight and poor diet quality can also trigger this process by increasing fat accumulation in our cells and damaging them (2). The exact mechanisms that are involved in these processes are still in research.

What decreases inflammation?

Research has found that adhering to a healthy diet, like the Mediterranean diet, characterized by high intake of fruit, vegetables, whole grains, fish, lean meats and nuts, can decrease inflammation and protect you against depressive symptoms and anxiety (3,4).

There is evidence that prebiotics, probiotics and synbiotics (a combination of prebiotics and probiotics) can also help lowering inflammation. In addition, you should avoid eating pro-inflammatory foods that have been found to increase the risk of inflammation, and with it mental disorders. Some of these are refined carbohydrates, beverages with a lot of sugar added like soda, juice and sports drinks, processed meat and foods high in saturated fats (5).

What are anti-inflammatory foods

Anti-inflammatory foods are the contrast of pro-inflammatory foods. These are foods that have been found to promote or induce low levels of inflammation in our body, which may protect us against neurological disorders. Briefly, these foods include fruits, vegetables, olive oil, fish and spices like curcuma (turmeric).

Here’s what YOU can do to minimize inflammation and improve your mental health.

Inflammation and Foods

This was co-authored by Josep Antoni Ramos-Quiroga, MD PhD psychiatrist and Head of Department of Psychiatry at Hospital Universitari Vall d’Hebron in Barcelona, Spain. He is also professor at Universitat Autònoma de Barcelona.

Sources

  1. Mitchell RHB, Goldstein BI. Inflammation in children and adolescents with neuropsychiatric disorders: A systematic review. J Am Acad Child Adolesc Psychiatry [Internet]. Elsevier Inc; 2014;53(3):274–96. Available from: http://dx.doi.org/10.1016/j.jaac.2013.11.013
  2. Ogłodek EA, Just MJ. The Association between Inflammatory Markers (iNOS, HO-1, IL-33, MIP-1β) and Depression with and without Posttraumatic Stress Disorder. Pharmacol Reports [Internet]. 2018;70:1065–72. Available from: https://www.sciencedirect.com/science/article/abs/pii/S1734114017305923
  3. Lassale C, Batty GD, Baghdadli A, Jacka F, Sánchez-Villegas A, Kivimäki M, et al. Healthy dietary indices and risk of depressive outcomes: a systematic review and meta-analysis of observational studies. Mol Psychiatry [Internet]. Springer US; 2018;1. Available from: http://www.nature.com/articles/s41380-018-0237-8
  4. Phillips CM, Shivappa N, Hébert JR, Perry IJ. Dietary inflammatory index and mental health: A cross-sectional analysis of the relationship with depressive symptoms, anxiety and well-being in adults. Clin Nutr. 2017;37.
  5. Shivappa N, Bonaccio M, Hebert JR, Di Castelnuovo A, Costanzo S, Ruggiero E, et al. Association of proinflammatory diet with low-grade inflammation: results from the Moli-sani study. Nutrition. 2018;54:182–8.

 

 

 

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Have you experienced drowsiness after eating a large meal? Has an important presentation made your stomach turn? Seeing a special someone made you feel butterflies in your stomach? If you have (and you most likely have), then you know how strong the connection between the brain and the gut is.

Scientists have found that many chronic metabolic diseases, type 2 diabetes, mood disorders and even neurological diseases, such as Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS) and multiple sclerosis, are often associated with functional gastrointestinal disorders (1). The importance of the association between the gut and the brain is gaining momentum with each new study. However, the way HOW the signaling between these two integral parts of the body exactly works hasn’t been clear until recently.

It was thought for a long time that the only “communication channel” between the gut and the brain was the passive release of hormones stimulated by the consumed nutrients. Hormones entered the bloodstream and slowly notified the brain that the stomach is full of nutrients and calories. This rather slow and indirect way of passing messages takes from minutes to hours.

But now, a recent study (2) has elegantly proven that the gut can message the brain in seconds! Using a rabies virus enhanced with green fluorescence, the scientists traced a signal as it traveled from the intestines to the brainstem of mice, crossing from cell to cell in under 100 milliseconds – faster than the blink of an eye.

The researchers had also noticed that the sensory cells lining the gut were quite similar to the receptors in the nose and on the tongue (3). The effects, however, differ. In the mouth, the taste of fatty acids triggers signals to increase hunger, whereas in the small intestine, fatty acids trigger signals of satiety. This means that the discovered “gut feeling” might be considered as a sixth sense, a way of how the brain is being signaled when the stomach is full.

This new knowledge will help to understand the mechanism of appetite, develop new and more effective appetite suppressants and help those struggling with weight and problematic eating patterns.

REFERENCES
(1) Pellegrini C et al (2018) Interplay among gut microbiota, intestinal mucosal barrier and enteric neuro-immune system: a common path to neurodegenerative diseases? Acta Neuropathol 136:345. doi:10.1007/s00401-018-1856-5

(2) Kaelberer et al (2018) A gut-brain neural circuit for nutrient sensory transduction. Science 361(6408):eaat5236. doi:10.1126/science.aat5236

(3) Bohórquez and Liddle (2015) The gut connectome: making sense of what you eat. J Clin Invest 125(3):888–890. doi:10.1172/JCI81121

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In studies about treatment for children diagnosed with Attention Deficit Hyperactivity Disorder (ADHD), it is important to use valid and reliable instruments to measure effects. A valid instrument can measure a difference in symptoms before and some time after the treatment has started. Usually questionnaires for parents and teachers are used.

In the TRACE project, currently running in the Netherlands, we are looking at the effectiveness of a dietary intervention versus care as usual, for children diagnosed with ADHD in the age group of 5-12 year old. In addition to the standard questionnaires, there is an observation instrument called the Disruptive Behavior Diagnostic Observation Schedule (DB-DOS). This instrument was added in the TRACE project as an objective measurement for changes in behavior.

DB-DOS, ADHDThe DB-DOS was originally developed to measure disruptive behavior disorders (DBD) in preschoolers1. This way, treatment effects are not only measured in an indirect way, through information of caregivers, but also in a direct observation in the clinical setting. However, the age range of the children in the TRACE project is different from the preschoolers the DB-DOS was originally intented for. That’s why the TRACE project added several tasks to the original DB-DOS, to make sure it elicits disruptive behaviours, as well as hyperactivity and impulsivity, and to make it suitable for older children. During the current trial we try to find out if the DB-DOS is also a valid measurement for older children, aged 5-12 years.

The DB-DOS uses three different interactional contexts: parent-child context, examiner-child context and parent-examiner-child context. Children will be asked to complete different tasks. Some are rather boring, or frustrating, to see if this may elicit attention problems, hyperactivity, impulsive behaviour or disruptive behaviors. The DB-DOS contains, for example, some tasks which can evoke anger or sadness and some tasks where children get the chance to cheat. The reaction of the child is observed from behind a one-way screen. The observation lasts about 60 minutes and afterwards the observed behavior is scored by the examiner through a coding system. With more evidence-based instruments, mental health problems can be targeted more efficiently and reliably.

Our final goal is earlier interventions which prevent mental health problems in these children getting more severe and spreading through other domains such as school, work, or social contacts.

We will keep you posted about the results of the DB-DOS in the TRACE project!

REFERENCE
1 Bunte, T. L., Laschen, S., Schoemaker, K., Hessen, D. J., Van der Heijden, P. G. M., & Matthys, W. (2013). Clinical Usefulness of Observational Assessment in the Diagnosis of DBD and ADHD in Preschoolers. Journal of Clinical Child & Adolescent Psychology, 42(6), p.p. 749-761.
http://dx.doi.org/10.1080/15374416.2013.773516

 

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Recently, the idea that gastrointestinal microbiota are able to affect host behaviour is gaining momentum and it is based on studies conducted with animal models but also in humans with neurological disorders. However, the mechanisms that underlay this complex interplay between gut, brain and microbiota are not completely understood. Here we discuss recent findings on how microbial products could potentially affect the gut-brain axis.

Intestinal microbiota grow through the fermentation of undigested carbohydrates that end up in the large intestine. It was shown that absence of microbes or disruption of the microbiota, led to increased populations of impaired microglia cells in mice. Microglia cells are the primary effector cells for immune signalling to the central nervous system. The presence of a complex microbiota community, was shown to be essential for proper microglia maturation and function [1].

The main products of microbial fermentation in the gut are; acetate, propionate and butyrate, collectively known as short chain fatty acids(SCFA’s). Their beneficial role in human physiology have been well described, and recently evidence suggests that these molecules are able to cross blood brain barrier [2]. Moreover, gut microbiota have been associated with the brain barrier integrity. Mice raised in absence of bacteria are reported to have reduced brain barrier integrity. Once colonized with either a butyrate or an acetate/propionate producing bacteria, significant improvements were reported in the barrier [3]. Notably the integrity of the blood-brain barrier from the germ free mice was able to be restored through the oral administration of butyrate.

Gut_Microbes and Mental HealthSCFA’s are among the molecules having the privilege to cross the blood brain barrier and access the brain directly, their role should be studied in detail.

Recent studies also demonstrate that gut microbes regulate levels of intestinal neurotransmitters. The enteric nervous system interacts with a plethora of neurotransmitters (more than 30 have been identified so far.) Actually, the bulk of serotonin production ~90%, a neurotransmitter associated with mood and appetite is located in the gut. Specialized cells known as enterochromaffin cells are the main serotonin producers in the gut. In the absence of intestinal microbiota gastrointestinal serotonin levels are depleted. However, they can be restored by the addition of a specific spore forming consortium of intestinal bacteria. Specific bacterial metabolites have been reported to mediate this effect [4].

Other intestinal microbiota have been reported also to regulate the levels of the GABA neurotransmitter. Reduced levels of GABA have been associated with anxiety, panic disorder and depression. Bacterial GABA producers have been known to exist for years but it was not until 2016 that a gut bacteria was identified as GABA consumer [5]. For example, decreased levels of bacterial GABA producers were identified in a human cohort of depressed individuals. Studies in mice reinforce these findings. Intervention with the lactic acid bacteria Lactobacillus rhamnosus (JB-1) in healthy mice reduced anxiety related symptoms (accompanied by a reduction in the mRNA expression of GABA receptors in the Central Nervous System.) Lactic acid producing bacteria have also been reported to produce GABA in several food products such as kimchi, fermented fish and cheese [6].

Collectively, our gut microbiota encodes for ~100 times more genes than the human genome. The potential for some of these microbial genes to produce compounds able to interact with the nervous system and regulate critical pathways implicated in the gut brain axis is realistic and worth being explored.

Authors Prokopis Konstanti, MSc and Clara Belzer, PhD are working in the Department of Molecular Ecology, Laboratory of Microbiology, Wageningen University, Netherlands.

Footnotes

  1. Erny, D., et al., Host microbiota constantly control maturation and function of microglia in the CNS. Nature neuroscience, 2015. 18(7): p. 965-977.
  2. Joseph, J., et al., Modified Mediterranean Diet for Enrichment of Short Chain Fatty Acids: Potential Adjunctive Therapeutic to Target Immune and Metabolic Dysfunction in Schizophrenia? Frontiers in Neuroscience, 2017. 11(155).
  3. Braniste, V., et al., The gut microbiota influences blood-brain barrier permeability in mice. Science translational medicine, 2014. 6(263): p. 263ra158-263ra158.
  4. Yano, J.M., et al., Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell, 2015. 161(2): p. 264-276.
  5. P. Strandwitz, K.K., D. Dietrich, D. McDonald, T. Ramadhar, E. J. Stewart, R. Knight, J. Clardy, K. Lewis; , Gaba Modulating Bacteria of the Human Gut Microbiome. 2016.
  6. Dhakal, R., V.K. Bajpai, and K.-H. Baek, Production of gaba (γ – Aminobutyric acid) by microorganisms: a review. Brazilian Journal of Microbiology, 2012. 43(4): p. 1230-1241.

 

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