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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Breaking news: It has long been assumed that the gut and the brain communicate not only via a slow, hormonal pathway, but that there must be an additional, faster association between gut and brain. Melanie Maya Kelberer and her colleagues from Duke University, NC, now managed to detect this connection. Their paper has just been published in the renowned journal ‘Science’.

By researching a mouse model, they were able to show that the gut and the brain are connected via one single synapse. This is how it works: A cell in the gut (the so-called enteroendocrine cell) transfers its information to a nerve ending just outside the gut. At the connecting nerve ending (the synapse), the neurotransmitter glutamate – the most important excitatory transmitter in the nervous system – passes on the information about our nutrition to small nerve endings of the vagal nerve, which spreads from the brain to the intestines.

Vagal nerveBy travelling along this vagal nerve, the information from the gut reaches the brainstem within milliseconds. The authors now state that a new name is needed for the enteroendocrine cells, now that they have been shown to be way more than that. The name ‘neuropod cells’ has been suggested. The authors interpret their findings as such, that this rapid connection between the gut and the brain helps the brain to make sense of what has been eaten. Through back-signalling, the brain might also influence the gut. In sum, this finding is an important step towards a better understanding of how the gut and the brain communicate. Findings such as this one help us to find ways to positively influence our brain states and our mental health by our food choices.

Read the original paper here: http://science.sciencemag.org/content/361/6408/eaat5236.long

Kaelberer, M.M., Buchanan, K. L., Klein, M. E., Barth, B. B., Montoya, M. M., Shen, X., and Bohórquez, D. V. (2018), A gut-brain neural circuit for nutrient sensory transduction, ​Science,
​ Vol. 361, Issue 6408

 

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The topic of adopting healthier diets is increasingly popular due to better awareness of issues like obesity, diet-related health problems and illnesses, and a general pursuit of better life quality. A large, longitudinal study in Estonia investigated how eating patterns have changed over the years, and which factors influence the food choices we make.

The Estonian Children Personality Behaviour and Health Study (ECPBHS) is a multidisciplinary study that has been going on for already 20 years. It started in 1998, when participants were 9 and 15 year-old schoolchildren from Tartu County in Estonia. The 1176 children that were included in the study in 1998 were tested again when they were 18, 25 and 33 years-old.

Through the ECPBHS, we have examined different aspects of both mental and physical health, risky behaviour, physical activity, psychosocial well-being, impulsivity and personality. An additional topic of study has also been nutrition.

To investigate whether the children in the study were eating healthy, we have analysed whether the nutrient and food intake comply with the Estonian dietary recommendations. When we compared our results with the previous studies carried out in Estonia1,2 we discovered that although the deficiency in many nutrient intakes showed fairly unhealthy food habits in Estonian schoolchildren3, there was a shift to a better average energy intake and consumption over time, and especially in comparison to the end of 1980s and the beginning of 1990s4. Throughout the years we have seen the tendency towards healthier food habits, but there is still overconsumption of fats. The consumption of fibre, as well as some of the vitamins and minerals, were below the recommendations3.

We know that the changes in society (including working patterns of men and women)5 can bring changes in the eating patterns, and when we looked at the teenagers’ eating habits6, we saw that the role of family was important in how teenagers’ eating habits were influenced. Although we saw that 18 year olds in 2001 and in 2007 were regularly eating three meals a day, there was a shift among boys to have more irregular breakfast consumption in 2007. This was offset by having school-lunch, which was higher in 2007 than in 2001.

teenage girl eating burger and softdrinkWe have also looked at the consumption of fast food and fizzy drinks and discovered that it was affected not only by age, gender, ethnic and urban environment, but it was also affected by mothers’ income and educational level7. We also found that children with certain gene polymorphism (ADRA2A C-1291G) consumed more ready-made sweet food products and sweet sour milk products.8 (Gene polymorphism (two alleles in one place) can cause abnormal gene expression or abnormal protein production, which may cause or can be associated with disease.)

What is important to remember, is that although our genes, family habits and society affect how we eat, we can still learn to make healthy food choices. So do not forget the basics: eat less sweets, and more vegetables and fruits. Fibres and fats are both important, but again, only to a certain amount.

Whatever diet one follows should be balanced, and combined with physical activity. These principles should also be taught to our children, so that they too could enjoy the benefits of a healthier diet and a more active lifestyle. Though, we have seen the tendency towards healthier food habits, there is still a room for improvement. Hopefully, we will see this improvement in our population study in the next few years.

 

Reference list:

  1. Saava, M., Pauts, V., Tšaiko, L., & Sink, R. (1995). Toitumine ja alimentaarsed ateroskleroosi riskitegurid koolieas. Eesti Arst, 4, 319-325.
  2. Grünberg, H., Mitt, K., & Thetloff, M. (1997). Food habits and dietary Intake of schoolchildren in Estonia. Scandinavian Journal of Nutrition, 41, 18-22.
  3. Gross, K. (2006). Eesti koolilaste toitainete ja toidugruppide tarbimine (BA thesis). University of Tartu.
  4. Villa, I., Alep, J., & Harro, M. (2002). Eesti koolilaste toitumine viimasel 15 aastal. Eesti Arst, 88(9), 607.
  5. Mestdag 2005; Lund & Gronow 2014
  6. Jõers-Türn, K. (2015). „Family factors influencing teenagers eating habit“ (MA thesis). University of Tartu.
  7. Alavere, H. (2007). Kiirtoidu ja gaseeritud jookide tarbimine ning seos insuliinresistentsusega Eesti koolilastel (MA thesis). University of Tartu.
  8. Mäestu, J., Villa, I., Parik, J., Paaver, M., Merenäkk,. L., Eensoo, D., Harro, M., & Harro, J. (2007). Human adrenergic α2A receptor C-1291G leads to higher consumption of sweet food products. Molecular Psychiatry 12, 520-521.
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Maladaptive or uncontrolled impulsivity and compulsivity lead to emotional and social maladjustment, e.g. addiction and crime, and underlie psychiatric disorders. Recently, alterations in microbiota composition have shown to have implications for brain and social behaviors as we have been explaining in our lasts blogs. The microbiota-gut-brain axis may be involved in this process but the mechanisms are not fully identified (1). The supplementation of probiotics can modulate the microbial community and now has been suspected to contribute to ameliorating symptoms of a psychiatric disease with possible influence on social behaviors (2). To date, no randomized controlled trial has been performed to establish feasibility and efficacy of this intervention targeting the reduction of impulsivity and compulsivity. This gave us the idea to perform a study to investigate the effects of supplementation with probiotics, working with adults with Attention Deficit Hyperactivity Disorder (ADHD) and Borderline Personality Disorder (BPD) which in most cases present high levels of impulsivity, compulsivity and aggression.

Probiotics for healthWe call our project PROBIA, which is an acronym of “PROBiotics for Impulsivity in Adults”. This study will be performed in three centers of Europe including, Goethe University in Frankfurt, Semmelweis University in Budapest and Vall d’Hebron Research Institute (VHIR) in Barcelona, the coordinator of the clinical trial. We are planning to start recruiting patients in January of 2019 and obtain the results in 2021. In our study, we will explore the effects of probiotics by measuring the change in ADHD or BPD symptoms, general psychopathology, health-related quality of life, neurocognitive function, nutritional intake, and physical fitness. The effect of the intervention on the microbiome, epigenetics, blood biomarkers, and health will be also explored by collecting blood, stool, and saliva samples.

We are looking forward to having the results of this amazing study in order to understand the mechanisms involved in the crosstalk between the intestinal microbiome and the brain. If improvement effects can be established in these patients, new cost-effective treatment will be available to this population.

 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. Desbonnet L, Clarke G, Shanahan F, Dinan TG, Cryan JF. Microbiota is essential for social development in the mouse. Mol Psychiatry [Internet]. The Author(s); 2013 May 21;19:146. Available from: http://dx.doi.org/10.1038/mp.2013.65
  2. Felice VD, O SM. The microbiome and disorders of the central nervous system. 2017 [cited 2017 Oct 16]; Available from: https://ac.els-cdn.com/S0091305717300242/1-s2.0-S0091305717300242-main.pdf?_tid=b52750d8-b2ae-11e7-819b-00000aab0f02&acdnat=1508185089_58e99184d2c0f677d79ff1dd88d02667

 

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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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We know that high-energy food (rich in refined sugars and fats) is addictive and can lead to an eating addiction and obesity. Addiction is a very severe disorder with chronic and relapsing components. People who suffer from addiction show compulsivity, persistence to seek the reward (food), and high motivation to overconsume in some cases.

Food Addictions in People and MiceTo study eating addiction, we have developed a mouse model that shows persistence to eat, high motivation for palatable food and resistance to punishment in obtaining the food. We have tested these three characteristics in several genetically identical animals and selected two extreme groups: Mice that are vulnerable to eating addiction and mice that are resilient to it.

Mice have more than 25,000 genes in their genome, and they can be turned on or turned off (‘expressed’ or ‘not expressed’) depending on certain needs or circumstances.

We are now investigating the activation status of a certain type of genes, the ones encoding the so-called microRNAs that are very important as they are involved in regulating the function of other genes. An alteration in the status of one of these genes can have numerous downstream consequences.

In particular, our studies highlighted several microRNA genes that are involved in multiple brain functions, like synaptic plasticity (variation in the strength of nerve signaling) or neuronal development. Now we will test these alterations in patients to try to find convergent abnormalities.

All this work is being done at the Department of Genetics, Microbiology & Statistics (Universitat de Barcelona) and at the Neuropharmacology lab at the Universitat Pompeu Fabra, both based in Catalonia.

Co-authored by Bru Cormand, Judit Cabana, Noelia Fernàndez

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Food is not only essential for our bodily functions, but also for our brain functioning and associated behavioural performance. Some studies have shown that eating more of a certain nutritional compound can enhance your performance. But is it really that simple? Can food supplements support our performance? While performing studies on the micronutrient tyrosine, I found out that it is not that simple, and I will tell you why.

Your food contains a range of nutrients that your body uses amongst others as energy sources and as building blocks for cells. For example, protein-rich food such as dairy, grains and seeds are made up of compounds called amino acids. Amino acids are used for different purposes in your body. Muscles use amino acids from your diet to grow. Some people take advantage of this process to increase muscle growth by eating extra protein in combination with exercise.

But amino acids also have a very important role for brain functioning; specific amino acids such as tryptophan, phenylalanine and tyrosine are precursors for neurotransmitters. Specifically tyrosine is a precursor for the neurotransmitter dopamine, which is crucially involved in cognitive processes such as short-term memory, briefly memorizing a phone number or grocery list. Ingested tyrosine from a bowl of yoghurt or a supplement is digested in your intestines, taken up into the bloodstream and then passes through the barrier between the blood stream and the brain (the blood-brain-barrier). In neurons in the brain, tyrosine is further processed and converted into dopamine. Here, dopamine influences the strength and pattern of neuronal activity and hereby contributes to cognitive performance such as short-term memory.

Short-term memory functions optimally most of the time, but can also be challenged. For example during stressful events like an exam or when faced with many tasks on a busy day, many people experience trouble remembering items. Another example is advancing age; elderly people often experience a decrease in their short-term memory capacity. These decrements in short-term memory have been shown to be caused by suboptimal levels of brain dopamine.

The intriguing idea arises to preserve or restore optimal levels of dopamine in the brain with a pharmacological tweak, or even better, using a freely available nutritional compound. Could it be that simple? Yes and no. Yes, if you eat high amounts of tyrosine, there will be more dopamine precursors going to your brain. But the effects on short-term memory vary between individuals and experiments.

Various experiments have been conducted using tyrosine supplementation to see if cognitive performance can be preserved, with mixed success.

In groups of military personnel, negative effects of stress or sleep deprivation on short-term memory were successfully countered. Subjects were asked to take an ice-cold water bath, known to induce stress, and to perform a short-term memory task [1]. In other experiments subjects remained awake during the night or performed challenging tasks on a computer in a noisy room, mimicking a cockpit [2,3].

The group that took tyrosine before or during these stressful interventions showed less decline in their short-term memory than the group that ingested a placebo compound. Tyrosine supplementation also benefitted performance on a cognitive challenge without a physical stressor, compared with performing a simpler task. Other experiments, without a physical or cognitive stressor didn’t show any differences in performance compared with a control group.

These results show that tyrosine supplementation can benefit performance on cognitive processes, such as short-term memory, but only during challenging or stressful situations that induce a shortage of brain dopamine (for review see 4,5).

However, results have also been shown to vary with age. Experiments in elderly people showed that tyrosine also influences the most challenging task compared with simple processes, but contrary to observations in younger adults, in many older adults tyrosine decreased rather than improved performance [6,7]! It seems that the effects seen in young(er) adults no longer hold in healthy aging adults. This can be due to changes in the dopamine system in the brain with aging, as well as changes in other bodily functions, such as the processing of protein and insulin. This doesn’t mean that tyrosine supplementation should be avoided all together for older adults. The results so far suggest that dosages should be adjusted downwards for the elderly body. Further testing is needed to conclude on the potential of tyrosine to support short-term memory in the elderly.

We can conclude that nutrients affect behavior, but importantly, these effects vary between individuals. So, unfortunately, one size does not fit all. To assure benefits from nutrient supplementation or diet rather than wasteful use or unintended effects, dosages should be carefully checked and circumstances of use should be considered.

REFERENCES
O’Brien, C., Mahoney, C., Tharion, W. J., Sils, I. V., & Castellani, J. W. (2007). Dietary tyrosine benefits cognitive and psychomotor performance during body cooling. Physiology and Behavior, 90(2–3), 301–307

Magill, R., Waters, W., Bray, G., Volaufova, J., Smith, S., Lieberman, H. R., … Ryan, D. (2003). Effects of tyrosine, phentermine, caffeine D-amphetamine, and placebo on cognitive and motor performance deficits during sleep deprivation. Nutritional Neuroscience, 6(4), 237–246.

Deijen, J. B., & Orlebeke, J. F. (1994). Effect of tyrosine on cognitive function and blood pressure under stress. Brain Research Bulletin, 33(3), 319–323.

van de Rest, O., van der Zwaluw, N. L., & de Groot, L. C. P. G. M. (2013). Literature review on the role of dietary protein and amino acids in cognitive functioning and cognitive decline. Amino Acids, 45(5), 1035–1045.

Jongkees, B. J., Hommel, B., Kuhn, S., & Colzato, L. S. (2015). Effect of tyrosine supplementation on clinical and healthy populations under stress or cognitive demands-A review. Journal of Psychiatric Research, 70, 50–57.

Bloemendaal, M., Froböse, M. I., Wegman, J., Zandbelt, B. B., van de Rest, O., Cools, R., & Aarts, E. (2018). Neuro-cognitive effects of acute tyrosine administration on reactive and proactive response inhibition in healthy older adults. ENeuro, 5(2).

van de Rest, O.& Bloemendaal, M., De Heus, R., & Aarts, E. (2017). Dose-dependent effects of oral tyrosine administration on plasma tyrosine levels and cognition in aging. Nutrients, 9(12).

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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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Psychobiotics are helpful bacteria (probiotics) or support for these bacteria (prebiotics) that influence the relationship between bacteria and brain. The human digestive system houses around 100 trillion of these bacteria, outnumbering the human body cells 10:1. Probiotics provide a great deal of functions vital to our well-being, like supporting the digestion process and improving the absorption of nutrients. Based on the latest research, helpful gut bacteria that can also positively affect the brain – psychobiotics – benefit people suffering from chronic stress, poor mood, or anxiety-like symptoms (1).

There are 3 ways psychobiotics can affect your mental health:

  • Brain chemicals like serotonin, dopamine, and noradrenaline can be produced in the intestines directly by gut microbiota.
  • Battling with and protecting from stress by modifying the level of stress hormones.
  • When an inflammation occurs, inflammatory agents are elevated throughout the body and brain and can cause depression and other mood and cognitive disorders. Psychobiotics can affect the brain by lowering inflammation.

Lactobacillus and Bifidobacterium are the most popular probiotics with respect to mental health (1).

Disruption of the balance of gut bacteria is quite common due to the use of different kinds of medications, antibiotics, artificial preservatives, poor food and water quality, herbicides, stress, and infections (2, 3, 4).

In order to support a healthy microbiota, one should start from eating a diverse range of foods rich in different plant sources. Foods that contain lots of fiber or are fermented also promote the growth of beneficial gut bacteria. Excessive consumption of sugar and artificial sweeteners should be minimized. Managing stress levels, exercising on a regular basis, not smoking and getting enough sleep are also important for keeping microbiota in good condition. When taking antibiotics, one should make sure to consume probiotics so the body can maintain the bacteria it needs to stay healthy.

For people needing help regarding mental health problems, psychobiotics may be a promising relief. Psychobiotics are well-adapted to the intestinal environment and naturally modulate gut–brain axis communications, thereby reducing the chance of adverse reactions.

It is possible that even simple prescribing of a particular diet may be sufficient to promote the selective proliferation of natural or therapeutically introduced psychobiotics (5). Further research focusing on the strain and dosage of psychobiotics, duration of treatment, and the nature of mental disorders will help to determine the most efficient ways of helping people to improve their mental health.

REFERENCES
Abhari A, Hosseini H (2018) Psychobiotics: Next generation treatment for mental disorders? J Clin Nutr Diet. 4:1. doi:10.4172/2472-1921.100063

Carding et al (2015) Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 26: 10.3402/mehd.v26.26191

Lozano et al (2018) Sex-dependent impact of Roundup on the rat gut microbiome. Toxicol Rep. 5:96–107. doi: 10.1016/j.toxrep.2017.12.005

Paula Neto et al (2017) Effects of food additives on immune cells as contributors to body weight gain and immune-mediated metabolic dysregulation. Front Immunol. 8:1478. doi:10.3389/fimmu.2017.01478

Kali (2016) Psychobiotics: An emerging probiotic in psychiatric practice. Biomed J. 39(3):223-224. doi:10.1016/j.bj.2015.11.004

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A hot topic these days, that one can hear more and more information about is the microbiota-gut-brain axis, the bidirectional interaction between the intestinal microbiota and the central nervous system nowadays, this has become a hot topic. We are becoming increasingly aware that gut microbiota play a significant role in modulating brain functions, behavior and brain development. Pre- and probiotics can influence the microbiota composition, so the question arises, can we have an impact on our mental health by controlling nutrition and using probiotics?

Burokas and colleagues aimed to investigate this possibility in their study (2017), where the goal was to test whether chronic prebiotic treatment in mice modifies behavior across domains relevant to anxiety, depression, cognition, stress response, and social behavior.

In the first part of the study, the researchers fed mice with prebiotics for 10 weeks. They were administered the prebiotics fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), a combination of both, or water. FOS and GOS are soluble fibers that are associated with the stimulation of beneficial bacteria such as bifidobacterium and lactobacillus.

Behavioral testing started from the third week including

  • the open field test (anxiety – amount of exploratory behavior in a new place),
  • novel object test (memory and learning – exploration time of a novel object in a familiar context), and
  • forced swimming test (depression-like behavior – amount of activity in the cylinder filled water).

Meanwhile, plasma corticosterone, gut microbiota composition, and cecal short-chain fatty acids were measured. Taken together, the authors found that the prebiotic FOS+GOS treatment exhibited both antidepressant and anxiolytic (anti-anxiety) effects. However, there were no major effects observed on cognition, nociception (response to pain stimulus), and sociability; with the exception of blunted aggressive behavior and more prosocial approaches.

In the second part, FOS+GOS or water-treated mice were exposed to chronic psychosocial stress. Behavior, immune, and microbiota parameters were assessed. Under stress, the microbiota composition of water-treated mice changed (decreased concentration of bifidobacterium and lactobacillus), which effect was reversed by treatment with prebiotics.

Furthermore, it was found that three weeks of chronic social stress significantly reduced social interaction, and increased stress indicators (basal corticosterone levels and stress-induced hyperthermia), whereas prebiotic administration protected from these effects.

After stimulation with a T-cell activator lectin (concanavalin A), the stressed, water-treated mice group presented increased levels of inflammatory cytokines (interleukin 6, tumor necrosis factor alpha), whereas in animals with prebiotics had these at normal levels.

Overall, these results suggest a beneficial role of prebiotic treatment in mice for stress-related behaviors and supporting the theory that modifying the intestinal microbiota via prebiotics represents a promising potential for supplement therapy in psychiatric disorders.

Watch YouTube Video:
https://youtu.be/E479yto8pyk

REFERENCES
Burokas, A., Arboleya, S., Moloney, R. D., Peterson, V. L., Murphy, K., Clarke, G., Stanton, C., Dinan, T. G., & Cryan, J. F. (2017). Targeting the Microbiota-Gut-Brain Axis: Prebiotics Have Anxiolytic and Antidepressant-like Effects and Reverse the Impact of Chronic Stress in Mice. Biological Psychiatry, 82(7), 472–487. https://doi.org/10.1016/j.biopsych.2016.12.031

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