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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ADHD and Exercise

ADHD is among the most common psychiatric disorders, with ~3% prevalence in adulthood and ~5% in childhood. ADHD has a high risk for comorbid conditions. Comorbid means that one psychiatric disorder often comes together with another psychiatric disorder. For instance mood, anxiety and substance use disorders have high comorbid rates in adults with ADHD.

Adults with ADHD are also at risk for obesity and major depressive disorders and adolescent ADHD predicts adult obesity: 40% of adults with ADHD are also obese. These are worrying numbers. Many adults who have ADHD suffer from these negative consequences that come with their mental illness.

There is a growing body of scientific evidence of the powerful effects of nutrition and lifestyle on mental health. Exercise is one of them.It helps prevent or manage a wide range of health problems and concerns, including stroke, obesity, metabolic syndrome, type 2 diabetes, depression, a number of types of cancer and arthritis. Besides that, regular exercise can help you sleep better, reduce stress, sharpen your mental functioning, and improve your sex life. Nearly all studies revolve around aerobic exercise which includes walking, jogging, swimming, and cycling.

Recent research shows that exercise might also have a positive effect on ADHD symptoms such as improving attention and cognition1,2 Additional research is needed to explore this effect further, but we can take a look at the mechanisms underlying this effect.

One of the parts in our brain that is affected by exercise is the prefrontal cortex. The prefrontal cortex plays an important role in controlling impulsive behavior and attention, and is positively influenced by exercise. Furthermore, dopamine and norepinephrine play an important role in attention regulation. Ritalin, among one of the most well-known medication for ADHD, also increases levels of dopamine.

When you exercise regularly, the basis levels of dopamine and norepinephrine rise, and even new dopamine receptors are created. These dopamine levels are also the reason why exercise therapy can be effective for people suffering from depression: low levels of dopamine are a predictor of depressive symptoms.

Taken together: people with ADHD are at risk for obesity and depression. Exercise has a positive influence on obesity, depression and ADHD. Wouldn’t it be great if we could treat people with ADHD with an exercise therapy?

The PROUD-study is currently studying the prevention of depressive symptoms, obesity and the improvement of general health in adolescents and young-adults with ADHD. PROUD establishes feasibility and effect sizes of two kinds of interventions: an aerobic exercise therapy and the effects of a bright light therapy.

Exercise and ADHDParticipants follow a 10 week exercise intervention in which they train three days a week: one day of only aerobic activities (20-40 min) and in two of these days, muscle-strengthening and aerobic activities (35 – 60 min). An app guides them through the exercises, and the intensity and duration of these exercises increase gradually. During a 24 week course changes in mood, condition, ADHD symptoms and body composition are measured.

I am really looking forward to the results of the effectiveness of this intervention in adolescents and adults with ADHD. It is great that this study tries to alter a lifestyle instead of temporarily symptom-reducing options. A healthy life is a happy life!

For more information about the PROUD-study see www.adhd-beweging-lichttherapie.nl (only in Dutch) or contact the researchers via proud@karakter.com. For more information about a healthy lifestyle and the positive effects on mental health, see our other blogs at https://newbrainnutrition.com/



  1. Kamp CF, Sperlich B, Holmberg HC (2014). Exercise reduces the symptoms of attention-deficit/hyperactivity disorder and improves social behaviour, motor skills, strength and neuropsychological parameters. Acta Paediatrica, 103, 709-714.


  1. Choi JW, Han DH, Kang KD, Jung HY, Renshaw, PF (2015). Aerobic exercise and attention deficit hyperactivity disorder: brain research. Med Sci Sports Exerc, 47, 33-39.
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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.

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.

(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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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.

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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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This month, August 2018, I started as dissemination manager at New Brain Nutrition. This means that I will make sure that the information generated in this research project is spread out to society. Together with the dissemination and communication team of New Brain Nutrition, I strive to inform and educate as many people as possible about how nutrition influences our gut, our brain and our mental health.

Now I didn’t study communication or marketing. Rather, I studied Cognitive Neuroscience and did a PhD on brain connectivity in adults with ADHD. But while doing this PhD research, I became very interested in science communication. I organised an open day, started a blog with fellow PhD students, and participated in science battles. And through these experiences I learned that for science communication the most important ingredient is a willingness to convey your story to someone else.

The art of storytelling is thought to be as old as humanity itself. People are better at remembering and comprehending stories [1] and stories attract more attention than what’s called ‘logical-scientific communication’ [2]. However, storytelling is often viewed as unfit for sharing scientific results, because a story provides a subjective interpretation of data [3]. In a good story, only the elements that contribute to the story are told, while the ones that do not match the narrative are left out. That surely is not what we want to do in science communication!

New Brain Nutrition Research through StorytellingHowever, I do think that scientists should use the art of storytelling in their science communication to non-expert audiences. There is just too much and too complex data and information out there. If we want people to hear about our findings, and understand what they mean, we need to help them to read, comprehend and remember this information. Narratives are often the best way to do this. When telling these stories, we need to make careful decisions about the goal of our story (do you want to persuade your audience of something, or is the goal comprehension?), the level of accuracy (can you use a metaphor that is not entirely accurate, in order to accurately describe a certain process in an understandable way?) and whether or not to leave out certain facts of the story [2]. These decisions can be difficult, and we might sometimes make the wrong decisions, but overall I believe that we can all learn the art of telling good, honest stories.

At the same time, science can be much more open and transparent about the data and the findings themselves. I therefore think that open science, including open access publications and data sharing, should go hand-in-hand with storytelling in science communication. Share your story, your interpretation of the data, with the public. Take them along in your reasoning, which you have developed over the years as an expert in your field. And at the same time, share your data and your findings so that those who want to can come up with their own interpretations and conclusions.

So that’s my goal: telling you the stories of our research. As accurately as possible, without hiding information or twisting plots, but in an interesting, engaging and comprehensible way. And I hope that this will be a dialogue rather than a monologue. Tell us what you think, what your questions are, what you find difficult to believe, what you want to know more about. Then together we can build the story of New Brain Nutrition.

This blogpost was inspired by a recent article in The Guardian: https://www.theguardian.com/commentisfree/2018/jul/20/our-job-as-scientists-is-to-find-the-truth-but-we-must-also-be-storytellers



[1] Schank, Roger C. & Abelson, Robert P. (1995) Knowledge and Memory:  The Real Story.  In: Robert S. Wyer, Jr (ed) Knowledge and Memory: The Real Story. Hillsdale, NJ. Lawrence Erlbaum Associates.  1-85. http://cogprints.org/636/1/KnowledgeMemory_SchankAbelson_d.html

[2] Dahlstrom, Michael F. (2014) Using narratives and storytelling to communicate science with nonexpert audiences. PNAS, 201320645. https://doi.org/10.1073/pnas.1320645111

[3] Katz, Yarden (2013) Against storytelling of scientific results. Nature methods, 10 (11). https://doi.org/10.1038/nmeth.2699


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In every classroom approximately two children are diagnosed with Attention Deficit Hyperactivity Disorder (ADHD). They struggle with attention problems and hyperactive and impulsive behavior. This has negative consequences for these children. For example, they can have difficulties learning, it puts them at risk for other psychiatric problems, and it can cause parent-child relationship problems. Therefore, children with ADHD do need some sort of treatment for optimizing the quality of their lives.

After psycho-education to the child, parents and teacher, medication is often the first choice of treatment because it is evidence-based. However, there is a growing group of parents that do not wish to medicate their child. They are concerned about the side and long-term effects. Thus, these parents seek other treatment. That is where they get stuck: which other effective treatments are available?

In order to develop new treatments, there is a growing field of research focusing on risk factors for ADHD symptoms. One of these risk factors that has been studied increasingly is nutrition. Nutrition plays a role in physical well-being, but could also play a role in psychological well-being and cognitive functioning. Consequently, dietary treatments could be an alternative treatment for children with ADHD. There is a long history of research in nutrition, but there is not enough evidence yet about the (cost-)effectiveness to implement dietary treatments in clinical health care.

Elimination DietSo far, studies examining the effectiveness of a so-called elimination diet showed the strongest effects (1). The aim of an elimination diet is to find out which products trigger ADHD symptoms. However, results of these studies are inconclusive because of several limitations. First, outcome measurements used in these studies were not objective. Second, studies suffered from a sample bias towards highly motivated and educated parents. Third, underlying mechanisms are still unknown. Fourth, long-term effects are unknown. Moreover, it is unknown if an elimination diet is more effective in reducing ADHD symptoms than a healthy diet based on the World Health Organization (WHO) guidelines (2).

We thought: can we take into account these limitations and examine the effectiveness of two dietary treatments? This resulted in the TRACE study: ‘Treatment of ADHD with Care as usual versus an Elimination diet’ (TRACE) study. This is the first study to determine the short- and long-term effectiveness and cost-effectiveness of two dietary treatments as initial addition to care as usual as a treatment trajectory for children with ADHD.

We will substantially improve upon previous studies by implementing the intervention in non-commercial mental health centers, including blinded and objective measurements, and comparing two dietary treatments with care as usual. Also, understanding the biological effects could inform clinicians to potential markers and targets for preventative or individualized treatment. For this reason, we also examine the underlying biological mechanisms (e.g. mechanisms in the gut and brain) of dietary treatments (TRACE-BIOME and TRACE-MRI studies). We collect blood, stool and saliva samples.

The TRACE study is a two arm randomized control trial: participants are randomized to either an elimination diet or a healthy diet. The comparator arm includes children who are being treated with care as usual. Currently, we included in each dietary treatment arm about half of the targeted participants (N=81 in each dietary group). In the care as usual group, we included about one third of the targeted participants (N=60).

We hope to finish inclusion around January 2020.   am really looking forward to the results and hope to share this with you in a couple of years! If you have any questions, feel free to contact us via trace@karakter.com


(1) Nigg, J. T., Lewis, K., Edinger, T., & Falk, M. (2012). Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms,         restriction diet, and synthetic food color additives. Journal of the American Academy of Child & Adolescent Psychiatry, 51(1), 86-97. https://doi.org/10.1016/j.jaac.2011.    10.015 . Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321798/

(2) Izquierdo Pulido, M. L., Ríos Hernández, A., Farran, A., & Alda, J. Á. (2015). The role of  diet and physical activity in children and adolescents with ADHD. Recent Advances in Pharmaceutical Sciences V, 2015, Research Signpost. Chapter 4, p. 51-64.  Link: http://diposit.ub.edu/dspace/bitstream/2445/67543/1/T_1444299316Munozv%204.pdf

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