A little while ago, this blog featured an entry by Annick Bosch on the TRACE study, an amazing intervention study using the Elimination Diet to treat ADHD in kids (https://newbrainnutrition.com/adhd-and-elimination-diet/). Very shortly summarized, the Elimination Diet entails that participants can only eat a very restricted set of foodstuffs for several weeks, which can greatly reduce the number of ADHD symptoms in some kids. Subsequently, new foodstuffs are added back into the diet one by one, all the time checking that ADHD symptoms do not return. This ensures that every child for which the Elimination Diet proves successful ends up with a unique diet which suppresses their ADHD symptoms.

Now this is a fascinating study, since it indicates a direct influence of diet on ADHD behavior. What we know from the neurobiology of ADHD, is that it is caused by a myriad of relatively small changes in the structure, connectivity and functioning of several brain networks 1. For the most common treatments of ADHD, like medication with methylphenidate 2, we can quite accurately see the changes these interventions have on brain functioning. However, for the Elimination Diet, this has not been studied before at all. This is why we are now starting with the TRACE-MRI study, where kids that participate in a diet intervention in the TRACE program, are also asked to join for two sessions in an MRI scanner. Once before the start of the diet, and once again after 5 weeks, when the strictest phase of the Elimination Diet concludes. In the MRI scanner, we will look at the structure of the brain, at the connectivity of the brain, and at the functioning of the brain using two short psychological tasks. We made a short vlog detailing the experience of some of our first volunteers for this MRI session.



With the addition of this MRI session, we hope to be able to see the changes in brain structure and function over the first 5 weeks of the diet intervention. This will help us establish a solid biological foundation of how diet can influence the brain in general, and ADHD symptoms specifically. It can also show us if the effect of the Elimination Diet is found in the same brain networks and systems which respond to medication treatment. And lastly, we can see if there is a difference in the brains for those participants for whom the diet has a strong effect versus those where the diet does little or nothing to improve their ADHD symptoms. This can then help us identify for which people a dietary intervention would be a good alternative to standard treatment.

We will update you on the TRACE-MRI study and on the developments in this field right here on this blog!


Faraone, S. V et al. Attention-deficit/hyperactivity disorder ­­­. Nat. Rev. Dis. Prim. 1, (2015).

Konrad, K., Neufang, S., Fink, G. R. & Herpertz-Dahlmann, B. Long-term effects of methylphenidate on neural networks associated with executive attention in children with ADHD: results from a longitudinal functional MRI study. J. Am. Acad. Child Adolesc. Psychiatry 46, 1633–41 (2007).

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Tips Against Overeating

Have you ever noticed that the type of food you eat can affect how you feel afterwards? Some food might make you wish to rest and relax, some food might give you the little extra energy you just needed. Evidence is accumulating that also in the long run, diet may play a pivotal role for your mental health. For example, it might have an effect on impulsive and compulsive behaviour [1].
But it’s not only the diet that affects our body, mind and brain – it’s also the amount of what we eat. Research shows that people don’t necessarily know what a suitable amount of food might be. Sure you can imagine that this can easily lead to obesity – which in turn can impair our general health.

A meta-analysis (that is, a study that investigates an effect among many independent studies that have been conducted so far) from 2018 came to the conclusion that serving size and the size of the tableware has an effect on the amount we eat: When offered larger-sized portions, packages or tableware, participants ate or drank more than when offered smaller-sized versions [2].

British nutritional scientists now developed a guideline for the British Nutrition Foundation (BNF) to help people estimate the suitable serving size. For example, they recommend that when having a pasta dish, you should take as much pasta for one person as fits into both of your hands (before cooking). A portion of fish or meat should be about half the size of your hand. However, this does not mean that when you eat more than one portion, you are an overeater.

According to their tipsheets, which can be found here,
one should compose his or her daily menu based on a mixture of different portions. For example, 3-4 portions of starchy carbohydrates (such as the above-mentioned pasta) are recommended daily. Their guidelines, however, offer a few handy (literally!) advises to help you get a sense of how much food you should consume, thus preventing you from overeating. With a few simple tips kept in mind, you can do some good for your physical and mental health, daily.

[1] Sarris J, Logan AC, Akbaraly TN, Amminger GP, Balanzá-Martínez V, Freeman MP, et al. Nutritional medicine as mainstream in psychiatry. Lancet Psychiatry. 2015; 2(3):271-4.
View here:

[2] Hollands GJ, Shemilt I, Marteau TM, Jebb SA, Lewis HB, Wei Y, Higgins JPT,
Ogilvie D. Portion, package or tableware size for changing selection and consumption of food, alcohol and tobacco. Cochrane Database of Systematic
Reviews 2015, Issue 9. Art. No.: CD011045. DOI: 10.1002/14651858.CD011045.pub2
View here:

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Increasing evidence is showing that the gut microbiota can alter the brain and behavior, and thus may play a role in the development of psychiatric and neurodevelopmental disorders, such as autism and schizophrenia.

Animal models are a useful tool to study this mechanism. For example, germ-free (GF) mice, which have never been exposed to microorganisms, are compared with mice exposed to microorganisms, known as conventional colonized mice (CC). Recent studies have schizophrenia and autismreported that GF animals show increased response to stress, as well as reduced anxiety and memory. In most cases, these alterations are restricted to males, in which there are higher incidence rates of neurodevelopmental disorders compared with females.

Mice, like humans, are a social species and are used to study social behavior. A recent study compared GF and CC mice using different sociability tests. GF mice showed impairments in social behavior compared with CC mice, particularly in males. Interestingly, they demonstrate that social deficits can be reversed by bacterial colonization of  the GF gut (GFC), achieving normal social behavior.

Microbiota seem to be crucial for social behaviors, including social motivation and preference for social novelty. Microbiota also regulate repetitive behaviors, characteristic of several disorders such as autism and schizophrenia.

Bacterial colonization can change brain function and behavior, suggesting that microbial-based interventions in later life could improve social impairments and be a useful tool to effect the symptoms of these disorders.

This blog was co-authored by Noèlia Fernàndez and Judit Cabana

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Real time measurements of intestinal
gases: a novel method to study how food is being digested

Researchers in Wageningen (The
Netherlands), have been able to identify for the first time, how gut microorganisms
process different types of carbohydrates by measuring in real time the intestinal
gases of mice. This is not only a novel method to understand how food is
digested but could also tell us more about the role of gut microorganisms in
gut health.

Intestinal gases

The intestinal microbiota is a diverse and
dynamic community of microorganisms which regulate our health status. The
advancement of biomolecular techniques and bioinformatics nowadays allows
researchers to explore the residents of our intestines, revealing what type of microorganisms
are there. However, studying only the microbial composition of an individual
provides limited insights on the mechanisms by which microorganisms can
interact with the rest of our body. For example, far less is understood about
the contribution of the gut microorganisms in the production of intestinal
gases such as hydrogen, methane and carbon dioxide through the breakdown of
food and how these gases affect the biochemical pathways of our bodies.

Intestinal gases consist mostly of
nitrogen, and carbon dioxide, which originate primarily from inhaled air. Hydrogen
and methane though, are produced as by-products of carbohydrate fermentation
(break down), by intestinal microorganisms. However, not all carbohydrates are
digested in the same way. For instance, food with simple sugars can be rapidly absorbed
in the small intestine unlike complex carbohydrates such as fibers, which reach
the colon where they are digested by the colonic microbiota.


Measuring hydrogen in mouse intestines

To study these interactions and gain
knowledge on how microorganisms process carbohydrates, the research team led by Evert van
Schothorst from the Human and Animal Physiology Group of Wageningen University
(WU) in collaboration with the WU-Laboratory of Microbiology fed mice two
different diets with the same nutritional values but with different types of carbohydrates
(1). The first diet contained amylopectin,
a carbohydrate which can be digested readily in the small intestine while the
second diet contained amylose, a slowly digestible carbohydrate that is
digested by intestinal microorganisms in the colon.

Animals fed the easily digestible carbohydrates
showed minimal production of hydrogen whereas the group fed with the complex
carbohydrates presented high levels of hydrogen. Moreover, the two groups were
characterized not only by distinct microbial composition (different types of
bacteria present) but also distinct metabolic profiles (short chain fatty acids),
suggesting that the type of carbohydrate strongly affects microbial composition
and function.

The importance of

Hydrogen consumption is essential in any anoxic
(without oxygen) microbial environment to maintain fermentative processes. In
the intestine it can be utilised through three major pathways for the
production of acetate, methane and hydrogen sulphide. These molecules are
critical mediators of gut homeostasis, as acetate is the most predominant short
chain fatty acid produced in mammals with evidence suggesting a role in inflammation and obesity (2). Methane, which is produced by a specific type of microorganisms,
called archaea, has been associated with constipation related diseases, such as
irritable bowel syndrome(3) and also recently with athletes’ performance (4)! Finally hydrogen sulphide
is considered to be a toxic gas, although recent findings support the notion
that it also has neuroprotective effects in neurodegenerative disorders such as
Parkinson and Alzheimer diseases (5).

To the best of our knowledge, this is the first time that food-microbiota interactions have been studied continuously, non-invasively and in real time in a mouse model. Hydrogen is a critical molecule for intestinal health and understanding its dynamics can provide valuable information about intestinal function, and deviations in conditions such as Crohn’s disease or irritable bowel syndrome (IBS).

Further reading

1. Fernández-Calleja, J.M., et al., Non-invasive continuous real-time in vivo analysis of microbial
hydrogen production shows adaptation to fermentable carbohydrates in mice.

Scientific reports, 2018. 8(1): p.


Perry, R.J., et al., Acetate mediates a
microbiome–brain–β-cell axis to promote metabolic syndrome.
Nature, 2016. 534(7606): p. 213

3. Triantafyllou, K., C. Chang, and M. Pimentel,
Methanogens, methane and gastrointestinal
Journal of neurogastroenterology and motility, 2014. 20(1): p. 31.

4. Petersen, L.M., et al., Community characteristics of the gut microbiomes of competitive
Microbiome, 2017. 5(1):
p. 98.

5. Cakmak,
Y.O., Provotella‐derived hydrogen sulfide, constipation,
and neuroprotection in Parkinson’s disease. Movement Disorders, 2015. 30(8): p.

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In my previous blogs, I explained the research questions of my study. This study will be performed in two cohorts which I will elaborate on in this current blog about early life nutrition and studying gut microbiota. The cohorts are called BIBO and BINGO.  

BIBO stands for ‘Basale Invloeden op de Baby’s Ontwikkeling’ (in English: basal influences on  infant’s development). Recruitment of this cohort started in 2006, and a total of 193 mothers and their infants were included. At age 10, 168 mothers and their children still joined the BIBO study; the attrition rate is thus low. The majority of the mothers are highly educated (76%). The number of boys (52%) and girls (48%) in this cohort are roughly equally divided. A unique aspect of the BIBO study is the number of stool samples collected in early life. Also, detailed information about early life nutrition has been recorded during the first six months of life (e.g. information on daily frequency of breastfeeding, formula feeding, and mixed feeding). Together, these stool samples and nutrition diaries provide important insights in the relations between early life nutrition and gut microbiota development. Data about children within the BIBO cohort will be collected at age 12,5 years and 14 years. At 12,5 years, the participants will be invited to the university for an fMRI scan (more information about the fMRI scan will be given in a future blog). At age 14, children’s impulsive behavior will be assessed by means of behavioral tests and (self- and mother-report) questionnaires.

BINGO stands for ‘Biologische INvloeden op baby’s Gezondheid en Ontwikkeling’ (in English: biological influences on infant’s health and development). When investigating biological influences on infant’s health and development, it is important to start before birth. Therefore, 86 healthy women were recruited during pregnancy. Recruitment took place in 2014 and 2015. One unique property of the BINGO cohort is the fact that not only mothers were recruited, but also their partners. The role of fathers is often neglected in research, and thus an important strength of this BINGO cohort. Another unique property is that samples of mothers’ milk were collected three times during the first three months of life, to investigate breast milk composition. As for many infants their diet early in life primarily consists of breast milk, it is interesting to relate breast milk composition to later gut microbiota composition and development. Currently, 79 mothers and children, and 54 fathers are still joining the BINGO study. The average age of the participants at the time of recruitment was 32 years for mothers and 33 years for the father. Majority of the parents within this cohort are highly educated (77%) and from Dutch origin (89%). The number of boys (52%) and girls (48%) in this cohort are roughly equally divided. At age 3, children’s impulsive behavior will be assessed by means of behavioral tests and mother-report questionnaires.

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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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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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