The Few-Foods Diet Approach
It has been suggested that for a subgroup of children and adolescents with ADHD, symptoms may be the result of hypersensitivity to certain foods (1). To define whether or not food is a trigger for ADHD, children can undergo an individualised few-foods diet procedure. The procedure starts with a highly restrictive phase, in which the child eats only very few foods. If the child responds well (i.e., if ADHD symptoms subside or even disappear), foods are re-introduced one by one to find which foods are causing the ADHD symptoms. The few-foods diet approach has been criticized for being too restrictive, making adherence to the diet extremely difficult – if not impossible – especially for young people. Recently, the inventors of the few-foods diet approach put their methods to the test in clinical practice (2). In this blog post I will talk you through the results of their test, focussing on two important questions: was the few-foods diet approach feasible for children/adolescents and their parents, and, perhaps more importantly, did the diet work?

Vegetables, Rice and Meat
A total of fifty-seven Dutch children with ADHD or longstanding behavioural problems enrolled in the study. Approximately half of the children were taking psychostimulants. After an elaborate inventory of the children’s habitual eating patterns, the children started on a five-week diet consisting of lettuce, carrots, cauliflower, cabbage, beet, rice, meat and water, complemented with limited amounts of potatoes, fruits, wheat, butter, corn and honey. If behaviour did not improve within two weeks, the diet was further restricted to vegetables, rice and meat only. To support their children, parents were encouraged to adhere to the diet as well and to remove all non-allowed foods from the house. After five weeks of the diet, the next phases of the study were tailored individually. While some returned to their habitual diets (for instance, because the few-foods diet did not work), others attempted to cease stimulant treatment while maintaining the few-foods diet, and yet others proceed to the reintroduction phase.

How Feasible is the Few-Foods Diet for Children and Their Parents?
Ninety-one percent of the children (52 out of 57) completed the first five weeks of the few-foods diet. Five children could not adhere to the strict diet and dropped out. Of the 52 children who completed the first five weeks of the few-foods diet, 21 children (40%) followed the most restricted diet consisting of only vegetables, rice and meat. Thus, the vast majority of children and parents made it through the first five weeks of the few-foods diet, even when the diet consisted of only a narrow selection of vegetables, rice and meat. This is an impressive achievement on the side of the children, their parents and the professionals guiding the families.

A crucial next question is whether the children and parents were willing to take the new diet forward. Adhering to a diet for five weeks can be challenging, but adhering for much longer – up to one and a half years – is something entirely different. Of the 34 children for whom the diet seemed to work, 26 were willing to enter the reintroduction phase. Two children for whom the diet had only a small beneficial effect started the reintroduction phase as well. Of the 28 children who entered the reintroduction phase, 14 (50%) were still following the few-foods diet six months later and another three children had stopped participating in the study but intended to continue following the few-foods diet. Thus, approximately half of the children who intended to follow the few-foods diet and who benefited from it managed to adhere to the diet for at least six months, while the other half of the children did not manage.

Does the Few-Foods Fiet Work?
After five weeks, 34 out of 57 children (60%) responded well to the few-foods diet, meaning that they experienced substantially fewer or less severe symptoms of ADHD. This group included 12 children who were taking psychostimulants at the start of the study and were able to stop taking medication while on the few-foods diet. The group of responders also included at least six children who responded favourably according to the study criteria, but not to their parents’ expectation. Thus, we conclude that after five weeks, approximately half of the children benefited from adhering to the stringent few-foods diet.

A Few Things to Keep in Mind
The outcomes of the study seem favourable: the vast majority of families managed to adhere to the few-foods diet during the first five weeks, and approximately half of the children responded beneficially to the few-foods diet. In fact, in many cases, taking psychostimulants was no longer necessary. There are, however, a few things to keep in mind when interpreting these results.

First, it is likely that parents who participated in the study were biased towards a positive outcome. In other words: it is likely that parents, whose report of their child’s behaviour was the primary outcome in the study, consciously or unconsciously wanted the few-foods diet to work. The parents had invested in the few-foods diet. Not only had they spent time and effort into their child’s (and oftentimes their entire family’s) adhering to the diet, but they had also invested financially: most health insurance companies in the Netherlands do not cover the few-foods diet, thus most parents had had to pay for the dietary treatment.

Second, the study was not blinded: practitioners, parents and children inevitably knew that they were undergoing the few-foods diet. Although blinding in a few-foods diet study such as this one is impossible, the absence of blinding does increase the risk of a placebo effect. In other words, as before, there is a reasonable chance that the diet works because the children and/or parents want or expect it to work.

Third, there is no control group in the study. Normally, to establish the effect of treatment A, one compares it to the (known) effect treatment B and/or to a placebo treatment. As a result of the absence of a control group, we don’t know what exactly is causing the effect of the few-foods diet. The beneficial effect could result from the lack of allergens in the few-foods diet, but it could also result from the increased parental guidance required for the child’s adherence to the few-foods diet.

In a new study (TRACE) performed by members of the Eat2beNICE consortium, we attempt to address these concerns. For instance, some of the children participating in the new study are instructed to follow a generally healthy diet rather than the few-foods diet. Comparing the outcomes in this control group to the outcomes of the children who followed the few-foods diet tells us whether the beneficial effect of the strict few-foods diet is indeed attributable to this particular diet. More information about the new TRACE study can be found here.

Yay or Nay?
In conclusion: in a subgroup of children whose ADHD symptoms stem from an allergic reaction to food allergens, the few-foods diet may offer a viable treatment option. Although the treatment is effective after five weeks, many children and their families do not manage to adhere to the diet in the long-term. We note that part of the beneficial effect of the few-foods diet is likely not attributable to the diet itself, but rather to non-specific factors including bias and a placebo effect.


(1) Pelsser LM, Frankena K, Toorman J, Savelkoul HF, Pereira RR, Buitelaar JK. A randomised controlled trial into the effects of food on ADHD. Eur Child Adolesc Psychiatry (2009) 18:12–9. 10.1007/s00787-008-0695-7

(2) Pelsser L, Frankena K, Toorman J, and Rodrigues Pereira R (2020). Retrospective Outcome Monitoring of ADHD and Nutrition (ROMAN): The Effectiveness of the Few-Foods Diet in General Practice. Front Psychiatry. 11: 96. doi: 10.3389/fpsyt.2020.00096

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Fish is an important component of a healthy diet. Especially fatty fish types such as herring, mackerel, sardines and salmon are often mentioned in relation to brain health. Many people take fish oil capsules aiming to improve their mood or feel more focused, or even in the hopes of preventing dementia. What makes fish, and especially fatty fish, so special?

Fatty Acids
Fatty fish is a rich source of polyunsaturated fatty acids, or PUFA’s (also called omega-3 fatty acids,ω−3 fatty acids, or n−3 fatty acids). PUFA’s come in different kinds, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and α-linolenic acid (ALA). The latter, ALA, is plant-based. It is found in walnuts, chia seed, flaxseed, and vegetable oils. The other two, EPA and DHA, are found in fatty fish. Fish do not produce PUFA’s themselves. Rather, PUFA’s accumulate in fish as they eat
algae or prey fish. In fact, nowadays, to pertain the health benefits of eating fatty fish despite most
consumption fish having lived in captivity, aquaculture feed is artificially enriched with fish oil [1].

Building Block of the Brain
PUFA’s are, quite literally, building blocks of the brain. Especially DHA is highly abundant in the
human brain, where it supports proper functioning of cell membranes. To obtain enough PUFA’s for
optimal functioning, our brains depend largely on what we eat. Mammals, including humans, are
unable to synthesize ALA. This is why ALA is referred to as an essential fatty acid . When ALA is ingested, however, our body can convert it to EPA and/or DHA. Therefore, strictly speaking, DHA and EPA are not essential fatty acids. However, ALA conversion to DHA or EPA is limited: even very high levels of ALA intake cannot fully compensate for the absence of DHA or EPA in a diet [2].

Deficiencies and supplementation
Most dietary advisory bodies recommend a minimum of 200 milligrams of omega-3 fatty acids per day, which equals about one portion of fatty fish per week (see for instance the Eatwell Guide [3]). Especially in countries where fish is not a standard meal component, it can be a challenge to meet this recommendation. For specific groups such as vegetarians or vegans, meeting the recommended intake is virtually impossible. If your diet is deficient in PUFA’s, taking fish oil capsules can be a solution. In fact, gelatin-free capsules are available for vegans and vegetarians, containing PUFA’s from algae rather than from fish.

Fish Oil Capsules to Treat ADHD Symptoms?
Most children in Western countries do not meet the guidelines regarding fatty fish intake [4]. Among youths with attention-deficit hyperactivity disorder (ADHD), even fewer meet the guidelines, resulting in lower PUFA blood-serum levels in children and adolescents with ADHD as compared to their peers without ADHD [5]. This has led researchers to believe that, possibly, low PUFA blood-serum levels may cause attention problems, hyperactivity, and impulsivity. If true, high intake of fatty fish or fish oil supplementation with capsules might reduce ADHD symptoms. To test this promising hypothesis, many researchers have measured symptoms in children and adolescents before and after several weeks of fish oil treatment. Unfortunately, when researchers reviewed all of these studies up until 2012, they concluded that the majority of studies found no beneficial effect of fish oil on ADHD symptoms [6]. Note, however, that this does not preclude the possibility that fish oil supplementation may have a beneficial effect for some children or adolescents with ADHD. Moreover, even if fish oil supplementation does not improve ADHD symptoms, supplementing PUFA deficiencies may provide other health benefits for this group. For instance, it may lower the risk of cardiovascular disease [7].


[2] Burns-Whitmore B, Froyen E, Heskey C, Parker T, San Pablo G (2019). Alpha-Linolenic and Linoleic Fatty Acids in the Vegan Diet: Do They Require Dietary Reference Intake/Adequate Intake Special Consideration? Nutrients, 11(10):E2365.


[4] Sichert-Hellert W, Wicher M, Kersting M. (2009). Age and time trends in fish consumption pattern of children and adolescents, and consequences for the intake of long-chain n-3 polyunsaturated fatty acids. Eur J Clin Nutr, 63(9):1071-5

[5] Burgess JR, Stevens L, Zhang W, Peck L (2000). Long-chain polyunsaturated fatty acids in children with attention-deficit hyperactivity disorder. Am J Clin Nutr, 71(1 Suppl):27S-30S

[6] Gillies D, Sinn JKH, Lad SS, Leach MJ, Ross MJ (2012). Polyunsaturated fatty acids (PUFA) for attention deficit hyperactivity disorder (ADHD) in children and adolescents. Cochrane Database of Systematic Reviews, 7:CD007986

[7] Abdelhamid AS, Brown TJ, Brainard JS, Biswas P, Thorpe GC, Moore HJ, Deane KHO, Summerbell CD, Worthington HV, Song F, Hooper L (2020). Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews, 3: CD003177

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Every day, our brain depends on what we eat. First and foremost, the brain needs tremendous amounts of energy, that can only be derived from food. While the human brain constitutes only two percent of the body’s weight, it consumes twenty percent of our daily energy intake [1]. When we eat too little, our brain is one of the first organs to suffer and send us warning signals: we become irritable, have difficulty concentrating, and feel dizzy or light-headed. In this blog I will explain how food in your stomach is transformed into electrical activity in your brain cells.

Like most other cells in the body, brain cells (or neurons) fuel their activities with glucose. The human brain needs around 100–150 grams of glucose per day [2]. Glucose is a sugar, and sugars are carbohydrates (along with starch and certain fibers). So how does our body turn food into glucose? As an example, let’s eat an imaginary banana of exactly one hundred grams. In the stomach, the banana is mixed with stomach acids to separate its components. After water (75%), our banana consists mostly of carbohydrates, namely starch (11%) and sugars (12%). The starch is passed on to the intestines, where it will be metabolized slowly. The sugars are broken down by the stomach. About half of the sugars in bananas are glucose; the other half is fructose, which is passed on to the liver. Thus, our imaginary banana provides us with approximately six grams of glucose. This glucose is absorbed by the stomach and small intestines, and released into the bloodstream.

Fun Fact: The ripening of bananas involves converting starch to sugar. This is why yellow bananas are much sweeter and easier to digest compared to unripe green bananas.

The blood-brain barrier
When the glucose has entered the bloodstream, it rapidly spreads through the body. The heart pumps the blood past all our organs, including the brain, supplying them with vital energy. The brain, however, is not easy to reach. Because the brain is so important, it is protected by a thick fence called the blood-brain barrier. Blood on one side and cerebrospinal fluid on the other, the blood-brain barrier prevents almost all molecules from crossing. Only specific molecules that are essential for proper brain functioning are allowed through. Glucose is such an essential molecule. A dedicated transporter (called GLUT1), similar to a port to which only glucose molecules have a key, helps the glucose molecules pass. It has been estimated that – as the brain is so energy-hungry – blood-brain barrier cells transport ten times their own weight of glucose every minute [3].

Having reached the cerebrospinal fluid, glucose is now very close to its destination: the inside of a brain cell. In fact, glucose molecules and brain cells are floating around in the same fluid. The glucose is transported once more, this time by a GLUT3 transporter, from the cerebrospinal fluid into the brain cell. There, it awaits glycolysis: the glucose molecule is broken down and releases free energy to the brain cell [4]. With this energy, the brain cell is able to communicate with other cells, which, in essence, is at the basis of neuronal functioning.

1. EE Benarroch (2014). Brain Glucose Transporters: Implications for Neurologic Disease. Neurology, 82 (15), 1374-9.

2. CW Kuzawa, HT Chugani, LI Grossman, L Lipovich, O Muzik, PR Hof, DE Wildman, CC Sherwood, WR Leonard, N Lange (2014). Metabolic Costs and Evolutionary Implications of Human Brain Development. Proc Natl Acad Sci U S A, 111 (36), 13010-5.

3. SG Patching (2017). Glucose Transporters at the Blood-Brain Barrier: Function, Regulation and Gateways for Drug Delivery. Mol Neurobiol, 54 (2), 1046-1077.

4. R Bailey (Nov 2019) “Glycolysis” ThoughtCo. Retrieved from on 9 Jan 2020.

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Stress tends to mess with our eating habits. In times of stress, some people eat more, while others eat less. The type of food people eat also changes: compared to non-stressed individuals, stressed individuals more often eat unhealthy foods.

Laboratory experiments have shown that stress causes people to make unhealthier food choices. In a typical experiment, participants are exposed to an acute stressor, for instance, they are asked to present themselves before strangers, or to solve a very difficult puzzle within an unrealistically short timeframe. Unknown to the participants, the most important part of the experiment takes place during the breaks, when they are offered food and drinks. Secretly, the researchers observe exactly what the participants eat and drink. They look for differences between those who were exposed to stress prior to the break, and those who were not. And indeed, researchers do typically find differences between these groups. For instance, women who were most sensitive to stress (as shown by an exaggerated cortisol response), also ate more calories in response to stress [1]. In a second experiment, participants who had just performed several difficult tasks in front of a judge, especially those who reported being subjected to chronic stress in daily life, ate more chocolate cake and fewer vegetables compared to non-stressed participants [2].

But how do such laboratory experiments relate to real-life? After all, for most of us, giving presentations is not the most influential stressor in our lives, and real-life situations are much more complex. To investigate how real-life stressors affect food choices, one needs so-called epidemiological studies. In such studies, large groups of people are followed over longer periods of time. At multiple time points, they are asked about their stress levels (including daily hassles, work-related stress, academic stress, etc.) as well as about their eating habits. Consistent with experimental studies, epidemiological studies have shown that, on average, diet quality is lower in people who report more stress (e.g. [3] [4]). However, the effects reported in real-life studies are much smaller compared to the effects reported in the lab: in real life, stress is only one among many factors influencing your food choices.

So exactly how big ís the effect of real-life stress on our real-life food choices? We investigated this in over a hundred thousand people from the North of the Netherlands. We found that exposure to stressful life events, such as the loss of a family member or being the victim of a crime, was associated with poorer diet quality; however, the effects of stress were relatively small. For instance: on average, most people reported having dealt with one stressful life event in the past year, and their average diet quality score (on a scale of 0-48) was 23.9 points. People who reported dealing with two instead of one stressful events had an average diet quality of 23.8 points. For comparison, the difference in diet quality between the average man (22.5 points) and the average woman (24.9 points) in our study was 27 times bigger [5].

To summarize, diet quality deteriorates in times of stress. However, in real life situations, with a multitude of other factors determining what, where and when we eat, the effect of stress alone is very small.

Do you want to learn more about brain changes underlying the effect of stress on food choices? Check out this blog: by Simone Demmel.

[1] Epel, E, Lapidus, R & McEwen, B, Brownell, K (2001). Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology, 26(1), 37-49

[2] Tryon, MS, DeCant, R, Laugero, KD (2013). Having your cake and eating it too: a habit of comfort food may link chronic social stress exposure and acute stress-induced cortisol hyperresponsiveness. Physiology and behavior, 114-115, 32-37

[3] Mikolajcyk, RT, Al Ansari, W & Maxwell, AE (2009). Food consumption frequency and perceived stress and depressive symptoms among students in three European countries. Nutrition Journal, 8(1),1-8

[4] O’Connor, D, Jones, F, Conner, M, McMillan, B, Ferguson, E (2008). Effects of daily hassles and eating style on eating behavior. Health Psychology, 27(1 supplement).

[5] Schweren et al., in preparation

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A healthy diet has numerous benefits. But what does a healthy diet consist of? And how do we, researchers, measure diet quality?

What’s considered a healthy diet in one country or culture, may not be regarded as such in another. For instance, low-fat and unsweetened dairy products are regarded as healthy in my country, the Netherlands, but not in many Asian countries where a vast proportion of the population is lactose intolerant. Differences in regional availability of foods further determine dietary habits across, and even within, countries. Fish, for example, is often at the core of a healthy diet in countries surrounded by water such as Japan (48.6 kg/year per person), but not in landlocked countries such as Hungary (5.1 kg/year per person) [1].

Here I will describe six common ways in which researchers may assess diet quality in Western populations.

1. Fruit and Vegetable Consumption

Probably the quickest way to obtain an estimate of an individual’s diet quality is by assessing fruit and vegetable consumption of the individual. Generally speaking, fruits and vegetables are high in healthy nutrients such as vitamins and fibers. Moreover, fruits and vegetables often replace unhealthier options such as energy-dense snacks. Finally, while fruit and vegetable consumption is only one aspect of diet quality, it has been shown to correlate with overall diet quality. Thus, fruit and vegetable consumption can be seen as a fast but crude way to assess diet quality.

2. Total Energy Intake

One could consider calculating total energy intake as an indicator of diet quality. Generally speaking, unhealthy foods are more energy-dense than healthy foods. Therefore, high-calorie diets likely contain more unhealthy foods. Of course, this is not necessarily the case; some foods, for instance avocado, are both energy-dense and nutrient-rich. Moreover, low energy intake may result in nutritional deficits. Therefore, total energy intake is not generally used as an indicator of diet quality.

3. Mediterranean Diet Score

The Mediterranean Diet Score (MDS) measures compliance to a Mediterranean-type diet, consisting of legumes, fruits, vegetables, unrefined cereals, olive oil and fish. Points are subtracted for dairy and meat [2]. The Mediterranean diet was inspired by the eating habits of Greece and Italy, where people seem to live longer and have lower risk of heart disease compared to other Western regions.

4. Western-Type Diet Score

A Western-style diet is a modern dietary pattern, that is sometimes referred to as the Standard American Diet. A Western diet consists of red and processed meats, pre-packaged foods, fried foods, whole-fat dairy products, refined grains, potatoes and sugar-sweetened beverages, among others [3]. Contrary to most diet quality scores, a higher Western diet score indicates a less healthy diet.

5. Healthy Eating Index

The Healthy Eating Index (HEI) measures how well an individual adheres to the key recommendations of the 2015 Dietary Guidelines for Americans. These guidelines are often used by US-based nutrition and health professionals, to help people to consume a healthful and nutritionally adequate diet. A total score is calculated based on nine advised food groups/components (including fruits and vegetables, whole grains, plant proteins), and four components that should be moderated (including salt and saturated fat) [4].

6. Dietary Approaches to Stop Hypertension

The dietary approaches to stop hypertension (DASH) dietary pattern emphasizes fruits, vegetables, low-fat dairy, whole grains, nuts and legumes, and limits saturated fat, cholesterol, red and processed meats, added sugars, and sugar-sweetened beverages. It was originally developed in the US to treat hypertension without medication [5]. Several medical associations and institutions have since incorporated the diet in their clinical guidelines [6]. 


[1] Ritchie & Roser (2019). Meat and Seafood Production & Consumption. Published online at Retrieved from: on 28 August 2019

[2] Dinu, Pagliai, Casini & Sofi (2018). Mediterranean diet and multiple health outcomes: an umbrella review of observational studies and randomised trials. European Journal of Clinical Nutrition, 72(1), 30-43. doi: 10.1038/ejcn.2017.58

[3] Cordain, Eaton, Sebastian, Mann, Lindeberg, Watkins et al. (2005). Origins and evolution of the Western diet: health implications for the 21st century. American Journal of Clinical Nutrition, 81(2), 341-354. doi: 10.1093/ajcn.81.2.341

[4] US Department of Agriculture, Food and Nutrition Service. Retrieved from on 28 August 2019

[5] Sacks, Svetkey, Vollmer, Appel, Bray, Harsha et al. (2001). Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. The New England Journal of Medicine, 344(1), 3-10. doi: 10.1056/NEJM200101043440101

[6] Chiavaroli, Viguiliouk, Nishi, Mejia, Rahelic, Kahleova et al. (2019). DASH Dietary pattern and cardiometabolic outcomes: an umbrella review of systematic reviews and meta-analyses. Nutrients, 11(2), 338. doi: 10.3390/nu11020338

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Why do we eat what we eat? What makes us choose an apple over chocolate cake, or the other way around? How do we decide whether or not to have that tempting dessert, despite feeling satiated after a hearty meal? I previously wrote about how our daily food choices are, at least in part, influenced by our genetic make-up, but there are many other factors determining what, when, where and why we eat. Today I will discuss the importance of personality traits.

Personality is a set of relatively stable traits, that together determine who we are. While some characteristics of us change day by day, or even hour by hour, others are more stable. For instance, although we all feel worried from time to time, you may – generally speaking – be easily worried or nervous. The famous Big Five model of personality proposes that all people can be described in terms of five traits: neuroticism, agreeableness, openness to experience, conscientiousness and extraversion. These five traits in turn host a number of more specific characteristics, such as impulsivity, self-consciousness, anger, excitement seeking and thoughtfulness.1

What does this have to do with eating habits? Well, as it turns out, specific personality traits are associated with different food choices. Most studies look at healthy versus unhealthy food choices. A healthy diet has consistently been associated with the Big Five trait “conscientiousness”, which includes characteristics such as self-discipline, diligence, thoughtfulness and goal-orientedness. An unhealthy diet, on the other hand, has been associated with neuroticism, stress-sensitivity and impulsivity.2 Impulsivity and neuroticism have also been linked to emotional eating, binge-eating, external eating and (not surprisingly) stress-eating and impulsive eating (e.g. 3).

So, among the numerous factors influencing what, when, where and why we eat, how important are personality traits? Imagine a test in which we ask participants to choose between an apple and chocolate cake. Indeed, knowing how impulsive, neurotic and conscientious these participants are helps us better predict what they’ll choose; however, the accuracy of our prediction would improve only very slightly compared to a prediction without knowing the participants’ personality. In my own study (which is ongoing and therefore yet unpublished), I found that those with an extremely high score on an impulsivity questionnaire (i.e. higher than 97% of all other participants), on average, consumed 2192 kcal per day, compared to an average of 2030 kcal/day for those with an extremely low impulsivity score (i.e. those scoring lower than 97% of all other participants). For self-discipline, a trait belonging to the conscientiousness domain, the effect was even smaller: extremely self-disciplined people on average consumed only 112 kcal per day less compared to people with an extreme lack of self-discipline. To give you an indication, 112 kcal equals about one medium-sized cookie, or one glass of orange juice. In other words, being a conscientious person doesn’t mean one will always choose the healthy option over the unhealthy one; nor will impulsive or neurotic people always choose chocolate over apples.

Mind you, the above reported findings are associations. Although it is compelling to think that impulsivity causes us to make unhealthy food choices, it may in fact be the other way around! Perhaps an unhealthy lifestyle makes us more impulsive. We do know, for instance, that certain mental health conditions can be improved by healthier diets, suggesting that what we eat can change the way we feel and behave (rather than the other way around). This question of “direction of causality” is an important and very challenging issue that we, researchers, urgently need to tackle.

Finally, a few words on attention-deficit hyperactivity disorder (ADHD); after all, impulsivity is one of its key symptoms. Does this mean that people with ADHD make less healthy food choices? Indeed, this seems to be the case. Studies have shown that – on average – people with ADHD have less healthy eating habits4, and are more prone to overweight and obesity5,6, compared to people without ADHD. However, other factors associated with ADHD may contribute to poorer eating habits as well. For instance, lower socio-economic status makes healthier foods less accessible to people with ADHD, as healthier foods are generally more expensive; also, lower levels of education may result in people with ADHD knowing less about healthy and unhealthy lifestyles.


  1. Costa, P.T., McCrae, R.R. (1992). Revised NEO Personality Inventory (NEO-PI-R) and NEO Five-Factor Inventory (NEO-FFI) manual. Odessa, FL: Psychological Assessment Resources
  2. Stevenson (2017). Psychological correlates of habitual diet in healthy adults. Psychological Bulletin, 143(1), 53-90
  3. Keller, C. & Siegrist, M. (2015). Does personality influence eating styles and food choices? Direct and indirect effects. Appetite, 84, 128-38
  4. Ríos-Hernández, A., Alda, J.A., Farran-Codina, A., Ferreira-García, E., Izquierdo-Pulido, M. (2017). The Mediterranean Diet and ADHD in Children and Adolescents. Pediatrics, 139(2)
  5. Bowling, A.B., Tiemeier, H.W., Jaddoe, V.W.V., Barker, E.D., Jansen, P.W. (2018). ADHD symptoms and body composition changes in childhood: a longitudinal study evaluating directionality of associations. Pediatric Obesity, 13(9):567-575
  6. Chen, Q., Hartman, C.A., Kuja-Halkola, R., Faraone, S.V., Almqvist, C., Larsson, H. (2018). Attention-deficit/hyperactivity disorder and clinically diagnosed obesity in adolescence and young adulthood: a register-based study in Sweden. Psychological Medicine, 1-9 (e-pub)
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We, human beings in Western society, make over 200 food choices each day (1). That’s a lot! Fortunately (or, according to others, unfortunately), we don’t actually have to think about each and every one of them, or at least not consciously. If our food choices are not so much a conscious decision, then how do we make them? A lot has been written about external factors influencing our food choices, for instance, alluring displays in supermarkets or the availability of unhealthy foods in our day-by-day environment. In this blog, I will address the potential role of genetics on food choices: to what extent do our genes determine what we eat?

Eating behaviours are complex, i.e. they are very diverse and influenced by many different factors. When we investigate complex behaviours, we are unlikely to find simple explanations. In other words: we do not expect to find one gene that makes me prefer pizza margarita over pizza fungi, nor will we find a single gene responsible for my triple-chocolate ice cream consumption. There are, however, some instances in which specific genes have relatively simple and straightforward effects on our food choices. This is the case when genetic variants code for food sensitivities.

A famous example is the LCT gene (or, more precisely, the C>T change at 13910 bases upstream of the LCT gene in the 13th intron of the MCM6 gene). The LCT gene codes for lactase persistence, or lactose tolerance after childhood. Worldwide, the majority of people (and most other mammals, for that matter) no longer tolerate dairy products after childhood. For them, consuming milk products causes nausea, bloating and cramping within 2-3 hours. As a result, they will soon learn not to consume dairy products. Those who have the lactase persistence gene, however, don’t have any problems digesting dairy products and, thus, are more likely to consume them (2). Geographical region is important here: while in Northern European countries such as the UK and Finland, 90-100% of people tolerate dairy products, in South-East Asia and Australia this number is close to 0% (3).

A similar situation seems to occur for genes coding for certain taste receptors on the tongue. The TAS2R38 gene, for instance, makes some people extremely sensitive to bitter taste. This, of course, will cause them to avoid bitter foods such as cruciferous vegetables (4). A recent study has even identified a small number of genes that together cause people to either love or hate marmite (5)! Another gene variant (CYP1A1), coding for caffeine clearance from the body, causes carriers to drink less or more coffee and tea (6).

Thus, when food sensitivities are involved, food choices can be driven by specific genes. Most food choices, however, have very little to do with food sensitivities and are much more complex. Pizza Margarita or Pizza Funghi? Triple-chocolate ice cream today or maybe tomorrow? While for such complex food choices there is no single gene responsible, our genetic make-up still does have influence. Typically, for complex behaviours, many different genes can be identified. While each gene individually contributes only a little bit, together they can actually have quite an effect on your food choices. For instance, a recent study identified seven genetic variants each having a small effect on carbohydrate intake. Taken together, genes explained 8% of the variation in carbohydrate intake between individuals (7).

In conclusion: while some genetic variants have rather drastic effects on our food choices, by giving us a physical adverse reaction to certain foods, there are only few of them. Most of our food choices are much more complex. These are influenced by multiple genes at the same time, and even together these genes have only limited influence.

1. Wansink, B., & Sobal, J. (2007). Mindless eating: The 200 daily food decisions we overlook. Environment and Behavior, 39(1), 106-123. doi: 10.1177/0013916506295573

2. Szilagyi, A. (2015). Adaptation to Lactose in Lactase Non Persistent People: Effects on Intolerance and the Relationship between Dairy Food Consumption and Evolution of Diseases. Nutrients, 7(8):6751-79. doi: 10.3390/nu7085309

3. Itan, Y., Jones, B.L., Ingram, C.J.E., Swallow, D.M. & Thomas, M.G. (2010). A worldwide correlation of lactase persistence phenotype and genotypes. BMC Evol Biol, 10:36. doi: 10.1186/1471-2148-10-36

4. Feeney, E., O’Brien, S., Scannell, A., Markey, A. & Gibney, E.R. (2011). Genetic variation in taste perception: does it have a role in healthy eating? Proc Nutr Soc, 70(1):135-43. doi: 10.1017/S0029665110003976.

5. Roos, T.R., Kulemin, N.A., Ahmetov, I.I., Lasarow, A. & Grimaldi, K. (2017). Genome-Wide Association Studies Identify 15 Genetic Markers Associated with Marmite Taste Preference. BioRxiv (preprint). doi: 10.1101/185629

6. Josse, A.R., Da Costa, L.A., Campos, H. & El-Sohemy, A. (2012). Associations between polymorphisms in the AHR and CYP1A1-CYP1A2 gene regions and habitual caffeine consumption. Am J Clin Nutr, 96(3):665-71. doi: 10.3945/ajcn.112.038794.

7. Meddens, S.F.W., de Vlaming, R., Bowers, P., Burik, C.A.P., Karlsson Linnér, R., Lee, C., et al. (2018). Genomic analysis of diet composition finds novel loci and associations with health and lifestyle. BioRxiv (preprint). doi: 10.1101/383406

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Loss of appetite is among the most common side effects of stimulant for ADHD. Across studies, approximately 20% of patients with ADHD who were treated with stimulants reported a loss of appetite [1,2]. Weight loss is also quite common, as are digestive problems [3]. Together, such side effects are often referred to as “gastro-intestinal adverse events”. But why do stimulants change the way we go about eating? And what could this tell us about ADHD itself?

Appetite can arise in response to physical cues, such as an empty stomach or low blood sugar. Psychological cues can also influence our appetite; for instance, we may get hungry when we watch other people eat, or when we are bored. For most people, eating is a pleasant and rewarding activity. In the human brain, pleasure, reward, craving and, thus, appetite, have everything to do with dopamine. More specifically, with dopamine levels in the striatum, a cluster of neurons at the very base of the forebrain. The striatum is strongly connected with the prefrontal cortex. The prefrontal cortex exercises cognitive control over the urges of the striatum: when we’re hungry, the striatum makes us crave high-caloric, high-fat, or sweet foods; at the same time, our more rational prefrontal cortex helps us make responsible food choices.

Interestingly, ADHD also has everything to do with dopamine and the striatum. Dopamine levels in the striatum are slightly ‘off’ in individuals with ADHD. As a result, people with ADHD feel a higher urge to seek pleasant experiences, and less prefrontal control over this urge. Impulsivity, a prominent feature of ADHD, can be viewed as a failure to sufficiently activate the prefrontal cortex. Finding a balance between pleasure-seeking on the one hand, and rational decision-making on the other, can be difficult for all of us. However, for people with ADHD whose dopamine balance is slightly off, making healthy, non-impulsive decisions about what to eat may be even more challenging. Indeed, overweight, obesity and diabetes seem to be more common in people with ADHD compared to people without ADHD [4].

Stimulants such as methylphenidate and dexamphetamine can restore the dopamine balance in the brain. This may result in less craving for food (as well as for other pleasant activities) and more control over impulsive urges. It is thus not very surprising that stimulant medications may cause a loss of appetite or even weight loss. Interestingly, stimulants are sometimes used to treat obesity and certain eating disorders as well. Especially for eating disorders involving impulsive eating, such as bulimia nervosa and binge-eating disorder, stimulant treatment could be promising. [5]

There is one other interesting angle on stimulants, dopamine, and eating. Did you know that most of the dopamine in your body is not located in the brain? In fact, a substantial proportion of all dopamine-related processes in the human body take place in the gut. Throughout the gastro-intestinal tract, dopamine receptors are abundant. Therefore, in addition to the indirect effects described above (i.e., via craving and/or impulse control), stimulants may have direct effects on eating behaviours as well. Unfortunately, we know very little about such direct effects.

[1] Storebø, Ramstad, Krogh, Nilausen, Skoog, Holmskov et al. (2015). Methylphenidate for attention-deficit/hyperactivity disorder in children and adolescents: Cochrane systematic review with meta-analyses and trial sequential analyses of randomised clinical trials. Cochrane Database Syst Rev (11):CD009885. doi: 10.1002/14651858.CD009885.pub2

[2] Storebø, Pedersen, Ramstad, Kielsholm, Nielsen, Krogh et al. (2018) Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents – assessment of adverse events in non-randomised studies. Cochrane Database Syst Rev 5:CD012069. doi: 10.1002/14651858.CD012069.pub2

[3] Holmskov, Storebø, Moreira-Maia, Ramstad, Magnusson, Krogh et al. (2017) Gastrointestinal adverse events during methylphenidate treatment of children and adolescents with attention deficit hyperactivity disorder: A systematic review with meta-analysis and Trial Sequential Analysis of randomised clinical trials. PLoS One 12(6):e0178187. doi: 10.1371/journal.pone.0178187

[4] Cortese, Moreira-Maia, St Fleur, Morcillo-Peñalver, Rohde & Faraone (2016). Association Between ADHD and Obesity: A Systematic Review and Meta-Analysis. Am J Psychiatry 173(1):34-43. doi: 10.1176/appi.ajp.2015.15020266

[5] Himmerich & Treasure (2018). Psychopharmacological advances in eating disorders. Expert Rev Clin Pharmacol, 11(1):95-108. doi: 10.1080/17512433.2018.1383895

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This project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 728018

New Brain Nutrition is a project and brand of Eat2BeNice, a consortium of 18 European University Hospitals throughout the continent.

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