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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