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 In my own study (which is ongoing and therefore yet unpublished), I found that those with an extremely high score on an impulsivity questionnaire (i.e. higher than 97% of all other participants), on average, consumed 2192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.

REFERENCES

  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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In our Eat2BeNice project, we want to know how lifestyle-factors, and nutrition contribute to impulsive, compulsive, and externalizing behaviours. The best way to investigate this is to follow lifestyle and health changes in individuals for a longer period of time. This is called a prospective cohort study, as it allows us to investigate whether lifestyle and nutrition events at one point in time are associated with health effects at a later point.

Luckily we can make use of the LifeGene project for this. LifeGene is a unique project that aims to advance the knowledge about how genes, environments, and lifestyle-factors affect our health. Starting from September 2009, individuals aged 18 to 45 years, were randomly sampled from the Swedish general population. Participants were invited to include their families (partner and children). All study participants will be prompted annually to respond to an update web-based questionnaire on changes in household composition, symptoms, injuries and pregnancy.

The LifeGene project (1) consists of two parts: First, a comprehensive web-based questionnaire to collect information about the physical, mental and social well-being of the study participants. Nine themes are provided for adults: Lifestyle (including detailed dietary intake and nutrition information), Self-care, Woman’s health, Living habits, Healthy history, Asthma and allergy, Injuries, Mental health and Sociodemographic. The partners and children receive questions about two to four of these themes. For children below the age of 15 the parents are requested to answer the questions for them.

The second part is a health test: at the test centres, the study participants are examined for weight, height, waist, hip and chest circumference, heart rate and blood pressure, along with hearing. Blood and urine samples are also taken at the test centres for analysis and bio-banking.

Up until 2019, LifeGene contains information from a total of 52,107 participants. Blood, serum and urine from more than 29,500 participants are stored in Karolinska Institute (KI) biobank. From these we can analyze genetic data and biomarkers for diabetes, heart disease, kidney disease and other somatic diseases. Based on LifeGene, we aim to identify nutritional and lifestyle components that have the most harmful or protective effects on impulsive, compulsive, and externalizing behaviors across the lifespan, and further examine whether nutritional factors are important mediators to link impulsivity, compulsivity and metabolic diseases(e.g. obesity, diabetes). We will update you on our results in the near future.

For more information, please go to the LifeGene homepage www.lifegene.se. LifeGene is an open-access resource for many national and international researchers and a platform for a myriad of biomedical research projects. Several research projects are underway at LifeGene https://lifegene.se/for-scientists/ongoing-research/.

This was co-authored by Henrik Larsson, professor in the School of Medical Science, Örebro University and Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Sweden.

AUTHORS:
Lin Li, MSc, PhD student in the School of Medical Science, Örebro University, Sweden.

Henrik Larsson, PhD, professor in the School of Medical Science, Örebro University and Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Sweden.

REFERENCES:

  1. Almqvist C, Adami HO, Franks PW, Groop L, Ingelsson E, Kere J, et al. LifeGene–a large prospective population-based study of global relevance. Eur J Epidemiol. 2011;26(1):67-77.
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Represented by a conscious propensity to harm others against their will, aggressiveness is a complex behavior depending on which environmental conditions we have been living in, and the kind of features we have inherited from our ancestors. Humans tend to be an aggressive species.

Among mammals, members of the same species cause only 0.3 percent of deaths of their conspecifics (a member of the same species) [1]. Astonishingly, in Homo sapiens, the rate is nearly 7 times higher, around 2% (1 in 50)!

More than 1.3 million people worldwide die each year because of violence in all of its forms (self-directed, interpersonal and collective), accounting for 2.5% of global mortality. There are two critical conditions that endorse aggressive behavior: being fiercely territorial and living in social groups.

From the evolutionary perspective, aggression is usually described as adaptive. Struggle for resources like habitat, mates and food have had a key role in forming aggressive behavior in humans. Genetic variants that promote aggression have been more likely to be passed on to the next generation because they have increased the chances of survival. Indeed, among tribes of extremely violent hunter-gatherers, men who committed acts of homicide had more children, as they were more likely to survive and have more offspring [2]. This lethal legacy may be the reason we are here today.

Although there are several biological aspects related to aggression, their predictive value continues to be rather low. It is possible to inherit a predisposition to acting violently, but scientists also emphasize that modeling violence in the home environment is the most certain way of propagating aggressive behavior. Children learn to act violently through the simple observation of aggressive models. The way parents manage the inevitable conflicts that arise between themselves and their children is central to the learning of aggression. When parents are unable to stop the child from escalating the intensity of conflict, and when they at least intermittently reinforce the child’s coercive behavior, the child learns that escalation is a viable method of resolving conflict. When this conflict strategy is applied to interactions with siblings or peers, and if it is also reinforced in these contexts, this conflict escalation is likely to include acts of aggression [3].

In addition to being hereditary and learned through social modeling, there is one other crucial component to aggressive behavior: self-control. In humans, the urge to react aggressively stems from the ancient parts located deep in the brain.

The structure capable of controlling those impulses is evolutionally much newer and located just behind the forehead – the frontal lobes. Unfortunately, this “top-down” conscious control of violent impulses is slower to act in contrast with the circuits of eruptive violence deep in the brain. People convicted of murder had been found to have reduced activity in the prefrontal cortex and increased activity in deeper regions [4]. Although there are plenty of examples of people with prefrontal cortex damage who do not commit violent acts, these findings clearly demonstrate that the damage to the prefrontal cortex impairs decision making and increases impulsive behavior.

Early physical aggression needs to be dealt with care. Long-term studies of physical aggression clearly indicate that most children, adolescents and even adults eventually learn to use alternatives to physical violence [5].

Aggression is part of the normal behavioral repertoire of most, if not all, species; however, when expressed in humans in the wrong context, aggression leads to social maladjustment and crime [6]. By identifying mechanisms that predispose people to the risk of being violent – even if the risk is small – we may eventually be able to tailor prevention programs to those who need them most.

This post is adapted from an earlier blog on MiND the Gap/

References

[1] Gómez, J. M., Verdú, M., González-Megías, A., Méndez, M. (2016). The phylogenetic roots of human lethal violence. Nature 538(7624), 233–237.

[2] Denson, T. F., Dobson-Stone, C., Ronay, R., von Hippel, W., Schira, M. M. (2014). A functional polymorphism of the MAOA gene is associated with neural responses to induced anger control. J Cogn Neurosci 26(7), 1418–1427.

[3] Hodges, E.V.E., Card, N.A., Isaacs, J. (2003). Learning of Aggression in the Home and the Peer Group. In: Heitmeyer, W., Hagan, J. (eds) International Handbook of Violence Research. Springer, Dordrecht.

[4] Raine, A., Buchsbaum, M., LaCasse, L. (1997). Brain abnormalities in murders indicated by positron emission tomography, Biol Psychiatry 42(6), 495–508.

[5] Lacourse, E., Boivin, M., Brendgen, M., Petitclerc, A., Girard, A., Vitaro, F., Paquin, S., Ouellet-Morin, I., Dionne, G., Tremblay, R. E. (2014). A longitudinal twin study of physical aggression during early childhood: Evidence for a developmentally dynamic genome. Psychol Med 44(12):2617–2627.

6] Asherson, P., Cormand, B. (2016). The genetics of aggression: Where are we now? Am J Med Genet B Neuropsychiatr Genet 171(5), 559–561.

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Rates of obesity and metabolic diseases are rapidly growing, and much attention is paid to study the effects of consumed foods on human health. We know already that dietary preferences can be a serious factor of diseases and even a cause of them, in a man. However, we do not know molecular and cellular mechanisms behind these effects. Thus, we do not know how these negative processes can be neutralized or diminished by preventive or curative interventions. As such mechanistic studies are needed.

These studies can be in principle carried out in vitro or in vivo. Food consumption and consumed nutrients affects both the brain and a periphery. Another words, these processes are systemic and involve a lot of interplay mechanisms. Consequently, in vitro approach has very limited potential to achieve research goal with studies on diets. For example, the use of a tissue from peripheral organs or brain, cell cultures or even mini-organs would not help to understand systemic mechanism.

With in vivo approach, human studies cannot help to understand the mechanisms and they exclude any interventions. The remaining solution then is the use of animal models – of course, in compliance with the three R’s principle1 (reduction, refinement, replacement). “Replacement” defines the choice of the object: to use the lowest phylogenetic ordered animal possible, when it’s impossible to use in vitro methodology or a non-animal model, to address a given scientific question.

The most commonly used animal in nutritional research is a mouse. Are mice perfect organisms to model dietary-induced disorders?

Like us, humans, mice are omnivore mammals, and almost all the genes in mice share functions with the genes in humans. In comparison to other mammals, mice have small size of the body (3000 times smaller than a human), and genetically identical mice (like human monozygotic twins) are available for experimental use. Basal metabolic rate per gram of body weight is 7 times greater in mice than in humans which speeds up the development of diet-induced disease. Because of the rapid generation and short life cycle (about 2 years) mice are used to study the effects of maternal diet in the offspring and model diet role in aging processes. Mice display complex behaviours, including social interactions, cognitive functions and emotionality, that are similar to human features.

The use of mice in nutritional research offers a unique tool: possibility to study the role of a given gene using genetic modification. Generation of mutant mice is well established in comparison with other mammalian species. Many genetically modified mouse models were developed over the years, including knockout mice in which genetic material is deleted, mice carrying additional genetic material or “humanized” models expressing human genes.

Numerous mouse models were generated to use in nutrition research. Probably the most popular model in diet research is diet-induced obesity model (DIO model)2 in which animal is fed high-fat or high-density diets – to mimic the most common cause of obesity in humans. Changes seen in DIO mice are remarkably consistent with those seen in obese patients. DIO mice are used to investigate mechanisms of obesity development and novel medication screening.

Another prominent example of a model in nutrition research is the ob/ob mouse3. Due to a mutation in hormone leptin these mice display severe obesity, insulin resistance and dyslipidemia. Studies performed on this model revealed new aspects of hypothalamus role in human energy metabolism.

Mouse model plays its role in development of anti-obesity and anti-diabetic medication. Information about the receptors and hormones that regulate food intake and energy balance can be used to choose a target for a new drug. For example, mice lacking serotonin 5-HT2C receptor were found to exhibit mild obesity and type 2 diabetes4, suggesting the role of this receptor in regulation of food intake. Recently appetite reducing drug (lorcaserin), 5-HT2C receptor agonist, was developed.

However, there are certain limitations in translating discoveries from mouse models to humans in nutrition research. There are clear differences in feeding patterns, nutrient metabolism and hormone control between humans and mice. In case those aspects are key features of the study, another available model could be used.

No model is perfectly mimicking all aspects of human disease. It is likely that better new models will be developed in the nearest future to study the human conditions not adequately replicated in mouse models. But for now, mouse model is a useful tool in studying dietary-induced diseases and it plays an important role in translational research and advancement of human health.

REFERENCES

  1. Tannenbaum, J. & Bennett, B. T. Russell and Burch’s 3Rs then and now: the need for clarity in definition and purpose. J. Am. Assoc. Lab. Anim. Sci. 54, 120–32 (2015).
  2. Hariri, N. & Thibault, L. High-fat diet-induced obesity in animal models. Nutr. Res. Rev. 23, 270–299 (2010).
  3. Ingalls, A. M., Dickie, M. M. & Snell, G. D. Obese, a new mutation in the house mouse. J. Hered. 41, 317–318 (1950).
  4. Tecott, L. H. et al. Eating disorder and epilepsy in mice lacking 5-HT2C serotonin receptors. Nature 374, 542–546 (1995).
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Feeling more happy after a run? Or feeling a bit blue during the dark winter days? Regular exercising and regular daylight exposure can influence your mood, behaviour and sleep-wake cycle 1,2,3. But can this also be used in a therapeutical setting, for instance in addition to or instead of the usual treatment with medication?

The PROUD trial aims to investigate the potential of bright light therapy and physical exercise to improve and prevent depression and obesity in adolescents and young adults with ADHD. This clinical trial is part of the CoCA research project, in which comorbid conditions of ADHD are investigated [insert hyperlink: https://coca-project.eu/coca-phase-iia-trial/study/]. In addition, we collect the stool samples of all participants in order to investigate the effects of physical exercise on the gut microbiome and how this is linked to behaviour. That part of the study is part of the Eat2beNICE research project.

Most people with Attention Deficit Hyperactivity Disorder (ADHD) receive medication to reduce their symptoms4. While this medication works well for many people, there is a lot of interest in other types of treatment. One reason for this is that people with ADHD suffer from additional conditions, such as depression5 and obesity6. The risk for developing these comorbid conditions is especially high during adolescence and young adulthood4.

Adolescents and young adults (age 14-45) with ADHD that want to participate are randomly assigned to one of three groups: 10-weeks of daily light therapy (30 minutes), 10-weeks of daily physical exercise (3x per day) or 10-week care as usual (for instance, the normal medication). The random assignment is very important here in order to compare the different interventions. We don’t want to have all people that like sports in the physical exercise group, because then we don’t know if the effects of the physical exercise are due to the intervention, or due to the fact that these people just like sports better.

Another nice feature of the study is that it uses a phone app (called m-Health). This app is used to remind the participants to do their exercise or light therapy, but it also gives feedback and summaries of how the participant is doing. The app is linked to a wrist sensor that measures activity and light.

The clinical trial is currently ongoing in London (England), Nijmegen (Netherlands), Frankfurt (Germany) and Barcelona (Spain). We can’t look at the results until the end of the trial, so for those we will need to wait until 2021. But in the mean time the PROUD-researchers have interviewed four participants. You can read these interviews here:

This blog is based on the blog “10 weeks of physical exercise or light therapy: what’s it like to participate in our clinical trial?” by Jutta Mayer and Adam Pawley, 9 Oct. 2018 on MiND the Gap – https://mind-the-gap.live/2018/10/09/10-weeks-of-physical-exercise-or-light-therapy/

REFERENCES

  1. Terman, M. Evolving applications of light therapy. Sleep Medicine Reviews. 2007; 11(6): 497-507.
  2. Stanton, R. & Reaburn, P. Exercise and the treatment of depression: A review of the exercise program variables. Journal of Science and Medicine in Sport. 2014; 17(2):177-182
  3. Youngstedt, S.D. Effects of exercise on sleep. Clinical Sports Medicine. 2005; 24(2):355-365.
  4. Cortese S, Adamo N, Del Giovane C, Mohr-Jensen C, Hayes AJ, Carucci S, et al. Comparative efficacy and tolerability of medications for attention-deficit hyperactivity disorder in children, adolescents, and adults: a systematic review and network meta-analysis. Lancet Psychiatry. 2018;5(9):727-738.
  5. Jacob CP, Romanos J, Dempfle A, Heine M, Windemuth-Kieselbach C, Kruse A, et al. Co-morbidity of adult attention-deficit/hyperactivity disorder with focus on personality traits and related disorders in a tertiary referral center. Eur Arch Psychiatry Clin Neurosci. 2007;257:309–17.
  6. Cortese S, Moreira-Maia CR, St Fleur D, Morcillo-Penalver C, Rohde LA, Faraone SV. Association between ADHD and obesity: a systematic review and meta-analysis. Am J Psychiatry. 2016;173:34–43.
  7. Meinzer MC, Lewinsohn PM, Pettit JW, Seeley JR, Gau JM, Chronis-Tuscano A, et al. Attention-deficit/hyperactivity disorder in adolescence predicts onset of major depressive disorder through early adulthood. Depress Anxiety. 2013;30:546–53
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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

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