Neurodevelopmental disorders such as attention deficit disorder (ADHD), autism spectrum disorder (ASS) and different types of anxiety disorders are associated with a higher risk of poor dietary, physical activity and sleep habits. Shaping behavior in children with neurodevelopmental symptoms can be challenging. How do parents experience shaping healthy habits in these children? What are tips and tricks to encourage your child to live healthy? We took together the results of a recent study conducted in Boston and our own results from a qualitative interview with parents of children that followed the TRACE-diet to help you encourage your child to be healthy.

What is hard?
For parents of children with a neurodevelopmental disorder (ND) it can be challenging to convince their children to make healthy choices. Some parents explain that taking an unhealthy option from a neurotypical child might also lead to an anger meltdown, but this meltdown is not comparable with a ND meltdown, which can last the whole day. Furthermore, children with ND can be more impulsive, which makes it harder for them to think before they choose. Other children with ND are resistant to change, and/or lack intrinsic motivation to change. The parents that tried taking their child to a health professional, reported a lack of clinical expertise among lifestyle experts to level with children with a neurodevelopmental disorder.

What is helpful?
Agency
Both studies found that allowing your kid agency in making choices is critical to create a healthy habit. It is important to limit the choices, otherwise your child will drown in options. Offer, for instance, a healthy snack and an unhealthy snack and let your child decide whether he/she wants the healthy snack now, or later.

Family engagement
Work as a team! This was a helpful strategy that was reported by most parents in the TRACE study. If you follow the diet with the whole family, the child does not feel left out or punished. Also, just not having snacks at home prevents your child from sneaking into the cabinet and taking one.

Positive reinforcement
It is important to define a goal together with your child. What are we working for? And for how long? You can help your child visualize this goal by making a calendar. Will your child only be rewarded at the end of the goal? Or are there also smaller sub-goals? For some children, a long-term goal such as “sleeping better” or “less belly pains” will be rewarding enough, but other children might need short-term goals.

The role of pets
In the Boston study, almost one-third of the parents reported that they used the role of pets to promote healthy habits. Animals can be used as a positive reinforcement for good choices, but they can also help to maintain healthy routines such as physical activity (walking the dog) and family engagement (walking the dog with the whole family).

 

REFERENCES

  1. Bowling, A. Blaine, R.E., Kaur, R., Davison, K.R. (2019). Shaping healthy habits in children with neurodevelopmental and mental health disorders: parent perceptions of barriers, facilitators and promising strategies. International Journal of Behavioral Nutrition and Physical Activity. 16:52.
  2. TRACE-study. For more information visit project-trace.nl
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According to the food and agriculture organization, about 1 billion people in the world were living in hunger or insecurity in the year 2010 (1). Additionally, 5 to 15 % of people in industrial countries experience food insecurity which makes it all the more a public health concern in Europe (2).

But, what exactly is food insecurity about?

Food insecurity means that the access to sufficient food, meeting the dietary and cultural needs and the individual food preferences for a healthy and active life is not possible. It is not only a lack of food, what`s more, is the feeling that the preferred food supply is not available or may be threatened in the future, which has, in turn, an effect on the eating behavior. That means even if food is sufficient, people may be food insecure, but not necessarily undernourished. Two risk groups are students, who do not have the money for buying their preferred food, and refugees, who can´t buy their traditional food in their new home towns. Food insecurity can result in a reduction on micro-and macronutrition intake. Macronutrients are large food components that the body needs to maintain its metabolism; it includes lipids (fats), sugars (carbohydrates) and proteins. Micronutritions, like vitamins, minerals (such as calcium or magnesium), trace elements (such as iron and zinc), are essential because, without them, numerous normal functions such as growth or energy production could not take place.

Effects on mental health

Food insecurity is also found more often in families with low social economic status (4). Researchers have found that food insecurity caused an increase of depression and anxiety symptoms (3). Furthermore the uncertainty of having food in the future produced stress and created desperation and hopelessness in the families. They perceived the situation as shameful and resigned or used drugs and alcohol to compensate. In addition to this ,children from food insecure families were also more likely to develop symptoms of depression/ anxiety, aggression and hyperactivity/inattention (2). However, when you control for many demographical and psychological variables such as immigrant status, family structure and income and paternal depression, only increased impulsive behavior and inattention seem to be specifically linked to food insecurity Another factor is maternal mental health. It has been shown that food insecurity is especially bad for children’s development if the mother has additional mental health problems like depression, domestic violence and psychosis.

Further insights can be derived from Canadian students (5). Here are financial constraints a primary contributing factor. It represents a barrier because often students can´t afford to buy qualitative and expensive food. Another important factor is insufficient time because the effort to buy, prepare and cook healthy meals takes time and requires planning. It may also be the limited access to culturally appropriate food. This could be a barrier especially for people from other countries, who don´t have the opportunity to buy their traditional food and spices in local supermarkets. In urban areas, more exotic and international food supply is possible, due to the higher demand. The consequences for students were feelings of shame, frustration and loneliness. Some have felt socially isolated, and in general the food insecurity was associated with high psychological stress. Nonetheless the students in the reports believed that the situation is temporary and that after university life gets better in terms of food quantity and quality. For now they accepted the current situation.

So overall, food insecurity may occur in different social classes, with different reasons and effects of varying intensity. It`s interesting to see that it can occur in developing countries and rich countries, and that it can have an influence on whole families and children of food insecure families and students. More studies about people with cultural issues (e.g. refugees) are needed.

So, if you have the chance:

Buy the food you prefer and take time for preparing your meal,                      to live your life as healthy as you want it to be!

REFERENCES

(1) Cole, S. M.; Gelson, T. (2011). The effect of food insecurity on mental health: Panel evidence from rural Zambia. Social Science & Medicine. 73 (7)1071-1079.

(2) Melchior M.; Chastang J.- F.; Falissard B.; Galera, C.; Tremblay, R.E.; Cote, S.M., Boivin, M. (2012). Food insecurity and children’s mental health: a prospective birth cohort study. PLoS One 7 (12).

(3) Weaver, L. J.; Hadley. C. (2009) Moving Beyond Hunger and Nutrition: A Systematic Review of the Evidence Linking Food Insecurity and Mental Health in Developing Countries, Ecology of Food and Nutrition, 48(4), 263-284.

(4) Melchior, M.; Caspi, A.; Howard, L.M.; Ambler, A.P.; Bolton, H.; Mountain, N; Moffitt, T.E. (2009) Mental health context of food insecurity: a representative cohort of families with young children. Pediatrics, 124 (4).

(5) Hattangadi, N.; Vogel, E.; Carroll, L. J.; Cote, T. (2019). “Everybody I Know Is Always Hungry…But Nobody Asks Why”: University Students, Food Insecurity and Mental Health. Sustainability. 11 (6).

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This week, my lab at the University of Canterbury published the first investigation1 into whether a mineral-vitamin supplement could change the bacteria in the microbiome of children with ADHD. Our preliminary data, based on our sample of 17 kids (half of whom were given micronutrients and half were given placebo for 10 weeks), hints at increased diversity and changes in the types of bacteria contained in the microbiome of the children exposed to the micronutrients. This type of study starts to moves us beyond the efforts to show that micronutrients benefit some people with psychiatric symptoms, and towards figuring out why they might exert their influence. So what does this mean?

First off, what is the microbiome?

The gut microbiome is defined as the trillions of microbes that inhabit the human digestive tract. In additional to playing a crucial role in digesting food, they also play pivotal roles in immune and metabolic functioning, gene expression, as well as playing a role in the expression of psychiatric symptoms through the gut-brain connection.2 We also know that they generate essential vitamins. When our microbiome gets into a state of dysbiosis (microbial imbalance), in addition to the physical symptoms like reflux, poor digestion, pain, constipation and/or diarrhoea, it is thought that dysbiosis can also lead to increased permeability of the gut wall, increased production of endotoxins, increased inflammation and decreased nutrient synthesis.

How do we learn about what bacteria are within and on us?

Research on the human microbiome has grown exponentially in the past decade. However, it was only recently that we could fairly cheaply quantify and describe the bugs contained within us. 16S rRNA sequencing (the technology we used) is a key methodology in identifying bacterial populations and allows scientists to easily and reliably characterize complex bacterial communities.3 This methodology is a simple and effective alternative to microbial culture, and provides detailed information about the various species of bacteria that are contained within our microbiome. The sequencing gives information on bacterial diversity, as well as details about the specific family (e.g., Bifidobacteriaceae), genus (e.g., Bifidobacterium), and species (e.g., Bifidobacterium Longom).

What about the microbiome of kids with ADHD?

What scientists are now wondering is whether people who suffer from specific psychiatric symptoms, like those associated with ADHD, have a different bacterial composition than those who don’t have these symptoms and whether these differences can help us understand the severity of the symptoms. In other words, is it possible that our bugs can make us impulsive? And if so, if we changed the bugs, can we become less impulsive?

There isn’t a huge literature exploring this topic in ADHD. Preliminary studies suggest that antibiotics in the first 6 months of life may increase risk of ADHD symptoms at 11 years of age,4 although this finding hasn’t been replicated.5 Another study found that the Phylum Actinobacteria is overrepresented in ADHD compared with controls.6 Other research suggests that reduced alpha diversity may exist in young patients with ADHD, specifically that boys with ADHD had more Bacteroidaceae relative to controls, with the species Neisseriaceae identified as a particularly promising ADHD-associated candidate.7 Although this finding of reduced alpha diversity was not observed in treatment-naïve children with ADHD, Jiang and colleagues noted that the more an individual had the species Faecalibacterium, the lower their ADHD severity.8

Overall, there are intriguing signals but the signals are not always replicating. Much more research with larger samples is needed to try to determine if there are reliable bacterial biomarkers. We also need to parse out the effect of diet, medications, age, ethnicity and gender on the results that have been reported. Further, we don’t know whether these differences are causal or a result of ADHD or completely irrelevant to the expression of the symptoms.

We still don’t know if changing the relative amount of a bacteria can change psychiatric symptoms. We know that diet manipulation can change levels of bacteria but whether those changes in bacteria are necessary for improvement in psychological states requires much more research.

So what did we find?

Looking at the microbiome over a short period of time with a small sample is challenging. There is such diversity in the bacteria within us and between us that it is a challenge to explore changes and also whether changes are meaningful. But we did observe some intriguing effects:

  1. The observed taxonomic units (OTU), a measure of community richness, significantly increased in treatment group but not in placebo group. We think this is a good thing.
  2. We observed significant greater decrease in abundance of genus Bifidobacterium from phylum Actinobacteria in active versus placebo and that the more it decreased, the more the ADHD symptom scores dropped. If Bifodobacterium is contributing to the symptoms of ADHD, this is a good thing.
  3. We also observed a significant positive correlation between Actinobacterium abundance and Clinician ADHD IV-RS rating scale before the intervention was introduced, which suggests that Actinobacterium may play a role in the expression of ADHD.

What does this mean?

The small sample makes it difficult to generalize from this study. However, these novel results provide a basis for future research on the biological connection between ADHD, diet and the microbiome. Previous research from our lab has shown that micronutrients do exert some positive effects on ADHD and associated symptoms.9 10 These findings suggest that micronutrient treatment may result in a more diverse microbiome which may in turn, have a positive effect on brain health.

What next?

The field of the microbiome is literally exploding with new studies out every day. The focus currently is trying to find ways to manipulate the microbiome for positive response. This has mainly been explored through either adding in bacteria (in the form of probiotics or psychobiotics if targeting psychological symptoms), diet manipulation, or more recently, fecal microbiota transplants. I do worry a bit that this search for the magic-bullet bacteria that causes distress may turn out to be as disappointing as the search was for candidate genes, but it is worth some effort to figure out if this is an important lead.

Eat2BeNice (New Brain Nutrition) plans to explore the role of the microbiome in multiple ways, including determining whether individuals with high impulsivity/compulsivity have a unique microbiome profile, whether targeted probiotics can improve impulsivity/compulsivity symptoms, and also whether improvement in impulsivity/compulsivity symptoms from diet manipulation and via the use of supplements can be explained via changes in the microbiome. Watch this space!

REFERENCES 

  1. Stevens AJ, Purcell RV, Darling KA, et al. Human gut microbiome changes during a 10 week Randomised Control Trial for micronutrient supplementation in children with attention deficit hyperactivity disorder. Sci Rep 2019;9(1):10128.
  2. Frye RE, Slattery J, MacFabe DF, et al. Approaches to studying and manipulating the enteric microbiome to improve autism symptoms. Microb Ecol Health Dis 2015;26:26878-78.
  3. Ames NJ, Ranucci A, Moriyama B, et al. The Human Microbiome and Understanding the 16S rRNA Gene in Translational Nursing Science. Nurs Res 2017;66(2):184-97.
  4. Slykerman RF, Coomarasamy C, Wickens K, et al. Exposure to antibiotics in the first 24 months of life and neurocognitive outcomes at 11 years of age. Psychopharmacology (Berl) 2019;236(5):1573-82.
  5. Axelsson PB, Clausen TD, Petersen AH, et al. Investigating the effects of cesarean delivery and antibiotic use in early childhood on risk of later attention deficit hyperactivity disorder. J Child Psychol Psychiatry 2019;60(2):151-59.
  6. Aarts E, Ederveen THA, Naaijen J, et al. Gut microbiome in ADHD and its relation to neural reward anticipation. PLoS One 2017;12(9):e0183509.
  7. Prehn-Kristensen A, Zimmermann A, Tittmann L, et al. Reduced microbiome alpha diversity in young patients with ADHD. PLoS One 2018;13(7):e0200728.
  8. Jiang HY, Zhou YY, Zhou GL, et al. Gut microbiota profiles in treatment-naive children with attention deficit hyperactivity disorder. Behav Brain Res 2018;347:408-13.
  9. Rucklidge JJ, Eggleston MJF, Johnstone JM, et al. Vitamin-mineral treatment improves aggression and emotional regulation in children with ADHD: a fully blinded, randomized, placebo-controlled trial. J Child Psychol Psychiatry 2018;59(3):232-46.
  10. Rucklidge JJ, Frampton CM, Gorman B, et al. Vitmain-mineral treatment of attention-deficit hyperactivity disorder in adults: double-blind randomised palcebo-controlled trial. The British Journal of Psychiatry 2014;204:306-15.
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For my research, I measured impulsive behaviour in 3-year-old children. Briefly, impulsivity is the opposite of inhibitory control. There are several forms of inhibitory control, and although there is no official categorisation of different forms of inhibitory control in young children, Anderson & Reidy (2012) defined five categories. The categories are:

  • Delay of gratification: the ability to resist direct temptation in order to receive a bigger reward after the delay.
  • Impulse control: the ability to inhibit an instinctive response.
  • Verbal inhibition: the ability to inhibit verbal responses.
  • Motoric inhibition: the ability to learn response sets that conflict with an established behaviour.
  • Go/No go: the ability to perform certain behaviour after being shown a certain stimuli but to inhibit that behaviour after being shown a different stimuli.

The Marshmallow test is a famous example of an inhibitory control task (more specifically: delay of gratification). For this task, a marshmallow is placed in front of the child. The child is told that if s/he refrains from eating the marshmallow while the examiner is gone, s/he will receive two marshmallows when the examiner returns. Another example of an inhibitory control task (more specifically: Go/No go) is the Bear/Dragon task. For this test, the child has to obey the commands (e.g. ‘hands on your head’) of the bear hand puppet, but must inhibit obeying the commands of the dragon hand puppet.

When comparing the Marshmallow task with the Bear/Dragon task, similarities and differences can be found. They are similar in the way that both tests require the child to inhibit their impulses. However, the Marshmallow task requires minimal working memory demand, while the Bear/Dragon task requires complex greater working memory demand (Petersen, Hoyniak, McQuillan, Bates, & Staples, 2016). The Bear/Dragon task is thus a complex inhibitory control task, because children are instructed to not only inhibit a prepotent response, but also to respond in a certain way to a salient, conflicting response option.

In my research, I used both behavioural tasks and parental report (both mothers and fathers) to assess inhibitory control. However, results from the behavioural tests and the parental questionnaires correlate poorly with each other; a finding which is also often reported in other studies. While behavioural tests show objective observations of the child’s behaviour, these observations are mostly only carried out at one specific time point (e.g. during a home visit). As such, the child’s performance might be prone to noise, such as that the child slept poorly the past night. Reports of behaviour, on the other hand, reflect the behaviour of the child during daily life. However, these reports can be prone to social desirable answering and parental perceptions of their child’s behaviour. By measuring inhibitory control with both behavioural tasks and parental reports, we obtain the most robust view of the child’s behaviour.

Overall, measuring inhibitory control behaviour in 3-year-olds can be challenging, but also a lot of fun! (Stay tuned for a blog on interesting anecdotes during my data collection.)

REFERENCES:

Anderson, P. J., & Reidy, N. (2012). Assessing Executive Function in Preschoolers. Neuropsychology Review, 22(4), 345–360. https://doi.org/10.1007/s11065-012-9220-3

Petersen, I. T., Hoyniak, C. P., McQuillan, M. E., Bates, J. E., & Staples, A. D. (2016). Measuring the development of inhibitory control: The challenge of heterotypic continuity. Developmental Review: DR, 40, 25–71. https://doi.org/10.1016/j.dr.2016.02.001

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Behavior results from the complex interplay between genes and environment. Our genes predispose us to how we act and feel, by influencing how our brain develops and functions. This way, certain genetic variants in our genome increase the risk of developing mental health problems (while others may decrease this risk). Whether someone actually develops a mental health disorder or not, depends on many other factors in our environment, such as stressors and experiences. Nonetheless, studying these genetic risk factors for mental health conditions is an important aspect of understanding these disorders.

As an example of such research, we have now identified several genetic risk factors that contribute to cocaine dependence. For this we combined genetic data from a lot of studies, including more than 6000 individuals. What’s even more interesting is that we found that the genetic variants that are related to cocaine dependence are correlated with the genetic risk factors for other conditions such as ADHD, schizophrenia and major depression. What this means is that certain small variations in DNA increase the risk for not just cocaine dependence, but actually several psychiatric conditions. Probably, there is a common biological mechanism that underlies all these conditions. Thanks to our genetic research, we are now only a small step closer towards unraveling these mechanisms.

We also wrote a blog post explaining our research findings. You can read it here: https://mind-the-gap.live/2019/07/04/cocaine-dependence-is-in-part-genetic-and-it-shares-genetic-risk-factors-with-other-psychiatric-conditions-and-personality-traits/

The original publication can be found here: https://www.sciencedirect.com/science/article/pii/S0278584619301101?via%3Dihub

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Probably the best known example on how the brain and mental health are linked to nutrition and our gut, and the one that we can all identify ourselves with, is stress. We all know it: studying 24/7 for an important exam, pressure in the job or even a house full of work. We have no time to think and – no – we definitely don’t have time to cook. But at the same time we are constantly hungry, craving for a snack. The fastest solution? The next best, nicest looking, edible piece of food we can find.

But why do we change our dietary habits during stress and what happens in our body? What are the consequences and what can we do to avoid this impulsive eating behavior?

A study from Yau and Potenza in 2013 states that about 20% of the population do not change their eating behavior during stress (good for them), while about 40% decrease and another 40% increase their caloric intake. But besides simply increasing the amount of food we consume, we also tend to choose more pleasurable and palatable food when we’re stressed. This usually leads to the consumption of unhealthy and calorie-dense foods, which unfortunately results in gaining weight (at least for most of us).

Stress can have many different causes, ranging from physical stressors like severe illnesses to emotional stressors such as the loss of a loved one. So far, it is known that acute and severe stressors tend to suppress appetite, which results from our evolutionary conserved ‘fight-or-flight’ reaction (Adams und Epel, 2007). On the other hand, lighter – but therefore often chronic – stressors (occurring on a daily basis) seem to increase our appetite, especially towards energy-dense foods. These two roughly categorized types of stress activate two different systems in our body, causing different stress responses:

  • Acute stressors activate the sympathetic adrenal medullary system
  • Chronic stressors activate the hypothalamic-pituitary-adrenal [HPA] axis (Torres & Nowson, 2007)

The sympathetic adrenal medullary system induces the release of adrenaline and noradrenaline. These are the ones increasing our heart rate right before we have to give a talk in front of a huge audience, while they, at the same time, reduce our drive to eat or even make us want to throw up… On the opposite side, the HPA-axis, activated by daily stressors, leads to the release of cortisol. And, cortisol can have some unwanted effects.

This hormone is known to stimulate our appetite by affecting our reward system, in a very similar way as alcohol and drugs affect this system. In the case of chronic stress, chocolate or chips can have the same effects as drugs: they make us feel better for a short amount of time. This “positive” feeling, that might reduce our stress level for a few moments, reinforces the consumption of sweets later on, thereby resulting in some kind of dependence. But as in all cases of addictions, this repeated stimulation of the reward system can lead to an adaptation, eventually increasing this compulsive behavior.

Knowing now that in some strange ways it is our body that makes us crave burgers and pizza in times of stress, what can we do to avoid gaining weight?

Well, the first thing is: listen to your body and try to understand what is going on. Ask yourself why you are stressed and if there is anything you can do to reduce it, like taking more breaks during the day. If this is not possible, try to find other ways to compensate: take walks, do more exercise, find something else that makes you feel better at the end of the day, besides that tasty chocolate donut and popcorn. Before snacking, hesitate and ask yourself if you are really hungry or just eating because you feel like it. And if you absolutely can’t resist, try to substitute the chocolate bar with healthier snacks, like dried fruits or nuts.

But finally, keeping all that in mind, don’t forget that food is not always your enemy and there is no problem with eating what you desire as long as it is in moderation.

REFERENCES:
Yau, Yvonne H. C.; Potenza, Marc N. (2013). Stress and Eating Behaviors. Minerva Endocrinol, 38(3): 255–267. Link: https://www.ncbi.nlm.nih.gov/pubmed/24126546

Adam, Tanja C.; Epel, Elissa S. (2007). Stress, eating and the reward system. Physiology & Behavior 91, 449–458. DOI: 10.1016/j.physbeh.2007.04.011

Torres, Susan J.; Nowson, Caryl A. (2007). Relationship between stress, eating behavior, and obesity. Nutrition Volume 23, Issues 11–12, Pages 887-894. DOI: 10.1016/j.nut.2007.08.008

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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.

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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