Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopment disorder characterized by inattention or hyperactivity–impulsivity, or both. It might seem paradoxical, but many studies indicate that individuals with a diagnosis of ADHD suffer from overweight and obesity. Therefore, it is important to understand the underlying mechanism that put individuals with ADHD at risk for obesity.

 Evidence from within-individual study
A systematic review and meta-analysis (1) based on 728,136 individuals from 42 studies, suggested a significant association between ADHD and obesity both in children/adolescents and adults. The pooled prevalence of obesity was increased by about 70% in adults with ADHD and 40% in children with ADHD compared with individuals without ADHD. However, due to the lack of longitudinal and genetically-informative studies, the meta-analysis was unable to explain the exact direction of association and the underlying etiologic mechanisms. There are several potential explanations:

  • ADHD causing obesity: The impulsivity and inattention components of ADHD might lead to disordered eating patterns and poor planning lifestyles, and further caused weight gain.
  • Obesity causing ADHD: Factors associated with obesity, for example dietary intake, might lead to ADHD-like symptoms through the microbiota-gut-brain axis.
  • ADHD and obesity may share etiological factors: ADHD and obesity may share dopaminergic dysfunctions underpinning reward deficiency processing. So the same biological mechanism may lead to both ADHD and obesity. This is difficult to investigate within individuals, but family studies can help to test this hypothesis.

We will further investigate these possibilities in the Eat2beNICE research project by using both perspective cohort study and twin studies.

Evidence from a recent within-family study
Recently, a population-based familial co-aggregation study in Sweden (2) was conducted to explore the role of shared familial risk factors (e.g. genetic variants, family disease history) in the association between ADHD and obesity. They identified 523,237 full siblings born during 1973–2002 for the 472,735 index males in Sweden, and followed them until December 3, 2009. The results suggest that having a sibling with overweight/obesity is a risk factor for ADHD. This makes it likely that biological factors (that are shared between family members) increase the risk for both ADHD and obesity.

Evidence from across-generation study
Given that both ADHD and obesity are highly heritable complex conditions, across-generation studies may also advance the understanding of the link between ADHD and obesity.

A population-based cohort study (3) based on a Swedish nationwide sample of 673,632individuals born during 1992-2004, was performed to explore the association between maternal pre-pregnancy obesity and risk of ADHD in offspring. The sibling-comparison study design was used to test the role of shared familial factors for the potential association. The results suggest that the association between maternal pre-pregnancy obesity and risk of ADHD in offspring might be largely explained by shared familial factors, for example, genetic factors transmitted from mother to child that contribute to both maternal pre-pregnancy obesity and ADHD.

Together, based on previous evidence from various study designs, there is evidence to suggest that the association between ADHD and obesity mainly is caused by shared etiological factors. However, future studies on different population are still needed to further test these findings.

REFERENCES:
1. 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. The American journal of psychiatry. 2016;173(1):34-43.

2. Chen Q, Kuja-Halkola R, Sjolander A, Serlachius E, Cortese S, Faraone SV, et al. Shared familial risk factors between attention-deficit/hyperactivity disorder and overweight/obesity – a population-based familial coaggregation study in Sweden. J Child Psychol Psychiatry. 2017;58(6):711-8.

3. Chen Q, Sjolander A, Langstrom N, Rodriguez A, Serlachius E, D’Onofrio BM, et al. Maternal pre-pregnancy body mass index and offspring attention deficit hyperactivity disorder: a population-based cohort study using a sibling-comparison design. Int J Epidemiol. 2014;43(1):83-90.

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Why 12 genetic markers for ADHD are exciting news for New Brain Nutrition

We are finally here: for the first time, genome-wide significant markers are identified that increase the risk for Attention Deficit / Hyperactivity Disorder (ADHD). This research was conducted by an international consortium of more than 200 experts on genetics and ADHD, and includes several researchers that are also involved in our Eat2beNICE project (the scientific basis of this New Brain Nutrition website). The findings were recently published in the prestigious journal “Nature Genetics” and will greatly advance the field of ADHD genetics research.

Why is this finding so important?

The genetics of ADHD are very complex. While ADHD is highly heritable, there are likely to be thousands of genes that contribute to the disorder. Each variant individually increases the risk by only a tiny fraction. To discover these variants, you therefore need incredibly large samples. Only then can you determine which variants are linked to ADHD. The now published study by Ditte Demontis and her team combined data from many different databases and studies, together including more than 55,000 individuals of whom over 22,000 had an ADHD diagnosis.

We can now be certain that the twelve genetic markers contribute to the risk of developing ADHD. Their influence is however very small, so these markers by themselves can’t tell if someone will have ADHD. What’s interesting for the researchers is that none of these markers were identified before in much smaller genetic studies of ADHD. So this provides many new research questions to further investigate the biological mechanisms of ADHD. For instance, several of the markers point to genes that are involved in brain development and neuronal communication.

Why are our researchers excited about this?

A second important finding from the study is that the genetic variants were not specific to ADHD, but overlapped with risk of lower education, higher risk of obesity, increased BMI, and type-2 diabetes. If genetic variants increase both your risk for mental health problems such as ADHD, and for nutrition-related problems such as obesity and type-2 diabetes, then there could be a shared biological mechanism that ties this all together.

We think that this mechanism is located in the communication between the gut and the brain. A complex combination of genetic and environmental factors influence this brain-gut communication, which leads to differences in behaviour, metabolism and (mental) health.genetic markers for adhd

The microorganisms in your gut play an important role in the interaction between your genes and outside environmental influences (such as stress, illness or your diet). Now that we know which genes are important in ADHD, we can investigate how their functioning is influenced by environmental factors. For instance, gut microorganisms can produce certain metabolites that interact with these genes.

The publication by Ditte Demontis and her co-workers is therefore not only relevant for the field of ADHD genetics, but brings us one step closer to understanding the biological factors that influence our mental health and wellbeing.

Further Reading

Demontis et al. (2018) Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature Genetics. https://www.nature.com/articles/s41588-018-0269-7

The first author of the paper, Ditte Demontis, also wrote a blog about the publication. You can read it here: https://mind-the-gap.live/2018/12/10/the-first-risk-genes-for-adhd-has-been-identified/

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Breaking news: It has long been assumed that the gut and the brain communicate not only via a slow, hormonal pathway, but that there must be an additional, faster association between gut and brain. Melanie Maya Kelberer and her colleagues from Duke University, NC, now managed to detect this connection. Their paper has just been published in the renowned journal ‘Science’.

By researching a mouse model, they were able to show that the gut and the brain are connected via one single synapse. This is how it works: A cell in the gut (the so-called enteroendocrine cell) transfers its information to a nerve ending just outside the gut. At the connecting nerve ending (the synapse), the neurotransmitter glutamate – the most important excitatory transmitter in the nervous system – passes on the information about our nutrition to small nerve endings of the vagal nerve, which spreads from the brain to the intestines.

Vagal nerveBy travelling along this vagal nerve, the information from the gut reaches the brainstem within milliseconds. The authors now state that a new name is needed for the enteroendocrine cells, now that they have been shown to be way more than that. The name ‘neuropod cells’ has been suggested. The authors interpret their findings as such, that this rapid connection between the gut and the brain helps the brain to make sense of what has been eaten. Through back-signalling, the brain might also influence the gut. In sum, this finding is an important step towards a better understanding of how the gut and the brain communicate. Findings such as this one help us to find ways to positively influence our brain states and our mental health by our food choices.

Read the original paper here: http://science.sciencemag.org/content/361/6408/eaat5236.long

Kaelberer, M.M., Buchanan, K. L., Klein, M. E., Barth, B. B., Montoya, M. M., Shen, X., and Bohórquez, D. V. (2018), A gut-brain neural circuit for nutrient sensory transduction, ​Science,
​ Vol. 361, Issue 6408

 

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The topic of adopting healthier diets is increasingly popular due to better awareness of issues like obesity, diet-related health problems and illnesses, and a general pursuit of better life quality. A large, longitudinal study in Estonia investigated how eating patterns have changed over the years, and which factors influence the food choices we make.

The Estonian Children Personality Behaviour and Health Study (ECPBHS) is a multidisciplinary study that has been going on for already 20 years. It started in 1998, when participants were 9 and 15 year-old schoolchildren from Tartu County in Estonia. The 1176 children that were included in the study in 1998 were tested again when they were 18, 25 and 33 years-old.

Through the ECPBHS, we have examined different aspects of both mental and physical health, risky behaviour, physical activity, psychosocial well-being, impulsivity and personality. An additional topic of study has also been nutrition.

To investigate whether the children in the study were eating healthy, we have analysed whether the nutrient and food intake comply with the Estonian dietary recommendations. When we compared our results with the previous studies carried out in Estonia1,2 we discovered that although the deficiency in many nutrient intakes showed fairly unhealthy food habits in Estonian schoolchildren3, there was a shift to a better average energy intake and consumption over time, and especially in comparison to the end of 1980s and the beginning of 1990s4. Throughout the years we have seen the tendency towards healthier food habits, but there is still overconsumption of fats. The consumption of fibre, as well as some of the vitamins and minerals, were below the recommendations3.

We know that the changes in society (including working patterns of men and women)5 can bring changes in the eating patterns, and when we looked at the teenagers’ eating habits6, we saw that the role of family was important in how teenagers’ eating habits were influenced. Although we saw that 18 year olds in 2001 and in 2007 were regularly eating three meals a day, there was a shift among boys to have more irregular breakfast consumption in 2007. This was offset by having school-lunch, which was higher in 2007 than in 2001.

teenage girl eating burger and softdrinkWe have also looked at the consumption of fast food and fizzy drinks and discovered that it was affected not only by age, gender, ethnic and urban environment, but it was also affected by mothers’ income and educational level7. We also found that children with certain gene polymorphism (ADRA2A C-1291G) consumed more ready-made sweet food products and sweet sour milk products.8 (Gene polymorphism (two alleles in one place) can cause abnormal gene expression or abnormal protein production, which may cause or can be associated with disease.)

What is important to remember, is that although our genes, family habits and society affect how we eat, we can still learn to make healthy food choices. So do not forget the basics: eat less sweets, and more vegetables and fruits. Fibres and fats are both important, but again, only to a certain amount.

Whatever diet one follows should be balanced, and combined with physical activity. These principles should also be taught to our children, so that they too could enjoy the benefits of a healthier diet and a more active lifestyle. Though, we have seen the tendency towards healthier food habits, there is still a room for improvement. Hopefully, we will see this improvement in our population study in the next few years.

 

Reference list:

  1. Saava, M., Pauts, V., Tšaiko, L., & Sink, R. (1995). Toitumine ja alimentaarsed ateroskleroosi riskitegurid koolieas. Eesti Arst, 4, 319-325.
  2. Grünberg, H., Mitt, K., & Thetloff, M. (1997). Food habits and dietary Intake of schoolchildren in Estonia. Scandinavian Journal of Nutrition, 41, 18-22.
  3. Gross, K. (2006). Eesti koolilaste toitainete ja toidugruppide tarbimine (BA thesis). University of Tartu.
  4. Villa, I., Alep, J., & Harro, M. (2002). Eesti koolilaste toitumine viimasel 15 aastal. Eesti Arst, 88(9), 607.
  5. Mestdag 2005; Lund & Gronow 2014
  6. Jõers-Türn, K. (2015). „Family factors influencing teenagers eating habit“ (MA thesis). University of Tartu.
  7. Alavere, H. (2007). Kiirtoidu ja gaseeritud jookide tarbimine ning seos insuliinresistentsusega Eesti koolilastel (MA thesis). University of Tartu.
  8. Mäestu, J., Villa, I., Parik, J., Paaver, M., Merenäkk,. L., Eensoo, D., Harro, M., & Harro, J. (2007). Human adrenergic α2A receptor C-1291G leads to higher consumption of sweet food products. Molecular Psychiatry 12, 520-521.
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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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