Recent research (1,2) on children and adolescents has reported that elevated levels of ADHD symptoms are positively associated with unhealthy dietary habits, including a higher consumption of refined sugars, processed food, soft drink, instant noodles, and a lower intake of vegetables and fruits. However, the link between low-quality diets and risk of ADHD in adults is still not well established, which would be further explored in the ongoing Eat2beNICE research project.

What is the underlying mechanism for an association between ADHD and unhealthy dietary habits? There is still no clear answer. Nemours’ potential biological pathways, by which dietary intake could have an impact on mental health, has been proposed in the literature (2). For example, iron and zinc are cofactors for dopamine and norepinephrine production (essential factors in the etiology of ADHD), so unbalanced diet with lower levels of iron and zinc may further contribute to the development of ADHD. However, we cannot overlook the possibility of a bi-directional relationship between diet quality and ADHD, especially when the interest in the concept of “food addiction” has received increased attention.

Food addiction refers to being addicted to certain foods (e.g. highly processed foods, highly palatable foods, sweet and junk foods) in a similar way as drug addicts are addicted to drugs. Animal models (3) have suggested that highly processed foods may possess addictive properties. Rats given high-sugar or high-fat foods display symptoms of binge eating, such as consuming increased quantities of food in short time periods, and seeking out highly processed foods despite negative consequences (e.g. electric foot shocks). One human study (4) found that individuals with high levels of ADHD-like traits (e.g. high levels of impulsively, disorganised, attention problems) were more likely to suffer from problematic eating behaviour with overconsumption of specific highly palatable foods in an addiction-like manner. Therefore, food addiction may, just as substance abuse, be over-represented among individuals with ADHD.

Thus, it seems there could be a vicious cycle between unhealthy dietary habits and ADHD: ADHD may lead to a worse choice of diet, lowering the health quality, which could eventually exacerbate ADHD symptoms. We will further test the bidirectional diet-ADHD associations in the ongoing Eat2beNice project.

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. Kim KM, Lim MH, Kwon HJ, Yoo SJ, Kim EJ, Kim JW, et al. Associations between attention-deficit/hyperactivity disorder symptoms and dietary habits in elementary school children. Appetite. 2018;127:274-9.

2. Rios-Hernandez A, Alda JA, Farran-Codina A, Ferreira-Garcia E, Izquierdo-Pulido M. The Mediterranean Diet and ADHD in Children and Adolescents. Pediatrics. 2017;139(2).

3. Gearhardt AN, White MA, Potenza MN. Binge Eating Disorder and Food Addiction. Curr Drug Abuse Rev. 2011;4(3):201-7.

4. Ptacek R, Stefano GB, Weissenberger S, Akotia D, Raboch J, Papezova H, et al. Attention deficit hyperactivity disorder and disordered eating behaviors: links, risks, and challenges faced. Neuropsychiatr Dis Treat. 2016;12:571-9.

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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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A hot topic these days, that one can hear more and more information about is the microbiota-gut-brain axis, the bidirectional interaction between the intestinal microbiota and the central nervous system nowadays, this has become a hot topic. We are becoming increasingly aware that gut microbiota play a significant role in modulating brain functions, behavior and brain development. Pre- and probiotics can influence the microbiota composition, so the question arises, can we have an impact on our mental health by controlling nutrition and using probiotics?

Burokas and colleagues aimed to investigate this possibility in their study (2017), where the goal was to test whether chronic prebiotic treatment in mice modifies behavior across domains relevant to anxiety, depression, cognition, stress response, and social behavior.

In the first part of the study, the researchers fed mice with prebiotics for 10 weeks. They were administered the prebiotics fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), a combination of both, or water. FOS and GOS are soluble fibers that are associated with the stimulation of beneficial bacteria such as bifidobacterium and lactobacillus.

Behavioral testing started from the third week including

  • the open field test (anxiety – amount of exploratory behavior in a new place),
  • novel object test (memory and learning – exploration time of a novel object in a familiar context), and
  • forced swimming test (depression-like behavior – amount of activity in the cylinder filled water).

Meanwhile, plasma corticosterone, gut microbiota composition, and cecal short-chain fatty acids were measured. Taken together, the authors found that the prebiotic FOS+GOS treatment exhibited both antidepressant and anxiolytic (anti-anxiety) effects. However, there were no major effects observed on cognition, nociception (response to pain stimulus), and sociability; with the exception of blunted aggressive behavior and more prosocial approaches.

In the second part, FOS+GOS or water-treated mice were exposed to chronic psychosocial stress. Behavior, immune, and microbiota parameters were assessed. Under stress, the microbiota composition of water-treated mice changed (decreased concentration of bifidobacterium and lactobacillus), which effect was reversed by treatment with prebiotics.

Furthermore, it was found that three weeks of chronic social stress significantly reduced social interaction, and increased stress indicators (basal corticosterone levels and stress-induced hyperthermia), whereas prebiotic administration protected from these effects.

After stimulation with a T-cell activator lectin (concanavalin A), the stressed, water-treated mice group presented increased levels of inflammatory cytokines (interleukin 6, tumor necrosis factor alpha), whereas in animals with prebiotics had these at normal levels.

Overall, these results suggest a beneficial role of prebiotic treatment in mice for stress-related behaviors and supporting the theory that modifying the intestinal microbiota via prebiotics represents a promising potential for supplement therapy in psychiatric disorders.

Watch YouTube Video:
https://youtu.be/E479yto8pyk

REFERENCES
Burokas, A., Arboleya, S., Moloney, R. D., Peterson, V. L., Murphy, K., Clarke, G., Stanton, C., Dinan, T. G., & Cryan, J. F. (2017). Targeting the Microbiota-Gut-Brain Axis: Prebiotics Have Anxiolytic and Antidepressant-like Effects and Reverse the Impact of Chronic Stress in Mice. Biological Psychiatry, 82(7), 472–487. https://doi.org/10.1016/j.biopsych.2016.12.031

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