Mens sana in corpore sano – healthy mind and healthy body

Food insecurity – defined as an individual or household lacking access to sufficient, safe, and nutritious food that meets individuals’ dietary needs – has been linked to children’s behavioral, academic, and emotional problems and an increased risk of the development of mental health disorders [1, 2].

In a Canadian study on food insecurity in young children, researchers found that children from food-insecure families were disproportionately likely to experience persistent symptoms of hyperactivity and inattention. These results were still true after controlling for immigrant status, family structure, maternal age at child’s birth, family income, maternal and paternal education, prenatal tobacco exposure, maternal and paternal depression and negative parenting [3].

Accordingly, a systematic review on food insecurity and attention-deficit hyperactivity disorder (ADHD) symptoms in children reported a predictive and inverse relationship between the two, with possible lasting impacts into adulthood. Authors concluded that evidence exists to hypothesize that childhood food insecurity is associated with predisposing or exacerbating ADHD symptoms in children [4].

In 2017 Dr. Raju, President of the Indian Psychiatric Society concluded in a speech on medical nutrition in mental health and disorders that there is growing evidence for a relationship between quality of diet and mental health. According to Raju, the importance of nutrients as important agents for prevention, treatment, or augmentation of treatment for mental disorders has been established. “Empathic interactions and rational nutrition along with specific pharmacological and physical interventions could form an ideal and humane patient-friendly package in psychiatric practice” [5].

Therefore, identifying families in risk of food insecurity and getting children and adolescents the best possible food supply could result in fewer children with ADHD symptoms.

REFERENCES:

  1. Althoff, R.R., M. Ametti, and F. Bertmann, The role of food insecurity in developmental psychopathology. Prev Med, 2016. 92: p. 106-109.
  2. Shankar, P., R. Chung, and D.A. Frank, Association of Food Insecurity with Children’s Behavioral, Emotional, and Academic Outcomes: A Systematic Review. J Dev Behav Pediatr, 2017. 38(2): p. 135-150.
  3. Melchior, M., et al., Food insecurity and children’s mental health: a prospective birth cohort study. PLoS One, 2012. 7(12): p. e52615.
  4. Lu, S., et al., The Relationship between Food Insecurity and Symptoms of Attention-Deficit Hyperactivity Disorder in Children: A Summary of the Literature. Nutrients, 2019. 11(3).
  5. Raju, M., Medical nutrition in mental health and disorders. Indian J Psychiatry, 2017. 59(2): p. 143-148.
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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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Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with an estimated prevalence rate of 5.3% among children and of about 2.5% among adults. It is characterized by a persistent pattern of inattention and/or hyperactivity-impulsivity, being associated with significant impairment of social, academic, and occupational functioning across the lifespan.

However, despite many efforts, the exact etiology of ADHD still remains unknown and data about modificable risk and protective factors are largely lacking. Recent evidence has suggested an association between inflammation, immunological disturbances and ADHD. Supporting this idea, an increased incidence of immune-mediated disorders (e.g. asthma, allergic rhinitis, atopic dermatitis, allergic conjunctivitis, psoriasis, thyrotoxicosis or type 1 diabetes) accompanied by elevated serum/plasma and cerebrospinal levels of inflammatory markers (especially interleukin (IL)-6) or auto-antibody levels (e.g. antibasal ganglia antibodies, antibodies against the dopamine transporter) have been found in these patients.

Importantly, recent studies have shown the gut flora as an important immunoregulator (1-3) and it is hypothesized that an imbalance in the gut microbiota (dysbiosis) may have a negative effect on cerebral development and behavior (4). About 95% of all circulating serotonin, dopamine or noradrenaline precursors are produced by our gut microbiota, being this ‘enteric nervous system’ bidirectional connected to the central nervous system through hormonal or immune/inflammatory pathways.

In line with this, recent findings suggest that some aliments as probiotics can not only revert dysbiosis, but also modulate brain neurodevelopment, activity and improve cognition, mood and behavior due to their immunoregulatory and anti-inflammatory properties (5-7).

Therefore, understanding the microbiota and how the gut connects to the brain would be important both for the better comprehension of the biological bases that underlie some psychiatric disorders such as ADHD, as for the future development of new evidenced-based drugs for these conditions.

This was co-authored by Josep Antoni Ramos-Quiroga, MD PhD psychiatrist and Head of Department of Psychiatry at Hospital Universitari Vall d’Hebron in Barcelona, Spain. He is also professor at Universitat Autònoma de Barcelona.

REFERENCES:

1. Felix KM, Tahsin S, Wu HJ. Host-microbiota interplay in mediating immune disorders. Ann N Y Acad Sci. 2018; 1417(1):57-70.

2. Yadav SK, Boppana S, Ito N, Mindur JE, Mathay MT, Patel A, et al. Gut dysbiosis breaks immunological tolerance toward the central nervous system during young adulthood. Proc Natl Acad Sci U S A.2017; 114(44): E9318-27.

3. Mandl T, Marsal J, Olsson P, Ohlsson B, Andreasson K. Severe intestinal dysbiosis is prevalent in primary Sjögren’s syndrome and is associated with systemic disease activity. Arthritis Res Ther.2017;19(1):237.

4. Rogers GB, Keating DJ, Young RL, Wong ML, Licinio J, Wesselingh S. From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways. Mol Psychiatry. 2016; 21(6):738-48.

5. Slykerman RF, Kang J, Van Zyl N, Barthow C, Wickens K, Stanley T, et al. Effect of early probiotic supplementation on childhood cognition, behavior and mood. A randomized, placebo-controlled trial. Acta Paediatr.2018; 107(12):2172-78.

6. Kane L, Kinzel J. The effects of probiotics on mood and emotion. JAAPA. 2018; 31(5):1-3.

7. Mayer EA. Gut feelings: the emerging biology of gut-brain communication. Nat Rev Neurosci.2011;12(8):453-66

 

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The food choices we make, how much we exercise and the amount of body fat we have affects our health already at a young age. Although seemingly healthy, our metabolism might tell a different story. This can already be seen at a young age.

The Estonian Children Personality Behaviour and Health Study (ECPBHS) started 20 years ago in 1998 and has since measured the participants’ body composition and assessed their metabolic abnormalities, such as insulin resistance and metabolic syndrome, at ages 15, 18, 25 and 33 years.

Insulin resistance is a state in which the body does not respond to normal levels of insulin efficiently, eventually causing a rise in blood sugar levels. It has been proposed that insulin resistance has a role in the development of several metabolic abnormalities what we know as metabolic syndrome1. These metabolic abnormalities include a large waistline (abdominal obesity), high levels of certain types of fat in the blood called triglycerides, a low level of HDL cholesterol, high blood pressure or usage of blood pressure medication and elevated fasting blood sugar levels or type 2 diabetes diagnosis2.

We have found that already at age 25, individuals who consumed more than 300 milligrams of cholesterol per day and had more than 4 hours of screen time were at higher risk of components of metabolic syndrome3. Insulin resistance was associated with male gender3,4, overweight and obesity, low physical activity levels and the consumption of lipids above the recommended daily energy intake*4. Individuals who consumed carbohydrates below the recommended daily energy intake*, were less likely to be insulin resistant. Already at age 25, insulin resistant individuals had higher serum cholesterol, lower HDL cholesterol, and higher triglyceride levels, fasting blood sugar and insulin levels. People who were overweight also had 4 times higher odds of insulin resistance and being obese increased the odds 12 times if compared to normal weight individuals4. From 15 to 25 years the occurrence of components of metabolic syndrome increased rapidly. At age 15 years 18% of participants had one or more metabolic abnormality and by age 25 years the number had doubled, whereas 5% already had metabolic syndrome.3 Individuals who were insulin resistant were more likely to have metabolic syndrome.4

Insulin resistance and the metabolic syndrome are risk factors for type 2 diabetes and cardiovascular disease later in life1. As we observed, one fifth of the adolescents already have at least one metabolic abnormality and the number of components of metabolic syndrome increases from adolescence to young adulthood. That is why it is important that healthy lifestyle habits should be introduced and encouraged already in early childhood. Although young people may seem to be healthy, the first signs of developing metabolic abnormalities may already be there.

*According to the Estonian nutrition and physical activity recommendations (2015), the recommended consumption of macronutrients from daily energy intake (E%) is as following: proteins 10–20%, lipids 25–35%, carbohydrates 50–60%5.

Written by:
Urmeli Joost, MSc is a PhD student at the Institute of Family Medicine and Public Health, University of Tartu, Estonia. Her main focus of research is the genetic, environmental and behavioural factors in obesity, dyslipidemia and glucose metabolism.

Inga Villa, MD, PhD is a Lecturer in Health Promotion at the Institute of Family Medicine and Public Health, University of Tartu, Estonia. Her main focus of research is nutrition, physical activity and sociocultural factors on health status and body composition.

REFERENCES
1. Xu, H., Li, X., Adams, H., Kubena, K. & Guo, S. Etiology of Metabolic Syndrome and Dietary Intervention. Int J Mol Sci 20, (2018).

2. Alberti, K. G. M. M. et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 120, 1640–1645 (2009).

3. Taimur, T. Metaboolse sündroomi komponentide levimus ja seosed toitumisega noorukieast täiskasvanueani. Tartu: Tartu Ülikooli peremeditsiini ja rahvatervishoiu instituut; 2018.

4. Joost U. Insuliinresistentsuse seosed elustiiliharjumustega noortel täiskasvanutel Eestis [masters thesis]. Tartu: Tartu Ülikooli tervishoiu instituut; 2015.

5. Pitsi, et al. Eesti toitumis- ja liikumissoovitused 2015. Tervise Arengu Instituut. Tallinn, 2017.

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Whenever I ask my patients, if they are eating their “5 a day”, the immediate answer is “Yes, sure”. However, sometimes I´m not sure if their “Yes, sure” belongs to their real eating behavior or if it is more like wishful thinking. This question applies for a broad range of behavior, like taking the stairs instead of the elevator, having enough sleep, walking the 10.000 steps a day etc.. But how can we be sure what people really do in their everyday life?

The answer is: Ambulatory Assessment

Ambulatory Assessment is the state of the art method for assessing current emotional states, feelings, and behavior in the natural environment of an individual’s everyday life. Equipped with smartphones and accelerometers, it is feasible to track how individuals feel at specific moments, what they are eating across a day and how they physically behave in real time and real life. Electronic e-diaries, provided by an App, prompt individuals whenever an event occur or randomly several times a day. Especially in patient groups with attention deficits, prompting short questionnaires several times a day show better recall than an extensive end-of-day questionnaire.

In the past, food-diaries were based on unhandy and retrospective paper-pencil-questionnaires or computer input. Nowadays, new technological opportunities pave the way to e-food-diaries on smartphones, enabling an immediate and flexible input capability. The design of e-food-diary-apps may be different, i.e., by photos, drop-down-menu, text, or voice records. Important is the documentation of what and how much the participants eat and drink and a database that can be connected to an international or national food code for data analysis.

In the Eat2beNICE research project, we assess food intake every time participants eat or drink by a drop-down-menu that leads from general to very detailed food-items and asks for general meal portions and amounts every time participants eat and drink across the day. If a participant cannot find a particular food-item, he or she has the opportunity to enter a free text message or to record a voice message. If participants forget to enter some foods and drinks across the day, they will receive a reminder in the evening to add forgotten items. This procedure enables very accurate tracking of participant’s food intake in our study.

To sum up, thanks to modern technology we can now accurately measure what a person feels, does and eats throughout the day. Of course, the design of an e-food-diary on the smartphone depends on the projects’- and samples’ requirements. Overall, it has to be easy to use, easy to implement in daily life and to be fun for the participants to obtain a high level of compliance and a high-quality database.

REFERENCES:
Ebner-Priemer, U. W., & Trull, T. J. (2009). Ambulatory Assessment: An Innovative and Promising Approach for Clinical Psychology. European Psychologist, 14, 109–119. https://doi.org/10.1027/1016-9040.14.2.109.

Engel, S. G., Crosby, Ross, Thomas, G., Bond, D., Lavender, J. M., Mason, T., . . . Wonderlich, Stephen. (2016). Ecological Momentary Assessment in Eating Disorder and Obesity Research: a Review of the Recent Literature. Current Psychiatry Reports, 18, 37. https://doi.org/10.1007/s11920-016-0672-7.

Fuller, N. R., Fong, M., Gerofi, J., Ferkh, F., Leung, C., Leung, L., . . . Caterson, I. D. (2017). Comparison of an electronic versus traditional food diary for assessing dietary intake-A validation study. Obesity Research & Clinical Practice, 11, 647–654. https://doi.org/10.1016/j.orcp.2017.04.001.

Smyth, J., Wonderlich, S., Crosby, R., Miltenberger, R., Mitchell, J., & Rorty, M. (2001). The use of ecological momentary assessment approaches in eating disorder research. The International Journal of Eating Disorders, 30, 83–95.

Stein, K. F., & Corte, C. M. (2003). Ecologic momentary assessment of eating-disordered behaviors. The International Journal of Eating Disorders, 34, 349–360. https://doi.org/10.1002/eat.10194.

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Have you ever noticed that the type of food you eat can affect how you feel afterwards? Some food might make you wish to rest and relax, some food might give you the little extra energy you just needed. Evidence is accumulating that also in the long run, diet may play a pivotal role for your mental health. For example, it might have an effect on impulsive and compulsive behaviour [1].
But it’s not only the diet that affects our body, mind and brain – it’s also the amount of what we eat. Research shows that people don’t necessarily know what a suitable amount of food might be. Sure you can imagine that this can easily lead to obesity – which in turn can impair our general health.

A meta-analysis (that is, a study that investigates an effect among many independent studies that have been conducted so far) from 2018 came to the conclusion that serving size and the size of the tableware has an effect on the amount we eat: When offered larger-sized portions, packages or tableware, participants ate or drank more than when offered smaller-sized versions [2].

British nutritional scientists now developed a guideline for the British Nutrition Foundation (BNF) to help people estimate the suitable serving size. For example, they recommend that when having a pasta dish, you should take as much pasta for one person as fits into both of your hands (before cooking). A portion of fish or meat should be about half the size of your hand. However, this does not mean that when you eat more than one portion, you are an overeater.

According to their tipsheets, which can be found here,
https://www.nutrition.org.uk/healthyliving/find-your-balance/portionwise.html
one should compose his or her daily menu based on a mixture of different portions. For example, 3-4 portions of starchy carbohydrates (such as the above-mentioned pasta) are recommended daily. Their guidelines, however, offer a few handy (literally!) advises to help you get a sense of how much food you should consume, thus preventing you from overeating. With a few simple tips kept in mind, you can do some good for your physical and mental health, daily.

REFERENCES
[1] Sarris J, Logan AC, Akbaraly TN, Amminger GP, Balanzá-Martínez V, Freeman MP, et al. Nutritional medicine as mainstream in psychiatry. Lancet Psychiatry. 2015; 2(3):271-4.
View here:
https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(14)00051-0/fulltext

[2] Hollands GJ, Shemilt I, Marteau TM, Jebb SA, Lewis HB, Wei Y, Higgins JPT,
Ogilvie D. Portion, package or tableware size for changing selection and consumption of food, alcohol and tobacco. Cochrane Database of Systematic
Reviews 2015, Issue 9. Art. No.: CD011045. DOI: 10.1002/14651858.CD011045.pub2
View here:
https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011045.pub2/full

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We have talked before about how ADHD has been associated with obesity and the mechanisms implicated on it. I would like to explain more about this important subject so you can understand what dietary changes you can make to avoid the risk of weight gain. Most of the authors attribute the presence of obesity in ADHD individuals to disorder eating patterns, especially overeating, that means that these people are eating a higher amount of calories per day in comparison of individuals without ADHD. When a person consumes more calories or food than their body needs they start to gaining weight and this happens to all kind of people, I’m not talking only about those who have ADHD, and that becomes a health problem.

Nevertheless, there is a recent study that suggests that ADHD-obesity relationship was linked to unhealthy food choices, rather than overeating behavior (1). This means that ADHD individuals are eating the same amounts of calories per day as healthy ones, but their food choices are not good enough to meet the dietary recommendations and can lead to nutritional deficiencies that have been observed on these patients (2,3). These kinds of patients tend to eat more processed meat, unhealthy snacks, and refined cereals; instead of consuming healthy food choices like vegetables, fruits, whole grains, nuts, and fish.

We can suggest that this problem it may be due to the fact that there is a lack of information related to nutrition, so it is easy to get confused on which food products are healthy and which are not.

When you go to the supermarket, you will find a lot of food options that have a label that says “light” or “healthy,” and you may buy them without analyzing if they are genuinely healthy.

So the question is “how can you know if a product is healthy or not?”

First of all, you should opt to buy fresh products such as fruits, vegetables and fish (foods that are rich in vitamins and minerals needed to maintain our mental health in good shape). And avoid consuming fast, packaged or canned food because these kinds of products contain a lot of sodium, sugar, fat, preservatives, additives and components that in high amounts can lead to health issues.

Second, if you need to buy food products that are packaged or canned, you should be able to read and understand the nutritional information and ingredients before you buy them to be sure they are the healthiest options on the market.

Here I share an example on what to search on nutrition facts labels of food products to make the right selection.

For more information on how to understand and use the nutrition facts label you can visit: www.fda.gov/food/labelingnutrition/ucm274593.htm#see3

This was co-authored by Josep Antoni Ramos-Quiroga, MD PhD psychiatrist and Head of Department of Psychiatry at Hospital Universitari Vall d’Hebron in Barcelona, Spain. He is also a professor at Universitat Autònoma de Barcelona.

REFERENCES
1. Hershko S, Aronis A, Maeir A, Pollak Y. Dysfunctional Eating Patterns of Adults With Attention Deficit Hyperactivity Disorder. J Nerv Ment Dis [Internet]. 2018;206(11):870–4.

2. Kotsi E, Kotsi E, Perrea DN. Vitamin D levels in children and adolescents with attention-deficit hyperactivity disorder (ADHD): a meta-analysis. Atten Defic Hyperact Disord [Internet]. Springer Vienna; 2018.

3. Landaas ET, Aarsland TIM, Ulvik A, Halmøy A, Ueland PM, Haavik J. Vitamin levels in adults with ADHD. Br J Psychiatry Open [Internet]. 2016;2(6):377–84.

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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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