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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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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MoBa is short for The Norwegian Mother and Child Cohort Study which is a large pregnancy observational study. During the years 1999-2008 pregnant women in Norway were recruited to the study. The study is conducted by the Norwegian Institute of Public Health. Questionnaires regarding health, diet and environment were sent out to the women during and after pregnancy. Women are sent regular follow-up questionnaires. As the child grows up, the child also completes questionnaires. In addition, the fathers were invited to participate with a questionnaire when their partner was pregnant. Biological samples were also collected from the mother, father and child. Today there are 114 500 children, 95 000 mothers and 75 000 fathers participating in the study.

https://www.fhi.no/en/studies/moba/

The study was set up to gain knowledge about the causes behind serious disease. The study is unique because it gathers information from fetal (in vitro) life and follows the offspring into adulthood. In this manner it is possible to look at early influences and later disease. The study is prospective, which means that information about mothers, fathers and their offspring is registered before a disease has manifested itself. With this design, women are asked questions several times during her pregnancy and do not have to try to remember what she did when looking back at her pregnancy.

MoBa is population-based and became nationwide with 50 participating hospitals in Norway. For more information on the many publications based on MoBa data, visit this link:

https://www.fhi.no/en/studies/moba/for-forskere-artikler/publications/

The participating women in MoBa also filled in a questionnaire about eating habits before and during pregnancy.

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Why do some people have a higher craving for carbohydrate-rich and junk-food than others? Why are weight-loss programs more effective in some individuals than others? And why are some people more physically active?

The dopamine system in the brain plays an important role in regulating how much you eat and whether or not you gain weight. When this system does not function optimally, people have a higher craving for junk-food, lower physical activity, and unsuccessful body weight control.

There are two mechanisms that determine food-related behaviour.

The more direct, homeostatic, mechanism constantly surveys the body’s energetic needs and holds them actively in balance. That is homeo-stasis.

The second non-homeostatic mechanism determines the way humans, and other animals, react to food: how willingly and often they will consume it again, and whether they feel anticipation or craving for it.

These behaviours are both largely regulated by the neurotransmitter dopamine, a chemical that conveys information in the brain. Once released by one nerve cell it binds to a receptor, a large molecule on the surface of the adjacent nerve cell, thus changing its functioning. A major component in eating-related behaviour is the dopaminergic D2 receptor (DRD2) that is most abundantly localized in striatum, a brain region activated by food anticipation and consumption1.

The function of the dopaminergic system affects eating and weight-related problems in four ways.

First, in some people, the dopamine system reacts more vigorously in response to food.

Second, this response leads to increased eating and possibly obesity.

Third, overeating and obesity lead to less efficient dopaminergic signaling.

Fourth, this lower dopaminergic signal needs to be compensated by more intense behaviour e.g., more eating2.

For example, in people with lower levels of dopamine D2 receptor, cravings for carbohydrate-rich food and junk-food are more prevalent3,4.

Besides eating-related behaviour, dopamine also affects health/obesity via voluntary physical activity, creating a vicious circle: obesity leads to weaker dopaminergic signal, especially lower levels of DRD2 receptor, and this, in turn, leads to decreased exercise and motivation for physical activity5–7.

Furthermore, individuals with lower levels of DRD2 receptors may benefit less from long-term weight loss programs and are less effective in weight maintenance8,9. Thus, dopamine affects body weight via choice of foods, physical activity, and body weight reduction efficacy. Despite the reasons for food-cravings, part of the solution is acknowledging and managing these impulses. Conscious action towards weight-reduction will lead to less pronounced food-cravings, which in turn leads to favourable solution of weight related problems10.

REFERENCES
1. Wise, R.A. Philos Trans R Soc Lond B Biol Sci 361, 1149–1158 (2006).
2. Alonso-Alonso, M. et al. Nutrition reviews 73, 296–307 (2015).
3. Lek, F.-Y., Ong, H.-H. & Say, Y.-H. Asia Pac J Clin Nutr 27, 707–717 (2018).
4. Yeh, J. et al. Asia Pac J Clin Nutr 25, 424–429 (2016).
5. Kravitz, A.V., O’Neal, T.J. & Friend, D.M. Front Hum Neurosci 10, 514–514 (2016).
6. Matikainen-Ankney, B.A. & Kravitz, A.V. Ann N Y Acad Sci 1428, 221–239 (2018).
7. Ruegsegger, G.N. & Booth, F.W. Front Endocrinol 8, 109–109 (2017).
8. Roth, C.L., Hinney, A., Schur, E.A., Elfers, C.T. & Reinehr, T. BMC Pediatr 13, 197–197 (2013).
9. Winkler, J.K. et al. Nutrition 28, 996–1001 (2012).
10. Smithson, E.F. & Hill, A.J. Eur J Clin Nutr 71, 625 (2016).

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We, human beings in Western society, make over 200 food choices each day (1). That’s a lot! Fortunately (or, according to others, unfortunately), we don’t actually have to think about each and every one of them, or at least not consciously. If our food choices are not so much a conscious decision, then how do we make them? A lot has been written about external factors influencing our food choices, for instance, alluring displays in supermarkets or the availability of unhealthy foods in our day-by-day environment. In this blog, I will address the potential role of genetics on food choices: to what extent do our genes determine what we eat?

Eating behaviours are complex, i.e. they are very diverse and influenced by many different factors. When we investigate complex behaviours, we are unlikely to find simple explanations. In other words: we do not expect to find one gene that makes me prefer pizza margarita over pizza fungi, nor will we find a single gene responsible for my triple-chocolate ice cream consumption. There are, however, some instances in which specific genes have relatively simple and straightforward effects on our food choices. This is the case when genetic variants code for food sensitivities.

A famous example is the LCT gene (or, more precisely, the C>T change at 13910 bases upstream of the LCT gene in the 13th intron of the MCM6 gene). The LCT gene codes for lactase persistence, or lactose tolerance after childhood. Worldwide, the majority of people (and most other mammals, for that matter) no longer tolerate dairy products after childhood. For them, consuming milk products causes nausea, bloating and cramping within 2-3 hours. As a result, they will soon learn not to consume dairy products. Those who have the lactase persistence gene, however, don’t have any problems digesting dairy products and, thus, are more likely to consume them (2). Geographical region is important here: while in Northern European countries such as the UK and Finland, 90-100% of people tolerate dairy products, in South-East Asia and Australia this number is close to 0% (3).

A similar situation seems to occur for genes coding for certain taste receptors on the tongue. The TAS2R38 gene, for instance, makes some people extremely sensitive to bitter taste. This, of course, will cause them to avoid bitter foods such as cruciferous vegetables (4). A recent study has even identified a small number of genes that together cause people to either love or hate marmite (5)! Another gene variant (CYP1A1), coding for caffeine clearance from the body, causes carriers to drink less or more coffee and tea (6).

Thus, when food sensitivities are involved, food choices can be driven by specific genes. Most food choices, however, have very little to do with food sensitivities and are much more complex. Pizza Margarita or Pizza Funghi? Triple-chocolate ice cream today or maybe tomorrow? While for such complex food choices there is no single gene responsible, our genetic make-up still does have influence. Typically, for complex behaviours, many different genes can be identified. While each gene individually contributes only a little bit, together they can actually have quite an effect on your food choices. For instance, a recent study identified seven genetic variants each having a small effect on carbohydrate intake. Taken together, genes explained 8% of the variation in carbohydrate intake between individuals (7).

In conclusion: while some genetic variants have rather drastic effects on our food choices, by giving us a physical adverse reaction to certain foods, there are only few of them. Most of our food choices are much more complex. These are influenced by multiple genes at the same time, and even together these genes have only limited influence.

REFERENCES
1. Wansink, B., & Sobal, J. (2007). Mindless eating: The 200 daily food decisions we overlook. Environment and Behavior, 39(1), 106-123. doi: 10.1177/0013916506295573

2. Szilagyi, A. (2015). Adaptation to Lactose in Lactase Non Persistent People: Effects on Intolerance and the Relationship between Dairy Food Consumption and Evolution of Diseases. Nutrients, 7(8):6751-79. doi: 10.3390/nu7085309

3. Itan, Y., Jones, B.L., Ingram, C.J.E., Swallow, D.M. & Thomas, M.G. (2010). A worldwide correlation of lactase persistence phenotype and genotypes. BMC Evol Biol, 10:36. doi: 10.1186/1471-2148-10-36

4. Feeney, E., O’Brien, S., Scannell, A., Markey, A. & Gibney, E.R. (2011). Genetic variation in taste perception: does it have a role in healthy eating? Proc Nutr Soc, 70(1):135-43. doi: 10.1017/S0029665110003976.

5. Roos, T.R., Kulemin, N.A., Ahmetov, I.I., Lasarow, A. & Grimaldi, K. (2017). Genome-Wide Association Studies Identify 15 Genetic Markers Associated with Marmite Taste Preference. BioRxiv (preprint). doi: 10.1101/185629

6. Josse, A.R., Da Costa, L.A., Campos, H. & El-Sohemy, A. (2012). Associations between polymorphisms in the AHR and CYP1A1-CYP1A2 gene regions and habitual caffeine consumption. Am J Clin Nutr, 96(3):665-71. doi: 10.3945/ajcn.112.038794.

7. Meddens, S.F.W., de Vlaming, R., Bowers, P., Burik, C.A.P., Karlsson Linnér, R., Lee, C., et al. (2018). Genomic analysis of diet composition finds novel loci and associations with health and lifestyle. BioRxiv (preprint). doi: 10.1101/383406

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Have you ever heard of the Okinawa Islands, located between Japan and Taiwan, which host one of the longest living people in the world? Even compared with the rest of Japan, to which the islands belong, people grow older on Okinawa.

On average, women become 86 years, men 78 years (1). And more than that, people there maintain a good health up until a very high age. So, what exactly is it that the Okinawans do differently? And what can we change in our lives to get the same positive effects for our health?

Research has extracted many factors that might contribute to this striking longevity, such as a constant moderate physical activity, lack of time pressure and the importance of a solid family structure (see also my blog on effective lifestyle changes here: https://newbrainnutrition.com/four-easy-rules-for-healthy-eating-and-lifestyle/).

What might be easier to change in our everyday lives, however, is the composition of the food we eat.

Let’s investigate what makes the Okinawan diet so healthy (2):

Their diet is rich in root vegetables, especially the very healthy sweet potato. (Who would have guessed that a vegetable carrying the term “sweet” could be more beneficial for your health than its common counterpart?). Sweet potatoes have a high content of dietary fibers, anti-oxidant vitamins A, C and E and anti-inflammatory properties.

They eat many legumes, such as soybeans.

An abundance of mostly green and yellow vegetables is eaten regularly.

Okinawans don’t abstain from meat, alcohol or tea. They consume it in moderation, choosing lean meat and products from the sea.

It seems that no food should be strictly avoided, but that it’s more like the phrase: “Eat everything in moderation and not in abundance.”

Different fruit and medicinal plants (like curcumin or bitter melon) further contribute to a healthy and diverse cuisine.

Altogether, their food is high in unrefined carbohydrates (refined carbohydrates occur e.g. in sweets or white bread, unrefined carbohydrates occur e.g. in brown rice or wholemeal bread) and they consume protein in moderate amounts and mostly plant-based (from legumes, vegetables, but also occasionally from fish or meat).

The Okinawan diet is characterized by a healthy fat profile: rich in omega-3 fatty acids (which occur in fatty fish like salmon, but also in seeds, like flaxseeds, and nuts), high in other polyunsaturated and monounsaturated fatty acids (occurring e.g. in olive oil or avocado, and low in saturated fats (e.g. occuring in butter).

Hence, its composition resembles that of the Mediterranean Diet, which also is associated with a lower risk of cardiovascular disease and other age- and lifestyle-related diseases (Download your free report on the current state of research on the Mediterranean diet here: https://newbrainnutrition.com/the-mediterranean-diet-and-depression-free-report-download/).

By changing our diet and adapting it to the Okinawan (or Mediterranean) diet, you could contribute to a long and healthy life.

Now you might ask how this relates to “new brain nutrition”? Well, a healthy diet affects our gut, which is linked closer to our brain than we originally have assumed (learn more here: https://newbrainnutrition.com/the-gut-brain-axis-an-important-key-to-your-health/​).

Hence, diet should have an impact on our brain health just as on our general health. Substances from fermented soy beans (so-called ​natto), for example, are said to have the potential to prevent the formation of plaque in the brain, which is related to Alzheimer’s disease.

Also, anti-inflammatory effects of a high polyunsaturated fatty acid consumption might have an effect on the production of neurotransmitters (essential for the transfer of information between nerve cells), which largely takes place in the gut.

Interestingly, due to a more western-style cuisine, the younger Okinawans are starting to face the same diseases such as diabetes, high blood pressure, etc, just as people from the rest of the world.

Diet matters. So: What changes in your diet do ​you​ want to start with?

Take the first step and try a typical Okinawa dish: Goya Champuru

1 Goya cucumber (may also be frozen)

1 block tofu, dried and as firm as possible approx. 80-100g

Shabu-Shabu meat (thinly sliced pork); cut meat into bite-sized pieces

1-2 tablespoons soy sauce

1-2 tablespoons rice wine (sake)

1/2 teaspoon salt

2 tablespoons neutral oil (must be suitable for frying!)

2 eggs

For vegetarians: Follow the same recipe, but replace Shabu-Shabu with chopped vegetables like carrots, onions, cabbage and bean sprouts or pumpkin.

Wash the Goya cucumber, cut it in half and remove the seeds with a spoon. Slice thinly, salt it, let it rest for a few minutes. Wash again, press firmly to remove as much water as possible.

Stir-fry the Shabu-Shabu in a tablespoon of oil, salt it afterward.

Add tofu and stir-fry it until it turns slightly dark. Put tofu and Shabu-Shabu aside.

In the same pan, heat another tablespoon of oil and stir-fry the Goya cucumber in high temperature.

Add the meat and tofu, then soy sauce and sake, stir.

Scramble two eggs and add them.

Stir and don’t let the food turn too dry.

Serve the Champuru with rice.

REFERENCES
(1) https://de.wikipedia.org/wiki/Präfektur_Okinawa

(2) Willcox DC; Scapagnini G; Willcox BJ. Healthy aging diets other than the Mediterranean: a focus on the Okinawan diet.Mech Ageing Dev. 2014; 136-137:148-62 (ISSN: 1872-6216); found here: https://www.sciencedirect.com/science/article/pii/S0047637414000037

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In every classroom, approximately two children are diagnosed with Attention Deficit Hyperactivity Disorder (ADHD). They struggle with attention problems and hyperactive and impulsive behavior. This has negative consequences for these children. For example, they can have difficulties learning, it puts them at risk for other psychiatric problems, and it can cause parent-child relationship problems. Therefore, children with ADHD do need some sort of treatment for optimizing the quality of their lives.

After psycho-education to the child, parents and teacher, medication is often the first choice of treatment because it is evidence-based. However, there is a growing group of parents that do not wish to medicate their child. They are concerned about the side and long-term effects. Thus, these parents seek other treatment. That is where they get stuck: which other effective treatments are available?

In order to develop new treatments, there is a growing field of research focusing on risk factors for ADHD symptoms. One of these risk factors that has been studies increasingly is nutrition. Nutrition plays a role in physical well-being, but could also play a role in psychological well-being and cognitive functioning. Consequently, dietary treatments could be an alternative treatment for children with ADHD. There is a long history of research in nutrition, but there is not enough evidence yet about the cost-effectiveness to implement dietary treatments in clinical health care.

So far, studies examining the effectiveness of a so-called elimination diet showed the strongest effects (1). The aim of an elimination diet is to find out which products trigger ADHD symptoms. However, results of these studies are inconclusive because of several limitations. First, outcome measurements used in these studies were not objective. Second, studies suffered from a sample bias towards highly motivated and educated parents. Third, underlying mechanisms are still unknown. Fourth, long-term effects are unknown. Moreover, it is unknown if an elimination diet is more effective in reducing ADHD symptoms than a healthy diet based on the World Health Organization (WHO) guidelines (2).

We thought: can we take into account these limitations ánd examine the effectiveness of two dietary treatments? This resulted in the TRACE study: ‘Treatment of ADHD with Care as usual versus an Elimination diet’ (TRACE) study. This is the first study to determine the short- and long-term effectiveness and cost-effectiveness of two dietary treatments as initial addition to care as usual as a treatment trajectory for children with ADHD. We will substantially improve upon previous studies by implementing the intervention in non-commercial mental health centers, including blinded and objective measurements, and comparing two dietary treatments with care as usual. Also, understanding the biological effects could inform clinicians to potential markers and targets for preventative or individualized treatment. For this reason, we also examine the underlying biological mechanisms (e.g. mechanisms in the gut and brain) of dietary treatments (TRACE-BIOME and TRACE-MRI studies). We collect blood, stool and saliva samples.

The TRACE study is a two-arm randomized control trial: participants are randomized to either an elimination diet or a healthy diet. The comparator arm includes children who are being treated with care as usual. Currently, we included in each dietary treatment arm about half of the targeted participants (N=81 in each dietary group). In the care as usual group, we included about one-third of the targeted participants (N=60). We hope to finish inclusion around January 2020.

I am really looking forward to the results and hope to share this with you in a couple of years! If you have any questions, feel free to contact us via trace@karakter.com

REFERENCES
(1) Nigg, J. T., Lewis, K., Edinger, T., & Falk, M. (2012). Meta-analysis of attention- deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives. Journal of the American Academy of Child & Adolescent Psychiatry, 51(1), 86-97. https://doi.org/10.1016/j.jaac.2011. 10.015 .
Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321798/

(2) Izquierdo Pulido, M. L., Ríos Hernández, A., Farran, A., & Alda, J. Á. (2015). The role of diet and physical activity in children and adolescents with ADHD. Recent Advances in Pharmaceutical Sciences V, 2015, Research Signpost. Chapter 4, p. 51-64.
Link: http://diposit.ub.edu/dspace/bitstream/2445/67543/1/T_1444299316Munozv%204.pdf

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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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Our body is colonized by trillions of microorganisms that are important for vital processes. Gut microbiota are the microorganisms living in the intestinal gut and play an essential role in digestion, vitamin synthesis and metabolism, among others. The mouth and the large intestine contain the vast majority of gut microbiota whether the stomach only contains few thousands of microorganisms, especially due to the acidity of its fluids. Microbiota composition is constantly changing, affecting the well-being and health of the individual.

Each individual has a unique microbiota composition, and it depends on several factors including diet, diseases, medication and also the genetics of the individual (host) (Figure). Some medicines, especially antibiotics, reduce bacterial diversity. Strong and broad spectrum antibiotics can have longer effects on gut microbiota, some of them up to several years. Genetic variation of an individual also affects the microbiota composition, and the abundance of certain microorganisms is partly genetically determined by the host.

The main contributor to gut microbiota diversity is diet, accounting for 57% of variation. Several studies have demonstrated that diet’s composition has a direct impact on gut microbiota. For example, an study performed on mice showed that “Western diet” (high-fat and sugar diet), alters the composition of microbiota in just one day! On the other hand, vegetarian and calorie restricted diet can also have an effect on gut microbiota composition.

Prebiotics and probiotics are diet strategies more used to control and reestablish the gut microbiota and improve the individual’s health. Probiotics are non-pathogenic microorganisms used as food ingredients (e.g. lactobacillus present in yoghurt) and prebiotics are indigestible food material (e.g. fibers in raw garlic, asparagus and onions), which are nutrients to increase the growth of beneficial microorganisms.

In the last years the new term psychobiotics has been introduced to define live bacteria with beneficial effects on mental health. Psychobiotics are of particular interest for improving the symptomatology of psychiatric disorders and recent preclinical trials have show promising results, particularly in stress, anxiety and depression.

Overall, these approaches are appealing because they can be introduced in food and drink and therefore provide a relatively non-invasive method of manipulating the microbiota.

AUTHORS:
Judit Cabana-Domínguez and Noèlia Fernàndez-Castillo

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