Have you ever done your weekly grocery shopping and ended up with more than actually written on your grocery list?
Everybody has at least once experienced how it is to buy food in a supermarket with hunger and buy much more than planned. The widely known recommendation: Never go grocery shopping when you are hungry!!!

But is it only a myth or is there a grain of truth in that advice?
What exactly is the issue with going grocery shopping when you are hungry? If you do you probably buy more food than you need and planned to buy. Additionally, unhealthy food might be much more attractive for you than healthy food. The consequence: you have more food at home, so you might eat more and unhealthier. Imagine you are hungry and are coming home from work after a stressful day and now you get to choose between a frozen pizza and a healthy meal that has not been prepared yet – What would you choose? In that situation, I think I would definitely choose the frozen pizza.

High-calorie food and unhealthy food are associated with obesity. Obesity research found a moderate relationship between obesity and emotional disorders like depressive disorder and anxiety disorder (1). Thus, having fast food frequently might not only affect your physical, but also your mental well-being.

Let’s rewind to grocery shopping, but now consider you are not hungry. You probably would only buy the things that are on your grocery list, and also rather healthy food than an unhealthy one. So now you come home hungry from a stressful day at work and you don’t have the choice between healthy and unhealthy food, and the temptation of the frozen pizza isn’t there. So you would start to prepare your healthy food and thus automatically eat healthier.

Coming back to the question if these scenarios are devised or true, and thus representative for weekly grocery shopping.
Research has shown that impulsivity, obesity, and food buying behavior are related. People with obesity are more impulsive than slim people. Also, impulsive people eat more than less impulsive people. Hunger influences food buying behavior and food consumption, especially of high caloric food. The relationship between impulsivity and buying food might be state dependent: researchers have found that impulsive people bought more calories, especially from snack food, but only when they were feeling hungry. This means that impulsivity and hunger interact in their influence on consumption. Obese people are found to show a preference for energy-dense, high-fat food and eat more of these foods, compared to slim people (2).

So what’s the conclusion?
Yes, hunger influences your grocery shopping, especially in interaction with impulsivity. If you consider yourself an impulsive person, you might be more prone to buying more than intended when you go shopping hungry.

So if you have the chance: only go shopping for groceries when you are full and focused. If you accidentally get into a hungry grocery shopping situation, keep this blog in mind and try to focus on your grocery list.

REFERENCES:
Scott, K. M., Bruffaerts, R., Simon, G. E., Alonso, J., Angermeyer, M., de Girolamo, G., … & Kessler, R. C. (2008). Obesity and mental disorders in the general population: results from the world mental health surveys. International journal of obesity32(1), 192.

Nederkoorn, C., Guerrieri, R., Havermans, R. C., Roefs, A., & Jansen, A. (2009). The interactive effect of hunger and impulsivity on food intake and purchase in a virtual supermarket. International journal of obesity33(8), 905.

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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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Feeling more happy after a run? Or feeling a bit blue during the dark winter days? Regular exercising and regular daylight exposure can influence your mood, behaviour and sleep-wake cycle 1,2,3. But can this also be used in a therapeutical setting, for instance in addition to or instead of the usual treatment with medication?

The PROUD trial aims to investigate the potential of bright light therapy and physical exercise to improve and prevent depression and obesity in adolescents and young adults with ADHD. This clinical trial is part of the CoCA research project, in which comorbid conditions of ADHD are investigated [insert hyperlink: https://coca-project.eu/coca-phase-iia-trial/study/]. In addition, we collect the stool samples of all participants in order to investigate the effects of physical exercise on the gut microbiome and how this is linked to behaviour. That part of the study is part of the Eat2beNICE research project.

Most people with Attention Deficit Hyperactivity Disorder (ADHD) receive medication to reduce their symptoms4. While this medication works well for many people, there is a lot of interest in other types of treatment. One reason for this is that people with ADHD suffer from additional conditions, such as depression5 and obesity6. The risk for developing these comorbid conditions is especially high during adolescence and young adulthood4.

Adolescents and young adults (age 14-45) with ADHD that want to participate are randomly assigned to one of three groups: 10-weeks of daily light therapy (30 minutes), 10-weeks of daily physical exercise (3x per day) or 10-week care as usual (for instance, the normal medication). The random assignment is very important here in order to compare the different interventions. We don’t want to have all people that like sports in the physical exercise group, because then we don’t know if the effects of the physical exercise are due to the intervention, or due to the fact that these people just like sports better.

Another nice feature of the study is that it uses a phone app (called m-Health). This app is used to remind the participants to do their exercise or light therapy, but it also gives feedback and summaries of how the participant is doing. The app is linked to a wrist sensor that measures activity and light.

The clinical trial is currently ongoing in London (England), Nijmegen (Netherlands), Frankfurt (Germany) and Barcelona (Spain). We can’t look at the results until the end of the trial, so for those we will need to wait until 2021. But in the mean time the PROUD-researchers have interviewed four participants. You can read these interviews here:

This blog is based on the blog “10 weeks of physical exercise or light therapy: what’s it like to participate in our clinical trial?” by Jutta Mayer and Adam Pawley, 9 Oct. 2018 on MiND the Gap – https://mind-the-gap.live/2018/10/09/10-weeks-of-physical-exercise-or-light-therapy/

REFERENCES

  1. Terman, M. Evolving applications of light therapy. Sleep Medicine Reviews. 2007; 11(6): 497-507.
  2. Stanton, R. & Reaburn, P. Exercise and the treatment of depression: A review of the exercise program variables. Journal of Science and Medicine in Sport. 2014; 17(2):177-182
  3. Youngstedt, S.D. Effects of exercise on sleep. Clinical Sports Medicine. 2005; 24(2):355-365.
  4. Cortese S, Adamo N, Del Giovane C, Mohr-Jensen C, Hayes AJ, Carucci S, et al. Comparative efficacy and tolerability of medications for attention-deficit hyperactivity disorder in children, adolescents, and adults: a systematic review and network meta-analysis. Lancet Psychiatry. 2018;5(9):727-738.
  5. Jacob CP, Romanos J, Dempfle A, Heine M, Windemuth-Kieselbach C, Kruse A, et al. Co-morbidity of adult attention-deficit/hyperactivity disorder with focus on personality traits and related disorders in a tertiary referral center. Eur Arch Psychiatry Clin Neurosci. 2007;257:309–17.
  6. 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. Am J Psychiatry. 2016;173:34–43.
  7. Meinzer MC, Lewinsohn PM, Pettit JW, Seeley JR, Gau JM, Chronis-Tuscano A, et al. Attention-deficit/hyperactivity disorder in adolescence predicts onset of major depressive disorder through early adulthood. Depress Anxiety. 2013;30:546–53
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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 have discussed the association between ADHD and obesity in our first blog (https://newbrainnutrition.com/adhd-and-obesity-does-one-cause-the-other/), briefly summarized, evidence from various study designs suggested that shared etiological factors might contribute to the above association. Recently, a large genome-wide association study (GWAS) on risk genes for ADHD reported a significant genetic correlation between ADHD and a higher risk of overweight and obesity, increased BMI, and higher waist-to-hip ratio, which further supported that there could be genetic overlap between obesity and ADHD (1).

Considering the previously described occurrence of unhealthy dietary intake in children and adolescents with ADHD in our second blog (https://newbrainnutrition.com/unhealthy-diets-and-food-addictions-in-adhd/), along with the fact that bad eating behaviours are crucial factors for the development of obesity, We can speculate that the shared genetic effects between ADHD and unhealthy dietary intake may also explain the potential bidirectional diet-ADHD associations. Is there any available evidence to support the above hypothesis?

To date, dopaminergic dysfunctions underpinning reward deficiency processing (or neural reward anticipation), was reported as a potential shared biological mechanism, through which the genetic variants could increase both the risk for ADHD and unhealthy dietary intake or obesity. Via the Gut-Brain axis, a two-way and high-speed connection, the gut can talk to the brain directly. According to the study (2), a higher proportion of bacteria that produce a substance that can be converted into dopamine was found in the intestines of people with ADHD than those without ADHD. Using functional magnetic resonance imaging (fMRI), they further found that the participants with more of these bacteria in their intestines displayed less activity in the reward sections of the brain, which constitutes one of the hallmarks of ADHD. We are therefore proposing the idea that there could be a biological pathway- ‘dietary habits-gut (microorganism)-reward system (dopamine)-ADHD’, through which the shared genetic effects between ADHD and unhealthy dietary intake may play a role.

In order to determine whether the genetic overlap between ADHD and dietary habits actually exists, we will in our next Eat2beNice project use twin methodology and unique data from the Swedish Twin Register. We will keep you updated!

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. Demontis D, Walters RK, Martin J, Mattheisen M, Als TD, Agerbo E, et al. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature genetics. 2019;51(1):63.

2. Aarts E, Ederveen TH, Naaijen J, Zwiers MP, Boekhorst J, Timmerman HM, et al. Gut microbiome in ADHD and its relation to neural reward anticipation. PLoS One. 2017;12(9):e0183509.

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Every child knows: sugar is bad for the teeth. Nutrition with a high amount of sugar does not only put you at a risk of dental cavities but also affects your physical and mental health, mood and memory.

Sick? Current researches associate sugar consumption with overweight and obesity, which increases the risk of various subsequent illnesses: diabetes type 2, cardiovascular diseases (risk for stroke and heart attack), dementia and cancer. (1)

Sad? In a study on patients with diabetes type 2 the level of blood sugar was manipulated. When the blood glucose was elevated (> 16,5 mmol/l) participants had a reduced energetic arousal and felt more sadness and anxiety (2).

Stupid? In a study on healthy adults memory skills and blood sugar levels were measured. Participants with higher blood sugar levels showed worse memory performance than adults with lower glucose levels. This difference was mediated by structural changes in the brain (3). Another study found that high blood sugar levels within the normal range (> 6.1 mmol) were associated with 6-10% loss in brain volume. The loss effected hippocampus and amygdala -areas that are important for learning, memory and cognitive skills (4).

The WHO recommends the intake of less than 10% or even better less than 5% free sugars of the daily total energy intake. For an adult that means less than 25 grams (6 teaspoons) per day (5). The problem is: there is a high amount of sugar in products where we don’t expect it.

So here are some tips to avoid sugar:
1. Pay attention to the ingredients list: There are many names to cover the total amount of contained sugar in products. Everything ending with “-ose” or “syrup” is sugar. The position on the list indicates the relative amount of a compound, so producers often mix different sugars in order to “hide” them at the end of the ingredients list. In “light” products the missing fat is often replaced by sugar. Better base your nutrition on staple foods like whole-grain food, fruits and vegetables to avoid hunger pangs as a response to changes in blood sugar level.

2. Avoid ready-made products such as pizza, sauces, soups or ketchup. You might be surprised how much sugar they contain! Also, many cereals and yoghurts contain high amounts of sugar. Prepare it yourself: Use unsweetened yoghurt and add your favourite fruits.
3. Step by step: Reduce your sugar intake slowly to be successful in the long term. For example, day by day put a bit less sugar into your coffee to get used to it.
4. Save on baking sugar: Just use less than stated in the recipe – it tastes just as good.
5. Replace sugary drinks with water or unsweetened teas. Add lemon, mint or pieces of fruit to your water.
6. Make it something special: If you don´t buy sweets you will be less tempted by them. It may be a good rule to eat cake and cookies only on special days or with friends.
7. Size does count: A small treat, when eaten attentive, will satisfy you better than the whole chocolate bar you consume while being absorbed by reading the newspaper, watching a movie, or driving your car.
8. Avoid sugar substitutes: Honey, agave syrup and fruit extract, etc have the same effects as refined sugars. It’s healthier to get used to less sweetness.
9. Experiment with spices: Instead of sugar, spices such as cinnamon, vanilla or cardamom can enhance flavor.
10. Eat fruits: Satisfy your sweet tooth with fruits instead of sugar.
Get to know the natural taste of your food 😊

Shortened version:
1. Pay attention to the ingredients list: Everything ending with “-ose” or “syrup” is sugar. In “light” products the missing fat is often replaced by sugar.
2. Avoid ready-made products such as pizza, sauces, soups or ketchup. Also, some cereals and yoghurts contain a relatively high amount of sugar.
3. Save on baking sugar: just use less than stated in the recipe – it tastes just as good.
4. Replace sugary drinks with water or unsweetened teas. Add lemon, mint or fruits to your water.
5. Avoid sugar substitutes: Honey, agave syrup and fruit extract, etc have the same effects as refined sugars. It’s healthier to get used to less sugar.
Get to know the natural taste of your food 😊

REFERENCES:
(1) Stanhope K. L. (2016). Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci, 53(1): 52-67. doi: 10.3109/10408363.2015.1084990.

(2) Sommerfield, A. J., Deary I. J. & Frier, B. M. (2004). Acute Hyperglycemia Alters Mood State and Impairs Cognitive Performance in People With Type 2 Diabetes. Diabetes Care, 27: 2335–2340.
doi: 10.2337/diacare.27.10.2335.

(3) Kerti, L., Witte, A. V., Winkler, A., Grittner, U., Rujescu, D. & Flöel, A. (2013). Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology, 81 (20), 1746- 1752.
doi: 10.1212/01.wnl.0000435561.00234.ee.

(4) Cherbuin, N., Sachdev, P. &Anstey, K. J. (2912). Higher normal fasting plasma glucose is associated with hippocampal atrophy: The PATH Study. Neurology, 79 (10): 1019- 1026.
doi: 10.1212/WNL.0b013e31826846de.

(5) WHO Library Cataloguing-in-Publication Data (2015). Guideline: Sugar intake for adults and children. World Health Organization.
Retrieved from: http://apps.who.int/iris/bitstream/handle/10665/149782/9789241549028_eng.pdf;jsessionid=3F96BB43E2B34C12341B1EB60F035587?sequence=1.

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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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Real time measurements of intestinal gases: a novel method to study how food is being digested

Researchers in Wageningen (The Netherlands), have been able to identify for the first time, how gut microorganisms process different types of carbohydrates by measuring in real time the intestinal gases of mice. This is not only a novel method to understand how food is digested but could also tell us more about the role of gut microorganisms in gut health.

Intestinal gases

The intestinal microbiota is a diverse and dynamic community of microorganisms which regulate our health status. The advancement of biomolecular techniques and bioinformatics nowadays allows researchers to explore the residents of our intestines, revealing what type of microorganisms are there. However, studying only the microbial composition of an individual provides limited insights on the mechanisms by which microorganisms can interact with the rest of our body. For example, far less is understood about the contribution of the gut microorganisms in the production of intestinal gases such as hydrogen, methane and carbon dioxide through the breakdown of food and how these gases affect the biochemical pathways of our bodies.

Intestinal gases consist mostly of nitrogen, and carbon dioxide, which originate primarily from inhaled air. Hydrogen and methane though, are produced as by-products of carbohydrate fermentation (break down), by intestinal microorganisms. However, not all carbohydrates are digested in the same way. For instance, food with simple sugars can be rapidly absorbed in the small intestine unlike complex carbohydrates such as fibers, which reach the colon where they are digested by the colonic microbiota.

Lower_digestive_system

Measuring hydrogen in mouse intestines

To study these interactions and gain knowledge on how microorganisms process carbohydrates, the research team led by Evert van Schothorst from the Human and Animal Physiology Group of Wageningen University (WU) in collaboration with the WU-Laboratory of Microbiology fed mice two different diets with the same nutritional values but with different types of carbohydrates (1). The first diet contained amylopectin, a carbohydrate which can be digested readily in the small intestine while the second diet contained amylose, a slowly digestible carbohydrate that is digested by intestinal microorganisms in the colon.

Animals fed the easily digestible carbohydrates showed minimal production of hydrogen whereas the group fed with the complex carbohydrates presented high levels of hydrogen. Moreover, the two groups were characterized not only by distinct microbial composition (different types of bacteria present) but also distinct metabolic profiles (short chain fatty acids), suggesting that the type of carbohydrate strongly affects microbial composition and function.

The importance of hydrogen

Hydrogen consumption is essential in any anoxic (without oxygen) microbial environment to maintain fermentative processes. In the intestine it can be utilised through three major pathways for the production of acetate, methane and hydrogen sulphide. These molecules are critical mediators of gut homeostasis, as acetate is the most predominant short chain fatty acid produced in mammals with evidence suggesting a role in inflammation and obesity (2). Methane, which is produced by a specific type of microorganisms, called archaea, has been associated with constipation related diseases, such as irritable bowel syndrome(3) and also recently with athletes’ performance (4)! Finally hydrogen sulphide is considered to be a toxic gas, although recent findings support the notion that it also has neuroprotective effects in neurodegenerative disorders such as Parkinson and Alzheimer diseases (5).

To the best of our knowledge, this is the first time that food-microbiota interactions have been studied continuously, non-invasively and in real time in a mouse model. Hydrogen is a critical molecule for intestinal health and understanding its dynamics can provide valuable information about intestinal function, and deviations in conditions such as Crohn’s disease or irritable bowel syndrome (IBS).

Further reading

1. Fernández-Calleja, J.M., et al., Non-invasive continuous real-time in vivo analysis of microbial hydrogen production shows adaptation to fermentable carbohydrates in mice. Scientific reports, 2018. 8(1): p. 15351.

https://www.nature.com/articles/s41598-018-33619-0

2. Perry, R.J., et al., Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome. Nature, 2016. 534(7606): p. 213

3. Triantafyllou, K., C. Chang, and M. Pimentel, Methanogens, methane and gastrointestinal motility. Journal of neurogastroenterology and motility, 2014. 20(1): p. 31.

4. Petersen, L.M., et al., Community characteristics of the gut microbiomes of competitive cyclists. Microbiome, 2017. 5(1): p. 98.

5. Cakmak, Y.O., Provotella‐derived hydrogen sulfide, constipation, and neuroprotection in Parkinson’s disease. Movement Disorders, 2015. 30(8): p. 1151-1151.

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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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ADHD and Exercise

ADHD is among the most common psychiatric disorders, with ~3% prevalence in adulthood and ~5% in childhood. ADHD has a high risk for comorbid conditions. Comorbid means that one psychiatric disorder often comes together with another psychiatric disorder. For instance mood, anxiety and substance use disorders have high comorbid rates in adults with ADHD.

Adults with ADHD are also at risk for obesity and major depressive disorders and adolescent ADHD predicts adult obesity: 40% of adults with ADHD are also obese. These are worrying numbers. Many adults who have ADHD suffer from these negative consequences that come with their mental illness.

There is a growing body of scientific evidence of the powerful effects of nutrition and lifestyle on mental health. Exercise is one of them.It helps prevent or manage a wide range of health problems and concerns, including stroke, obesity, metabolic syndrome, type 2 diabetes, depression, a number of types of cancer and arthritis. Besides that, regular exercise can help you sleep better, reduce stress, sharpen your mental functioning, and improve your sex life. Nearly all studies revolve around aerobic exercise which includes walking, jogging, swimming, and cycling.

Recent research shows that exercise might also have a positive effect on ADHD symptoms such as improving attention and cognition1,2 Additional research is needed to explore this effect further, but we can take a look at the mechanisms underlying this effect.

One of the parts in our brain that is affected by exercise is the prefrontal cortex. The prefrontal cortex plays an important role in controlling impulsive behavior and attention, and is positively influenced by exercise. Furthermore, dopamine and norepinephrine play an important role in attention regulation. Ritalin, among one of the most well-known medication for ADHD, also increases levels of dopamine.

When you exercise regularly, the basis levels of dopamine and norepinephrine rise, and even new dopamine receptors are created. These dopamine levels are also the reason why exercise therapy can be effective for people suffering from depression: low levels of dopamine are a predictor of depressive symptoms.

Taken together: people with ADHD are at risk for obesity and depression. Exercise has a positive influence on obesity, depression and ADHD. Wouldn’t it be great if we could treat people with ADHD with an exercise therapy?

The PROUD-study is currently studying the prevention of depressive symptoms, obesity and the improvement of general health in adolescents and young-adults with ADHD. PROUD establishes feasibility and effect sizes of two kinds of interventions: an aerobic exercise therapy and the effects of a bright light therapy.

Exercise and ADHDParticipants follow a 10 week exercise intervention in which they train three days a week: one day of only aerobic activities (20-40 min) and in two of these days, muscle-strengthening and aerobic activities (35 – 60 min). An app guides them through the exercises, and the intensity and duration of these exercises increase gradually. During a 24 week course changes in mood, condition, ADHD symptoms and body composition are measured.

I am really looking forward to the results of the effectiveness of this intervention in adolescents and adults with ADHD. It is great that this study tries to alter a lifestyle instead of temporarily symptom-reducing options. A healthy life is a happy life!

For more information about the PROUD-study see www.adhd-beweging-lichttherapie.nl (only in Dutch) or contact the researchers via proud@karakter.com. For more information about a healthy lifestyle and the positive effects on mental health, see our other blogs at https://newbrainnutrition.com/

 

References

  1. Kamp CF, Sperlich B, Holmberg HC (2014). Exercise reduces the symptoms of attention-deficit/hyperactivity disorder and improves social behaviour, motor skills, strength and neuropsychological parameters. Acta Paediatrica, 103, 709-714.

 

  1. Choi JW, Han DH, Kang KD, Jung HY, Renshaw, PF (2015). Aerobic exercise and attention deficit hyperactivity disorder: brain research. Med Sci Sports Exerc, 47, 33-39.
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