Having Attention Deficit / Hyperactivity Disorder (ADHD) can be quite a burden to someone’s quality of life. People with ADHD generally have problems with regulating their attention and their impulses, resulting in concentration and memory problems as well as reckless behaviour [1]. Luckily, this condition is receiving more attention these days, and an increasing number of people are receiving adequate treatment in the form of medication and/or behavioural therapy. But what is much less known is that many people with ADHD also suffer from other mental and somatic conditions.

The research consortium Comorbid Conditions of ADHD (“CoCA”) investigates the prevalence and the mechanisms of ADHD comorbidity [2]. This research focusses on the four most prevalent comorbidities: depression, anxiety, substance abuse, and obesity. It is important to learn more about these conditions in the context of ADHD, as this can raise awareness among health care professionals. For instance, it can happen that an adult seeks treatment for depression, while this person also has undiagnosed ADHD. What’s more, the ADHD may even be the underlying cause of the depressive symptoms. In this case, it might be better to treat the ADHD symptoms first.

A first step to raise awareness is to map out how often these comorbidities occur together with ADHD. For this, the researchers from the CoCA project have made use of several very large population datasets that contain information of millions of people. From these datasets they can find patterns of ADHD comorbidity. This way they have shown that indeed depression, anxiety, substance use disorder and severe obesity are much more frequent in individuals with an ADHD diagnosis.

Other patterns that emerge from this data is that depression, anxiety and obesity are more frequent in women compared to men in the general population, and this sex-difference is also present amongst individuals with ADHD. This means that when a woman with ADHD seeks treatment, it is especially important to be aware of these other conditions that may increase symptoms and reduce the quality of life.

To learn more about the prevalence of ADHD comorbidities, you can watch this webinar. Here dr. Catharina Hartman and myself explain and discuss the first findings from the CoCA project.

 

REFERENCES:

[1] https://newbrainnutrition.com/adhd/

[2] www.coca-project.eu

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Crohn’s disease is a chronic inflammatory condition affecting the gastrointestinal tract – causing injuries or wounds anywhere in between the mouth and anus. Symptoms usually start in young adults, but can also occur in children or later in life. Often, it takes quite some time until a doctor diagnoses it because of the wide variety of symptoms.

Patients suffering from Crohn’s disease often experience diarrhea, stomach pain, and unwanted weight loss. Furthermore, and these are all unspecific symptoms, they might report fever, fatigue, problems with their skin, joints or eyes. Symptoms come and go and might be severe at one point and relatively mild at another [1].

It is currently not completely understood what causes the disease. Data suggest a combination of genetic and environmental factors, like smoking, oral contraceptive, and antibiotic use. On the other hand, being exposed to pets and farm animals is believed to decrease the risk. Furthermore, a high fiber intake, fruit consumption, and physical activity have also been linked to a risk reduction [2,3].

Therapeutic options to treat Crohn’s disease are different types of medication, and treatment decisions are guided by the age of the patient, symptoms, and extent of the disease. Corticosteroids, immunomodulators, and biologics (these are monoclonal antibodies) are often used, sometimes also in combination [4].

Another possible treatment option is to provide nutrients that directly influence the intestines. This is called enteral nutrition. The benefit of this is that it avoids the side effects of medication – which is especially relevant for children. A recent Chinese meta-analysis of data even reports that exclusive enteral nutrition was equally effective as corticosteroid medication when given to children with Crohn’s disease [5, 6].

But what exactly is enteral nutrition and how does it work?

Over a period of 6-8 weeks, enteral nutrition provides the complete daily nutritional requirements through liquid formulations delivered orally or through nasogastric or gastrostomy tubes [7]. Beforehand, malnutrition and individual caloric needs need to be identified by a dietician. The treatment influences the bacterial milieu, shifting away from a pro-inflammatory state. It is established as a primary therapy in children, while it is less used in adults due to patients’ preference and availability of other therapeutic options such as biologics. Overall, enteral nutrition should be discussed with patients and offered especially if they desire a non-pharmacological therapy [8].

REFERENCES:

[1] Veauthier, B. and J.R. Hornecker, Crohn’s Disease: Diagnosis and Management. Am Fam Physician, 2018. 98(11): p. 661-669.

[2] Ananthakrishnan AN. Epidemiology and risk factors for IBD. Nat Rev Gastroenterol Hepatol. 2015;12(4):205–217

[3] Cholapranee A, Ananthakrishnan AN. Environmental hygiene and risk of inflammatory bowel diseases: a systematic review and meta-analysis. Inflamm Bowel Dis. 2016;22(9):2191–2199.

[4] National Institute for Health and Care Excellence. Crohn’s disease: management. https://www.nice.org.uk/guidance/ng129. Accessed February 06, 2020.

[5] Shaikhkhalil, A.K. and W. Crandall, Enteral Nutrition for Pediatric Crohn’s Disease: An Underutilized Therapy. Nutr Clin Pract, 2018. 33(4): p. 493-509.

[6] Yu, Y., K.C. Chen, and J. Chen, Exclusive enteral nutrition versus corticosteroids for treatment of pediatric Crohn’s disease: a meta-analysis. World J Pediatr, 2019. 15(1): p. 26-36.

[7] Wall C.L., Day A.S., Gearry R.B. Use of exclusive enteral nutrition in adults with crohn’s disease: A review. World J. Gastroenterol. 2013; 19:7652–7660. doi: 10.3748/wjg.v19.i43.7652.

[8] Hansen, T. and D.R. Duerksen, Enteral Nutrition in the Management of Pediatric and Adult Crohn’s Disease. Nutrients, 2018. 10(5).

 

 

 

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Insulin and diabetes
Insulin is a peptide hormone produced by beta cells of the pancreas. It regulates the metabolism by promoting the absorption of glucose from the blood into liver, fat and skeletal muscle cells. When the blood glucose level is high, the beta cells secrete insulin into the blood, and when glucose levels are low, the secretion of insulin is inhibited. If the pancreas produces little or no insulin, it results in type 1 diabetes, while insulin resistance – a condition in which cells fail to respond normally to the insulin – is characteristic for type 2 diabetes.

Insulin signaling in the brain
The brain was traditionally considered to be an insulin‐insensitive organ. While insulin and insulin receptors in the brain were discovered in 19781,2, this discovery was not appreciated until recently, when the role of insulin signaling was shown in disorders of the central nervous system. There are two types of insulin receptor, differing in functionality and distribution: 1) peripheral tissues express predominantly IR‑B, which targets metabolic effects of insulin, and 2) neurons express exclusively the IR‐A. The insulin receptor belongs to the family of tyrosine kinase receptors and is structurally similar to the receptors of neurotrophins, which play an important role in survival, development and the functioning of neurons. Impaired insulin signaling in the brain, which is commonly termed as ‘central insulin resistance’ is now viewed as a pathogenetic mechanism of neurodevelopmental, neurodegenerative and neuropsychiatric disorders

Insulin and excitotoxicity
A recent study showed that insulin can protect against glutamate excitotoxicity4. Excitotoxicity is a pathological process, by which excessive activation of glutamate receptors allows high levels of calcium ions to enter the cell and activate enzymes that damage the cell. This process is implicated in neurodegenerative disorders such as Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, Parkinson’s disease, and Huntington’s disease, affective disorders, traumatic brain injury, stroke.

In this study, effects of short-term insulin exposure on several parameters of excitotoxicity were investigated in cultured rat neurons. Insulin prevented the onset of so-called delayed calcium deregulation, the postulated point-of-no-return in the mechanisms of excitotoxicity. Additionally, insulin improved depletion of the brain-derived neurotrophic factor, which is a critical neuroprotector in excitotoxicity. Also, insulin improved the viability of cells exposed to glutamate. Thus, this study showed that short-term insulin exposure is protective against excitotoxicity, one of the key mechanisms of neurodegeneration, which opens new therapeutic possibilities.

Insulin and Therapeutic Possibilities
Thus, insulin supplementation or enhancement of insulin receptor functioning can be considered as a potential therapy for neurodegenerative and neuropsychiatric disorders. Extensive experimental work is ongoing in order to further uncover the underlying mechanisms of this new function of insulin in the brain and develop effective therapies of neurodegeneration.

REFERENCES:
[1] J. Havrankova, D. Schmechel, J. Roth, M. Brownstein, Identification of insulin in rat brain, Proc. Natl. Acad. Sci. 75 (1978) 5737–5741. doi:10.1073/pnas.75.11.5737.
[2] J. Havrankova, J. Roth, M. Brownstein, Insulin receptors are widely distributed in the central nervous system of the rat, Nature. 272 (1978) 827–829. doi:10.1038/272827a0.
[3] I. Pomytkin, J.P. Costa-Nunes, V. Kasatkin, E. Veniaminova, A. Demchenko, A. Lyundup, K.-P. Lesch, E.D. Ponomarev, T. Strekalova, Insulin receptor in the brain: Mechanisms of activation and the role in the CNS pathology and treatment, CNS Neurosci. Ther. (2018). doi:10.1111/cns.12866.
[4] I. Krasil’nikova, A. Surin, E. Sorokina, A. Fisenko, D. Boyarkin, M. Balyasin, A. Demchenko, I. Pomytkin, V. Pinelis, Insulin protects cortical neurons against glutamate excitotoxicity, Front. Neurosci. 13 (2019). doi:10.3389/fnins.2019.01027.

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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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The bacteria in your gut affect blood insulin levels and may influence your chances of developing type 2 diabetes

Developing type 2 diabetes is for a large part influenced by your diet but also genes. However, a recent study has now shown that your gut microorganisms might also play an important role in the risk of developing type 2 diabetes (T2D). The article published in Nature Genetics entitled “Causal relationships among the gut microbiome, short-chain fatty acids (SCFA’s) and metabolic diseases”, claims evidence that bacterial metabolites such as SCFA’s are able to influence insulin levels and increase the risk of getting T2D.

Various studies have suggested that increased SCFA production benefits the host by exerting anti-obesity and antidiabetic effects, however, results of different studies are not always in agreement. Moreover, there is also evidence that increased production of SCFAs in the gut might be related to obesity, due to energy accumulation. Resolving these conflicting findings requires a detailed understanding of the causal relationships between the gut-microbiome and host energy metabolism, and the present study contributes to this.

The authors analyzed data from a large population study based in Groningen (The Netherlands), comprising 952 individuals with known genetic data, as well as information on parameters associated with metabolic traits such as BMI and insulin sensitivity. In addition, data were acquired for the type and the function of the bacteria which were present in the gut of the study participants. Combining this data, the authors tried to answer the question of whether changes in microbiome features causally affect metabolic traits or vice versa?

A technique called Mendelian randomization (MR) which is increasingly accepted to establish cause-effect relationships in the onset of diseases was applied. The primary outcome of the analysis was that host genes influence the production of the SCFA butyrate in the gut, which is associated with improved insulin response in the blood after an oral glucose tolerance test. In addition, abnormalities in the production or absorption of propionate, another SCFA, were causally related to an increased risk of T2D.

So far available data suggest that overweight humans or those with type 2 diabetes may have different microorganisms in their gut compared to healthy people. These microorganisms which are commonly found in healthy people are absent from the T2D patients. Whether the differences in the microbiota between healthy and T2D patients are an effect of the disease development or account for causality is challenging to be answered. With the data from the present study, authors are able to go one step further and demonstrate potential routes by which microorganisms are able to regulate our metabolic status underlying their importance for our wellbeing.

Collectively the present article suggests that production of bacterial SCFA’s play a pivotal role in the regulation of metabolic traits such as blood insulin levels and are associated with the onset of T2D.

Since the study was observational and did not include any T2D patients, confirmation of the results is essential. Follow up studies including T2D patients would be highly informative. With the rising prevalence of obesity in adults, which is reaching epidemic levels, the prevalence of T2D will also continue to rise. In the past years, scientists have mainly focused on the role of human gene data, but this has not led to major breakthroughs. Perhaps knowledge of the microbiome will elucidate molecular mechanisms which can be translated to novel effective treatments for metabolic disorders such as T2D.

REFERENCES
Sanna, S., van Zuydam, N. R., Mahajan, A., Kurilshikov, A., Vila, A. V., Võsa, U., . . . Oosting, M. (2019). Causal relationships among the gut microbiome, short-chain fatty acids and metabolic diseases. Nature genetics, 1.

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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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