The prevalence of overweight and obesity has increased worldwide and is affecting millions of adults and children 1. The development of obesity is complex with factors like genetics, individual metabolism, dietary and physical activity choices, food and water availability, education and culture, playing a role 2. Several genome wide association studies have revealed an association between obesity and the gene encoding the transcription factor AP-2 beta (TFAP2B) 3,4. TFAP2B plays an important role during early stages of pregnancy in the development of different parts of the nervous system5. It has been demonstrated that overexpression of TFAP2B in fat cells causes a decrease in the production and release of adiponectin, a protein hormone which is involved in glucose metabolism6, and a diminished response to insulin7. But how does TFAP2B contribute to the development of obesity?

We have now shown in our ECPBHS study a very clear association between one TFAP2B variation (intron 2 VNTR) and measures of obesity and insulin resistance. Our findings have just recently published in the International Journal of Obesity8.

We found that men, who inherited the same variant of that gene from both parents (called 5/5 homozygotes), had significantly higher body weight, body mass index, proportion of body fat and insulin resistance, throughout adolescence to young adulthood. Strikingly, women that were 5/5 homozygotes had the same effects, but these appeared later, in young adulthood.

We hypothesized that the people who are TFAP2B 5/5 homozygotes have a higher risk of obesity because they consume more food. But we found the opposite: by age 25 male 5/5 homozygotes had smaller daily calorie intake and consumption of fats and carbohydrates. In females, these differences in caloric and macronutrient intake, were not observed. We therefor think that the risk is not related to increased food intake, but to differences in metabolism.

In conclusion, the gene TFAP2B increases the risk of obesity, abdominal obesity and insulin resistance in this sample, and is probably related to differences in metabolism. We should consider implementing lifestyle interventions already in childhood for individuals who are 5/5 homozygotes, to reduce the effect of TFAP2B on body weight. The physiological role of TFAP2B in body weight regulation and insulin resistance still needs further research.

REFERENCES:

  1. GBD 2015 Obesity Collaborators, Afshin A, Forouzanfar MH, et al. Health Effects of Overweight and Obesity in 195 Countries over 25 Years. N Engl J Med. 2017; 377: 13-27. doi:10.1056/NEJMoa1614362
  2. Lee BY, Bartsch SM, Mui Y, Haidari LA, Spiker ML, Gittelsohn J. A systems approach to obesity. Nutr Rev. 2017; 75: 94-106. doi:10.1093/nutrit/nuw049
  3. Locke AE, Kahali B, Berndt SI, et al. Genetic studies of body mass index yield new insights for obesity biology. Nature. 2015; 518: 197-206. doi:10.1038/nature14177
  4. Felix JF, Bradfield JP, Monnereau C, et al. Genome-wide association analysis identifies three new susceptibility loci for childhood body mass index. Hum Mol Genet. 2016; 25: 389-403. doi:10.1093/hmg/ddv472
  5. Moser M, Rüschoff J, Buettner R. Comparative analysis of AP-2α and AP-2β gene expression during murine embryogenesis. Developmental Dynamics. 1997; 208: 115-124. doi:10.1002/(SICI)1097-0177(199701)208:1<115::AID-AJA11>3.0.CO;2-5
  6. Ikeda K, Maegawa H, Ugi S, et al. Transcription factor activating enhancer-binding protein-2beta. A negative regulator of adiponectin gene expression. J Biol Chem. 2006; 281: 31245-31253. doi:10.1074/jbc.M605132200
  7. Tao Y, Maegawa H, Ugi S, et al. The transcription factor AP-2beta causes cell enlargement and insulin resistance in 3T3-L1 adipocytes. Endocrinology. 2006; 147: 1685-1696. doi:10.1210/en.2005-1304
  8. Joost U, Villa I, Comasco E, Oreland L, Veidebaum T, Harro J. Association between Transcription Factor AP-2B genotype, obesity, insulin resistance and dietary intake in a longitudinal birth cohort study. Int J Obes [in press]. doi:10.1038/s41366-019-0396-y
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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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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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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 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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This project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 728018

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