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

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

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

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

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

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

They eat many legumes, such as soybeans.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

1 Goya cucumber (may also be frozen)

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

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

1-2 tablespoons soy sauce

1-2 tablespoons rice wine (sake)

1/2 teaspoon salt

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

2 eggs

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

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

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

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

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

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

Scramble two eggs and add them.

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

Serve the Champuru with rice.

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

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

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Recently, I participated in the Radboud Talks 2019, a scientific pitch competition, where I was lucky to be one of the eight finalists.

Why Radboud Talks? It is a perfect opportunity to share my work/ideas with the world and to gain more experience regarding presentation skills. They organized two workshops beforehand, where I had the opportunity to learn presentation techniques from professionals (actors and science communication advisors). We also received a lot of feedback, so I really learned a lot about how to present my scientific work to a general audience.

Below you can find the video from the preliminaries based on which I was chosen as a finalist. There you can hear about my research project which is about gut bacteria and their potential role in ADHD (Attention Deficit Hyperactivity Disorder). ADHD is a common worldwide neurodevelopmental disorder. Every person with ADHD has a unique combination of symptoms and challenges. Importantly, it has a significant social impact on patients’ lives, causing disruption at school, work and relationships. Despite its societal importance, progress in understanding disease biology has been slow.

 

The study of the human microbiome has become a very popular topic, because of their revealed importance in human physiology and health maintenance. Numerous studies have reported that gut bacteria may have an effect on our mental health. Some studies showed a potential role of gut bacteria in a psychiatric disorder like depression, autism or Parkinson (1). Above all, diet showed to have a profound effect of ADHD symptoms. This was earlier described in this blog: https://newbrainnutrition.com/investigating-the-effects-of-a-dietary-intervention-in-adhd-on-the-brain/ and we know that diet is one of the main factors influencing gut bacteria. Taking all together, I am curious (and investigating) if gut bacteria play a role in ADHD and if yes what kind of effect do they have on ADHD symptoms.

REFERENCES:
Bastiaanssen, T., Cowan, C., Claesson, M. J., Dinan, T. G., & Cryan, J. F. (2018). Making Sense of … the Microbiome in Psychiatry. The international journal of neuropsychopharmacology22(1), 37–52. doi:10.1093/ijnp/pyy067

 

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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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Why 12 genetic markers for ADHD are exciting news for New Brain Nutrition

We are finally here: for the first time, genome-wide significant markers are identified that increase the risk for Attention Deficit / Hyperactivity Disorder (ADHD). This research was conducted by an international consortium of more than 200 experts on genetics and ADHD, and includes several researchers that are also involved in our Eat2beNICE project (the scientific basis of this New Brain Nutrition website). The findings were recently published in the prestigious journal “Nature Genetics” and will greatly advance the field of ADHD genetics research.

Why is this finding so important?

The genetics of ADHD are very complex. While ADHD is highly heritable, there are likely to be thousands of genes that contribute to the disorder. Each variant individually increases the risk by only a tiny fraction. To discover these variants, you therefore need incredibly large samples. Only then can you determine which variants are linked to ADHD. The now published study by Ditte Demontis and her team combined data from many different databases and studies, together including more than 55,000 individuals of whom over 22,000 had an ADHD diagnosis.

We can now be certain that the twelve genetic markers contribute to the risk of developing ADHD. Their influence is however very small, so these markers by themselves can’t tell if someone will have ADHD. What’s interesting for the researchers is that none of these markers were identified before in much smaller genetic studies of ADHD. So this provides many new research questions to further investigate the biological mechanisms of ADHD. For instance, several of the markers point to genes that are involved in brain development and neuronal communication.

Why are our researchers excited about this?

A second important finding from the study is that the genetic variants were not specific to ADHD, but overlapped with risk of lower education, higher risk of obesity, increased BMI, and type-2 diabetes. If genetic variants increase both your risk for mental health problems such as ADHD, and for nutrition-related problems such as obesity and type-2 diabetes, then there could be a shared biological mechanism that ties this all together.

We think that this mechanism is located in the communication between the gut and the brain. A complex combination of genetic and environmental factors influence this brain-gut communication, which leads to differences in behaviour, metabolism and (mental) health.genetic markers for adhd

The microorganisms in your gut play an important role in the interaction between your genes and outside environmental influences (such as stress, illness or your diet). Now that we know which genes are important in ADHD, we can investigate how their functioning is influenced by environmental factors. For instance, gut microorganisms can produce certain metabolites that interact with these genes.

The publication by Ditte Demontis and her co-workers is therefore not only relevant for the field of ADHD genetics, but brings us one step closer to understanding the biological factors that influence our mental health and wellbeing.

Further Reading

Demontis et al. (2018) Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nature Genetics. https://www.nature.com/articles/s41588-018-0269-7

The first author of the paper, Ditte Demontis, also wrote a blog about the publication. You can read it here: https://mind-the-gap.live/2018/12/10/the-first-risk-genes-for-adhd-has-been-identified/

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Breaking news: It has long been assumed that the gut and the brain communicate not only via a slow, hormonal pathway, but that there must be an additional, faster association between gut and brain. Melanie Maya Kelberer and her colleagues from Duke University, NC, now managed to detect this connection. Their paper has just been published in the renowned journal ‘Science’.

By researching a mouse model, they were able to show that the gut and the brain are connected via one single synapse. This is how it works: A cell in the gut (the so-called enteroendocrine cell) transfers its information to a nerve ending just outside the gut. At the connecting nerve ending (the synapse), the neurotransmitter glutamate – the most important excitatory transmitter in the nervous system – passes on the information about our nutrition to small nerve endings of the vagal nerve, which spreads from the brain to the intestines.

Vagal nerveBy travelling along this vagal nerve, the information from the gut reaches the brainstem within milliseconds. The authors now state that a new name is needed for the enteroendocrine cells, now that they have been shown to be way more than that. The name ‘neuropod cells’ has been suggested. The authors interpret their findings as such, that this rapid connection between the gut and the brain helps the brain to make sense of what has been eaten. Through back-signalling, the brain might also influence the gut. In sum, this finding is an important step towards a better understanding of how the gut and the brain communicate. Findings such as this one help us to find ways to positively influence our brain states and our mental health by our food choices.

Read the original paper here: http://science.sciencemag.org/content/361/6408/eaat5236.long

Kaelberer, M.M., Buchanan, K. L., Klein, M. E., Barth, B. B., Montoya, M. M., Shen, X., and Bohórquez, D. V. (2018), A gut-brain neural circuit for nutrient sensory transduction, ​Science,
​ Vol. 361, Issue 6408

 

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A hot topic these days, that one can hear more and more information about is the microbiota-gut-brain axis, the bidirectional interaction between the intestinal microbiota and the central nervous system nowadays, this has become a hot topic. We are becoming increasingly aware that gut microbiota play a significant role in modulating brain functions, behavior and brain development. Pre- and probiotics can influence the microbiota composition, so the question arises, can we have an impact on our mental health by controlling nutrition and using probiotics?

Burokas and colleagues aimed to investigate this possibility in their study (2017), where the goal was to test whether chronic prebiotic treatment in mice modifies behavior across domains relevant to anxiety, depression, cognition, stress response, and social behavior.

In the first part of the study, the researchers fed mice with prebiotics for 10 weeks. They were administered the prebiotics fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), a combination of both, or water. FOS and GOS are soluble fibers that are associated with the stimulation of beneficial bacteria such as bifidobacterium and lactobacillus.

Behavioral testing started from the third week including

  • the open field test (anxiety – amount of exploratory behavior in a new place),
  • novel object test (memory and learning – exploration time of a novel object in a familiar context), and
  • forced swimming test (depression-like behavior – amount of activity in the cylinder filled water).

Meanwhile, plasma corticosterone, gut microbiota composition, and cecal short-chain fatty acids were measured. Taken together, the authors found that the prebiotic FOS+GOS treatment exhibited both antidepressant and anxiolytic (anti-anxiety) effects. However, there were no major effects observed on cognition, nociception (response to pain stimulus), and sociability; with the exception of blunted aggressive behavior and more prosocial approaches.

In the second part, FOS+GOS or water-treated mice were exposed to chronic psychosocial stress. Behavior, immune, and microbiota parameters were assessed. Under stress, the microbiota composition of water-treated mice changed (decreased concentration of bifidobacterium and lactobacillus), which effect was reversed by treatment with prebiotics.

Furthermore, it was found that three weeks of chronic social stress significantly reduced social interaction, and increased stress indicators (basal corticosterone levels and stress-induced hyperthermia), whereas prebiotic administration protected from these effects.

After stimulation with a T-cell activator lectin (concanavalin A), the stressed, water-treated mice group presented increased levels of inflammatory cytokines (interleukin 6, tumor necrosis factor alpha), whereas in animals with prebiotics had these at normal levels.

Overall, these results suggest a beneficial role of prebiotic treatment in mice for stress-related behaviors and supporting the theory that modifying the intestinal microbiota via prebiotics represents a promising potential for supplement therapy in psychiatric disorders.

Watch YouTube Video:
https://youtu.be/E479yto8pyk

REFERENCES
Burokas, A., Arboleya, S., Moloney, R. D., Peterson, V. L., Murphy, K., Clarke, G., Stanton, C., Dinan, T. G., & Cryan, J. F. (2017). Targeting the Microbiota-Gut-Brain Axis: Prebiotics Have Anxiolytic and Antidepressant-like Effects and Reverse the Impact of Chronic Stress in Mice. Biological Psychiatry, 82(7), 472–487. https://doi.org/10.1016/j.biopsych.2016.12.031

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