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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The occurrence of placebo effects has been known for a very long time. A first “trick trial” concerning it took place in the late 1500s when instead of holy water, ordinary water was placed in a religious flask and given to a girl who was said to be possessed by the devil – which caused her to contort in pain. Likewise, when priests read a Latin text to the women, misinforming her that it was the Holy Scripture (while in actuality, it was Virgil’s Aeneid) she nonetheless squirmed in agony1.

The placebo effect can be viewed as controversial: on one hand, when doing placebo-controlled pharmacological trials, a strong placebo effect is dreaded as it might lead to a smaller effect size of the active agent and consecutively to failed trials and limits in drug development. In recent years, several psychopharmacological trials have failed to establish new therapy options due to “placebo response rates ruining drug development” ².

There have been multiple interesting outcomes from trials focusing especially on the placebo effect.

When informing a patient that he would be receiving analgesics, the intravenous application of isotonic saline had the same response as a hidden application of 6-8mg morphine³. A trial focusing on migraine patients and treating them with either placebo or rizatriptan found that the efficacies of the active agent labeled as placebo and placebo labeled as rizatriptan were similar. Furthermore, even open-label placebo was superior to no treatment. Authors concluded that increasing “positive” information incrementally boosted the efficacy of both placebo and medication during migraine attacks4. Furthermore, depending on the efficiency of a medication, 20-85% of its “treatment impact” have been found the be caused by placebo effect5.

When talking about placebo, one shouldn’t forget its “evil brother” nocebo, as – like Hansen et al. (2017) expressed in their journal article – you cannot have a placebo without a nocebo effect.

After a lumbar puncture, half of the patients who were told they might experience a headache afterward did have one, whereas of the control group (patients not warned about this side effect), all but one of thirteen remained headache-free6. A meta-analysis of patient expectancy and post-chemotherapy nausea reported a robust positive association between both, suggesting that patients with stronger expectancies experience more chemotherapy-induced nausea7.

In conclusion, the way clinicians introduce a new treatment and explain desired effects and possible side effects shapes the therapeutic outcome more than we believe. Even though physicians, of course, cannot hide possible side effects when informing about treatment options, it is very important to stress positive effects and avoid using words painting negative pictures. Instead of telling a patient “this medication can lead to bleedings”, one might rephrase and say “due to this, blood clotting might be impaired”.

Don’t forget though: as mentioned above, even when knowing they were receiving placebo, pain reduced in patients suffering from migraines compared to pain increasing in the no-treatment group. Therefore, believing that a drug or diet or any other kind of treatment can and will work is one of the most important steps you can take towards it actually helping you.

REFERENCES:
1   Kaptchuk, T.J., C.E. Kerr, and A. Zanger, Placebo controls, exorcisms, and the devil. Lancet, 2009. 374(9697): p. 1234-5.
2  Stahl, S.M. and G.D. Greenberg, Placebo response rate is ruining drug development in psychiatry: why is this happening and what can we do about it? Acta Psychiatr Scand, 2019. 139(2): p. 105-107.
3  Levine, J.D., et al., Analgesic responses to morphine and placebo in individuals with postoperative pain. Pain, 1981. 10(3): p. 379-89.
4  Kam-Hansen, S., et al., Altered placebo and drug labeling changes the outcome of episodic migraine attacks. Sci Transl Med, 2014. 6(218): p. 218ra5.
5   Hansen, E., N. Zech, and K. Meissner, [Placebo and nocebo : How can they be used or avoided?]. Internist (Berl), 2017. 58(10): p. 1102-1110.
6   Daniels, A.M. and R. Sallie, Headache, lumbar puncture, and expectation. Lancet, 1981. 1(8227): p. 1003.
7   Colagiuri, B. and R. Zachariae, Patient expectancy and post-chemotherapy nausea: a meta-analysis. Ann Behav Med, 2010. 40(1): p. 3-14.

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When exposed to UVB-radiation, the human body produces vitamin D out of cholesterol. Vitamin D is therefore also known as the “sunshine vitamin”. Healthy vitamin D levels in people are thought to play a role in preventing several health problems, such as cardiovascular diseases, osteoporosis, mood disorders, diabetes and other autoimmune diseases [1]. In a previous post, Dr. Faraone also outlines the association between vitamin D and ADHD in children and adolescents [2]. In most western countries, the beneficial effects of vitamin D are well-established. Pregnant women are even advised to add vitamin D supplementation to their diet to stimulate the fetal growth [3].

People that live further from the equator, have fewer hours of UVB-radiation and are more prone to vitamin D insufficiency. For example, residents of northern Canada and Norway have very little UVB exposure during November through February. During those months, vitamin D intake is even more important.

Residents of the arctic circle, whose families have lived there for generations after generations, have diets that are traditionally relatively high in vitamin D. The diet contains among other things: liver, trout, Atlantic salmon, seals and whales. As younger generations gradually shift away from the traditional diet, vitamin D insufficiency becomes more common among northern residents [5]. It is yet unclear if the decline in traditional diets will be accompanied by a rise in vitamin D insufficiency-related health problems. However, it is well established that several of these health problems have been uncommon among northern residents in the past [6].

Research shows that in countries further away from the equator, vitamin D levels are steady with regular UVB-exposure: Going outdoors around noon, sun bed use (with caution) and sun seeking holidays. And in the UVB-scarce months, regular vitamin D intake becomes in particular important to prevent from low vitamin D levels and its possible consequences [4].

References

[1] Wessels I, & Rink L (2019) . Micronutrients in autoimmune diseases: possible therapeutic benefits of zinc and vitamin D. J Nutr Biochem. Oct 30;77:108240. doi:10.1016/j.jnutbio.2019.108240. [Epub ahead of print]

[2] https://newbrainnutrition.com/adhd-and-vitamin-d-deficiency/

[3] Gallo S, McDermid JM, Al-Nimr RI, Hakeem R, Moreschi JM, Pari-Keener M, Stahnke B, Papoutsakis C, Handu D, Cheng FW (2019). Vitamin D Supplementation during Pregnancy: An Evidence Analysis Center Systematic Review and Meta-Analysis. J Acad Nutr Diet. Oct 25. pii: S2212-2672(19)30849-4. doi: 10.1016/j.jand.2019.07.002. [Epub ahead of print]

[4] Brustad M1, Edvardsen K, Wilsgaard T, Engelsen O, Aksnes L, Lund E (2007). Seasonality of UV-radiation and vitamin D status at 69 degrees north. Photochem Photobiol Sci. 2007 Aug;6(8):903-8. Epub 2007 Jun 27.

[5] El Hayek Fares J, & Weiler HA(2016). Implications of the nutrition transition for vitamin D intake and status in Aboriginal groups in the Canadian Arctic. Nutr Rev. 2016 Sep;74(9):571-83. doi: 10.1093/nutrit/nuw020.

[6] Dewailly E Blanchet C Lemieux S et al (2001). n-3 Fatty acids and cardiovascular disease risk factors among the Inuit of Nunavik . Am J Clin Nutr. 74 : 464 – 473 .[/st_text][/st_column][/st_row]

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I have noticed a growing number of companies offering to measure nutrient levels and then offering a personalized treatment approach to address deficiencies identified. I have also been sent individual blood results from members of the public and asked whether the results can be used to direct the best treatment. Others contact me and tell me their nutrient levels are “normal” so their doctor told them there was no need for additional nutrients.

It is a reasonable question because there are many studies that suggest that people with psychological problems such as ADHD have lower levels of nutrients in their blood relative to the nonclinical population. What we don’t know is whether it is necessary to be deficient in order to benefit from additional nutrients than what you can get out of your diet.

So what does the research say?

Our lab at the University of Canterbury in New Zealand is one of a few that has specifically investigated whether nutrient levels are predictive of response to a broad spectrum micronutrient intervention. It is important to note that not many labs take this approach, that is giving a combination of nutrients together and then assess treatment response. Many researchers make the assumption that one must be deficient to benefit from nutrients, and therefore select people for the deficiency and only treat them. We treat everyone, regardless of identified deficiency, and then assess whether the deficiency predicts who will respond and who won’t.

Overall, our research shows that the effect, if there is one, is weak, and certainly not useful at an individual level as a good predictor of treatment outcome.

Here is what we did: We assessed some key nutrients pre-treatment via serum/plasma. We measured vitamin B12, vitamin D, zinc, copper, folate, ferritin, potassium, sodium, calcium, and homocysteine. We have looked at two data sets – an adult study and a child study, both comparing vitamins/minerals to placebo in the treatment of symptoms associated with ADHD.

Findings from the adult ADHD trial:

Participants improved significantly on all outcome measures after exposure to the micronutrients for 8 weeks; 61% were identified as responders.

But, there was no relationship between baseline functioning and baseline nutrient levels. This was a bit surprising given that studies have identified deficiencies in magnesium, zinc and iron in children with ADHD. Surprisingly, we didn’t find that these nutrient levels were highly correlated with ADHD symptoms.

Very few predictors were identified. We found that greater pre-treatment with ferritin predicted who would be an ADHD responder. We wondered if those with higher ferritin had higher inflammation and therefore responded more rapidly to the treatment as the micronutrients may have improved inflammation.

Lower pre-treatment vitamin D predicted greater change on a measure of mood. This finding is not unexpected as low vitamin D levels have been associated with low mood. Pre-treatment copper gave us a signal, but it was weak and mixed.

Micronutrient supplementsIt is important to note that while there were these small signals, there were still many people with normal levels of these nutrients who benefitted from the nutrient approach, only there were fewer relative to those with vitamin D and copper deficiencies.

No other relationships between baseline nutrient levels and treatment response were identified. In other words, zinc, iron and vitamin B12 pre-treatment did not predict who would benefit and who would not. Further, there were no specific demographic variables (age, socio-economic status, gender, marital status, education) which contraindicated micronutrient treatment for ADHD in adults.

Findings from the child trial:

We identified that 49% of the children responded to the micronutrient intervention. Substantial nutrient deficiencies pre-treatment were observed only for vitamin D (13%) and copper (15%), otherwise most children entered the trial with nutrient levels falling within expected ranges. Lower pre-treatment folate and B12 levels, being female, greater severity of symptoms and co-occurring disorders pre-treatment, more pregnancy complications and fewer birth problems were identified as possible predictors of greater improvement for some but not all outcome measures although predictive values of all of them were weak. Lower IQ and higher BMI predicted greater improvement in aggression.

It is important to note that levels of folate pre-treatment for ADHD responders was within the normal reference range for folate (>8nmol/L). In other words, the blood tests did not identify responders as deficient in folate, just lower relative to non-responders. Note though, that there were many children with higher B12 and folate who did benefit from the nutrient treatment. No other relationships between pre-treatment nutrient levels and treatment response were identified.

It is also important to point out that across two studies, replication did not occur and any findings we did observe were incredibly modest. As such, they could not be used at an individual level to reliably identify who might benefit from this treatment approach. We see this as good news as it means people don’t have to feel they need to get expensive testing done before trying nutrients. The bad news is that the search is still on to figure out why some people respond and some don’t.

Although not reported in these trials, we have also looked at the predictive value of nutrient levels recorded from hair samples and similarly, the levels were also not overly helpful at predicting treatment response.

Do nutrient levels have to change for benefit to occur?

Now this is a tricky question. But we have now published a study looking at this very question, that is, whether change in a nutrient biomarker is correlated with improvement in mental health. Our overall findings were that they were not.

I think this type of question stems from research in medicine such as physicians tracking cholesterol levels in order to determine whether they are associated with the progression of disease (such as incidence of stroke). Change in cholesterol levels are used to estimate risk for future cardiovascular events.

In the mental health world, at best, they are weakly correlated with improvement in symptoms and probably not that helpful. We investigated whether changes in serum nutrient levels mediate clinical response to a micronutrient intervention for ADHD. Data were compiled from two ADHD trials (8-10 weeks), one in adults (n = 53) and one in children (n = 38). Seven outcomes included change in ADHD symptoms, mood, overall functioning (all clinician-rated) as well as response status. Change in serum/plasma nutrient levels (vitamins B12 and D, folate, ferritin, iron, zinc, and copper) were considered putative mediators.

We found that a decrease in ferritin and an increase in copper were weakly associated with greater likelihood of being identified as an ADHD responder; none of the other nutrient biomarkers served as mediators. Perhaps we need to look to see if other tissue (like hair or microbiome samples) might be more useful. Monitoring these biomarkers is unlikely helpful in understanding clinical response to a broad-spectrum micronutrient approach.

Blood levels don’t necessarily tell us what is going on in the brain and what nutrients are being used and what isn’t being used. We didn’t look at ALL nutrients so it may be we missed an important biomarker. It may be ratios are more important. But next time a professional is keen to track nutrient levels as a proxy for response, perhaps be a bit sceptical about whether the data support such testing.

Is the term deficiency accurate?

The term “deficiency”, as is often used in the ADHD literature when discussing nutrient levels, may be problematic. Although research shows that the ADHD group mean nutrient levels are often below control group means, the ADHD means are typically still falling within the normal reference range, potentially challenging the use of the term “nutrient deficiency” when attempting to investigate causes of ADHD and in relation to predicting response to nutrients. Given that reference ranges are generally defined as the set of values that 95 percent of the normal population falls within, this does not necessarily mean that these ranges are best equipped to identify what is required for optimal health for any particular individual.

Had functional ranges (the range used to assess risk for disease before the disease develops) been used in these studies, many more would have been identified with “deficiencies”. An important hypothesis which requires further investigation is that some individuals may have suboptimal nutrition for brain health despite having nutrient levels within the reference range. In other words, they might have a nutrient deficiency relative to their metabolic needs rather than relative to general population levels.

It is exciting that the EAT2BeNice consortium (NewBrainNutrition) will be looking at nutrient levels alongside other biomarkers so we can confirm whether these results are replicable. Hopefully some of the other biomarkers will prove more useful at predicting treatment response. Afterall, it is a valid clinical question to wonder – when a treatment works, who does it work for and why? These types of data inform clinical practice and can help the consumer decide whether you should go for that expensive testing, or not bother. At this stage, I wouldn’t bother.

References

  1. Rucklidge JJ, Johnstone JM, Gorman B, Boggis A, Frampton CM. Moderators of treatment response in adults with ADHD treated with a vitamin-mineral supplement. Prog Neuropsychopharmacol Biol Psychiatry. 2014;50:163-71.
  2. Rucklidge JJ, Eggleston MJF, Darling K, Stevens A, Kennedy M, Frampton CM. Can we predict treatment response in children with ADHD to a vitamin-mineral supplement? An investigation into pre-treatment nutrient serum levels, MTHFR status, clinical correlates and demographic variables. Prog Neuropsychopharmacol Biol Psychiatry. 2018.
  3. Rucklidge JJ, Eggleston MJF, Boggis A, Darling K, et al. Do Changes in Blood Nutrient Levels Mediate Treatment Response in Children and Adults With ADHD Consuming a Vitamin–Mineral Supplement? Journal of Attention Disorders. 2019. 0:1087054719886363.

 

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Meet Tim: he is an 8-year-old boy, living in the Netherlands with his parents and younger sister. A couple of years ago, Tim was diagnosed with Attention Deficit Hyperactivity/Impulsivity Disorder (ADHD). His psychologist recommended to participate in the TRACE study: this study examines the short- and long-term effects of dietary treatments in children with ADHD. In addition, the TRACE-BIOME study examines the underlying mechanisms of a dietary treatment. For this, we collect blood, stool and saliva samples and we perform a fMRI. These measurements might, among other things, shed light on the role of the brain-gut-axis.

But what’s it like to participate in a clinical trial? First of all, Tim was allocated to one of the two TRACE dietary treatments: an elimination diet or a healthy diet. Tim was allocated to the elimination diet. If we want to know if this diet is effective for Tim, we have to do a lot of different assessments (Figure 1).

Figure 1: assessments TRACE study
The TRACE Study, New Brain Nutrition

 

 

 

Before the baseline, 5 week and 1-year assessments, a couple of measurements already take place:

  • Tim wears an Actigraph one week before the assessment, which measures motor activity and sleep-wake rhythm;
  • Parents collect a stool sample from Tim in which his microbiota can be assessed;
  • Parents and teachers fill out different questionnaires about Tim’s behavior, but also about for example parenting styles;
  • Parents keep track of a food diary: what does Tim eat during two weekdays and one weekend day?

Before starting the elimination diet, Tim’s parents have a consult with one of the TRACE dieticians, so that they can prepare changing the diet of Tim. Then, it is time for the baseline assessment. Tim and his mother meet the researcher at the hospital for the blood venipuncture. He also has to chew on a cotton pad to collect a saliva sample. After this, they walk to Karakter which is a center for Child and Adolescent Psychiatry. The researcher measures his weight, length, blood pressure and heart rate. Next, Tim has to perform a task on the laptop which he really likes! This task assesses cognitive functions such as sustained attention, working memory and cognitive flexibility. After the computer task there is time for a break. Next, they start with a behavioral observation. In this task, Tim first plays with his mother and then with the researchers. The different tasks try to elicit ADHD symptoms and emotion (dys)regulation behavior. Finally, the MRI researcher takes Tim and his mother to the fMRI scanner in which he has to do two different tasks. All in all, the assessment takes about 4 hours.

After 5 weeks of the diet, it is time for the second assessment which is the same as the baseline assessment. The researcher has calculated, based on the parent and teacher questionnaires, if there is a significant response to the diet. Tim shows a 40% reduction of ADHD symptoms, which is a significant response! Therefore, they continue the diet. After 4 and 8 months of the diet, his parents receive some online questionnaires. Finally, after one year they are invited for the final assessment, which is again the same as the baseline assessment (without the fMRI).

 

The following YouTube video explains the assessments described above, in Dutch: ADHD en voeding: TRACE-onderzoek testdag

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When we are under high stress, we can often reach for foods that are “comforting” (like cookies, donuts, cake, pastries, and chocolate bars), but these foods may not be the best choice for feeding your brain under stressful and demanding circumstances. Comfort foods are often calorie-rich but nutrient-poor.

Further, under high stress (and it doesn’t actually matter what has caused the high stress, whether it be a natural disaster like an earthquake or fire, or witnessing something really traumatic), the reactions our body goes through can be quite similar. We release adrenaline. This is part of our natural alarm response system.

Adrenaline is an essential neurotransmitter that is released as part of the fight-flight response. It enables our body to get us to safety, shut down non-essential functions, and make sure the muscles needed for fight or flight get activated. Cortisol, a hormone, is also essential for the alarm system to function optimally.

Unfortunately, over extended periods of time, the alarm system can go into over-drive, and this is one factor that can lead to re-experiencing memories, flashbacks, hypervigilance, being on edge all the time, feeling anxious and panicky when reminded of the traumatic event, struggling with sleeping and having nightmares.

Making neurotransmitters and hormones requires micronutrients, which are numerous kinds of vitamins and minerals. This is a well-established scientific fact. Micronutrients like zinc, calcium, magnesium, iron, and niacin are all essential for making neurotransmitter chemicals for the brain and the body. If your body is depleted of these nutrients, then either it won’t have sufficient nutrients to make these essential chemicals, or it will redirect all resources to the fight or flight response (as it is so vital for survival) and there won’t be much left for ensuring optimal brain function to do things like concentrate, regulate moods and sleep.

Consequently, as micronutrients get depleted at a high rate during times of stress, we need to replenish them in greater quantity from our food (and perhaps other sources).

Where can we get these micronutrients from?

Answer: Nutrient-dense foods; real food, not ultra-processed foods.
Compare a banana to a cookie; one obtains far more of these micronutrients (like potassium, magnesium, folate) that are required for brain function from a banana. Eating kale chips over potato chips would also provide more nutrients. Reaching for a carrot stick and dipping it in hummus would be better for your brain than gorging down a commercial meat pie (although meat pies can be healthy if they contain lots of vegetables too). Choosing nuts and seeds over pretzels would also give you better brain food.

Overall, to cope well with stress your goal should be to increase intake of plant food and food high in nutrient density while still getting adequate protein, fats and carbs. Fish is a great source of protein and of essential fatty acids, which are also vital for brain function. In eating these types of foods, you would be shifting your diet from a Western type of diet (ultra-processed, high in sugar) to a Mediterranean-style diet (high in fruits and veggies, fish, nuts, healthy fats and low in processed foods).

Therefore, stop counting calories and start focussing on nutrients, especially nutrients that are good for your brain!

Would this be sufficient to sooth the over-activated alarm system in a situation of high and chronic stress? Possibly, although some people might need more nutrients than what they can get out of their diet, even if it is a healthy one. There are many reasons for this, some of which reflect reduced nutrient density in modern foods, some of which are due to our own specific genetic make-up, and some have to do with the health of our microbiome (the millions of helpful bacteria that live inside us, especially in our gut).

If you do need to consume more nutrients than what you can source from your diet, or you are struggling with cooking due to your particular circumstances and the stresses you are experiencing, or you are time poor because of family or work demands, what do you take in terms of a supplement? Research from the Mental Health and Nutrition Lab in Christchurch, NZ found that following the Christchurch earthquakes as well as other research on stressed communities shows that B vitamins, in particular, can be helpful. A recently published meta-analysis confirmed the positive effect of B vitamins on reducing stress. In addition, some may find a reduction of intrusive thoughts require additional minerals as well.

Nutrition resources for psychologists and mental health professionals working with people struggling with anxiety post-trauma:

When working with people struggling with stress/anxiety, research shows that it is essential that their diet includes foods that are nutrient-dense. This means being aware of foods that are high in vitamins and minerals as well as being a good source of fats, proteins and carbohydrates.

You can ask some simple questions:

  • How many times a week do you eat fast food meals or snacks?
  • How many regular fizzy drinks do you drink each day?
  • Snacks? Favourite Foods? Problem Foods?
  • Any restrictions? Allergies? Aversions?
  • How many servings of fruit do you eat each day?
  • How many servings of vegetables do you eat each day?
  • How often do you eat red meat (good source of iron, folate)?
  • Do you eat fish? (good to know if they are vegan, vegetarian, or gluten-free)

These questions can start the conversation to find out if they are eating nutrient dense foods.

Here are some basic tips:

  1. Start with whole foods diet approach including good fats, nuts, seeds, fish, a modest amount of meat, vegetables, fruit, whole grains
  2. Shifting towards eating “real” as opposed to processed foods naturally eliminates unnecessary food additives such as artificial colours, flavours, sweeteners and preservatives that do not add nutritional value and may contribute to psychiatric symptoms in some people
  3. Limit sugar intake (sugar is everywhere in processed foods, energy/fizzy drinks – encourage clients to look at labels to spot the hidden sugar)
  4. watch caffeine and alcohol intake doesn’t creep up
  5. Eat a good solid nutrient-dense breakfast: e.g., omelette with vegetables, muesli (oats, nuts, raisins) with milk, yogurt, fresh fruit
  6. If your client is struggling with cooking or a change in diet is not working enough to reduce psychological symptoms, you can consider suggesting supplements as there has been a lot of research on them. If suggesting supplements, stick to the data and published research, the best research is on adding additional B vitamins (like Blackmores or Berocca). For more information please email the Mental Health and Nutrition Research Group: mentalhealthnutrition@canterbury.ac.nz

Here are some useful resources:

A recent radio interview about dietary patterns and stress: https://www.radionz.co.nz/national/programmes/nights/audio/2018687489/nutrition-during-times-of-stress-and-trauma

Harvard Medical School has put together lots of resources on healthy eating, including the healthy eating plate: www.health.harvard.edu/staying-healthy/healthy-eating-plate

The Helfimed trial was a successful trial that showed the benefit of assisting people suffering from depression to nudge over to a more Mediterranean-based diet. They have lots of recipes on their website: http://helfimed.org/cgi-sys/suspendedpage.cgi

The Mood and Food Centre in Melbourne often blogs on diet-related topics. Check out their website: http://foodandmoodcentre.com.au/

Dr Drew Ramsey has some excellent resources on eating well on a budget: https://drewramseymd.com/uncategorized/brain-food-budget/

There are lots of great resources at this site: https://www.getselfhelp.co.uk/freedownloads.htm

Books that we have enjoyed reading on nutrition and mental health that do have some scientific basis to their recommendations:

  • Brain Changer – Prof Felice Jacka
  • Finally Focused – Dr James Greenblatt
  • The Mad Diet – Suzanne Lockhart
  • The anti-anxiety food solution –Trudy Scott
  • What the FAT? – Prof Grant Schofield (also includes recipes)

Rachel Kelly has devised a cookbook directly focused on eating foods that will contain nutrients help you feel mentally better:

https://www.rachel-kelly.net/books-apps/

How to eat well on a budget:
From the British Dietetic Association: A healthy diet can be more expensive than a diet made up of more refined foods. Fish, fruit and vegetables can be particularly pricey. However, by cutting down on sugary drinks and snacks, takeaways and alcohol, you can save money to be spent on healthier items. Take care to buy only as much as you know you can use within the next few days to reduce waste. You can also cut your costs by taking advantage of special promotions and by shopping at market stalls which are often cheaper than supermarkets.

If you live alone you could save money by splitting purchases with friends (larger pack sizes are usually cheaper) or by cooking several portions of a dish and freezing some of them. This also saves fuel and saves you the effort of preparing meals every day. Frozen fruit and vegetables are often cheaper than fresh produce and are usually just as good nutritionally (with no wastage). Fresh fruit and vegetables are usually cheapest when they are in season.

Also, research from Australia has shown that a Mediterranean style diet was cheaper than a poor quality diet.

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Stress tends to mess with our eating habits. In times of stress, some people eat more, while others eat less. The type of food people eat also changes: compared to non-stressed individuals, stressed individuals more often eat unhealthy foods.

Laboratory experiments have shown that stress causes people to make unhealthier food choices. In a typical experiment, participants are exposed to an acute stressor, for instance, they are asked to present themselves before strangers, or to solve a very difficult puzzle within an unrealistically short timeframe. Unknown to the participants, the most important part of the experiment takes place during the breaks, when they are offered food and drinks. Secretly, the researchers observe exactly what the participants eat and drink. They look for differences between those who were exposed to stress prior to the break, and those who were not. And indeed, researchers do typically find differences between these groups. For instance, women who were most sensitive to stress (as shown by an exaggerated cortisol response), also ate more calories in response to stress [1]. In a second experiment, participants who had just performed several difficult tasks in front of a judge, especially those who reported being subjected to chronic stress in daily life, ate more chocolate cake and fewer vegetables compared to non-stressed participants [2].

But how do such laboratory experiments relate to real-life? After all, for most of us, giving presentations is not the most influential stressor in our lives, and real-life situations are much more complex. To investigate how real-life stressors affect food choices, one needs so-called epidemiological studies. In such studies, large groups of people are followed over longer periods of time. At multiple time points, they are asked about their stress levels (including daily hassles, work-related stress, academic stress, etc.) as well as about their eating habits. Consistent with experimental studies, epidemiological studies have shown that, on average, diet quality is lower in people who report more stress (e.g. [3] [4]). However, the effects reported in real-life studies are much smaller compared to the effects reported in the lab: in real life, stress is only one among many factors influencing your food choices.

So exactly how big ís the effect of real-life stress on our real-life food choices? We investigated this in over a hundred thousand people from the North of the Netherlands. We found that exposure to stressful life events, such as the loss of a family member or being the victim of a crime, was associated with poorer diet quality; however, the effects of stress were relatively small. For instance: on average, most people reported having dealt with one stressful life event in the past year, and their average diet quality score (on a scale of 0-48) was 23.9 points. People who reported dealing with two instead of one stressful events had an average diet quality of 23.8 points. For comparison, the difference in diet quality between the average man (22.5 points) and the average woman (24.9 points) in our study was 27 times bigger [5].

To summarize, diet quality deteriorates in times of stress. However, in real life situations, with a multitude of other factors determining what, where and when we eat, the effect of stress alone is very small.

Do you want to learn more about brain changes underlying the effect of stress on food choices? Check out this blog: https://newbrainnutrition.com/stress-and-nutrition-hungry-brain/ by Simone Demmel.

REFERENCES:
[1] Epel, E, Lapidus, R & McEwen, B, Brownell, K (2001). Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology, 26(1), 37-49

[2] Tryon, MS, DeCant, R, Laugero, KD (2013). Having your cake and eating it too: a habit of comfort food may link chronic social stress exposure and acute stress-induced cortisol hyperresponsiveness. Physiology and behavior, 114-115, 32-37

[3] Mikolajcyk, RT, Al Ansari, W & Maxwell, AE (2009). Food consumption frequency and perceived stress and depressive symptoms among students in three European countries. Nutrition Journal, 8(1),1-8

[4] O’Connor, D, Jones, F, Conner, M, McMillan, B, Ferguson, E (2008). Effects of daily hassles and eating style on eating behavior. Health Psychology, 27(1 supplement).

[5] Schweren et al., in preparation

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What is vitamin B1 (thiamine)?

Thiamine, which is also known as vitamin B1, is an essential micronutrient, which is required for metabolism, enzymatic processes and conduction of nerve signals. All living organisms use thiamine, but it can be made only in bacteria, fungi and plants. In humans, gastrointestinal microbiota also produces thiamine, but not enough for the organism functioning. Thus, we, as well as other animals must obtain vitamin B1 from the diet.

Thiamine deficiency

Deficiency of thiamine can affect the cardiovascular, nervous and immune systems. A severe and chronic form is known as beriberi. Wet beriberi affects cardiovascular system resulting in tachycardia, high arterial and venous pressures, leg swelling. Dry beriberi affects nervous system resulting in impairment of sensory, motor and reflex functions and altered mental status. Worldwide thiamine deficiency is most widely reported in populations where primary food source are polished rice and grains. In Western countries, it most commonly affects people suffering from alcoholism or chronic illness. Thiamine deficiency in patients with alcohol use disorder often lead to Kosakoff syndrome, a chronic disease with severe memory loss and learning problems.

Food sources of thiamine

It is very easy to add foods rich with thiamine to the diet. Food sources of thiamine include beef, pork, eggs, liver, nuts, oats, oranges, seeds, legumes and yeast. Such foods as rice, pasta, breads, cereals and flour are often fortified with vitamin B1 as the processing involved in creating these products removes thiamine. Thiamine supplements and medications are available on market to treat or prevent thiamine deficiency. Remarkably, B1 is well tolerated and has almost no side effects.

Bioavailable analogues of Thiamine

Analogues of vitamin B1, such as benfotiamine or dibenzoyl thiamine, have improved bioavailability, due to their higher lipid solubility, which facilitate permeation in cell membranes. As a result, they provide higher levels of thiamine in muscle, brain and liver. This can be the reason of their higher effectiveness.

Thiamine as medication

Thiamine was the first of the water-soluble vitamins to be discovered, and since early 20th century it was extensively studied. Most commonly thiamine supplementation is used to treat syndromes associated with severe thiamine deficiency and during pregnancy and lactating due to increased need for this vitamin. Rapid recovery can occur within hours if thiamine is given intravenously. If concentrated thiamine supplements are not available, diets rich with thiamine will also lead to recovery, though at a slower rate.

New properties of thiamine

Recently, other important roles of thiamine including the regulation of oxidative stress were discovered [1]. As emotional stress is associated with oxidative stress in the brain, it was hypothesized that thiamine can counteract negative effects of the stress. And indeed, in studies on mice thiamine precluded negative changes in mood and emotionality, as well as neuroinflammation and oxidative stress caused by stress [2,3]. It also ameliorated cellular proliferation and neurogenesis in the hippocampus under stress conditions. In agreement with animal studies, vitamin B1 was also able to ameliorate symptoms of major depressive disorder in patients [4] or work stress-related mood swings [5].

Thus, thiamine was shown as a promising treatment for the depressive-like changes and excessive aggression, caused by stress. Hopefully, new studies on thiamine will be conducted in the nearest future to show novel properties of this vitamin.

 

References

[1]      L. Bettendorff, P. Wins, Biological functions of thiamine derivatives: Focus on non-coenzyme roles, OA Biochem. 1 (2013).

[2]      N. Markova, N. Bazhenova, D.C. Anthony, J. Vignisse, A. Svistunov, K.-P. Lesch, L. Bettendorff, T. Strekalova, Thiamine and benfotiamine improve cognition and ameliorate GSK-3β-associated stress-induced behaviours in mice, Prog. Neuro-Psychopharmacology Biol. Psychiatry. 75 (2017) 148–156.

[3]      A. Gorlova, D. Pavlov, D.C. Anthony, E.D. Ponomarev, M. Sambon, A. Proshin, I. Shafarevich, D. Babaevskaya, K.-P. Lesсh, L. Bettendorff, T. Strekalova, Thiamine and benfotiamine counteract ultrasound-induced aggression, normalize AMPA receptor expression and plasticity markers, and reduce oxidative stress in mice, Neuropharmacology. (2019).

[4]      A. Ghaleiha, H. Davari, L. Jahangard, M. Haghighi, M. Ahmadpanah, M.A. Seifrabie, H. Bajoghli, E. Holsboer-Trachsler, S. Brand, Adjuvant thiamine improved standard treatment in patients with major depressive disorder: results from a randomized, double-blind, and placebo-controlled clinical trial, Eur. Arch. Psychiatry Clin. Neurosci. 266 (2016) 695–702.

[5]      C. Stough, A. Scholey, J. Lloyd, J. Spong, S. Myers, L.A. Downey, The effect of 90 day administration of a high dose vitamin B-complex on work stress, Hum. Psychopharmacol. Clin. Exp. 26 (2011) 470–476.

 

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Children with ADHD who keep taking micronutrients over one year are mostly in remission in their symptoms with no side effects

The results from a University of Canterbury (UC) study into the longer term effects of micronutrients on ADHD symptoms in children was recently published in the Journal of Child and Adolescent Psychopharmacology.  

This study was led by Dr Kathryn Darling at the Mental Health and Nutrition Lab in Christchurch (under the supervision of Eat2BeNice Scientist Julia Rucklidge) and looked at the long-term effects of a broad-spectrum micronutrient (vitamins and minerals) in attention-deficit/hyperactivity disorder (ADHD) treatment.

Eighty-four of the 93 children who entered a 10-week randomised controlled trial (micronutrients versus placebo), followed by a 10 week phase of all children taking micronutrients, then completed follow-up assessments after 12 months. This allowed us to gather valuable information about what happens when people choose to stay on or come off the micronutrient treatment.

The study showed that children who benefit in the short term from taking a broad-spectrum vitamin/mineral formula maintain those benefits or continue to improve when they keep taking it longer term, without side effects.

Continued micronutrient treatment was associated with improvements in ADHD symptoms which were similar to, or greater than, those associated with stimulant medication. Unlike stimulant medications, micronutrients were associated with improvements, rather than worsening, in mood and anxiety. This indicates that micronutrients can be a serious treatment option for those who choose not to take medications. Micronutrients may be especially helpful for children with ADHD who also have difficulties with mood or anxiety.

Other key findings from this research:

  • Those who continued to take micronutrients did not have any ongoing side effects.
  • Children who continued to take micronutrients and children who changed to medications (like methylphenidate/Ritalin/Concerta) either stayed well or continued to show improvement in ADHD symptoms at 12-month follow-up assessment, while those who stopped treatment altogether did not.
  • Children who switched from micronutrients to medications like methylphenidate/Ritalin were more likely to have problems with mood or anxiety at the 12-month follow-up assessment, which were worse than at the end of the micronutrient trial. After the end of the trial, mood and anxiety symptoms had generally continued to improve for the children who stayed on micronutrients, and mostly stayed the same for those who stopped treatment.
  • The most common reasons people stopped taking micronutrients were the cost and number of pills to swallow.
  • Based on dominant treatment, more of those who stayed on trial micronutrients (84%) were identified as “Much” or “Very Much” improved overall relative to baseline functioning, compared to 50% of those who switched to psychiatric medications and only 21% of those who discontinued treatment. Fifteen (79%) of those still taking micronutrients, 8 (42%) of those using medications, and 7 (23%) of those who discontinued treatment were considered in remission based on parent-reported ADHD. Those who stayed on micronutrients were more likely to have failed medication treatment in the past.

It is important to note that these findings are reporting on group averages, so the effect of micronutrients or other treatments for any specific child may have been different. People do respond differently to any form of treatment – perhaps they benefited across all areas of functioning or perhaps had no benefit at all.

This study is limited due to its naturalistic observational status but allows us to evaluate effectiveness in the real world. No funds were received from the manufacturer of the micronutrients.

If you want to know more about the micronutrients we studied, email mentalhealthnutrition@canterbury.ac.nz

 

Reference:

Darling, K. A., Eggleston, M. J., Retallick-Brown, H., & Rucklidge, J. J. (2019). Mineral-Vitamin Treatment Associated with Remission in Attention-Deficit/Hyperactivity Disorder Symptoms and Related Problems: 1-Year Naturalistic Outcomes of a 10-Week Randomized Placebo-Controlled Trial. Journal of child and adolescent psychopharmacology.

https://doi.org/10.1089/cap.2019.0036

 

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Meet Tim: he is an 8-year-old boy, living in the Netherlands with his parents and younger sister. A couple of years ago, Tim was diagnosed with Attention Deficit Hyperactivity/Impulsivity Disorder (ADHD). His psychologist recommended to participate in the TRACE study: this study examines the short- and long term effects of dietary treatments in children with ADHD. In addition, the TRACE-BIOME study examines the underlying mechanisms of a dietary treatment. For this, we collect blood, stool, and saliva samples and we perform a fMRI. These measurements might, among other things, shed light on the role of the brain-gut-axis.

But what’s it like to participate in a scientific study? First of all, Tim was allocated to one of the two TRACE dietary treatments: an elimination diet or a healthy diet. Tim was allocated to the elimination diet. If we want to know if this diet is effective for Tim, we have to do a lot of different assessments (Figure 1).

Figure 1: assessments TRACE study

 

 

           

 

 

 

 


Before the baseline, 5 week and 1-year assessments, a couple of measurements already take place:

  • Tim wears an Actigraph one week before the assessment, which measures motor activity and sleep-wake rhythm;
  • Parents collect a stool sample from Tim in which his microbiota can be assessed;
  • Parents and teachers fill out different questionnaires about Tim’s behavior, but also about, for example, parenting styles;
  • Parents keep track of a food diary: what does Tim eat during two weekdays and one weekend day?

Before starting the elimination diet, Tim’s parents have a consult with one of the TRACE dieticians, so that they can prepare changing the diet of Tim. Then, it is time for the baseline assessment. Tim and his mother meet the researcher at the hospital for the blood venipuncture. He also has to chew on a cotton pad to collect a saliva sample. After this, they walk to Karakter which is a center for Child and Adolescent Psychiatry. The researcher measures his weight, length, blood pressure and heart rate. Next, Tim has to perform a task on the laptop which he really likes! This task assesses cognitive functions such as sustained attention, working memory, and cognitive flexibility. After the computer task, there is time for a break. Next, they start with behavioral observation. In this task, Tim first plays with his mother and then with the researchers. The different tasks try to elicit ADHD symptoms and emotion (dys)regulation behavior. Finally, the MRI researcher takes Tim and his mother to the fMRI scanner in which he has to do two different tasks. All in all, the assessment takes about 4 hours.

After 5 weeks of the diet, it is time for the second assessment which is the same as the baseline assessment. The researcher has calculated, based on the parent and teacher questionnaires, if there is a significant response to the diet. Tim shows a 40% reduction of ADHD symptoms, which is a significant response! Therefore, they continue the diet. After 4 and 8 months of the diet, his parents receive some online questionnaires. Finally, after one year they are invited for the final assessment, which is again the same as the baseline assessment (without the fMRI).

The following movie explains the assessments described above, in Dutch: 

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