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3535The Autism Revolution: Whole Body Strategies for Making Life All It Can BeThe Autism Revolution: Whole Body Strategies for Making Life All It Can BeMartha HerbertMartha Herbert01/08/2013
Prof Martha Herbert gave a keynote presentation at the 'Changing the Course of Autism' conference that took place in Edinburgh, UK, in June 2013. She was asked to give an overview of what she'd be talking about at the opening ceremony for the event, at the Scottish Parliament. You can watch the video of this here.
Move beyond conventional thinking about autism . . .
After years of treating patients and analyzing scientific data, prominent Harvard Medical School researcher and clinician Dr. Martha Herbert offers a revolutionary new view of autism. Autism is not hardwired into a child’s genes and destined to remain fixed forever, as parents are often told. Instead, Dr. Herbert approaches autism as a collection of challenges, many of which can be tackled in a deliberate and methodical way. Her recommendations aim to provide optimal nutrition, reduce toxic exposures, shore up the immune system, reduce stress, and open the door to learning and creativity—all by understanding and truly meeting your child’s needs.
Drawing from the newest research, technologies, and insights, as well as inspiring case studies of both children and adults, Dr. Herbert guides you through small changes that can create a substantial difference in your loved one with autism. A paradigm-changing book that offers hope and healing for the millions of people with autism in their lives, The Autism Revolution shows that there’s plenty you can do every day to reduce vulnerability, feel better and live life to its fullest.
3541Bondi et al 2013 - Adolescent Behavior and Dopamine Availability Are Uniquely Sensitive to Dietary Omega-3 Fatty Acid DeficiencyAdolescent Behavior and Dopamine Availability Are Uniquely Sensitive to Dietary Omega-3 Fatty Acid DeficiencyAdolescent Behavior and Dopamine Availability Are Uniquely Sensitive to Dietary Omega-3 Fatty Acid DeficiencyBondi CO, Taha AY, Tock JL, Totah NK, Cheon Y, Torres GE, Rapoport SI, Moghaddam B25/07/2013Biol Psychiatry. 2013 Jul 25. pii: S0006-3223(13)00578-7. doi: 10.1016/j.biopsych.2013.06.007
BACKGROUND: Understanding the nature of environmental factors that contribute to behavioral health is critical for successful prevention strategies in individuals at risk for psychiatric disorders. These factors are typically experiential in nature, such as stress and urbanicity, but nutrition-in particular dietary deficiency of omega-3 polyunsaturated fatty acids (n-3 PUFAs)-has increasingly been implicated in the symptomatic onset of schizophrenia and mood disorders, which typically occurs during adolescence to early adulthood. Thus, adolescence might be the critical age range for the negative impact of diet as an environmental insult.
METHODS: A rat model involving consecutive generations of n-3 PUFA deficiency was developed on the basis of the assumption that dietary trends toward decreased consumption of these fats began 4-5 decades ago when the parents of current adolescents were born. Behavioral performance in a wide range of tasks as well as markers of dopamine-related neurotransmission was compared in adolescents and adults fed n-3 PUFA adequate and deficient diets.
RESULTS: In adolescents, dietary n-3 PUFA deficiency across consecutive generations produced a modality-selective and task-dependent impairment in cognitive and motivated behavior distinct from the deficits observed in adults. Although this dietary deficiency affected expression of dopamine-related proteins in both age groups in adolescents but not adults, there was an increase in tyrosine hydroxylase expression that was selective to the dorsal striatum.
CONCLUSIONS: These data support a nutritional contribution to optimal cognitive and affective functioning in adolescents. Furthermore, they suggest that n-3 PUFA deficiency disrupts adolescent behaviors through enhanced dorsal striatal dopamine availability.
Addiction, anxiety, cognition, fatty acids, nutrition, schizophrenia
http://www.ncbi.nlm.nih.gov/pubmed/?term=Adolescent+Behavior+and+Dopamine+Availability+Are+Uniquely+Sensitive+to+Dietary+Omega-3+Fatty+Acid+DeficiencyView this and related abstracts via PubMed here
3526Musci et al 2013 - Internalizing Antecedents and Consequences of Binge-Eating Behaviors in a Community-Based, Urban Sample of African American FemalesInternalizing Antecedents and Consequences of Binge-Eating Behaviors in a Community-Based, Urban Sample of African American FemalesInternalizing Antecedents and Consequences of Binge-Eating Behaviors in a Community-Based, Urban Sample of African American Females.Musci RJ, Hart SR, Ialongo N20/07/2013Prevention Science, 2013; DOI: 10.1007/s11121-013-0411-9
The etiology of problem-eating behaviors is often overlooked in research as it typically shares many symptoms with other more common psychiatric illnesses. Binge-eating problems are at the forefront of the popular media because of the connection to obesity; therefore, increased knowledge of binge eating problems, particularly the internalizingantecedents and consequences will have implications in a multitude of domains, including prevention programs aimed at physical and mental health. The current study examines the antecedents of binge-eatingbehaviors by exploring how the growth of internalizing symptoms influences the proximal outcome of a binge-eating inventory in a longitudinal sample of AfricanAmerican girls. Additional consequences of binge-eating problems are also explored. This study focuses on binge-eating problems in order to present valuable information for prevention scientists who wish to develop target individuals at high risk for internalizing problems such as suicide.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Internalizing+Antecedents+and+Consequences+of+Binge-Eating+Behaviors+in+a+Community-Based%2C+Urban+Sample+of+African+American+FemalesView this and related abstracts on PubMed here
3714Keeney et al 2013 - Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine nitration and proteomics changes in levels of key proteins in brain: implications for low vitamin D-dependent age-related cognitive decline.Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine nitration and proteomics changes in levels of key proteins in brain: implications for low vitamin D-dependent age-related cognitive decline.Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine nitration and proteomics changes in levels of key proteins in brain: implications for low vitamin D-dependent age-related cognitive decline.Keeney JT, Förster S, Sultana R, Brewer LD, Latimer CS, Cai J, Klein JB, Porter NM, Allan Butterfield D.18/07/2013Free Radic Biol Med.65324-34. Epub 2013 Jul 18.
In addition to the well-known effects of vitamin D (VitD) in maintaining bone health, there is increasing appreciation that this vitamin may serve important roles in other organs and tissues, including the brain.
Given that VitD deficiency is especially widespread among the elderly, it is important to understand how the range of serum VitD levels that mimic those found in humans (from low to high) affects the brain during aging from middle age to old age.
To address this issue, 27 male F344 rats were split into three groups and fed isocaloric diets containing low (100 IU/kg food), control (1000 IU/kg food), or high (10,000 IU/kg food) VitD beginning at middle age (12 months) and continued for a period of 4-5 months. We compared the effects of these dietary VitD manipulations on oxidative and nitrosative stress measures in posterior brain cortices.
The low-VitD group showed global elevation of 3-nitrotyrosine compared to control and high-VitD-treated groups. Further investigation showed that this elevation may involve dysregulation of the nuclear factor κ-light-chain enhancer of activated B cells (NF-κB) pathway and NF-κB-mediated transcription of inducible nitric oxide synthase (iNOS) as indicated by translocation of NF-κB to the nucleus and elevation of iNOS levels.
Proteomics techniques were used to provide insight into potential mechanisms underlying these effects. Several brain proteins were found at significantly elevated levels in the low-VitD group compared to the control and high-VitD groups. Three of these proteins, 6-phosphofructokinase, triose phosphate isomerase, and pyruvate kinase, are involved directly in glycolysis. Two others, peroxiredoxin-3 and DJ-1/PARK7, have peroxidase activity and are found in mitochondria. Peptidyl-prolyl cis-trans isomerase A (cyclophilin A) has been shown to have multiple roles, including protein folding, regulation of protein kinases and phosphatases, immunoregulation, cell signaling, and redox status.
Together, these results suggest that dietary VitD deficiency contributes to significant nitrosative stress in brain and may promote cognitive decline in middle-aged and elderly adults.
3530Santos Vaz et al 2013 - Dietary Patterns, n-3 Fatty Acids Intake from Seafood and High Levels of Anxiety Symptoms during Pregnancy: ALSPAC findingsDietary Patterns, n-3 Fatty Acids Intake from Seafood and High Levels of Anxiety Symptoms during Pregnancy: Findings from the Avon Longitudinal Study of Parents and ChildrenDietary Patterns, n-3 Fatty Acids Intake from Seafood and High Levels of Anxiety Symptoms during Pregnancy: Findings from the Avon Longitudinal Study of Parents and Children Juliana dos Santos Vaz, Gilberto Kac, Pauline Emmett, John M Davies, Jean Golding, Joseph R Hibbeln13/07/2013PLOS One
Little is known about relationships between dietary patterns, n-3 polyunsaturated fatty acids (PUFA) intake and excessive anxiety during pregnancy.
To examine whether dietary patterns and n-3 PUFA intake from seafood are associated with high levels of anxiety during pregnancy.
Pregnant women enrolled from 1991–1992 in ALSPAC (n 9,530). Dietary patterns were established from a food frequency questionnaire using principal component analysis. Total intake of n-3 PUFA (grams/week) from seafood was also examined. Symptoms of anxiety were measured at 32 weeks of gestation with the Crown-Crisp Experiential Index; scores =9 corresponding to the 85th percentile was defined as high anxiety symptoms. Multivariate logistic regression models were used to estimate the OR and 95% CI, adjusted by socioeconomic and lifestyle variables.
Multivariate results showed that women in the highest tertile of the health-conscious (OR 0.77; 0.65–0.93) and the traditional (OR 0.84; 0.73–0.97) pattern scores were less likely to report high levels of anxiety symptoms. Women in the highest tertile of the vegetarian pattern score (OR 1.25; 1.08–1.44) were more likely to have high levels of anxiety, as well as those with no n-3 PUFA intake from seafood (OR 1.53; 1.25–1.87) when compared with those with intake of >1.5 grams/week.
The present study provides evidence of a relationship between dietary patterns, fish intake or n-3 PUFA intake from seafood and symptoms of anxiety in pregnancy, and suggests that dietary interventions could be used to reduce high anxiety symptoms during pregnancy.
ALSPAC; omega-3, anxiety; maternal diet, pregnancy, fish and seafood, dietary patternshttp://www.ncbi.nlm.nih.gov/pubmed/23874437View this and related abstracts via PubMed here. Free full text of this article is available online.
350912 July 2013 - Gov UK - The School Food PlanSchool Food PlanA plan of action designed to improve the quality and take-up of school food and put the kitchen at the heart of school life is published. 12/07/2013
The ‘School food plan’, written by Leon restaurant founders Henry Dimbleby and John Vincent, includes a range of actions to drive up standards and divert some of the £1 billion parents currently spend on packed lunches back into the system.
A year ago, Secretary of State for Education Michael Gove asked Henry and John to work with schools, councils, caterers, parents and government to set out how to increase the number of children eating good food in schools.
The actions set out today in the plan include: £16.1 million of new money to boost take up in schools and ensure thousands of children get healthy breakfast; a checklist for headteachers to help improve the ‘food culture’ in their schools, and the launch of 2 flagship London boroughs to help prove that better school food can have a significant impact on children’s health and attainment.
Henry Dimbleby said:
While we have been hugely impressed by the energy and enthusiasm we have witnessed among school cooks, teachers and others working to make school food great, our findings are clear - not enough children are eating well and not enough money is going into the school food system to ensure that it can provide great food and pay its way.
That’s why we have got to make a change. We need to ensure that children have the fuel they need in order to be happy and healthy and perform well at school. The best schools worry about what’s going on in children’s bodies as well as their minds.
This is a series of actions, each of which is the responsibility of a named person or organisation, to transform what children eat at school and how they learn about food.
John Vincent said:
Increasing take-up is not something that can be done from the top-down. It requires a cultural change within each school.
It means cooking food that is both appetising and nutritious, making the dining hall a welcoming place, keeping queues down, getting the price right, allowing children to eat with their friends; getting them interested in cooking and growing.
We know from our experience that this change is led by headtachers and we hope they help to take this plan forward to make a real and lasting change.
Welcoming the plan, Michael Gove said:
The whole virtue of the ‘School food plan’ is that it’s there to help - it emphasises the vital importance of making sure food is high quality and tasty and creating a culture in your school where everyone appreciates the importance of food.
What I’d like to see is more children eating school lunches and fewer having packed lunches, and more children feeling healthier and more energetic throughout the day.
I would like to thank John and Henry for the hard work that went into this this plan and believe we now have a set of actions that can make a real difference in schools right across the country.
Mayor of London, Boris Johnson, said:
This is an ambitious plan that sets out a blueprint from which we can get kids to eat more healthily and to learn more about food.
All the evidence suggests that if kids have a healthy school meal they’ll do better in the classroom and that’s something which is in everyone’s long-term interest.
Through our forthcoming pilot we want London boroughs to help show the rest of the country that the link between great food and academic achievement is inextricable.
Actions in the plan include:
A £16.1 million injection of cash from the Department for Education over the next 2 years. This includes £11.8 million that organisations such as the Children’s Food Trust and the Food For Life Partnership can bid for to help turn around schools that are struggling with their lunch service, £3.15 million to ensure healthy breakfasts are available for thousands of children who arrive at school hungry.
A practical checklist for headteachers, listing the most important things they or their team can do to that can make a big difference to take-up and food culture in schools. The checklist is based on the examples of what is working well that the reviewers have seen during their trips to over 60 schools in the country. They are designed to be pinned up in the head’s office and the kitchen. Suggested actions include:
Lowering the price of school meals - consider subsidising school meals for your reception and year 7 classes for the first term, or offer discounts for parents of multiple children or those whose children eat a school lunch every day.
Teachers should be encouraged to eat with the children in the dining hall.
Have a stay-on-site rule for break and lunch time.
Have a cashless payment system to shorten queuing times and prevent free school meal children from being stigmatised.
Offer after school cooking lessons for parents with their children.
Make sure packed lunches are not more exciting than school lunches. Ban sugary drinks, crisps and confectionery, or offer prizes and other incentives for bringing in a healthy lunch. Or ban packed lunches altogether.
Watch what gets served at mid-morning break. Many children eat their main meal at this time which too often means filling up on pizza, paninis or cake.
The launch of 2 flagship London boroughs to help prove that better school food can have a significant impact on children’s health and attainment. Every school in each area will receive co-ordinated support from expert organisations such as the Children’s Food Trust to improve the quality and take up of school meals and spread great food culture through the wider community. The Department for Education and the Mayor’s Office will jointly fund the boroughs.
The Department for Education will test and introduce a set of revised food based standards (built on a nutritional framework), with the intention of applying them to maintained schools and all new academies and free schools by September 2014.
Ofsted will amend its guidance to inspectors to consider behaviour and culture in the dining hall and the way a school promotes healthy lifestyles.
Co-founder of Innocent smoothies Richard Reed and branding expert Wally Olins will help devise a strategy to improve the image of school food, and Jamie Oliver has agreed to help through his media work.
Ensuring cooking is in the curriculum for all children up to the age of 14. The new curriculum will emphasise the importance of cooking nutritious, savoury dishes, understanding where food comes from, and taking pleasure in the creative arts of the kitchen.
The government will investigate the case for extending free school meals entitlement.
Other actions in the plan include:
including food and nutrition in headteacher training
action to ensure small schools are funded fairly
a 5 measure test to judge whether the ‘School food plan’ is working
a new ‘what works well’ website to share best practice
In addition, in September Change4Life - the government’s biggest existing public awareness campaign - will launch a new ‘Back to School’ pledge. This will consist of 5 healthy behaviours, one of which will be a promise by parents to give their child a school dinner.
Over the course of the last year Henry and John have:
held more than 100 meetings with experts, representative groups and organisations working with schools to improve their food culture
organised 7 regional events around England, attended by nearly 500 people and representatives from over 150 schools
visited more than 60 schools to eat their food, attend lessons and discuss issues with children, parents, cooks, teachers, business managers, teachers and heads
held 20 focus groups with children
convened an expert panel to develop the plan
commissioned primary research including a representative survey of 400 headteachers’ views on school food
Key facts and figures:
The obesity rate in the UK has risen from 6% of the population in 1980 to 27% today, and almost 20% of children are already obese by the time they leave primary school.
Across the country, take-up of school food remains stubbornly low. The majority of children - 57% - either bring in a packed lunch or buy something outside school (almost always junk food).
Many parents mistakenly imagine that a packed lunch is the healthiest option. In fact, it is far easier to get the necessary nutrients into a cooked meal.
Only 1% of packed lunches meet the nutritional standards that currently apply to school food and two-thirds contain sweets, sugary drinks and savoury snacks such as crisps.
Parents currently spend almost £1 billion a year on packed lunches; persuading just a fraction of them to switch to school food would lead to healthier children who are able to concentrate better and work harder.
http://www.schoolfoodplan.com/Visit the School Food Plan website hereSchool_Food_Plan_2013.pdfDownload a copy of The School Food Plan hereSchool Food Plan smaller.jpgSchool Food Plan logo
3519Lyall K et al 2013 - Maternal dietary fat intake in association with autism spectrum disordersMaternal dietary fat intake in association with autism spectrum disordersMaternal dietary fat intake in association with autism spectrum disordersLyall K, Munger KL, O'Reilly EJ, Santangelo SL, Ascherio A27/06/2013Am J Epidemiol. 2013 Jul 15;178(2):209-20. doi: 10.1093/aje/kws433. Epub 2013 Jun 27.
Our goal in this study was to determine whether maternalfatintake before or during pregnancy was associated with risk of autismspectrum disorder (ASD) in the offspring. Our primary analysis included 317 mothers who reported a child with ASD and 17,728 comparison mothers from the Nurses' Health Study II (index births in 1991-2007). Dietary information was collected prospectively through a validated food frequency questionnaire. Binomial regression was used to estimate crude and adjusted risk ratios. Maternalintake of linoleic acid was significantly inversely associated with ASD risk in offspring, corresponding to a 34% reduction in risk in the highest versus lowest quartiles of intake. Mothers in the lowest 5% of ω-3 fatty acid intake had a significant increase in offspring ASD risk as compared with the remaining distribution (risk ratio = 1.53, 95% confidence interval: 1.00, 2.32); this association was also seen in the subgroup of women (86 cases and 5,798 noncases) for whom dietary information during pregnancy was available (risk ratio = 2.42, 95% confidence interval: 1.19, 4.91). Thus, variations in intake of polyunsaturated fats within the range commonly observed among US women could affect fetal brain development and ASD risk. Because the number of women with diet assessed during pregnancy was small, however, these results should be interpreted cautiously.
autism, dietary fat, linoleic acid, polyunsaturated fatty acids, ?-3 fatty acids, ?-6 fatty acidshttp://www.ncbi.nlm.nih.gov/pubmed/?term=Maternal+Dietary+Fat+Intake+in+Association+With+Autism+Spectrum+DisordersView this and related abstracts via PubMed here
3522Lennerz et al 2013 - Effects of dietary glycemic index on brain regions related to reward and craving in menEffects of dietary glycemic index on brain regions related to reward and craving in menEffects of dietary glycemic index on brain regions related to reward and craving in menLennerz BS, Alsop DC, Holsen LM, Stern E, Rojas R, Ebbeling CB, Goldstein JM, Ludwig DS26/06/2013Am J Clin Nutr. 2013 Jun 26.
Qualitative aspects of diet influence eating behavior, but the physiologic mechanisms for these calorie-independent effects remain speculative.
We examined effects of the glycemicindex (GI) on brain activity in the late postprandial period after a typical intermeal interval.
With the use of a randomized, blinded, crossover design, 12 overweight or obese men aged 18-35 y consumed high- and low-GI meals controlled for calories, macronutrients, and palatability on 2 occasions. The primary outcome was cerebral blood flow as a measure of resting brain activity, which was assessed by using arterial spin-labeling functional magnetic resonance imaging 4 h after test meals. We hypothesized that brain activity would be greater after the high-GI meal in prespecified regions involved in eating behavior, reward, and craving.
Incremental venous plasma glucose (2-h area under the curve) was 2.4-fold greater after the high- than the low-GI meal (P = 0.0001). Plasma glucose was lower (mean ± SE: 4.7 ± 0.14 compared with 5.3 ± 0.16 mmol/L; P = 0.005) and reported hunger was greater (P = 0.04) 4 h after the high- than the low-GI meal, respectively. At this time, the high-GI meal elicited greater brain activity centered in the right nucleus accumbens (a prespecified area; P = 0.0006 with adjustment for multiple comparisons) that spread to other areas of the right striatum and to the olfactory area.
Compared with an isocaloric low-GI meal, a high-GI meal decreased plasma glucose, increased hunger, and selectively stimulated brainregions associated with reward and craving in the late postprandial period, which is a time with special significance to eating behavior at the next meal. This trial was registered at clinicaltrials.gov as NCT01064778.
3564Lassek & Gaulin 2013 - Maternal milk DHA content predicts cognitive performance in a sample of 28 nationsMaternal milk DHA content predicts cognitive performance in a sample of 28 nationsMaternal milk DHA content predicts cognitive performance in a sample of 28 nationsLassek WD, Gaulin SJ.25/06/2013Matern Child Nutr. 2013 Jun 25. doi: 10.1111/mcn.12060. [Epub ahead of print]
Convergent evidence from neuronal biology and hominin brain hypertrophy suggests that omega-3 fatty acids are a limiting resource for neural and cognitive development in Homo sapiens, and therefore that children from populations with higher omega-3 availability should display superior cognitive performance.
Using multiple regression, we tested this prediction in a sample of 28 countries, with Programme for International Student Assessment (PISA) math scores in 2009 as an index of cognitive performance, and country-specific breast milk levels of omega-3 docosahexaenoic acid (DHA) as an index of omega-3 availability.
Breast milk DHA makes a highly significant contribution to math scores (β = 0.462, P = 0.006), greater in magnitude than the control variables of per capita Gross Domestic Product (PCGDP) and educational expenditures per pupil.
Together, dietary fish (positively) and total fat (negatively) explain 61% of the variance in maternal milk DHA in a larger sample of 39 countries.
dietary fat, omega-3, fish and seafood, breastmilk, infant feeding, cognition, observational study, human study, cross-national comparison http://www.ncbi.nlm.nih.gov/pubmed/23795772View this and related abstracts via PubMed here
3555Montgomery et al 2013 - Low blood Long Chain Omega-3 Fatty Acids in UK Children Are Associated with Poor Cognitive Performance and Behavior: A Cross-Sectional Analysis from the DOLAB StudyLow blood Long Chain Omega-3 Fatty Acids in UK Children Are Associated with Poor Cognitive Performance and Behavior: A Cross-Sectional Analysis from the DOLAB StudyLow blood Long Chain Omega-3 Fatty Acids in UK Children Are Associated with Poor Cognitive Performance and Behavior: A Cross-Sectional Analysis from the DOLAB StudyPaul Montgomery, Jennifer R. Burton, Richard P. Sewell, Thees F. Spreckelsen, Alexandra J. Richardson24/06/2013PLoS One Published June 24
Omega-3 long-chain polyunsaturated fatty acids (LC-PUFA), especially DHA (docosahexaenonic acid) are essential for brain development and physical health. Low blood Omega-3 LC-PUFA have been reported in children with ADHD and related behavior/learning difficulties, as have benefits from dietary supplementation. Little is known, however, about blood fatty acid status in the general child population. We therefore investigated this in relation to age-standardized measures of behavior and cognition in a representative sample of children from mainstream schools.
493 schoolchildren aged 7–9 years from mainstream Oxfordshire schools, selected for below average reading performance in national assessments at age seven.
Whole blood fatty acids were obtained via fingerstick samples. Reading and working memory were assessed using the British Ability Scales (II). Behaviour (ADHD-type symptoms) was rated using the revised Conners’ rating scales (long parent and teacher versions). Associations were examined and adjusted for relevant demographic variables.
DHA and eicosapentaenoic acid (EPA), accounted for only 1.9% and 0.55% respectively of total blood fatty acids, with DHA showing more individual variation. Controlling for sex and socio-economic status, lower DHA concentrations were associated with poorer reading ability (std. OLS coeff. = 0.09, p < .042) and working memory performance (0.14, p?
In these healthy UK children with below average reading ability, concentrations of DHA and other Omega-3 LC-PUFA were low relative to adult cardiovascular health recommendations, and directly related to measures of cognition and behavior. These findings require confirmation, but suggest that the benefits from dietary supplementation with Omega-3 LC-PUFA found for ADHD, Dyspraxia, Dyslexia, and related conditions might extend to the general school population.
Previous studies have shown links between low omega-3 status and behaviour and learning difficulties in children with ADHD and related conditions. Importantly, this study extends these findings into the general school population.
Simple associations alone are never enough to provide definitive evidence of a causal link, i.e. 'correlation is not causation'. However, these findings do suggest that the benefits from dietary supplementation with Omega-3 LC-PUFA already shown for ADHD, DCD, Dyslexia, and related conditions might extend to the general school population.
This proposal was supported by the results of the subsequent DOLAB intervention trial. This was a randomised controlled trial (i.e. a study design that CAN provide definitive evidence of causality), involving 362 of the children who took part in the observational study reported here.
FAB Associate members can access further information on the findings from the DOLAB studies by logging in to the FAB Audio/Video Library.
Here, you can watch and listen to the presentations given at the special FAB Research conference held on September 4th 2013 in London.
omega-3, RCT, children, behaviour, cognition, reading, working memory, ADHD, dyslexia, blood fatty acids, blood biochemical study, observational study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/23826114View this and related abstracts via PubMed here. Free full text of this article is available online.
3574Markers of Celiac Disease and Gluten Sensitivity in Children with Autism.Markers of Celiac Disease and Gluten Sensitivity in Children with Autism.Markers of Celiac Disease and Gluten Sensitivity in Children with Autism.Lau NM, Green PH, Taylor AK, Hellberg D, Ajamian M, Tan CZ, Kosofsky BE, Higgins JJ, Rajadhyaksha AM, Alaedini A.18/06/2013PLoS One. 8(6):e66155. June 18 2013.
Gastrointestinal symptoms are a common feature in children with autism, drawing attention to a potential association with celiac disease or gluten sensitivity. However, studies to date regarding the immune response to gluten in autism and its association with celiac disease have been inconsistent. The aim of this study was to assess immune reactivity to gluten in pediatric patients diagnosed with autism according to strict criteria and to evaluate the potential link between autism and celiac disease.
Study participants included children (with or without gastrointestinal symptoms) diagnosed with autism according to both the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADI-R) (n?=?37), their unaffected siblings (n?=?27), and age-matched healthy controls (n?=?76). Serum specimens were tested for antibodies to native gliadin, deamidated gliadin, and transglutaminase 2 (TG2). Affected children were genotyped for celiac disease associated HLA-DQ2 and -DQ8 alleles.
Children with autism had significantly higher levels of IgG antibody to gliadin compared with unrelated healthy controls (p<0.01). The IgG levels were also higher compared to the unaffected siblings, but did not reach statistical significance. The IgG anti-gliadin antibody response was significantly greater in the autistic children with gastrointestinal symptoms in comparison to those without them (p<0.01). There was no difference in IgA response to gliadin across groups. The levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2, did not differ between patients and controls. An association between increased anti-gliadin antibody and presence of HLA-DQ2 and/or -DQ8 was not observed.
A subset of children with autism displays increased immune reactivity to gluten, the mechanism of which appears to be distinct from that in celiac disease. The increased anti-gliadin antibody response and its association with GI symptoms points to a potential mechanism involving immunologic and/or intestinal permeability abnormalities in affected children.
Gluten, coeliac disease, celiac disease, autism, children, biochemical study, immune system, anti-gliadin antibodies, biomarkers, gut permeability, experimental study, human study, observational studyhttp://www.ncbi.nlm.nih.gov/pubmed/23823064View this and related abstracts via PubMed here. Free full text of this article is available online.
The catalytic properties of many enzymes depend on the participation of vitamins as obligatory cofactors.
Vitamin B12 (cobalamin) and folic acid (folate) deficiencies in infants and children classically present with megaloblastic anemia and are often accompanied by neurological signs. A number of rare inborn errors of cobalamin and folate absorption, transport, cellular uptake, and intracellular metabolism have been delineated and identification of disease-causing mutations has improved our ability to diagnose and treat many of these conditions.
Two inherited defects in biotin metabolism are known, holocarboxylase synthetase and biotinidase deficiency. Both lead to multiple carboxylase deficiency manifesting with metabolic acidosis, neurological abnormalities, and skin rash.
Thiamine-responsive megaloblastic anemia is characterized by megaloblastic anemia, non-type I diabetes, and sensorineural deafness that responds to pharmacological doses of thiamine (vitamin B1).
Individuals affected with inherited vitamin E deficiencies including ataxia with isolated vitamin E deficiency and abetalipoproteinemia present with a spinocerebellar syndrome similar to patients with Friedreich's ataxia.
If started early, treatment of these defects by oral or parenteral administration of the relevant vitamin often results in correction of the metabolic defect and reversal of the signs of disease, stressing the importance of early and correct diagnosis in these treatable conditions.
vitamins, Vit-B, Vit-E, Vit-B12, biotin,folate, folic acid, neurological symptoms, infants, metabolic disorders, dietary deficiencies, supplementation, human studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/23622402View this and related abstracts via PubMed here.
3473Bath et al 2013 - Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC)Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC)Iodine and pregnancySarah C Bath PhD a, Colin D Steer MSc b, Prof Jean Golding FMedSci b, Pauline Emmett PhD b, Prof Margaret P Rayman DPhil 22/05/2013The Lancet, Early Online Publication, 22 May 2013
As a component of thyroid hormones, iodine is essential for fetal brain development. Although the UK has long been considered iodine replete, increasing evidence suggests that it might now be mildly iodine deficient. We assessed whether mild iodine deficiency during early pregnancy was associated with an adverse effect on child cognitive development.
We analysed mother—child pairs from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort by measuring urinary iodine concentration (and creatinine to correct for urine volume) in stored samples from 1040 first-trimester pregnant women. We selected women on the basis of a singleton pregnancy and availability of both a urine sample from the first trimester (defined as =13 weeks' gestation; median 10 weeks IQR 9—12) and a measure of intelligence quotient (IQ) in the offspring at age 8 years. Women's results for iodine-to-creatinine ratio were dichotomised to less than 150 µg/g or 150 µg/g or more on the basis of WHO criteria for iodine deficiency or sufficiency in pregnancy. We assessed the association between maternal iodine status and child IQ at age 8 years and reading ability at age 9 years. We included 21 socioeconomic, parental, and child factors as confounders.
The group was classified as having mild-to-moderate iodine deficiency on the basis of a median urinary iodine concentration of 91·1 µg/L (IQR 53·8—143; iodine-to-creatinine ratio 110 µg/g, IQR 74—170). After adjustment for confounders, children of women with an iodine-to-creatinine ratio of less than 150 µg/g were more likely to have scores in the lowest quartile for verbal IQ (odds ratio 1·58, 95% CI 1·09—2·30; p=0·02), reading accuracy (1·69, 1·15—2·49; p=0·007), and reading comprehension (1·54, 1·06—2·23; p=0·02) than were those of mothers with ratios of 150 µg/g or more. When the less than 150 µg/g group was subdivided, scores worsened ongoing from 150 µg/g or more, to 50—150 µg/g, to less than 50 µg/g.
Our results show the importance of adequate iodine status during early gestation and emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient. Iodine deficiency in pregnant women in the UK should be treated as an important public health issue that needs attention.
3561Douad et al 2013 - Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatmentPreventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatmentPreventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatmentDouaud G, Refsum H, de Jager CA, Jacoby R, Nichols TE, Smith SM, Smith AD.20/05/2013Proc Natl Acad Sci U S A.110(23)9523-8. Epub 2013 May 20
Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)?
One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y.
Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe.
In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment.
We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline.
Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.
3681Stonehouse et al 2013 - DHA supplementation improved both memory and reaction time in healthy young adults: a randomized controlled trial.DHA supplementation improved both memory and reaction time in healthy young adults: a randomized controlled trial.Omega-3 DHA and memoryStonehouse W, Conlon CA, Podd J, Hill SR, Minihane AM, Haskell C, Kennedy D.01/05/2013Am J Clin Nutr. May;97(5)1134-43. doi: 10.3945/ajcn.112.053371. Epub 2013 Mar 20.
Docosahexaenoic acid (DHA) is important for brain function, and its status is dependent on dietary intakes. Therefore, individuals who consume diets low in omega-3 (n-3) polyunsaturated fatty acids may cognitively benefit from DHA supplementation. Sex and apolipoprotein E genotype (APOE) affect cognition and may modulate the response to DHA supplementation.
We investigated whether a DHA supplement improves cognitive performance in healthy young adults and whether sex and APOE modulate the response.
Healthy adults (n = 176; age range: 18-45 y; nonsmoking and with a low intake of DHA) completed a 6-mo randomized, placebo-controlled, double-blind intervention in which they consumed 1.16 g DHA/d or a placebo. Cognitive performance was assessed by using a computerized cognitive test battery. For all tests, z scores were calculated and clustered into cognitive domains as follows: episodic and working memory, attention, reaction time (RT) of episodic and working memory, and attention and processing speed. ANCOVA was conducted with sex and APOE as independent variables.
RTs of episodic and working memory improved with DHA compared with placebo
3524Mimouni-Bloch et al 2013 - Breastfeeding May Protect from Developing Attention-Deficit/Hyperactivity DisorderBreastfeeding May Protect from Developing Attention-Deficit/Hyperactivity Disorderbreastfeeding and adhdMimouni-Bloch A, Kachevanskaya A, Mimouni FB, Shuper A, Raveh E, Linder N06/04/2013Breastfeeding Medicine, 2013; : 130410052833002 DOI: 10.1089/bfm.2012.0145
Abstract Introduction: Breastfeeding has a positive influence on physical and mental development. Attention-deficit/hyperactivitydisorder (ADHD) is a common neurobehavioral disorder with major social, familial, and academic influences. The present study aimed to evaluate whether ADHD is associated with a shorter duration of breastfeeding. Subjects and Methods: In this retrospective matched study, children 6-12 years old diagnosed at Schneider's Children Medical Center (Petach Tikva, Israel) with ADHD between 2008 and 2009 were compared with two control groups. The first one consisted of healthy (no ADHD) siblings of ADHD children; the second control group consisted of children without ADHD who consulted at the otolaryngology clinic. A constructed questionnaire about demographic, medical, and perinatal findings, feeding history during the first year of life, and a validated adult ADHD screening questionnaire were given to both parents of every child in each group. Results: In children later diagnosed as having ADHD, 43% were breastfed at 3 months of age compared with 69% in the siblings group and 73% in the control non-related group (p=0.002). By 6 months of age 29% of ADHD children were breastfed compared with 50% in the siblings group and 57% in the control non-related group (p=0.011). A stepwise logistic regression that included the variables found to be significant in univariate analysis demonstrated a significant association between ADHD and lack of breastfeeding at 3 months of age, maternal age at birth, male gender, and parental divorce. Conclusions: Children with ADHD were less likely to breastfeed at 3 months and 6 months of age than children in the two control groups. We speculate that breastfeeding may have a protective effect from developing ADHD later in childhood.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Breastfeeding+May+Protect+from+Developing+Attention-Deficit%2FHyperactivity+DisorderView this abstract and related articles on Pubmed here
3696Crawford & Say 2013 - Vitamin B12 deficiency presenting as acute ataxia.Vitamin B12 deficiency presenting as acute ataxia.Vitamin B12 deficiency and motor coordination problemsCrawford JR, Say D.26/03/2013BMJ Case Rep. Mar 26
A previously healthy 7-year-old Caucasian boy was hospitalised for evaluation of acute ataxia and failure to thrive, initially suspicious for an intracranial mass.
Weight and body mass index were below the third percentile and he demonstrated loss of joint position and vibratory sense on examination. Laboratory studies revealed megaloblastic anaemia while an initial MRI of the brain showed no evidence of mass lesions or other abnormalities.
A dietary history revealed the child subscribed to a restrictive vegan diet with little to no intake of animal products or other fortified foods. The child was diagnosed with presumed vitamin B12 deficiency and was treated with intramuscular B12 injections.
Neurological symptoms resolved promptly within several days after starting therapy. This case underlines the importance of assessing nutritional status in the evaluation of neurological dysfunction in the pediatric patient.
Vit-B12, B12 deficiency, neurological symptoms, ataxia, dyspraxia, vegan diet, case study, human studyhttp://www.ncbi.nlm.nih.gov/pubmed/23536622View this and related abstracts via PubMed here
3652Petrof et al 2013 - Microbial ecosystems therapeutics: a new paradigm in medicine?Microbial ecosystems therapeutics: a new paradigm in medicine?Microbial ecosystems therapeutics: a new paradigm in medicine?Petrof EO, Claud EC, Gloor GB, Allen-Vercoe E11/03/2013Benef Microbes. 2013 Mar 1;4(1):53-65. doi: 10.3920/BM2012.0039
Increasing evidence indicates that the complex microbial ecosystem of the human intestine plays a critical role in protecting the host against disease. This review discusses gut dysbiosis (here defined as a state of imbalance in the gut microbial ecosystem, including overgrowth of some organisms and loss of others) as the foundation for several diseases, and the applicability of refined microbial ecosystem replacement therapies as a future treatment modality. Consistent with the concept of a 'core' microbiome encompassing key functions required for normal intestinal homeostasis, 'Microbial Ecosystem Therapeutics' (MET) would entail replacing a dysfunctional, damaged ecosystem with a fully developed and healthy ecosystem of 'native' intestinal bacteria. Its application in treating Clostridium difficile infection is discussed and possible applications to other diseases such as ulcerative colitis, obesity, necrotising enterocolitis, and regressive-type autism are reviewed. Unlike conventional probiotic therapies that are generally limited to a single strain or at most a few strains of bacteria 'Microbial Ecosystem Therapeutics' would utilise whole bacterial communities derived directly from the human gastrointestinal tract. By taking into account the intrinsic needs of the entire microbial ecosystem, MET would emphasise the rational design of healthy, resilient and robust microbial communities that could be used to maintain or restore human health. More than simply a new probiotic treatment, this emerging paradigm in medicine may lead to novel strategies in treating and managing a wide variety of human diseases.
Human gut microbiota, dysbiosis, complex probioticshttp://www.ncbi.nlm.nih.gov/pubmed/23257018View this and related abstracts via PubMed here
3651Herberling et al 2013 - Hypothesis for a systems connectivity model of Autism Spectrum Disorder pathogenesis: links to gut bacteria, oxidative stress, and intestinal permeabilityHypothesis for a systems connectivity model of Autism Spectrum Disorder pathogenesis: links to gut bacteria, oxidative stress, and intestinal permeabilityHypothesis for a systems connectivity model of Autism Spectrum Disorder pathogenesis: links to gut bacteria, oxidative stress, and intestinal permeabilityHeberling CA, Dhurjati PS, Sasser M08/03/2013Medical Hypotheses80, Issue 3264-270Elsevier Limited
Autism Spectrum Disorders are neurodevelopmental disorders with symptoms that include cognitive impairments, stereotyped behaviors, and impairments in social skills. The dramatic increase in incidence of autism in recent years has created an increased need to find effective treatments. This paper proposes a hypothesis for a systems model of the connections between Autism Spectrum Disorder pathogenesis routes observed in recent studies. A combination treatment option is proposed to combat multiple pathogenesis mechanisms at once. Autism has been cited as being linked to gastrointestinal symptoms and is thought to be caused by a combination of genetic predisposition and environmental factors. Neuroinflammation as a result of increased gastrointestinal permeability has been noted as being a likely cause of Autism Spectrum Disorders, with possible primary causes stemming from abnormal intestinal bacteria and/or sulfur metabolic deficiencies. Our pathogenesis model proposes a circular relationship: oxidative stress and sulfur metabolic deficiencies could cause changes in colonic bacterial composition; and environmental bacterial contaminants could lead to elevated oxidative stress in individuals. It would thus be a self-perpetuating process where treatment options with single targets would have short-lived effects. It is believed that bacterial toxins, oxidative stress and dietary allergens such as gluten could all lead to increased epithelial permeability. Therefore, we propose a combination treatment to combat intestinal permeability, abnormal bacteria and/or bacterial overgrowth, and sulfur metabolic deficiencies. It is our hope that the proposed model will inspire new studies in finding effective treatments for individuals with Autism Spectrum Disorders. We suggest possible future studies that may lend more credibility to the proposed model.
Autism Spectrum Disorder, Neuroinflammation, Gastrointestinal permeability; Epithelial permeabilityhttp://www.ncbi.nlm.nih.gov/pubmed/23273906View this and related abstracts via PubMed here
3697Syed & Lioutas 2013 - Tobacco-alcohol amblyopia: a diagnostic dilemmaTobacco-alcohol amblyopia: a diagnostic dilemmaTobacco-alcohol amblyopia: a diagnostic dilemmaSyed S, Lioutas V.07/03/2013J Neurol Sci. 327(1-2)41-5. Epub 2013 Mar 7.
Tobacco alcohol amblyopia is an outdated term for a rare condition characterized by visual impairment due to tobacco and alcohol abuse usually associated with nutritional deficiencies. The more accurate term used now is Nutritional Optic Neuropathy. The visual impairment generally presents as a centrocecal scotoma. Its pathophysiology is poorly understood but it is generally attributed to toxic effects of cyanide and B12 deficiency.
61 year old male presented with one month history of altered mental status and progressive, painless, bilateral vision loss in the setting of severe alcohol and tobacco abuse and poor nutrition. Patient developed loss of central vision in the left-eye and blurring of vision in the right-eye after 1 week, which was reduced to only perception of hand movements by the time of presentation.
His BMI was 19.3 with an emaciated appearance. On ophthalmological exam, visual-acuity was 20/200 (right) and 20/300 (left), with a left central scotoma and normal fundoscopic exam. Neurological examination was significant for confabulation and gait instability consistent with Wernickes Korsakoff. Workup included negative imaging and normal B12, folate and thiamine levels, undetectable cyanide levels, and negative Leber's Hereditary Optic Neuropathy mutation.
He was discharged after 30 days, after a steady reversal of his symptoms in the setting of abstinence and nutritional supplementation. A diagnosis of tobacco alcohol amblyopia was made by exclusion and by history.
This case of tobacco alcohol amblyopia has an atypical presentation because of normal fundoscopic exam, undetectable cyanide levels and normal B12 levels. It reinforces the need for biomarkers for this disease. Nutritional fortification has made these cases rare, but a neurological perspective may be essential for accurate diagnosis, treatment and positive outcome for these patients.
Tobacco alcohol amblyopia can be a difficult diagnosis due to lack of biomarkers and rare occurrence. A neurologist can facilitate diagnosis in atypical cases.
tobacco, alchohol, addiction, nutritional deficiencies, neurological symptoms, vision, cognition, motor co-ordination, case study, human study, diagnosishttp://www.ncbi.nlm.nih.gov/pubmed/23477666View this and related abstracts via PubMed here
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