359911 Dec 2013 - BBC News - Ulcer drugs linked to vitamin B12 deficiencyVitamin B12 deficiencyPeople who took tablets known as proton pump inhibitors (PPIs) or histamine antagonists (H2RAs) were more likely to lack enough vitamin B12 for good health.12/12/2013
Medication used to treat stomach ulcers may cause potentially harmful vitamin B12 deficiency, say experts.
A US study of 200,000 people in the Journal of the American Medical Association found the link.
Left untreated, B12 deficiency can lead to dementia and neurological problems.
The study authors say doctors should still prescribe these medicines, but that they should weigh possible harms against any benefits in patients who need the drugs for prolonged periods of time.
More investigations are needed to fully evaluate the risk which appears to be in people who take these medications for two or more years, they say.
Link not proof
The Kaiser Permanente researchers found that the link with B12 deficiency increased with dose and was stronger in women and younger age groups.
But the overall risk was still low.
PPIs and H2RAs are commonly prescribed for patients with symptoms of stomach ulcers such as heartburn and indigestion.
The tablets are also widely available to buy without a prescription, 'over-the-counter' at pharmacies.
They work by reducing the amount of acid made by your stomach.
Stomach acid is needed for us to absorb vitamin B12 from our food, such as meat, fish and dairy.
If identified, most cases of B12 deficiency can be easily treated by giving supplements or an injection of vitamin B12.
But symptoms, such as lethargy, can be vague and overlooked.
Prof Mark Pritchard of the British Society of Gastroenterology said people should not be concerned by the findings.
"Only patients who had taken these tablets for more than two years were at risk and only a minority of patients on long-term proton pump inhibitors showed evidence of vitamin B12 deficiency."
He said people taking ulcer medications could ask their GP for a simple blood test to measure vitamin B12 levels if they are worried.
http://www.bbc.co.uk/news/health-25314643View this news item on the BBC website here
3649Dalton et al 2013 - Gut Permeability in Autism Spectrum DisordersGut Permeability in Autism Spectrum DisordersGut Permeability in Autism Spectrum DisordersDalton N, Chandler S, Turner C, Charman T, Pickles A, Loucas T, Simonoff E, Sullivan P, Baird G12/12/2013Autism Res. 2013 Dec 12. doi: 10.1002/aur.1350
To test whether gut permeability is increased in autism spectrum disorders (ASD) by evaluating gut permeability in a population-derived cohort of children with ASD compared with age- and intelligence quotient-matched controls without ASD but with special educational needs (SEN).
PATIENTS AND METHODS:
One hundred thirty-three children aged 10-14 years, 103 with ASD and 30 with SEN, were given an oral test dose of mannitol and lactulose and urine collected for 6 hr. Gut permeability was assessed by measuring the urine lactulose/mannitol (L/M) recovery ratio by electrospray mass spectrometry-mass spectrometry. The ASD group was subcategorized for comparison into those without (n = 83) and with (n = 20) regression.
There was no significant difference in L/M recovery ratio (mean (95% confidence interval)) between the groups with ASD: 0.015 (0.013-0.018), and SEN: 0.014 (0.009-0.019), nor in lactulose, mannitol, or creatinine recovery. No significant differences were observed in any parameter for the regressed versus non-regressed ASD groups. Results were consistent with previously published normal ranges. Eleven children (9/103 = 8.7% ASD and 2/30 = 6.7% SEN) had L/M recovery ratio > 0.03 (the accepted normal range cut-off), of whom two (one ASD and one SEN) had more definitely pathological L/M recovery ratios > 0.04.
There is no statistically significant group difference in small intestine permeability in a population cohort-derived group of children with ASD compared with a control group with SEN. Of the two children (one ASD and one SEN) with an L/M recovery ratio of > 0.04, one had undiagnosed asymptomatic celiac disease (ASD) and the other (SEN) past extensive surgery for gastroschisis.
autism, autism spectrum disorders, gut permeability, lactulose/mannitol ratiohttp://www.ncbi.nlm.nih.gov/pubmed/24339339View this and related abstracts via PubMed here
3639de Theije et al 2013 - Altered gut microbiota and activity in a murine model of autism spectrum disordersAltered gut microbiota and activity in a murine model of autism spectrum disorders.Altered gut microbiota and activity in a murine model of autism spectrum disorders.de Theije CG, Wopereis H, Ramadan M, van Eijndthoven T, Lambert J, Knol J, Garssen J, Kraneveld AD, Oozeer R11/12/2013Brain Behav Immun. 2013 Dec 11. pii: S0889-1591(13)00590-4. doi: 10.1016/j.bbi.2013.12.005
Autism spectrum disorder (ASD) is a heterogeneous group of complex neurodevelopmental disorders with evidence of genetic predisposition. Intestinal disturbances are reported in ASD patients and compositional changes in gut microbiota are described. However, the role of microbiota in brain disorders is poorly documented. Here, we used a murine model of ASD to investigate the relation between gut microbiota and autism-like behaviour. Using next generation sequencing technology, microbiota composition was investigated in mice in utero exposed to valproic acid (VPA). Moreover, levels of short chain fatty acids (SCFA) and lactic acid in caecal content were determined. Our data demonstrate a transgenerational impact of in utero VPA exposure on gut microbiota in the offspring. Prenatal VPA exposure affected operational taxonomic units (OTUs) assigned to genera within the main phyla of Bacteroidetes and Firmicutes and the order of Desulfovibrionales, corroborating human ASD studies. In addition, OTUs assigned to genera of Alistipes, Enterorhabdus, Mollicutes and Erysipelotrichalis were especially associated with male VPA-exposed offspring. The microbial differences of VPA in utero-exposed males deviated from those observed in females and was (i) positively associated with increased levels of caecal butyrate as well as ileal neutrophil infiltration and (ii) inversely associated with intestinal levels of serotonin and social behaviour scores. These findings show that autism-like behaviour and its intestinal phenotype is associated with altered microbial colonization and activity in a murine model for ASD, with preponderance in male offspring. These results open new avenues in the scientific trajectory of managing neurodevelopmental disorders by gut microbiome modulation.
Autism spectrum disorders, Butyrate, Gut microbiota, Neurodevelopment, Prenatal, Short chain fatty acids, Valproatehttp://www.ncbi.nlm.nih.gov/pubmed/24333160View this and related abstracts via PubMed here
363710 Dec 2013 - Medical News Today - Autism-like behaviors in mice alleviated by probiotic therapyAutism-like behaviors in mice alleviated by probiotic therapyAutism spectrum disorder (ASD) is diagnosed when individuals exhibit characteristic behaviors that include repetitive actions, decreased social interactions, and impaired communication. Curiously, many individuals with ASD also suffer from gastrointestinal (GI) issues, such as abdominal cramps and constipation.10/12/2013
Autism spectrum disorder (ASD) is diagnosed when individuals exhibit characteristic behaviors that include repetitive actions, decreased social interactions, and impaired communication. Curiously, many individuals with ASD also suffer from gastrointestinal (GI) issues, such as abdominal cramps and constipation.
Using the co-occurrence of brain and gut problems in ASD as their guide, researchers at the California Institute Technology (Caltech) are investigating a potentially transformative new therapy for autism and other neurodevelopmental disorders.
The gut microbiota - the community of bacteria that populate the human GI tract - previously has been shown to influence social and emotional behavior, but the Caltech research, published online in the December 5 issue of the journal Cell, is the first to demonstrate that changes in these gut bacteria can influence autism-like behaviors in a mouse model.
"Traditional research has studied autism as a genetic disorder and a disorder of the brain, but our work shows that gut bacteria may contribute to ASD-like symptoms in ways that were previously unappreciated," says Professor of Biology Sarkis K. Mazmanian. "Gut physiology appears to have effects on what are currently presumed to be brain functions."
To study this gut-microbiota-brain interaction, the researchers used a mouse model of autism previously developed at Caltech in the laboratory of Paul H. Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences. In humans, having a severe viral infection raises the risk that a pregnant woman will give birth to a child with autism. Patterson and his lab reproduced the effect in mice using a viral mimic that triggers an infection-like immune response in the mother and produces the core behavioral symptoms associated with autism in the offspring.
In the new Cell study, Mazmanian, Patterson, and their colleagues found that the "autistic" offspring of immune-activated pregnant mice also exhibited GI abnormalities. In particular, the GI tracts of autistic-like mice were "leaky," which means that they allow material to pass through the intestinal wall and into the bloodstream. This characteristic, known as intestinal permeability, has been reported in some autistic individuals. "To our knowledge, this is the first report of an animal model for autism with comorbid GI dysfunction," says Elaine Hsiao, a senior research fellow at Caltech and the first author on the study.
To see whether these GI symptoms actually influenced the autism-like behaviors, the researchers treated the mice with Bacteroides fragilis, a bacterium that has been used as an experimental probiotic therapy in animal models of GI disorders.
The result? The leaky gut was corrected.
In addition, observations of the treated mice showed that their behavior had changed. In particular, they were more likely to communicate with other mice, had reduced anxiety, and were less likely to engage in a repetitive digging behavior.
"The B. fragilis treatment alleviates GI problems in the mouse model and also improves some of the main behavioral symptoms," Hsiao says. "This suggests that GI problems could contribute to particular symptoms in neurodevelopmental disorders."
With the help of clinical collaborators, the researchers are now planning a trial to test the probiotic treatment on the behavioral symptoms of human autism. The trial should begin within the next year or two, says Patterson.
"This probiotic treatment is postnatal, which means that the mother has already experienced the immune challenge, and, as a result, the growing fetuses have already started down a different developmental path," Patterson says. "In this study, we can provide a treatment after the offspring have been born that can help improve certain behaviors. I think that's a powerful part of the story."
The researchers stress that much work is still needed to develop an effective and reliable probiotic therapy for human autism - in part because there are both genetic and environmental contributions to the disorder, and because the immune-challenged mother in the mouse model reproduces only the environmental component.
"Autism is such a heterogeneous disorder that the ratio between genetic and environmental contributions could be different in each individual," Mazmanian says. "Even if B. fragilis ameliorates some of the symptoms associated with autism, I would be surprised if it's a universal therapy - it probably won't work for every single case."
The Caltech team proposes that particular beneficial bugs are intimately involved in regulating the release of metabolic products (or metabolites) from the gut into the bloodstream. Indeed, the researchers found that in the leaky intestinal wall of the autistic-like mice, certain metabolites that were modulated by microbes could both easily enter the circulation and affect particular behaviors.
"I think our results may someday transform the way people view possible causes and potential treatments for autism," Mazmanian says.
36218 Dec 2013 - The Guardian - Healthy diet may prevent dementia, say doctorsHealthy diet may prevent dementiaIn a letter to Jeremy Hunt, doctors say persuading people to eat a Mediterranean diet is 'best strategy available'08/12/2013
The battle against dementia should be refocused away from "dubious" drugs to the benefits of a Mediterranean diet, a group of doctors and health workers said ahead of an international summit.
In a letter to the health secretary, Jeremy Hunt, they said persuading people to eat fresh fruits and vegetables, nuts, fish and olive oil was "possibly the best strategy currently available".
Dementia experts from G8 countries will gather in London this week for a meeting convened by the prime minister, David Cameron, as part of the UK's presidency of the group of leading economies.
Hunt has called dementia a health and care "timebomb" with the number of people living with the condition expected to triple worldwide to 135 million by 2050, according to a recent report.
There is also a lack of diagnosis in England and Wales – with fewer than half of cases formally recognised by GPs and patchy performance across different areas. Critics of current policies are also concerned about high levels of anti-psychotic drug prescription.
Among signatories to the letter were former chair of the Royal College of General Practitioners, professor Clare Gerada, the chair of the National Obesity Forum, professor David Haslam, professor of Clinical Epidemiology at the University of Liverpool Simon Capewell and London cardiologist Dr Aseem Malhotra.
They said successfully encouraging people on to a healthier diet could have a far greater impact in the fight to reduce the dramatically increasing rates of the disease than pharmaceutical and medical interventions and "the dubious benefit of most drugs". It can also protect against coronary heart disease, hypertension and diabetes.
Research by the University of Exeter's Medical School found a majority of studies suggested the diet could improve cognitive function, lower rates of decline and reduce the risk of Alzheimer's disease.
However, results for mild cognitive impairment – the stage before Alzheimer's or dementia, when someone could be experiencing some cognitive difficulties – were inconsistent.
Dr Malhotra said: "The evidence base for the Mediterranean diet, in preventing all of the chronic diseases that is plaguing the western world is overwhelming.
"This includes cardiovascular disease, type 2 diabetes, Alzheimer's and cancer.
"Policymakers and the public need to know that such a diet is far more potent than the often dubious benefit of many medications and without side-effects."
Dr Simon Poole, a leading advocate of the Mediterranean diet who organised the letter, said: "Educating all generations, including our children, in the importance of a good diet in maintaining health in old age is a project which will take years, but is absolutely essential.
"We are calling upon policymakers to not only support the care and treatment of those who are already suffering from dementia, but to make significant investments in work which will see benefits beyond the period of one or two parliaments."
http://www.theguardian.com/society/2013/dec/08/healthy-diet-prevent-dementia-jeremy-hunt-mediterranean?dm_i=8UC,22KZ0,13QKDE,7GZOU,1View this news item in the Guardian online here
3638de Theije et al 2013 - Intestinal inflammation in a murine model of autism spectrum disordersIntestinal inflammation in a murine model of autism spectrum disordersIntestinal inflammation in a murine model of autism spectrum disordersde Theije CG, Koelink PJ, Korte-Bouws GA, Lopes da Silva S, Korte SM, Olivier B, Garssen J, Kraneveld AD07/12/2013Brain Behav Immun. 2013 Dec 7. pii: S0889-1591(13)00589-8. doi: 10.1016/j.bbi.2013.12.004
Autism spectrum disorder (ASD) is a cluster of neurodevelopmental disorders characterized by impairments in communication, social interest and stereotypical behaviour. Dysfunction of the intestinal tract is reported in patients with ASD and implicated in the development and severity of ASD symptoms. However, more research is required to investigate the association of intestinal problems with ASD and the potential underlying mechanisms. The purpose of this study was to investigate comorbid symptoms of intestinal inflammation in a murine model of ASD induced by prenatal exposure to valproic acid (VPA). Pregnant BALB/c females were treated subcutaneously with 600mg/kg VPA or phosphate buffered saline on gestational day 11. Offspring were housed with their mother until weaning on postnatal day 21 (P21). All pups were exposed to a social behaviour test on P28. Inflammatory correlates and activity of the serotonergic system were measured in brain and intestinal tissue. Here we demonstrate, in addition to reduced social behaviour and increased expression of neuroinflammatory markers in the brain, that VPA in utero- exposed male offspring showed epithelial cell loss and neutrophil infiltration in the intestinal tract. Furthermore, reduced levels of serotonin were not only observed the prefrontal cortex and amygdala of VPA in utero- exposed males, but also in the small intestine. Overall, we demonstrate that gender-specific inflammatory conditions are present in the small intestines of VPA in utero- exposed mice and are accompanied by a disturbed serotonergic system in the brain as well as in the intestinal tract.
Autism spectrum disorders, Gut-brain axis, Intestinal tract, Neurodevelopment, Prenatal, Serotonin, Valproic acidhttp://www.ncbi.nlm.nih.gov/pubmed/24321212View this and related abstracts via PubMed here
3640Peters et al 2013 - Rigid-Compulsive Behaviors are Associated with Mixed Bowel Symptoms in Autism Spectrum DisorderRigid-Compulsive Behaviors are Associated with Mixed Bowel Symptoms in Autism Spectrum Disorder.Rigid-Compulsive Behaviors are Associated with Mixed Bowel Symptoms in Autism Spectrum Disorder.Peters B, Williams KC, Gorrindo P, Rosenberg D, Lee EB, Levitt P, Veenstra-Vanderweele J.29/11/2013J Autism Dev Disord. 2013 Nov 29
Based on clinical experience, we hypothesized that rigid-compulsive behaviors are associated with severe constipation and co-occurring diarrhea or underwear staining in children with autism spectrum disorder. Using data from the Autism Treatment Network, we evaluated the association between these gastrointestinal symptoms and measures of rigid compulsive behavior in children ages 2-17. Following statistical correction, four of five primary measures were significantly associated with constipation and diarrhea or underwear staining, including parental report of repetitive behavior, parental report of compulsive behavior, clinician diagnosis of obsessive-compulsive disorder, and report of rituals observed on the autism diagnostic observation schedule. This association could point to a causal connection between these symptoms or to a common biological pathway that impacts both gut and brain.
Constipation, diarrhea, http://www.ncbi.nlm.nih.gov/pubmed/24293040View this and related abstracts via PubMed here
3644de Theije 2013 - Food allergy and food-based therapies in neurodevelopmental disordersFood allergy and food-based therapies in neurodevelopmental disordersFood allergy and food-based therapies in neurodevelopmental disordersde Theije CG, Bavelaar BM, Lopes da Silva S, Korte SM, Olivier B, Garssen J, Kraneveld AD27/11/2013Pediatr Allergy Immunol. 2013 Nov 17. doi: 10.1111/pai.12149
Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are neurodevelopmental disorders which occur in childhood and may persist into adulthood. Although the etiology of these disorders is largely unknown, genetic and environmental factors are thought to play a role in the development of ASD and ADHD. Allergic immune reactions, in prenatal and postnatal phases, are examples of these environmental factors, and adverse reactions to foods are reported in these children. In this review, we address the clinical and preclinical findings of (food) allergy in ASD and ADHD and suggest possible underlying mechanisms. Furthermore, opportunities for nutritional interventions in neurodevelopmental disorders are provided.
attention deficit hyperactivity disorder, autism spectrum disorder, food allergy, food-based therapy, gut-brain axis, neurodevelopmenthttp://www.ncbi.nlm.nih.gov/pubmed/24236934View this and related abstracts via PubMed here
360025 Nov 2013 - BBC World Service - Discovery - Gut MicrobiotaGut microbiotaAdam Hart discovers the role gut microbes play in our health and development, and asks if we should consider ourselves an ecosystem rather than an individual?25/11/2013
Excellent podcast of 27 minutes duration which you can download here:
35927 Nov 2013 - BBC News - US moves to ban trans fats in foodstrans fatsUS food safety officials have taken steps to ban the use of trans fats, saying they are a threat to health.09/11/2013
Trans fats, also known as partially hydrogenated oils, are no longer "generally recognised as safe", said the Food and Drug Administration (FDA).
The regulator said a ban could prevent 7,000 deaths and 20,000 heart attacks in the US each year.
The FDA is opening a 60-day consultation period on the plan, which would gradually phase out trans fats.
"While consumption of potentially harmful artificial trans fat has declined over the last two decades in the United States, current intake remains a significant public health concern," FDA Commissioner Margaret Hamburg said in a statement.
"The FDA's action today is an important step toward protecting more Americans from the potential dangers of trans fat."
'Industrially produced ingredient'
If the agency's plan is successful, the heart-clogging oils would be considered food additives and could not be used in food unless officially approved.
The ruling does not affect foods with naturally occurring trans fats, which are present in small amounts in certain meat and dairy products.
Foods containing trans fat
Some processed baked goods such as cakes, cookies, pies
Microwave popcorn, frozen pizza, some fast food
Margarine and other spreads, coffee creamer
Refrigerator dough products such as cinnamon rolls
Source: US Food and Drug Administration
Nutritionists have long criticised their use, saying they contribute to heart disease more than saturated fat.
Some companies have already phased out trans fats, prompted by new nutritional labels introduced in 2006 requiring it to be listed on food packaging.
New York City and some other local governments have also banned it.
But trans fats persist primarily in processed foods - including some microwave popcorns and frozen pizzas - and in restaurants that use the oils for frying.
According to the FDA, trans fat intake among Americans declined from 4.6g per day in 2003 to around 1g per day in 2012.
The American Heart Association said the FDA's proposal was a step forward in the battle against heart disease.
"We commend the FDA for responding to the numerous concerns and evidence submitted over the years about the dangers of this industrially produced ingredient," said its chief executive, Nancy Brown.
Outgoing New York Mayor Michael Bloomberg, who led the charge to ban trans fats in that city, said the FDA plan "deserves great credit".
"The groundbreaking public health policies we have adopted here in New York City have become a model for the nation for one reason: they've worked," he said.
In the UK, it is more than 3 years since NICE (the UK's independent medical advisory body), urged the government to ban industrially-produced trans fats. Their advice followed the World Health Orgnaisation's recognition in 2009 that trans fats are a toxin. See: BBC News - Medics call for ban on trans-fats in UK food
Instead, however, the UK govt chose to rely purely on 'voluntary agreements' with industry to reduce or remove trans fats. According to expert commentators, this still leaves the UK population exposed to unnecessary and serious health risks.
35914 Nov 2013 - BBC News - Recession hits family spending on fresh foodrecession and family spending on foodMany young families cut back on fresh fruit and vegetables and switched to less healthy processed food as the recession squeezed budgets, a UK study of 15,000 households' data suggests.04/11/2013By Christine Jeavans
It showed rising food prices and stagnating wages had led people to buy less food and choose cheaper products.
The Institute for Fiscal Studies said pensioners, single parent households and families had the biggest drop in the nutritional quality of their diets.
Food campaigners expressed concern.
The Children's Food Trust said the move to processed food was a "huge worry".
The report's authors used food purchasing data from 15,850 British households from 2005 to 2012, enabling them to analyse the impact on spending of the recession.
They found that households spent 8.5% less on food in real terms across the period as disposable incomes failed to keep pace with rising food prices.
Food prices rose by 33% between 2007 and 2013, official figures show. Butter, meat and fruit prices all increased by more than average while processed food rose by 28%.
The IFS researchers found that on every measure, pensioner households, single parents and families with young children experienced a worse-than-average decline in nutritional quality.
Pensioners tended to increase their purchases of fatty foods while households with young children chose more sugary products.
IFS research economist Kate Smith, one of the authors of the report, said: "Over the recession households have responded to higher food prices and the squeezes on their incomes by switching to cheaper calories.
"This has coincided with a fall in the nutritional quality of foods purchased, with moves away from fresh fruit and vegetables and towards processed foods. As a result, the average saturated fat and sugar content of food purchases has increased over this period."
Children's Food Trust chief executive Linda Cregan said: "Feeding children well is absolutely crucial for their future health - these figures are an indication of just how tough this has become for many families in recent years.
"Some of the trends in this report are a huge worry - we need to see the foods children eat containing less saturated fat, salt and sugar, not more."
Long-term calorie fall
A second report from the IFS, looked at longer term trends.
Between 1980 and 2009, households bought 15% to 30% fewer calories, but average weight continued to climb.
During this time there was a big rise in snacking and eating out, but an even bigger fall in calories bought for the home during the 30-year period.
"We were surprised to find that there has been a substantial decline in total calories purchased at a time when obesity has increased," said one of this study's authors Melanie Luhrmann.
"This does not mean that poor diet plays no part in rising obesity. But understanding the interaction between diet and physical activity is clearly crucial."
Both reports are being presented as part of the Economic and Social Research Council's Festival of Social Science in London.
http://www.bbc.co.uk/news/health-24773201View this news item on the BBC News website here
3646Wang et al 2013 - Increased abundance of Sutterella spp. and Ruminococcus torques in feces of children with autism spectrum disorderIncreased abundance of Sutterella spp. and Ruminococcus torques in feces of children with autism spectrum disorderIncreased abundance of Sutterella spp. and Ruminococcus torques in feces of children with autism spectrum disorderWang L, Christophersen CT, Sorich MJ, Gerber JP, Angley MT, Conlon MA04/11/2013Mol Autism. 2013 Nov 4;4(1):42
A recent report indicated that numbers of Sutterella spp. are elevated in gastrointestinal biopsies taken from children with autism spectrum disorder (ASD). We have recently reported changes in the numbers of some bacteria within the stool of ASD children, and now examine whether numbers of Sutterella spp. and some other mucosa-associated bacteria linked with gastrointestinal disease (Ruminococcus gnavus and Ruminococcus torques) are also altered in the stool of these children.
We show that numbers of Sutterella spp. are elevated in feces of ASD children relative to controls, and that numbers of R. torques are higher in the children with ASD with a reported functional gastrointestinal disorder than those without such a disorder.
We show further evidence of changes in the gut microbiota of children with ASD and confirm that the abundance of Sutterella spp. is altered in stool.
Autism spectrum disorder, Gut, Feces, Microbiota, Sutterellahttp://www.ncbi.nlm.nih.gov/pubmed/24188502View this and related abstracts via PubMed here
350529 Oct 2013 - FAB EVENT - Feeding Healthy Minds - Maternal and Infant Nutrition and Children's Brain DevelopmentFAB EventOrganised by Food and Behaviour Research29/10/201329/10/2013
This event has now taken place.
Programme and Abstracts
A document with the programme, speaker details and abstracts, summarising the content of the day's presentations may be downloaded at the link below.
FAB Research Audio/Video Library
This event was fully filmed and the presentations will shortly be available to view in the FAB Research Audio/Video Library.
Access to this resource is restricted to FAB Associate Members only. If you would like to learn more about becoming a FAB Research Assoicate please see Subscribe to FAB Research.
About the event:
We are enormously proud to be hosting this opportunity for you to hear from some of the world’s leading experts on the role of nutrition in brain development and function, and its importance for mothers and infants.
Hear the latest evidence on how the diets that mothers eat before and during pregnancy can have a lifelong impact on their children's health and development - and find out what kinds of diets are likely to promote the best, and the worst, outcomes.
The programme for the day has been designed for a multi-disciplinary audience of professionals, policy makers, researchers from academia and industry, and others concerned with the health, education and welfare of mothers, babies and young children. It will give all participants the chance to hear about and discuss the latest evidence and insights into the modern maternal diet and its lasting legacy.
Is it true that pregnant mothers whose diets are high in fat and sugar will have already programmed their babies to crave high fat, high sugar foods by the time they are weaned?
What are the likely consequences for their children's behavioural and cognitive development if mothers consume a typical modern, western-type diet during pregnancy?
Which nutrients and dietary fats are particularly important in early life, and why?
Which ones are lacking from many mothers' and infants' diets - and what are the likely consequences for both the mothers' mental health and their children's future cognitive development and wellbeing?
What are the best ways to ensure an adequate intake, for mothers and for young infants?
Improving mothers' and children's food choices – what can be done, and who should be doing it?
This event will provide you with opportunities not only to learn from the latest research findings, but also to ask your own questions and get answers that may influence some of the decisions you have to make every day.
Speakers and Presentations:
Early Life Nutrition and Mental Health: An Overview Dr Alex Richardson (Founder/Trustee of FAB Research; Senior Research Fellow, University of Oxford; Author of ‘They Are What You Feed Them’)
The Essentiality of Omega-3 DHA for Human Brain Development: The Marine Food Chain and the Implications for Maternal Nutrition Professor Michael A Crawford (Imperial College, London; Institute of Brain Chemistry and Human Nutrition)
Dietary Needs for Omega-3 During Pregnancy and Infancy Professor Sheila Innis (Faculty of Medicine, Department of Paediatrics & Faculty of Agricultural Sciences, Foods, Nutrition and Health, Child and Family Research Institute, University of British Columbia)
Omega-3 and the Brain: Fish and Seafood Intakes During Pregnancy and Child Development Outcomes Captain Joseph Hibbeln MD (Acting Chief of Section of Nutritional Neurosciences, Laboratory of Membrane Biophysics and Biochemistry, National Institute on Alcohol Abuse and Alcoholism at the National Institutes of Health, Bethesda, Maryland, USA)
Breastfeeding and Children’s Intelligence: Omega-3 and Gene-Nutrient Interactions Dr Pauline Emmett(Senior Research Fellow at the Centre for Child and Adolescent Health in Bristol. Former head of Nutrition Research for the Avon Longitudinal Study of Parents and Children (ALSPAC) based in Bristol)
Effect of inadequate iodine status in pregnant women on cognitive outcomes in their children. Findings from the Avon Longitudinal Study of Parents and Children (ALSPAC) Dr Sarah Bath(Post-doctoral Research Fellow, Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey)
Translating Research into Practice for Families and Children – A Dietitian’s Perspective David Rex (Dietitian, Health & Social Care – Children’s Services, Highland Council, Inverness)
9.30am to 4.30pm35-43 Lincoln’s Inn Fields, London WC2A 3PEThe Royal College of SurgeonsFiona O'Fee or Ruth Whitfieldadmin@fabresearch.org01463 667318Programme and All Abstracts.pdfDownload the conference programme and abstracts hereBooking Form.docxiStock_000002860334Small.jpgBreastfeeding
3648Stice et al 2013 - Relative ability of fat and sugar tastes to activate reward, gustatory, and somatosensory regionsRelative ability of fat and sugar tastes to activate reward, gustatory, and somatosensory regionsRelative ability of fat and sugar tastes to activate reward, gustatory, and somatosensory regionsStice E, Burger KS, Yokum S16/10/2013Am J Clin Nutr. 2013 Dec;98(6):1377-84. doi: 10.3945/ajcn.113.069443. Epub 2013 Oct 16.
Although the intake of high-fat and high-sugar food activates mesolimbic reward, gustatory, and oral somatosensory brain regions, contributing to overeating, few studies have examined the relative role of fat and sugar in the activation of these brain regions, which would inform policy, prevention, and treatment interventions designed to reduce obesity.
We evaluated the effect of a high-fat or high-sugar equicaloric chocolate milkshake and increasing fat or sugar milkshake content on the activation of these regions.
Functional magnetic resonance imaging was used to assess the neural response to the intake of high-fat/high-sugar, high-fat/low-sugar, low-fat/high-sugar, and low-fat/low-sugar chocolate milkshakes and a tasteless solution in 106 lean adolescents (mean ± SD age = 15.00 ± 0.88 y). Analyses contrasted the activation to the various milkshakes.
High-fat compared with high-sugar equicaloric milkshakes caused greater activation in the bilateral caudate, postcentral gyrus, hippocampus, and inferior frontal gyrus. High-sugar compared with high-fat equicaloric milkshakes caused greater activation in the bilateral insula extending into the putamen, the Rolandic operculum, and thalamus, which produced large activation regions. Increasing sugar in low-fat milkshakes caused greater activation in the bilateral insula and Rolandic operculum; increasing fat content did not elicit greater activation in any region.
Fat caused greater activation of the caudate and oral somatosensory regions than did sugar, sugar caused greater activation in the putamen and gustatory regions than did fat, increasing sugar caused greater activity in gustatory regions, and increasing fat did not affect the activation. Results imply that sugar more effectively recruits reward and gustatory regions, suggesting that policy, prevention, and treatment interventions should prioritize reductions in sugar intake.
http://www.ncbi.nlm.nih.gov/pubmed/24132980View this and related abstracts via PubMed here
3647De Angelis et al 2013 - Fecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specifiedFecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specifiedFecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specifiedDe Angelis M, Piccolo M, Vannini L, Siragusa S, De Giacomo A, Serrazzanetti DI, Cristofori F, Guerzoni ME, Gobbetti M, Francavilla R09/10/2013PLoS One. 2013 Oct 9;8(10):e76993. doi: 10.1371/journal.pone.0076993
This study aimed at investigating the fecal microbiota and metabolome of children with Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and autism (AD) in comparison to healthy children (HC). Bacterial tag-encoded FLX-titanium amplicon pyrosequencing (bTEFAP) of the 16S rDNA and 16S rRNA analyses were carried out to determine total bacteria (16S rDNA) and metabolically active bacteria (16S rRNA), respectively. The main bacterial phyla (Firmicutes, Bacteroidetes, Fusobacteria and Verrucomicrobia) significantly (P<0.05) changed among the three groups of children. As estimated by rarefaction, Chao and Shannon diversity index, the highest microbial diversity was found in AD children. Based on 16S-rRNA and culture-dependent data, Faecalibacterium and Ruminococcus were present at the highest level in fecal samples of PDD-NOS and HC children. Caloramator, Sarcina and Clostridium genera were the highest in AD children. Compared to HC, the composition of Lachnospiraceae family also differed in PDD-NOS and, especially, AD children. Except for Eubacterium siraeum, the lowest level of Eubacteriaceae was found on fecal samples of AD children. The level of Bacteroidetes genera and some Alistipes and Akkermansia species were almost the highest in PDD-NOS or AD children as well as almost all the identified Sutterellaceae and Enterobacteriaceae were the highest in AD. Compared to HC children, Bifidobacterium species decreased in AD. As shown by Canonical Discriminant Analysis of Principal Coordinates, the levels of free amino acids and volatile organic compounds of fecal samples were markedly affected in PDD-NOS and, especially, AD children. If the gut microbiota differences among AD and PDD-NOS and HC children are one of the concomitant causes or the consequence of autism, they may have implications regarding specific diagnostic test, and/or for treatment and prevention.
Autism spectrum disorder, Pervasive developmental disorder, Gut, Feces, Microbiota, Metabolomehttp://www.ncbi.nlm.nih.gov/pubmed/24130822View this and related abstracts via PubMed here
3569Tolmunen et al 2004 - Dietary folate and the risk of depression in Finnish middle-aged men. A prospective follow-up study.Dietary folate and the risk of depression in Finnish middle-aged men. A prospective follow-up study.Dietary folate and the risk of depression in Finnish middle-aged men. A prospective follow-up study.Tolmunen T, Hintikka J, Ruusunen A, Voutilainen S, Tanskanen A, Valkonen VP, Viinamäki H, Kaplan GA, Salonen JT23/09/2013Psychother Psychosom. 2004 Nov-Dec;73(6):334-9.
Several cross-sectional studies have focused on the low blood folate levels of depressive patients. Nevertheless, no prospective studies have been published on the association between dietary folate and depression.
We studied the association between dietary folate and cobalamin and receiving a discharge diagnosis of depression in a prospective follow-up setting. Our cohort was recruited between 1984 and 1989 and followed until the end of 2000, and it consisted of 2,313 men aged between 42 and 60 years from eastern Finland.
The mean intake of folate in the whole cohort was 256 microg/day (SD=76). Those below the median of energy-adjusted folate intake had higher risk of getting discharge diagnosis of depression (RR 3.04, 95% CI: 1.58, 5.86) during the follow-up period than those who had a folate intake above the median. This excess risk remained significant after adjustment for current socioeconomic status, the baseline HPL depression score, the energy-adjusted daily intake of fibre and vitamin C, and the total fat intake.
A low dietary intake of folate may be a risk factor for severe depression. This also indicates that nutrition may have a role in the prevention of depression.
356516 Sept 2013 - Medical Xpress - Diet is associated with the risk of depressionDiet and depressionA healthy diet may reduce the risk of severe depression, according to a prospective follow-up study of more than 2,000 men conducted at the University of Eastern Finland. In addition, weight loss in the context of a lifestyle intervention was associated with a reduction in depressive symptoms.16/09/2013
"The study reinforces the hypothesis that a healthy diet has potential not only in the warding off of depression, but also in its prevention," says Ms Anu Ruusunen, MSc, who presented the results in her doctoral thesis in the field of nutritional epidemiology.
Depressed individuals often have a poor quality of diet and decreased intake of nutrients. However, it has been unclear whether the diet and the intake of foods and nutrients are associated with the risk of depression in healthy individuals.
Those following a healthy diet are less at risk
A healthy diet characterized by vegetables, fruits, berries, whole-grains, poultry, fish and low-fat cheese was associated with a lower prevalence of depressive symptoms and a lower risk of depression during the follow-up period.
Increased intake of folate was also associated with a decreased risk of depression. Vegetables, fruits, berries, whole-grains, meat and liver are the most important dietary sources of folate. In addition, increased coffee consumption was non-linearly associated with a decreased risk of depression.
In addition, participation in a three-year lifestyle intervention study improved depression scores with no specific group effect. Furthermore, a reduction in the body weight was associated with a greater reduction in depressive symptoms.
Junk food, sugar and processed meats may increase depressive symptoms
Adherence to an unhealthy diet characterized by a high consumption of sausages, processed meats, sugar-containing desserts and snacks, sugary drinks, manufactured foods, French rolls and baked or processed potatoes was associated with an increased prevalence of elevated depressive symptoms.
Contrary to some earlier observations, vitamin B12 intake, serum concentrations of n-3 PUFAs, serum ratio of n-6 to n-3 PUFAs, tea drinking and total caffeine intake were not related to the risk of depression in this study.
The study was based on the population-based Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study. The participants, over 2,000 middle-aged or older Finnish men were followed-up for an average of 13-20 years.
3570Ruusunen A, 2013 - Diet and Depression: An Epidemiological StudyRuusunen A, 2013 - Diet and Depression: An Epidemiological StudyRuusunen A, 2013 - Diet and Depression: An Epidemiological StudyAna Ruusunen13/09/2013University of Eastern Finland, Dissertations in Health Sciences, No 185
The association between diet and depression has previously mainly been studied in cross-sectional studies, and only few prospective studies have been published. The evidence suggests that folate and long-chain n-3 polyunsaturated fatty acids (PUFAs) may be connected to the decreased risk of depression. Furthermore, only few studies have concentrated on the association between general dietary patterns and depression.
The aim of this thesis was to investigate whether dietary intake of folate and vitamin B12, serum concentrations of n-3 PUFAs, consumption of coffee and tea, or caffeine intake are associated with the risk of getting a discharge diagnosis of severe depression in population based sample (the Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study, n=2,077- 2,313, works I, II and III) of middle-aged or older Eastern Finnish men during an average of 13-20 years of follow-up. In addition, the study focused on examining if dietary patterns are associated with the prevalence of depressive symptoms or the risk of depression requiring hospital treatment (the KIHD Study, n=1,003, work IV). Finally, the aim was to investigate how an intensive lifestyle intervention affects the depressive symptoms in an intervention study design (the Finnish Diabetes Prevention Study (DPS), n=140, work V).
It was observed that increased intake of folate and healthy dietary patterns (consumption of vegetables, fruits, berries, whole-grains, poultry, fish and low-fat cheese) were associated with a lower risk of depression. In addition, increased coffee consumption was non-linearly associated with a decreased risk of depression. Vitamin B12 intake, serum concentrations of n-3 PUFAs, serum ratio of n-6 to n-3 PUFAs, tea drinking and caffeine intake were not related to the risk of depression. Adherence to unhealthy dietary pattern (consumption of sausages, processed meats, sugar-containing desserts and snacks, sugary drinks, manufactured foods, French rolls and baked or processed potatoes) was associated with an increased prevalence of elevated depressive symptoms. In addition, participation in the three-year lifestyle intervention study improved depression scores with no specific group effect, although clinically non-significantly. Reduction of body weight was associated with a greater reduction in depressive symptoms.
The results of this thesis indicate that diet, especially a healthy diet rich in folate, and a dietary pattern rich in vegetables, fruits, berries, whole-grains, poultry, fish and low-fat cheese, may be protective against depression. N-3 PUFAs may not have a role in the prevention of depression, at least not in middle-aged or older men with generally low circulating concentrations of n-3 PUFAs.
3645Berk et al 2013 - So depression is an inflammatory disease, but where does the inflammation come from?So depression is an inflammatory disease, but where does the inflammation come from?So depression is an inflammatory disease, but where does the inflammation come from?Berk M, Williams LJ, Jacka FN, O'Neil A, Pasco JA, Moylan S, Allen NB, Stuart AL, Hayley AC, Byrne ML, Maes M12/09/2013BMC Med. 2013 Sep 12;11:200. doi: 10.1186/1741-7015-11-200
We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder. The obvious question this poses is 'what is the source of this chronic low-grade inflammation?'
This review explores the role of inflammation and oxidative and nitrosative stress as possible mediators of known environmental risk factors in depression, and discusses potential implications of these findings. A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency.
The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.
Depression, Inflammation, Cytokines, Diet, Obesity, Exercise, Smoking, Vitamin D, Dental cares, Sleep, Atopic, Gut, Oxidative stresshttp://www.ncbi.nlm.nih.gov/pubmed/24228900View this and related abstracts via PubMed here
3705Weijing et al 2013 - Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humansOral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humansOral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humansWeijing Cai, Jaime Uribarri, Li Zhu, Xue Chen, Shobha Swamy, Zhengshan Zhao, Fabrizio Grosjean, Calogera Simonaro, George A. Kuchel, Michal Schnaider-Beeri, Mark Woodward, Gary E. Striker12/09/2013www.pnas.org/lookup/suppl/doi:10.1073/pnas.1316013111/-/DCSupplemental.
Age-associated dementia and Alzheimer’s disease (AD) are currently epidemic. Neither their cause nor connection to the metabolic syndrome (MS) is clear. Suppression of deacetylase survival factor sirtuin 1 (SIRT1), a key host defense, is a central feature of AD. Age-related MS and diabetes are also causally associated with suppressed SIRT1 partly due to oxidant glycotoxins advanced glycation end products (AGEs). Changes in the modern diet include excessive nutrient-bound AGEs, such as neurotoxic methyl-glyoxal derivatives (MG). To determine whether dietary AGEs promote AD, we evaluated WT mice pair-fed three diets throughout life: low-AGE (MG−), MG-supplemented low-AGE (MG+), and regular (Reg) chow. Older MG+-fed mice, similar to old Reg controls, developed MS, increased brain amyloid-β42, deposits of AGEs, gliosis, and cognitive deficits, accompanied by suppressed SIRT1, nicotinamide phosphoribosyltransferase, AGE receptor 1, and PPARγ. These changes were not due to aging or caloric intake, as neither these changes nor the MS were present in age-matched, pair-fed MG− mice. The mouse data were enhanced by significant temporal correlations between high circulating AGEs and impaired cognition, as well as insulin sensitivity in older humans, in whom dietary and serum MG levels strongly and inversely associated with SIRT1 gene expression. The data identify a specific AGE (MG) as a modifiable risk factor for AD and MS, possibly acting via suppressed SIRT1 and other host defenses, to promote chronic oxidant stress and inflammation. Because SIRT1 deficiency in humans is both preventable and reversible by AGE reduction, a therapeutic strategy that includes AGE reduction may offer a new strategy to combat the epidemics of AD and MS.
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