366122 Jan 2014 - FoodNavigator - Food 'compensation' means diet drinks are not a weight loss solution, warn researchersFood 'compensation' means diet drinks are not a weight loss solution, warn researchersOverweight and obese adults who drink sugar-free or diet beverages consume more calories from food than overweight people who drink regular soda, according to new data.22/01/2014By Nathan Gray
The results of a large US-based study involving more than 23,000 adults has suggested that people who are overweight or obese drink more sugar-free beverages than people of a healthy weight. However, the study which examined patterns in adult diet beverage consumption and calorie intake, also found that overweight and obese adults who drink diet beverages consume more calories from food than obese or overweight adults who drink 'regular soda' or other sugar sweetened beverages (SSBs) - thus counterbalancing any reduction in calorie intake from drinking the sugar-free beverage.
http://www.foodnavigator.com/Science-Nutrition/Food-compensation-means-diet-drinks-are-not-a-weight-loss-solution-warn-researchers?utm_source=copyright&utm_medium=OnSite&utm_campaign=copyrightView the full news item here on FoodNavigator
3665Potalla et al 2013 - Higher RBC EPA + DHA corresponds with larger total brain and hippocampal volumes: WHIMS-MRI StudyHigher RBC EPA + DHA corresponds with larger total brain and hippocampal volumes: WHIMS-MRI Study.Higher RBC EPA + DHA corresponds with larger total brain and hippocampal volumes: WHIMS-MRI Study.Pottala JV, Yaffe K, Robinson JG, Espeland MA, Wallace R, Harris WS22/01/2014Neurology. 2014 Jan 22.
To test whether red blood cell (RBC) levels of marine omega-3 fatty acids measured in the Women's Health Initiative Memory Study were related to MRI brain volumes measured 8 years later.
RBC eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and MRI brain volumes were assessed in 1,111 postmenopausal women from the Women's Health Initiative Memory Study. The endpoints were total brain volume and anatomical regions. Linear mixed models included multiple imputations of fatty acids and were adjusted for hormone therapy, time since randomization, demographics, intracranial volume, and cardiovascular disease risk factors.
In fully adjusted models, a 1 SD greater RBC EPA + DHA (omega-3 index) level was correlated with 2.1 cm3 larger brain volume (p = 0.048). DHA was marginally correlated (p = 0.063) with total brain volume while EPA was less so (p = 0.11). There were no correlations between ischemic lesion volumes and EPA, DHA, or EPA + DHA. A 1 SD greater omega-3 index was correlated with greater hippocampal volume (50 mm3, p = 0.036) in fully adjusted models. Comparing the fourth quartile vs the first quartile of the omega-3 index confirmed greater hippocampal volume (159 mm3, p = 0.034).
A higher omega-3 index was correlated with larger total normal brain volume and hippocampal volume in postmenopausal women measured 8 years later. While normal aging results in overall brain atrophy, lower omega-3 index may signal increased risk of hippocampal atrophy. Future studies should examine whether maintaining higher RBC EPA + DHA levels slows the rate of hippocampal or overall brain atrophy.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Higher+RBC+EPA+%2B+DHA+corresponds+with+larger+total+brain+and+hippocampal+volumesView this and related abstracts via PubMed here
366016 Jan 2014 - ScienceDaily - Altering the Community of Gut Bacteria Promotes Health and Increases Lifespangut bacteriaScientists at the Buck Institute for Research on Aging have promoted health and increased lifespan in Drosophila by altering the symbiotic, or commensal, relationship between bacteria and the absorptive cells lining the intestine. The research, appearing in the January 16, 2014 edition of Cell, provides a model for studying many of the dysfunctions that are characteristic of the aging gut and gives credence to the growing supposition that having the right balance of gut bacteria may be key to enjoying a long healthy life.16/01/2014
Even though recent research in humans has linked the composition of gut flora with diet and health in the elderly and the list of age-related diseases associated with changes in gut bacteria include cancer, diabetes, and inflammatory bowel disease, lead author and Buck faculty Heinrich Jasper, PhD, says there is no systematic understanding of how we go from having a young, healthy gut to one that is old and decrepit. "Our study explores age-related changes in the gut that include increased oxidative stress, inflammation, impaired efficiency of the immune response, and the over-proliferation of stem cells," said Jasper. "It puts these changes into a hierarchical, causal relationship and highlights the points where we can intervene to rescue the negative results of microbial imbalance."
Jasper says the bacterial load in fly intestines increases dramatically with age, resulting in an inflammatory condition. The imbalance is driven by chronic activation of the stress response gene FOXO (something that happens with age), which suppresses the activity of a class of molecules (PGRP-SCs, homologues of PGLYRPs in humans) that regulate the immune response to bacteria. PGRP-SC suppression deregulates signaling molecules (Rel/NFkB) that are important to mount an effective immune response to gut bacteria. The resulting immune imbalance allows bacterial numbers to expand, triggering an inflammatory response that includes the production of free radicals. Free radicals, in turn, cause over-proliferation of stem cells in the gut, resulting in epithelial dysplasia, a pre-cancerous state.
Jasper said the most exciting result of their study occurred when his group increased the expression of PGRP-SC in epithelial cells of the gut, which restored the microbial balance and limited stem cell proliferation. This enhancement of PGRP-SC function, which could be mimicked by drugs, was sufficient to increase lifespan of flies. "If we can understand how aging affects our commensal population -- first in the fly and then in humans -- -- our data suggest that we should be able to impact health span and life span quite strongly, because it is the management of the commensal population that is critical to the health of the organism."
http://www.sciencedaily.com/releases/2014/01/140116130646.htm?utm_source=Email+Campaign&utm_medium=email&utm_campaign=10491-310688-NH-eNews+-+21st+January+2014View this news item and related new articles on ScienceDaily here
36269 Jan 2014 - BBC News - Campaigners vow to cut sugar in foodSugarA campaign group has been formed to reduce the amount of sugar added to food and soft drinks in an effort to tackle obesity and diabetes in the UK.09/01/2014
Action on Sugar has been set up by the team behind Consensus Action on Salt and Health (Cash), which has pushed for cuts to salt intake since the 1990s.
The new group aims to help people avoid "hidden sugars" and get manufacturers to reduce the ingredient over time.
It believes a 20% to 30% reduction in three to five years is within reach.
Like Cash, Action on Sugar will set targets for the food industry to add less sugar bit by bit so that consumers do not notice the difference in taste.
It says the reduction could reverse or halt the obesity epidemic and would have a significant impact in reducing chronic disease in a way that "is practical, will work and will cost very little".
The group listed flavoured water, sports drinks, yoghurts, ketchup, ready meals and even bread as just a few everyday foods that contain large amounts of sugar.
A favourite tactic of Cash has been to name and shame products with large quantities of salt.
Action on Sugar chairman Graham MacGregor, who is professor of cardiovascular medicine at the Wolfson Institute of Preventive Medicine and set up Cash in 1996, said: "We must now tackle the obesity epidemic both in the UK and worldwide.
"This is a simple plan which gives a level playing field to the food industry, and must be adopted by the Department of Health to reduce the completely unnecessary and very large amounts of sugar the food and soft drink industry is currently adding to our foods."
Dr Aseem Malhotra, a cardiologist and science director of Action on Sugar, said: "Added sugar has no nutritional value whatsoever and causes no feeling of satiety.
"Aside from being a major cause of obesity, there is increasing evidence that added sugar increases the risk of developing type 2 diabetes, metabolic syndrome and fatty liver."
36279 Jan 2014 - The Guardian - Obesity experts campaign to cut sugar in food by up to 30%SugarDoctors say marketing ploys to cut calories are ineffective, now industry must slowly lower sugar content of processed foods09/01/2014by Sarah Boseley, Health Editor
Obesity experts are launching a campaign to put pressure on the government and industry to cut the sugar content of food and drinks by up to 30%. The high-profile scientists and doctors behind Action on Sugar say that gradual cuts in the amount of sugar in ready meals, cereals, sweets and soft drinks will not be noticed by the public, but will result in a reduction in the calories we all consume.
A 20-30% reduction in sugar over time will cut our calorie intake by about 100kcal a day – and more for those who consume a lot of sugar.
That is enough to halt or even reverse the obesity epidemic and reduce the toll of diabetes and other disease, say the doctors, who include Robert Lustig, author of Fat Chance: The Bitter Truth About Sugar, and Professors John Wass, academic vice-president of the Royal College of Physicians, Philip James of the International Association for the Study of Obesity and Sir Nicholas Wald of the Wolfson Institute of Preventive Medicine.
Action on Sugar aims to do what a similar campaign launched in the 1990s called Cash (Consensus Action on Salt and Health) successfully did for salt levels in our food. It is chaired by Professor Graham MacGregor, who also heads Cash.
"Provided the sugar reductions are done slowly, people won't notice," he said. "In most products in the supermarkets, the salt has come down by between 25% and 40%."
People had not noticed the difference. Kellogg's Cornflakes contain 60% less salt than they used to.
The government's strategy against obesity has been to agree voluntary curbs on marketing to children and calorie reduction through a public health "responsibility deal".
But MacGregor and others say it is not working and has had no effect on calorie intake. "We must start to slowly reduce the amount of calories people consume by slowly taking out added sugar from foods and soft drinks," he said.
The industry argues that sugars are forms of carbohydrate, which we need in our diet, and that we should cut calories by eating less, but there is no specific reason to target sugar.
"Sugars, or any other nutrient for that matter, consumed as part of a varied and balanced diet are not a cause of obesity, to which there is no simple or single solution," said the Food and Drink Federation. "That's why the food industry has been working on a range of initiatives with other players to tackle obesity and diet-related diseases."
The sugars in food and drinks are listed on the label, they said, so everybody can see what is in the products they buy. The industry has worked to reduce salt levels and saturated fats, but there is no evidence that sugars are particularly harmful, it said.
Aseem Malhotra, cardiologist and science director of the new group, disagrees, pointing to studies that suggest sugar increases the risk of diabetes, regardless of whether or not a person is overweight.
"Added sugar has no nutritional value and the body doesn't need any added sugar," he said. Claims by industry that sugar was needed for energy were untrue, he added.
The campaign is worried about hidden sugars in processed foods, such as the nine teaspoons in a standard 330ml can of Coke, the six teaspoons in a Muller Crunch Corner strawberry shortcake yoghurt, and the six in a 375g portion of Sharwood's sweet and sour chicken with rice. A serving of Kellogg's Frosties contains four teaspoons and Heinz classic tomato soup has four teaspoons in 300g.
Saturated fat contains more calories per gram than sugar, but Lustig, professor of paediatric endocrinology at the University of California, San Francisco, said that not all calories were the same.
"The science says that sugar is different – that sugar is dangerous exclusive of its calories, just like alcohol," he said. He called sugar "the alcohol of childhood", which was likely to put children at greater risk of fatty liver disease and diabetes.
Yoni Freedhoff, assistant professor of medicine at the University of Ottawa, Canada, another adviser to the group, said: "Not only has added sugar found its way into virtually everything we eat, but worse still, the use of sugar as a means to pacify, entertain and reward children has become normalised to the point that questioning our current sugary status quo often inspires anger and outrage."
Simon Capewell, professor of clinical epidemiology at Liverpool University, called sugar the new tobacco. "Everywhere, sugary drinks and junk foods are now pressed on unsuspecting parents and children by a cynical industry focused on profit not health," he said.
The Department of Health said: "Helping people eat fewer calories, including sugar, is a key part of the responsibility deal and our efforts to reduce obesity. There are 38 businesses signed up to reduce calories, but we want to go further still, and are discussing this with the food industry.
"As part of the responsibility deal calorie reduction pledge, Coca Cola has reduced calories in some of its soft drinks brands by at least 30%. Mars has reduced its single chocolate portions to no more than 250 calories, and Tesco has reduced the number of calories sold in its own brand soft drinks by over one billion."
http://www.theguardian.com/society/2014/jan/09/obesity-campaign-cut-sugar-processed-foodsView this item and related stories in The Guardian here
3301About the FAB Research Audio/Video LibraryAbout the FAB Research Audio/Video LibraryAudio Video08/01/2014
The FAB Research Audio/Video Library was set up in April 2013 and is an area where our Associate Members may access audio and video material, and other accompanying resources if available, from recent and past events and webinars.
With Prof Robert Lustig MD; Prof Jason Halford; Prof David Haslam; Dr Alex Richardson; Prof Jack Winkler; Prof Michael Yudkin
If you would like to access the FAB Research Audio/Video Library and hear the full presentations given by Professor Robert Lustig and all the speakers at this event, and enjoy continuous unrestricted access to our growing library of media and resources, please join us as a FAB Associate Member.
36697 Jan 2014 - MedXpress - Several forms of Vitamin E protect against memory disorders Vitamin E, Antioxidants, age-related cognitive impairment and dementia 07/01/2014
Elderly people with high serum vitamin E levels are less likely to suffer from memory disorders than their peers with lower levels, according to a study published recently inExperimental Gerontology. According to the researchers, various forms of vitamin E seem to play a role in memory processes. The study was carried out in cooperation between the University of Eastern Finland, the Finnish National Institute for Health and Welfare, Karolinska Institutet, and the University of Perugia.
Studies investigating the link between vitamin E and memory disorders have usually focused on a single form of vitamin E, namely α-tocopherol, which is also used in vitamin E supplements. However, vitamin E exists in eight different natural forms, tocopherols and tocotrienols, all of which have antioxidant properties.
This recently published study comprises a sample of 140 over 65-year-old Finnish persons with no memory impairment at the onset of the study. During the eight-year follow-up, it was discovered that higher total serum levels of vitamin E, and higher levels of γ-tocopherol, β-tocotrienol and total tocotrienols in particular, seemed to protect against memory disorders. According to the researchers, the results show that the entire vitamin E family plays a role in memory processes. Accordingly, measuring the levels of vitamin E from serum is the most reliable way to determine whether they are sufficiently high.
The study comprised part of the more extensive Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study, which focuses on the association between the risk factors of cardiovascular diseases and memory disorders.
Research often ignores the fact that Vitamin E is not a single substance, but actually includes 8 different substances (4 tocopherols and 4 tocotrienols). In this study, all forms of Vitamin E were assessed in a sample of elderly people with no memory impairment, who were then followed up over 8 years. The researchers found that higher initial blood levels of total Vitamin E were associated with lower risks of developing Mild Cognitive Impairment or Alzheimer's Disease.
36327 Jan 2014 - Science-Based Medicine - Vitamin E for Alzheimer’sVitamin E for Alzheimer’s07/01/2014By Harriet Hall
Recently you may have seen headlines like “Vitamin E slows decline in patients with mild Alzheimer’s” or “There’s still no cure for Alzheimer’s disease, but the latest hope for slowing its progression is already on drugstore shelves.” They were referring to an article in the January 1, 2014 issue of the Journal of the American Medical Association (JAMA) announcing the results of the TEAM-AD VA Cooperative Randomized Trial of vitamin E and memantine (Namenda) for Alzheimer’s disease (AD).
The study attracted a lot of media attention. Most of the news reports I have seen were accurate and cautious, explaining the nuances of the study rather than suggesting that everyone should run out and buy vitamin E; but I wouldn’t be surprised to learn that a lot of readers ignored the fine print and did just that. It would be interesting to track sales of vitamin E and see if there was a bump following the publicity.
We know of no treatment that will delay, prevent or cure Alzheimer’s disease, or that affects the underlying disease process. It’s a tragic, frustrating disease that takes away the very things that make us who we are: memory and personality. It is affecting more and more people as the numbers of elderly increase. Available prescription medications are only modestly effective in slowing functional decline and delaying the need for institutionalization. They are expensive, they don’t help everyone, and when they do help, they only help for a limited time. It is very exciting to think an inexpensive vitamin could help patients with mild to moderate AD, but we must resist the temptation to read too much into this study.
The study was a large, rigorous, multicenter randomized placebo-controlled trial with 33 authors, carried out at 14 Veterans Affairs (VA) medical centers. It enrolled 613 patients age 53 to 96 with a diagnosis of possible or probable AD of mild to moderate severity who were already taking an acetylcholinesterase inhibitor (AChEI). 65% were on Donepezil, 32% on Galantamine, and 3% on Rivastigmine); 97% were male, 86% were white, 13% black, and 11% Hispanic. (Note: these were classified as possible or probable cases, since definitive diagnosis of AD is only possible at autopsy.)
Participants were randomized to one of four groups:
- Alpha tocopherol (vitamin E) 1,000 IU twice a day + memantine-matching placebo - Memantine 10 mg twice a day + vitamin E-matching placebo - Both vitamin E and memantine - Two placebos
Primary outcome measure was the Alzheimer’s Disease Cooperative Study/Activities of Daily Living Inventory (ADCS-ADL), a validated questionnaire that assesses functional abilities to perform activities of daily living. A difference of 2 points on this scale is generally considered significant because it potentially represents, for example, a loss of dressing or bathing independently. Secondary outcome measures included tests of cognitive function and dementia severity, memory, language and praxis functions, assessment of psychological and behavioral problems, the time required for caregivers to assist patients in major areas of daily activities, and a measure of functional dependence.
Annual assessments included physical exams, review of concomitant medications, blood concentrations of the study drugs to assess adherence, and careful questioning about adverse experiences. 42% of subjects failed to complete the trial, most commonly due to death (50%), withdrawal of consent (30%) and adverse events possibly related to the study medication (1%). Mean follow-up time was 2.27 years.
All participants got worse over the period of the study. Subjects in the vitamin E group had a significantly slower decline than those in the placebo group (3.15 units less on the ADCS-ADL Inventory, annual rate of decline 19% less, delay in progression of 6.2 months). There was no significant difference between the placebo group and the memantine or memantine + vitamin E groups. The group taking both vitamin E and memantine did significantly worse than the group taking vitamin E alone.
Adherence was estimated at 65-68%, which isn’t all that bad considering the age of patients and the effects of Alzheimer’s.
Secondary outcomes showed no significant differences between the four groups except that caregiver hours increased less in the vitamin E group than in the memantine group.
Safety: there were no significant differences between groups for serious adverse events. The annual mortality rate was 7.3% for vitamin E, 11.3% for memantine, 9% for vitamin E + memantine, and 9.4% for placebo.
They concluded that 2,000 IU of vitamin E significantly delayed clinical progression in activities of daily living in patients with mild to moderate AD who were also taking AChEI. Paradoxically, the combination of memantine and vitamin E had less effect than either drug alone; the authors could not think of a plausible mechanism for this finding. No significant changes were seen in cognition or memory, but the researchers considered the 6.2-month delay in progression of functional loss to be of more practical importance. Mortality rate was reduced with vitamin E, in contrast to a previous meta-analysis of vitamin E studies that had showed an increase in all-cause mortality with doses typically lower than the 2,000 IU used in this study. Interestingly, only one study in that meta-analysis involved Alzheimer’s patients, and that one also showed a decrease in mortality.
An accompanying editorial praised the study as reflecting the best in trials of AD therapy, especially because of its size, duration, and separation from commercial motivation; but it characterized the therapeutic effect as “modest” and more relevant to functional disability than to any effect on the disease process itself. They pointed out that functional ability is non-specific (decreasing with age as well as with disease), that the primary outcome was not confirmed by any of the secondary outcomes, and that the mechanism of vitamin E in AD is uncertain. Memantine is only approved for moderate to severe AD, and this study confirms that it is not indicated for milder disease. The results for vitamin E are encouraging, but can’t be extrapolated to situations other than the specific ones in the study. Another opinion
An ND quoted on one website said “This new study demonstrates that scientists seeking to slam the door on vitamins, and new vitamin research, is the antithesis of what science is all about.” He is responding to a straw man. Several recent studies and editorials have discouraged indiscriminate use of multivitamins in healthy populations, especially as a substitute for a nutritious diet. But no one has recommended we stop studying individual vitamins for new indications where there is preliminary evidence that they might be helpful in specific populations or diseases.
This study is encouraging, but it doesn’t mean everyone should start taking high doses of vitamin E to ward off Alzheimer’s. And it would be premature to incorporate vitamin E into routine treatment of Alzheimer’s patients on the basis of this one study. There are too many unanswered questions. Women and minority groups were underrepresented, the interaction with memantine is puzzling, the secondary outcomes didn’t support the primary outcome, the beneficial effect on mortality may not be generalizable to all AD patients, and interactions with other medications or illnesses have not been studied.
I agree with the Alzheimer’s Association’s call for caution:
No one should take vitamin E to treat Alzheimer’s disease except under the supervision of a physician. Vitamin E — especially at the high doses used in the ADCS study — can negatively interact with other medications, including those prescribed to keep blood from clotting or to lower cholesterol.
36311 Jan 2014 - BBC News - Vitamin E 'beneficial' in dementiaVitamin E 'beneficial' in dementiaA daily dose of vitamin E could help people with dementia, research suggests.01/01/2014
A study in the journal JAMA found people with mild to moderate Alzheimer's disease on high doses of vitamin E had a slower rate of decline than those given a dummy pill.
They were able to carry out everyday tasks for longer and needed less help from carers, say US researchers.
The Alzheimer's Society said the dosage was very high and might not be safe.
In the study, 613 people with mild to moderate Alzheimer's disease received either a daily dose of vitamin E, a dementia drug treatment known as memantine, a combination of vitamin E and memantine, or placebo.
Changes in their ability to carry out everyday tasks - such as washing or dressing - were measured over an average of two years.
The study found participants receiving vitamin E had slower functional decline than those receiving placebo, with the annual rate of decline reduced by 19%.
Those on vitamin E (also known as alpha tocopherol) also needed less help from carers.
"These findings suggest that alpha tocopherol is beneficial in mild to moderate Alzheimer's disease by slowing functional decline and decreasing caregiver burden," said a team led by Dr Maurice Dysken of Minneapolis VA Health Care System.
Commenting on the study, Dr Doug Brown, director of research and development at the Alzheimer's Society, said treatments which can help people with dementia carry out everyday tasks are key to enabling those with the condition to live well for as long as possible.
But he said more research was needed to see if vitamin E really does have benefits for people with dementia, and whether it would be safe to be taking such a high dose on a daily basis.
"It is vitally important that people always seek advice from their doctor before considering taking supplements," he said.
"In this instance, the dosage of vitamin E taken by participants was much higher than the recommended daily allowance and was at a level that could be significantly harmful for some."
Dr Eric Karran, director of research at Alzheimer's Research UK, said the trial suggested vitamin E may modestly slow the decline in day-to-day functioning in people with mild to moderate Alzheimer's, but without having an effect on memory and thinking skills.
He said it was too early to recommend vitamin E as a treatment.
"Until the findings from this trial have been replicated, we would not encourage people to take high doses of vitamin E supplements to try to prevent or treat Alzheimer's," he added.
"If people are concerned about their vitamin intake or diet, they should talk to their GP."
3633Dysken et al 2014 - Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trialEffect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trialEffect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial.Dysken MW, Sano M, Asthana S, Vertrees JE, Pallaki M, Llorente M, Love S, Schellenberg GD, McCarten JR, Malphurs J, Prieto S, Chen P, Loreck DJ, Trapp G, Bakshi RS, Mintzer JE, Heidebrink JL, Vidal-Cardona A, Arroyo LM, Cruz AR, Zachariah S, Kowall NW, Chopra MP, Craft S, Thielke S, Turvey CL, Woodman C, Monnell KA, Gordon K, Tomaska J, Segal Y, Peduzzi PN, Guarino PD01/01/2014JAMA. 2014 Jan 1;311(1):33-44. doi: 10.1001/jama.2013.282834
Although vitamin E and memantine have been shown to have beneficial effects in moderately severe Alzheimer disease (AD), evidence is limited in mild to moderate AD.
To determine if vitamin E (alpha tocopherol), memantine, or both slow progression of mild to moderate AD in patients taking an acetylcholinesterase inhibitor.
DESIGN, SETTING, AND PARTICIPANTS:
Double-blind, placebo-controlled, parallel-group, randomized clinical trial involving 613 patients with mild to moderate AD initiated in August 2007 and concluded in September 2012 at 14 Veterans Affairs medical centers.
Participants received either 2000 IU/d of alpha tocopherol (n = 152), 20 mg/d of memantine (n = 155), the combination (n = 154), or placebo (n = 152).
MAIN OUTCOMES AND MEASURES:
Alzheimer's Disease Cooperative Study/Activities of Daily Living (ADCS-ADL) Inventory score (range, 0-78). Secondary outcomes included cognitive, neuropsychiatric, functional, and caregiver measures.
Data from 561 participants were analyzed (alpha tocopherol = 140, memantine = 142, combination = 139, placebo = 140), with 52 excluded because of a lack of any follow-up data. Over the mean (SD) follow-up of 2.27 (1.22) years, ADCS-ADL Inventory scores declined by 3.15 units (95% CI, 0.92 to 5.39; adjusted P = .03) less in the alpha tocopherol group compared with the placebo group. In the memantine group, these scores declined 1.98 units less (95% CI, -0.24 to 4.20; adjusted P = .40) than the placebo group's decline. This change in the alpha tocopherol group translates into a delay in clinical progression of 19% per year compared with placebo or a delay of approximately 6.2 months over the follow-up period. Caregiver time increased least in the alpha tocopherol group. All-cause mortality and safety analyses showed a difference only on the serious adverse event of "infections or infestations," with greater frequencies in the memantine (31 events in 23 participants) and combination groups (44 events in 31 participants) compared with placebo (13 events in 11 participants).
CONCLUSIONS AND RELEVANCE:
Among patients with mild to moderate AD, 2000 IU/d of alpha tocopherol compared with placebo resulted in slower functional decline. There were no significant differences in the groups receiving memantine alone or memantine plus alpha tocopherol. These findings suggest benefit of alpha tocopherol in mild to moderate AD by slowing functional decline and decreasing caregiver burden.
http://www.ncbi.nlm.nih.gov/pubmed/24381967View this and related research papers here
3642Stilling et al 2013 - Microbial genes, brain & behaviour - epigenetic regulation of the gut-brain axisMicrobial genes, brain & behaviour - epigenetic regulation of the gut-brain axisMicrobial genes, brain & behaviour - epigenetic regulation of the gut-brain axisStilling RM, Dinan TG, Cryan JF27/12/2013Genes Brain Behav. 2014 Jan;13(1):69-86. doi: 10.1111/gbb.12109
To date, there is rapidly increasing evidence for host-microbe interaction at virtually all levels of complexity, ranging from direct cell-to-cell communication to extensive systemic signalling, and involving various organs and organ systems, including the central nervous system. As such, the discovery that differential microbial composition is associated with alterations in behaviour and cognition has significantly contributed to establishing the microbiota-gut-brain axis as an extension of the well-accepted gut-brain axis concept. Many efforts have been focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome to neurodevelopmental disorders such as autism. There is also a growing appreciation of the role of epigenetic mechanisms in shaping brain and behaviour. However, the role of epigenetics in informing host-microbe interactions has received little attention to date. This is despite the fact that there are many plausible routes of interaction between epigenetic mechanisms and the host-microbiota dialogue. From this new perspective we put forward novel, yet testable, hypotheses. Firstly, we suggest that gut-microbial products can affect chromatin plasticity within their host's brain that in turn leads to changes in neuronal transcription and eventually alters host behaviour. Secondly, we argue that the microbiota is an important mediator of gene-environment interactions. Finally, we reason that the microbiota itself may be viewed as an epigenetic entity. In conclusion, the fields of (neuro)epigenetics and microbiology are converging at many levels and more interdisciplinary studies are necessary to unravel the full range of this interaction.
Anxiety, Gut, HDAC, cognition, depression, epigenetics, germ-free, histone modification, hologenome, learning, microbiome, microbiota, nucleomodulin, probiotic, stresshttp://www.ncbi.nlm.nih.gov/pubmed/24286462View this and related abstracts via PubMed here
3634Wang et al 2013 - The role of microbiome in central nervous system disordersThe role of microbiome in central nervous system disordersThe role of microbiome in central nervous system disordersWang Y, Kasper LH25/12/2013Brain Behav Immun. 2013 Dec 25. pii: S0889-1591(13)00600-4. doi: 10.1016/j.bbi.2013.12.015
Mammals live in a co-evolutionary association with the plethora of microorganisms that reside at a variety of tissue microenvironments. The microbiome represents the collective genomes of these co-existing microorganisms, which is shaped by host factors such as genetics and nutrients but in turn is able to influence host biology in health and disease. Niche-specific microbiome, prominently the gut microbiome, has the capacity to effect both local and distal sites within the host. The gut microbiome has played a crucial role in the bidirectional gut-brain axis that integrates the gut and central nervous system (CNS) activities, and thus the concept of microbiome-gut-brain axis is emerging. Studies are revealing how diverse forms of neuro-immune and neuro-psychiatric disorders are correlated with or modulated by variations of microbiome, microbiota-derived products and exogenous antibiotics and probiotics. The microbiome poises the peripheral immune homeostasis and predisposes host susceptibility to CNS autoimmune diseases such as multiple sclerosis. Neural, endocrine and metabolic mechanisms are also critical mediators of the microbiome-CNS signaling, which are more involved in neuro-psychiatric disorders such as autism, depression, anxiety, stress. Research on the role of microbiome in CNS disorders deepens our academic knowledge about host-microbiome commensalism in central regulation and in practicality, holds conceivable promise for developing novel prognostic and therapeutic avenues for CNS disorders.
Central nervous system, Gut–brain axis, Microbiome, Neuro-immune disorders, Neuro-psychiatric disordershttp://www.ncbi.nlm.nih.gov/pubmed/24370461View this abstract and related citations in PubMed here
3636Malkki H 2013 - Neurodevelopmental disorders: Human gut microbiota alleviate behavioural symptoms in a mouse model of autism spectrum disorderNeurodevelopmental disorders: Human gut microbiota alleviate behavioural symptoms in a mouse model of autism spectrum disorder.Neurodevelopmental disorders: Human gut microbiota alleviate behavioural symptoms in a mouse model of autism spectrum disorder.Malkki H24/12/2013Nat Rev Neurol. 2013 Dec 24. doi: 10.1038/nrneurol.2013.267
This paper was commented on in:
Nature Reviews Neurology (2013)doi:10.1038/nrneurol.2013.267 - Published online 24 December 2013:
Some of the core behavioural alterations in autism spectrum disorder (ASD) can be corrected by probiotic bacteria that ameliorate ASD-associated gastrointestinal (GI) dysfunction, a new study in mice suggests.
For the study, published in Cell, Elaine Hsiao and colleagues at the California Institute of Technology (Pasadena, CA, USA) used the maternal immune activation (MIA) mouse model of ASD to assess the role of the gut–brain axis in ASD.
Besides increased anxiety, stereotypical behaviour, altered sensorimotor gating, and impaired social interaction and communication—behavioural symptoms typical of ASD—the MIA offspring showed altered gut microbiota, increased gut permeability and elevated microbiota-related serum metabolites. These findings are in line with studies that report a subset of individuals with ASD experience GI problems.
“Our findings reveal that certain beneficial gut bacteria may influence behaviours relevant to neurodevelopmental disorders, and raise the exciting prospect that probiotics could be a safe and effective treatment for some cases of autism,” Hsiao contends.
http://www.ncbi.nlm.nih.gov/pubmed/24366270View this and related abstracts via PubMed here
3728Wang et al 2013 - Resolution of inflammation is altered in Alzheimer's diseaseResolution of inflammation is altered in Alzheimer's disease.Resolution of inflammation is altered in Alzheimer's disease.Hjorth E, Cortés-Toro V, Eyjolfsdottir H, Graff C, Nennesmo I, Palmblad J, Eriksdotter M, Sambamurti K, Fitzgerald JM, Serhan CN, Granholm24/12/2013Alzheimers Dement. 2014 Feb 12. pii: S1552-5260(14)00030-2. doi: 10.1016/j.jalz.2013.12.024. [Epub ahead of print]
Resolution is the final stage of the inflammatory response, when restoration of tissue occurs. Failure may lead to chronic inflammation, which is known as part of the pathology in the brain of individuals with Alzheimer's disease (AD).
Specialized pro-resolving mediators (SPMs), receptors, biosynthetic enzyme, and downstream effectors involved in resolution were analyzed in postmortem hippocampal tissue from AD patients and non-AD subjects. SPMs were analyzed in cerebrospinal fluid (CSF).
SPMs and SPM receptors were detected in the human brain. Levels of the SPM lipoxin A4 (LXA4) were reduced in AD, both in the CSF and hippocampus. An enzyme involved in LXA4 synthesis and two SPM receptors were elevated in AD brains. LXA4 and RvD1 levels in CSF correlated with Mini-Mental State Examination (MMSE) scores.
A resolution pathway exists in the brain and the alterations described herein strongly suggest a dysfunction of this pathway in AD. MMSE correlations suggest a connection with cognitive function in AD.
15-Lipoxygenase-2, ALX/FPR2, ChemR23, ELISA, FPRL1, Human, Immunohistochemistry, Lipoxin A(4), Mild cognitive impairment, Resolvin D1, Specialized pro-resolving mediators, Tauhttp://www.ncbi.nlm.nih.gov/pubmed/24530025View this and related abstracts on PubMed here
364119 Dec 2013 - NC Research Campus - Omega-3 Intake Linked to Higher Cognition in Infants, Toddlers and Young ChildrenOmega-3 Intake Linked to Higher Cognition in Infants, Toddlers and Young ChildrenAdults may be aware of the amount of omega-3 and other fatty acids in their diet, but most may not be thinking about the impact of fatty acids on their children, especially their cognitive abilities. 19/12/2013by Carol L. Cheatham, Ph.D
The role of fatty acids and nutrients like choline, iron, and zinc on the cognitive abilities of children is exactly what Carol L. Cheatham, Ph.D., developmental cognitive neuroscientist with the UNC Chapel Hill Nutrition Research Institute (NRI) at the NC Research Campus, thinks about every day. Her most recent research studies prove just how critical fatty acids are to the cognitive development and cognitive functioning of infants, toddlers and young children.
More Omega-3 for Young Children
Kelly Will, a graduate student in Cheatham’s laboratory, conducted a study on the effect of the ratio of omega-6 and omega-3 fatty acids and the cognitive abilities of children seven to nine years of age. The results were recently published in The American Journal of Clinical Nutrition.
In the study, Will gathered dietary data so that she knew the ratio of each child’s omega-6 to omega-3 intake. After taking a set of neuropsychological tests, Cheatham said, “She found that the children who were eating too many omega-6 in comparison to omega-3 had slower speed of processing on working memory and planning problems.”
The comparison is important because omega-6, which is found in meats and refined vegetable oil is more abundant in the Western diet. Research has connected the over-consumption of omega-6 fatty acids to chronic inflammation, an underlying factor in heart disease, cancer and other common diseases. Omega-3 fatty acids are linked to the regulation of blood clotting and are considered heart healthy because they lower fats or triglycerides in the blood including the “bad” low-density lipoprotein (LDL) cholesterol. Unfortunately, the typical American diet includes relatively few foods that are rich in omega-3 compared to those high in omega-6.
“Think of omega-6 fatty acids as French fries and omega-3 as vegetables,” Cheatham said. “Intake needs to be in balance because the metabolic pathways share the same enzymes. If the pathways get out of balance because you are eating more omega-6 than omega-3, the enzymes get used up, and you won’t be able to make your own DHA because you will be out of the things you need to make it.”
http://www.ncresearchcampus.net/partners-and-research/latest-research/omega-3-intake-linked-to-higher-cognitionRead the full news item online here
3635Hsiao et al 2013 - Microbiota modulate behavioral and physiological abnormalities associated with neurodevelopmental disordersMicrobiota modulate behavioral and physiological abnormalities associated with neurodevelopmental disordersMicrobiota modulate behavioral and physiological abnormalities associated with neurodevelopmental disordersHsiao EY, McBride SW, Hsien S, Sharon G, Hyde ER, McCue T, Codelli JA, Chow J, Reisman SE, Petrosino JF, Patterson PH, Mazmanian SK19/12/2013Cell. 2013 Dec 19;155(7):1451-63. doi: 10.1016/j.cell.2013.11.024. Epub 2013 Dec 5
Neurodevelopmental disorders, including autism spectrum disorder (ASD), are defined by core behavioral impairments; however, subsets of individuals display a spectrum of gastrointestinal (GI) abnormalities.
We demonstrate GI barrier defects and microbiota alterations in the maternal immune activation (MIA) mouse model that is known to display features of ASD.
Oral treatment of MIA offspring with the human commensal Bacteroides fragilis corrects gut permeability, alters microbial composition, and ameliorates defects in communicative, stereotypic, anxiety-like and sensorimotor behaviors.
MIA offspring display an altered serum metabolomic profile, and B. fragilis modulates levels of several metabolites. Treating naive mice with a metabolite that is increased by MIA and restored by B. fragilis causes certain behavioral abnormalities, suggesting that gut bacterial effects on the host metabolome impact behavior.
Taken together, these findings support a gut-microbiome-brain connection in a mouse model of ASD and identify a potential probiotic therapy for GI and particular behavioral symptoms in human neurodevelopmental disorders.
For an accessible news summary of this research, see:
autistic spectrum disorder, gut permeability, microbiota, maternal immune activation, gut-microbiome-brain connection, probiotic therapyhttp://www.ncbi.nlm.nih.gov/pubmed/24315484View this and related abstracts via PubMed here
3612Guidelines for FAB Research SponsorshipGuidelines for FAB Research SponsorshipGuidelines for FAB Research Sponsorship18/12/2013
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360817 Dec 2013 - University of New South Wales - Junk food can harm memory in a weekJunk food and memoryEven a short-term diet of junk food can have a detrimental effect on the brain's cognitive ability, according to UNSW research.17/12/2013
For the first time, researchers have shown that rats fed a diet high in fat and sugar had impaired memory after just a week.
Interestingly, the results were similarly poor for the rats fed a healthy diet and given access to sugar water to drink.
The work has been published in the journal Brain, Behavior and Immunity.
The cognitive impairment related to place recognition, with the animals showing poorer ability to notice when an object had been shifted to a new location. These animals also had inflammation of the hippocampal region of the brain, which is associated with spatial memory.
"We know that obesity causes inflammation in the body, but we didn't realise until recently that it also causes changes in the brain," says one of the authors Professor Margaret Morris from UNSW Medicine.
"What is so surprising about this research is the speed with which the deterioration of the cognition occurred," says Professor Morris, from the School of Medical Sciences. "Our preliminary data also suggests that the damage is not reversed when the rats are switched back to a healthy diet, which is very concerning."
Some aspects of the animals' memories were spared, regardless of their diets. All the animals were equally able to recognise objects after eating either the "healthy", "cafeteria" (high in fat and sugar, including cake, chips and biscuits) or "healthy with sugar" regimes.
The change in the animals' memory appeared even prior to the emergence of weight differences between the animals.
Ongoing work will attempt to establish how to stop the inflammation in the brain of animals with the unhealthy diets.
"We suspect that these findings may be relevant to people," says Professor Morris. "While nutrition affects the brain at every age, it is critical as we get older and may be important in preventing cognitive decline. An elderly person with poor diet may be more likely to have problems. "
The research builds on previous work that has implications for obesity.
"Given that high energy foods can impair the function of the hippocampus, if you eat a lot of them it may contribute to weight gain, by interfering with your episodic memory," says Professor Morris.
"People might be less aware of their internal cues like hunger pangs and knowing when they have had enough," she said.
360514 Dec 2013 - NY Times - The Selling of Attention Deficit DisorderADHD; Attention Deficit DisorderThe Number of Diagnoses Soared Amid a 20-Year Drug Marketing Campaign14/12/2013
After more than 50 years leading the fight to legitimize attention deficit hyperactivity disorder, Keith Conners could be celebrating.
Severely hyperactive and impulsive children, once shunned as bad seeds, are now recognized as having a real neurological problem. Doctors and parents have largely accepted drugs like Adderall and Concerta to temper the traits of classic A.D.H.D., helping youngsters succeed in school and beyond.
But Dr. Conners did not feel triumphant this fall as he addressed a group of fellow A.D.H.D. specialists in Washington. He noted that recent data from the Centers for Disease Control and Prevention show that the diagnosis had been made in 15 percent of high school-age children, and that the number of children on medication for the disorder had soared to 3.5 million from 600,000 in 1990. He questioned the rising rates of diagnosis and called them “a national disaster of dangerous proportions.”
“The numbers make it look like an epidemic. Well, it’s not. It’s preposterous,” Dr. Conners, a psychologist and professor emeritus at Duke University, said in a subsequent interview. “This is a concoction to justify the giving out of medication at unprecedented and unjustifiable levels.”
The rise of A.D.H.D. diagnoses and prescriptions for stimulants over the years coincided with a remarkably successful two-decade campaign by pharmaceutical companies to publicize the syndrome and promote the pills to doctors, educators and parents. With the children’s market booming, the industry is now employing similar marketing techniques as it focuses on adult A.D.H.D., which could become even more profitable.
Few dispute that classic A.D.H.D., historically estimated to affect 5 percent of children, is a legitimate disability that impedes success at school, work and personal life. Medication often assuages the severe impulsiveness and inability to concentrate, allowing a person’s underlying drive and intelligence to emerge.
But even some of the field’s longtime advocates say the zeal to find and treat every A.D.H.D. child has led to too many people with scant symptoms receiving the diagnosis and medication. The disorder is now the second most frequent long-term diagnosis made in children, narrowly trailing asthma, according to a New York Times analysis of C.D.C. data.
Behind that growth has been drug company marketing that has stretched the image of classic A.D.H.D. to include relatively normal behavior like carelessness and impatience, and has often overstated the pills’ benefits. Advertising on television and in popular magazines like People and Good Housekeeping has cast common childhood forgetfulness and poor grades as grounds for medication that, among other benefits, can result in “schoolwork that matches his intelligence” and ease family tension.
A 2002 ad for Adderall showed a mother playing with her son and saying, “Thanks for taking out the garbage.”
The Food and Drug Administration has cited every major A.D.H.D. drug — stimulants like Adderall, Concerta, Focalin and Vyvanse, and nonstimulants like Intuniv and Strattera — for false and misleading advertising since 2000, some multiple times.
Sources of information that would seem neutral also delivered messages from the pharmaceutical industry. Doctors paid by drug companies have published research and delivered presentations that encourage physicians to make diagnoses more often that discredit growing concerns about overdiagnosis.
http://www.nytimes.com/2013/12/15/health/the-selling-of-attention-deficit-disorder.html?_r=0View this and related news items in the NY Times here
360613 Dec 2013 - NY Times - In Food Cravings, Sugar Trumps FatFood cravingsWhat makes a milkshake so irresistible? Is it the sweet flavor that our taste buds are after? Or the smooth and creamy texture? Or perhaps it is the copious blend of fat and sugar?13/12/2013
An intriguing new study suggests that what really draws people to such treats, and prompts them to eat much more than perhaps they know they should, is not the fat that they contain, but primarily the sugar.
The new research tracked brain activity in more than 100 high school students as they drank chocolate-flavored milkshakes that were identical in calories but either high in sugar and low in fat, or vice versa. While both kinds of shakes lit up pleasure centers in the brain, those that were high in sugar did so far more effectively, firing up a food-reward network that plays a role in compulsive eating.
To their surprise, the researchers found that sugar was so powerful a stimulus that it overshadowed fat, even when the two were combined in large amounts. High sugar shakes that were low in fat ramped up the reward circuitry just as strongly as the more decadent shakes that paired sugar and fat in large quantities, suggesting that fat was a runner-up to sugar, said Eric Stice, the lead author of the study, which was funded by the National Institutes of Health and published in The American Journal of Clinical Nutrition.
“We do a lot of work on the prevention of obesity, and what is really clear not only from this study but from the broader literature over all is that the more sugar you eat, the more you want to consume it,” said Dr. Stice, a senior research scientist at the Oregon Research Institute. “As far as the ability to engage brain reward regions and drive compulsive intake, sugar seems to be doing a much better job than fat.”
The new findings add to a growing number of brain studies that are providing a more complex understanding of what drives people to overeat in the first place.
Heavily processed foods loaded with fat and sugar activate and potentially alter the same reward regions in the brain that are hijacked by alcohol and drugs of abuse. Though the extent to which these foods can provoke addictive behavior remains controversial, the results may help explain why millions of people who diet and struggle to lose weight ultimately fail.
“The obesity epidemic and the problems with overeating don’t have too much to do with people overeating fruits and healthy foods. They have a lot to do with people overeating excess sugars and fats,” said Nicole Avena, a faculty member at the New York Obesity Research Center at Columbia University, who was not involved in the new study.
Dr. Avena said that people “can have all the willpower in the world. But if the brain reward system is being activated in a way that causes them to have a battle against their willpower, then it can be very difficult for them to control their intake.”
Public health officials often tell Americans to avoid fattening sodas, snacks and fast foods, but the relative roles of fat and sugar in influencing the brain and potentially behavior have remained uncertain.
Dr. Stice and his colleagues sought to learn more by recruiting 106 healthy teenagers — 47 male and 59 female — and asking them to sip different milkshakes as they lay in functional magnetic resonance imaging machines.
The milkshakes were all made with chocolate syrup and an ice cream base. But the fat content was manipulated in different conditions by using either half and half or 2 percent milk, and the sweetness was manipulated by varying the simple syrup content.
Low fat, low sugar milkshakes activated regions of the brain associated with taste and sensation, but they had no impact on reward regions.
Relatively high fat, low sugar milkshakes, however – with 9 grams of fat and 7 grams of sugar per 100 milliliters (less than half a cup) – did engage part of the reward circuitry. And a high sugar shake that had triple that amount of sugar but only a quarter of the fat had an even greater impact, lighting up such brain structures as the putamen, insula and rolandic operculum.
These brain regions, called the food-reward system, control our desire for food: the more active they are, the more we want to eat. The researchers found that increasing the fat content of a high sugar shake did not activate the reward region any further.
Dr. Stice said he was surprised because he expected fat would be a stronger stimulus than sugar. But he also noted that the human brain is hardwired to prefer sweet flavors.
“When we’re children, we prefer high sugar foods right away, but not high fat,” he said. “We develop preferences for fat, but we’re basically born with a preference for sugar.”
Dr. Stice said the bulk of brain research on fat and sugar was pointing to the idea that addressing societal problems with overeating should start with sugar.
“If you look at our American diet, most people are consuming considerably more sugar than fat,” he said. “We’ve really ramped up the sugar in our diets, but we’ve backed off on fat.”
In her own research, Dr. Avena has found that sugar and fat influence brain chemistry and behavior when consumed in large quantities. Animals given small amounts of each do not show many changes. But when they are given unlimited access to either, those that gorge on sugar in particular show changes in their opiate receptors — which help regulate pain, reward and euphoria — and when the sugar is suddenly taken away, they show signs of withdrawal.
Another researcher who has studied the impact of fat and sugar on the brain in people, Dr. David Ludwig, said it was not so much the “immediate hedonic response” to junk food that drives overconsumption, but its impact on the brain and the body over several hours.
Dr. Ludwig and his colleagues showed in brain imaging studies on adults that high sugar milkshakes stimulate reward regions but also cause spikes and drops in blood sugar levels. Four hours later, they showed, these blood sugar drops stimulate changes in brain activity that induce cravings — and those cravings are typically for foods that can quickly restore blood sugar levels, like desserts, starches and sweets.
“These foods themselves are not inherently addictive through their taste per se,” said Dr. Ludwig, the director of the New Balance Foundation Obesity Prevention Center at Boston Children’s Hospital. “It’s the effects that they have on our metabolism. If our blood sugar is stable, we can walk by a bakery and be much less tempted than if our blood sugar is crashing. Your brain knows these foods are going to rescue low blood sugar. But then this sets up the next cycle.”
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