1441Whiteley et al 2010 - The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disordersThe ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disordersGluten- and casein-free diets for autistic spectrum disorderWhiteley P, Haracopos D, Knivsberg AM, Reichelt KL, Parlar S, Jacobsen J, Seim A, Pedersen L, Schondel M, Shattock P.01/04/2010Nutr Neurosci. 13(2):87-100.
There is increasing interest in the use of gluten- and casein-free diets for children with autism spectrum disorders (ASDs). We report results from a two-stage, 24-month, randomised, controlled trial incorporating an adaptive 'catch-up' design and interim analysis.
Stage 1 of the trial saw 72 Danish children (aged 4 years to 10 years 11 months) assigned to diet (A) or non-diet (B) groups by stratified randomisation. Autism Diagnostic Observation Schedule (ADOS) and the Gilliam Autism Rating Scale (GARS) were used to assess core autism behaviours, Vineland Adaptive Behaviour Scales (VABS) to ascertain developmental level, and Attention-Deficit Hyperactivity Disorder - IV scale (ADHD-IV) to determine inattention and hyperactivity.
Participants were tested at baseline, 8, and 12 months. Based on per protocol repeated measures analysis, data for 26 diet children and 29 controls were available at 12 months. At this point, there was a significant improvement to mean diet group scores (time*treatment interaction) on sub-domains of ADOS, GARS and ADHD-IV measures.
Surpassing of predefined statistical thresholds as evidence of improvement in group A at 12 months sanctioned the re-assignment of group B participants to active dietary treatment. Stage 2 data for 18 group A and 17 group B participants were available at 24 months. Multiple scenario analysis based on inter- and intra-group comparisons showed some evidence of sustained clinical group improvements although possibly indicative of a plateau effect for intervention.
Our results suggest that dietary intervention may positively affect developmental outcome for some children diagnosed with ASD. In the absence of a placebo condition to the current investigation, we are, however, unable to disqualify potential effects derived from intervention outside of dietary changes.
Further studies are required to ascertain potential best- and non-responders to intervention. The study was registered with ClincialTrials.gov, number NCT00614198.
autism, gluten, casein, GF/CF diet, human study, dietary interventionhttp://www.ncbi.nlm.nih.gov/pubmed/20406576View this and related abstracts via PubMed here
1771Rajendran & Kumar 2010 - Role of diet in the management of inflammatory bowel diseaseRole of diet in the management of inflammatory bowel diseaseRole of diet in the management of inflammatory bowel diseaseRajendran N, Kumar D.28/03/2010World J Gastroenterol. 16(12):1442-8.
Many studies have looked at connections between diet, etiology, signs and symptoms associated with inflammatory bowel disease (IBD). Although these connections are apparent to clinicians, they are difficult to prove qualitatively or quantitatively.
Enteral feeding and polymeric diets are equally effective at bringing about remission in Crohn's disease (CD). Parenteral feeding is also effective, although none of these methods is as effective as corticosteroid therapy. However, enteral feeding is preferred in the pediatric population because linear growth is more adequately maintained via this route.
Exclusion diets in patients brought into remission using an elemental diet have been shown to maintain remission for longer periods. Studies that aim to isolate culpable food groups have shown that individuals react differently on exposure to or exclusion of various foods. The commonly identified food sensitivities are cereals, milk, eggs, vegetables and citrus fruits.
Studies that have looked at gut mucosal antigen behavior have shown higher rectal blood flow, in response to specific food antigens, in those with CD over healthy subjects. Exclusion of sugar shows little evidence of amelioration in CD. Omega 3 fatty acids show promise in the treatment of IBD but await larger randomized controlled trials.
Patients frequently notice that specific foods cause aggravation of their symptoms. Whilst it has been difficult to pinpoint specific foods, with advances in the laboratory tests and food supplements available, the aim is to prolong remission in these patients using dietary measures, and reduce the need for pharmacotherapy and surgical intervention.
Inflammatory Bowel Disease, IBD, Crohn's disease, ulcerative colitis, diet, dietary intervention, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20333783View this and related abstracts via PubMed here
1726Moltó-Puigmartí et al 2010 - FADS1 FADS2 gene variants modify the association between fish intake and the DHA proportions in human milkFADS1 FADS2 gene variants modify the association between fish intake and the docosahexaenoic acid proportions in human milkFADS1 FADS2 gene variants modify the association between fish intake and the docosahexaenoic acid proportions in human milkMoltó-Puigmartí C, Plat J, Mensink RP, Müller A, Jansen E, Zeegers MP, Thijs C.24/03/2010Am J Clin Nutr. 91(5):1368-76. Epub 2010 Mar 24.
BACKGROUND: The genes encoding Delta(5)- and Delta(6)-desaturases (FADS1 FADS2 gene cluster) were reported to be associated with n-3 (omega-3) and n-6 (omega-6) fatty acid proportions in human plasma, tissues, and milk. Docosahexaenoic acid (DHA) can be supplied especially by dietary fish or fish oil and synthesized from alpha-linolenic acid through a pathway involving these desaturases.
OBJECTIVE:We evaluated whether FADS gene variants modify the effect of maternal fish and fish-oil intake on plasma and milk DHA proportions.
DESIGN:FADS1 rs174561, FADS2 rs174575, and intergenic rs3834458 single nucleotide polymorphisms were genotyped in 309 women from the KOALA Birth Cohort Study in The Netherlands. Plasma was collected at 36 wk of pregnancy, and milk was collected at 1 mo postpartum. Fish and fish-oil intake was assessed by using a food-frequency questionnaire at 34 wk of pregnancy and updated for the week of milk collection. Gene-diet interactions were tested by linear regression analysis.
RESULTS:DHA proportions were lower in women homozygous for the minor allele than in women who were homozygous for the major allele (DHA proportions in plasma phospholipids: P < 0.01; DHA proportions in milk: P < 0.05). Fish intake ranged from 0 to 2.5 portions of fatty fish/wk, and 12 women took fish-oil supplements during pregnancy. DHA proportions in plasma phospholipids increased with increasing fish and fish-oil intake, irrespective of the genotype. DHA proportions in milk increased only with fish and fish-oil intake in the major-allele carriers.
CONCLUSION: Lower proportions of DHA in milk from women who were homozygous for the minor allele could not be compensated for by increasing fish and fish-oil intake, possibly because of limited incorporation into milk.
genetics, FADS genes, desaturase, EFA-HUFA conversion, dietary intake, fish, DHA, RBCFA, human study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/20335541View this and related abstracts via PubMed here
1436Benton 2010 - The influence of dietary status on the cognitive performance of childrenThe influence of dietary status on the cognitive performance of childrenThe influence of dietary status on the cognitive performance of childrenBenton D.17/03/2010Mol Nutr Food Res.Jan 13. [Epub ahead of print]
The rapid rate of growth of the brain during the last third of gestation and the early postnatal stage makes it vulnerable to an inadequate diet, although brain development continues into adulthood and micronutrient status can influence functioning beyond infancy. Certain dietary deficiencies during the first 2 years of life, for example iodine and iron, create problems that are not reversed by a later adequate diet. It is important that the intake of micronutrients varies greatly between individuals as they are essential for metabolism in general and in particular cell division and hence growth. In developing countries, there is consistent evidence that the adequacy of diet has lasting implications for cognitive development. In particular, attention has been directed to protein-calorie malnutrition and more specifically the intake of iron, iodine and vitamin A, a deficiency of which damages eyesight. In industrialized countries variations in diet are less influential, although a few well-designed studies have reported that multivitamin and mineral supplementations influence anti-social behaviour and intelligence. In the short term, there is increasing evidence that the missing of breakfast has negative consequences late in the morning. A working hypothesis is that meals of a low rather than high glycaemic load are beneficial.
diet, cognition, children, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20077417View this and related abstracts via PubMed here
1452Kamphuis & Scheltens 2010 - Can Nutrients Prevent or Delay Onset of Alzheimer's Disease?Can Nutrients Prevent or Delay Onset of Alzheimer's Disease?Can Nutrients Prevent or Delay Onset of Alzheimer's Disease?Kamphuis PJ, Scheltens P.17/03/2010J Alzheimers Dis. 2010 Feb 24. [Epub ahead of print]
Age-related changes in nutritional status can play an important role in brain functioning. Specific nutrient deficiencies in the elderly, including omega-3 fatty acids, B-vitamins, and antioxidants among others, may exacerbate pathological processes in the brain.
Consequently, the potential of nutritional intervention to prevent or delay cognitive impairment and the development of Alzheimer's disease (AD) is a topic of growing scientific interest. This review summarizes epidemiological studies linking specific nutritional deficiencies to mild cognitive impairment (MCI), as well as completed and ongoing nutritional studies in prevention of MCI and AD.
Processes that underlie AD pathogenesis include: membrane/synaptic degeneration, abnormal protein processing (amyloid-beta, tau), vascular risk factors (hypertension, hypercholesterolemia), inflammation, and oxidative stress. Consideration of mechanistic evidence to date suggests that several nutritional components can effectively counteract these processes, e.g., by promoting membrane formation and synaptogenesis, enhancing memory/behavior, improving endothelial function, and cerebrovascular health.
The literature reinforces the need for early intervention in AD and suggests that multi-nutritional intervention, targeting multiple aspects of the neurodegenerative process during the earliest possible phase in the development of the disease, is likely to have the greatest therapeutic potential.
diet, nutrients, Alzheimer's disease, ARCD, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20182021View this and related abstracts via PubMed here
1450Nones et al 2010 - Flavonoids and Astrocytes Crosstalking: Implications for Brain Development and PathologyFlavonoids and Astrocytes Crosstalking: Implications for Brain Development and Pathology Flavonoids and Astrocytes Crosstalking: Implications for Brain Development and PathologyNones J, Stipursky J, Costa SL, Gomes FC.17/03/2010Neurochem Res. Mar 9. [Epub ahead of print]
Flavonoids are naturally occurring polyphenolic compounds that are present in a variety of fruits, vegetables, cereals, tea, and wine, and are the most abundant antioxidants in the human diet. Evidence suggests that these phytochemicals might have an impact on brain pathology and aging; however, neither their mechanisms of action nor their cell targets are completely known.
In the mature mammalian brain, astroglia constitute nearly half of the total cells, providing structural, metabolic, and trophic support for neurons. During the past few years, increasing knowledge of these cells has indicated that astrocytes are pivotal characters in neurodegenerative diseases and brain injury.
Most of the physiological benefits of flavonoids are generally thought to be due to their antioxidant and free-radical scavenging effects; however, emerging evidence has supported the hypothesis that their mechanism of action might go beyond these properties. In this review, we focus on astrocytes as targets for flavonoids and their implications in brain development, neuroprotection, and glial tumor formation.
Finally, we will briefly discuss the emerging view of astrocytes as essential characters in neurodegenerative diseases, and how a better understanding of the action of flavonoids might open new avenues to develop therapeutic approaches to these pathologies.
diet, antioxidants, flavanoids, flavonoids, brain development, brain function, astrocytes, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20213345View this and related abstracts via PubMed here
1451Oster & Pillot 2010 - DHA and synaptic protection in Alzheimer's disease miceDocosahexaenoic acid and synaptic protection in Alzheimer's disease mice Docosahexaenoic acid and synaptic protection in Alzheimer's disease miceOster T, Pillot T.17/03/2010Biochim Biophys Acta. 2010 Mar 6. [Epub ahead of print]
Alzheimer's disease (AD) is a major public health concern due to longer life expectancy in the Western countries. Amyloid-beta (Abeta) oligomers are considered the proximate effectors in the early stages of AD. AD-related cognitive impairment, synaptic loss and neurodegeneration result from interactions of Abeta oligomers with the synaptic membrane and subsequent activation of pro-apoptotic signalling pathways. Therefore, membrane structure and lipid status appear determinant in Abeta-induced toxicity.
Numerous epidemiological studies have highlighted the beneficial influence of docosahexaenoic acid (DHA, C22:6 n-3) on the preservation of synaptic function and memory capacities in aged individuals or upon Abeta exposure, whereas its deficiency is presented as a risk factor for AD. An elevated number of studies have been reporting the beneficial effects of dietary DHA supplementation on cognition and synaptic integrity in various AD models.
1445Yaqoob & Shaikh 2010 - The nutritional and clinical significance of lipid rafts.The nutritional and clinical significance of lipid rafts. The nutritional and clinical significance of lipid rafts.
Yaqoob P, Shaikh SR.17/03/2010Curr Opin Clin Nutr Metab Care. 13(2)156-66.
PURPOSE OF REVIEW: Lipid rafts are potentially modifiable by diet, particularly (but not exclusively) by dietary fatty acids. This review examines the potential for dietary modification of raft structure and function in the immune system, brain and retinal tissue, the gut, and in cancer cells.
RECENT FINDINGS: In-vitro and ex-vivo studies suggest that dietary n-3 polyunsaturated fatty acids (PUFAs) may exert immunosuppressive and anticancer effects through changes in lipid raft organization. In addition, gangliosides and cholesterol may modulate lipid raft organization in a number of tissues, and recent work has highlighted sphingolipids in membrane microdomains as potential targets for inhibition of tumor growth. The roles of fatty acids and gangliosides, especially in relation to lipid rafts, in cognitive development, age-related cognitive decline, psychiatric disorders, and Alzheimer's disease are poorly understood and require further investigation. The roles of lipid rafts in cancer, in microbial pathogenesis, and in insulin resistance are starting to emerge, and indicate compelling evidence for the growing importance of membrane microdomains in health and disease.
SUMMARY: In-vitro and animal studies show that n-3 PUFAs, cholesterol, and gangliosides modulate the structure and composition of lipid rafts, potentially influencing a wide range of biological processes, including immune function, neuronal signaling, cancer cell growth, entry of pathogens through the gut barrier, and insulin resistance in metabolic disorders. The physiological, clinical, and nutritional relevance of these observations remains to be determined.
lipids, diet, nutrition, neuronal membrane structure, review http://www.ncbi.nlm.nih.gov/pubmed/20010096View this and related abstracts via PubMed here
1449Sullivan et al 2010 - High-Fat Diet during Pregnancy Causes Perturbations in the Serotonergic System and Increased Anxiety-Like Behavior in OffspringChronic Consumption of a High-Fat Diet during Pregnancy Causes Perturbations in the Serotonergic System and Increased Anxiety-Like Behavior in Nonhuman Primate Offspring. Chronic Consumption of a High-Fat Diet during Pregnancy Causes Perturbations in the Serotonergic System and Increased Anxiety-Like Behavior in Nonhuman Primate Offspring.Sullivan EL, Grayson B, Takahashi D, Robertson N, Maier A, Bethea CL, Smith MS, Coleman K, Grove KL.10/03/2010J Neurosci. 30(10)3826-30.
Childhood obesity is associated with increased risk of behavioral/psychological disorders including depression, anxiety, poor learning, and attention deficit disorder. As the majority of women of child-bearing age are overweight or obese and consume a diet high in dietary fat, it is critical to examine the consequences of maternal overnutrition on the development of brain circuitry that regulates offspring behavior.
Using a nonhuman primate model of diet-induced obesity, we found that maternal high-fat diet (HFD) consumption caused perturbations in the central serotonergic system of fetal offspring. In addition, female infants from HFD-fed mothers exhibited increased anxiety in response to threatening novel objects.
These findings have important clinical implications as they demonstrate that exposure to maternal HFD consumption during gestation, independent of obesity, increases the risk of developing behavioral disorders such as anxiety.
diet, dietary fat, maternal obesity, nutritional programming, behaviour, anxiety, depression, experimental study, animal study http://www.ncbi.nlm.nih.gov/pubmed/20220017View this and related abstracts via PubMed here
1899Collison et al 2010 - Dietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memoryDietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memoryDietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memoryCollison KS, Makhoul NJ, Inglis A, Al-Johi M, Zaidi MZ, Maqbool Z, Saleh SM, Bakheet R, Mondreal R, Al-Rabiah R, Shoukri M, Milgram NW, Al-Mohanna FA.01/03/2010Physiol Behav. 99(3):334-42. Epub 2009 Nov 27.
Recent evidence suggests that intake of excessive dietary fat, particularly saturated fat and trans-hydrogenated oils (trans-fatty acids: TFA) can impair learning and memory. Central obesity, which can be induced by neonatal injections of monosodium Glutamate (MSG), also impairs learning and memory.
To further clarify the effects of dietary fat and MSG, we treated C57BL/6J mice with either a TFA-enriched diet, dietary MSG, or a combination of both and examined serum lipid profile and spatial memory compared to mice fed standard chow. Spatial learning was assessed at 6, 16 and 32 weeks of age in a Morris Water Maze (MWM). The subjects were given four days of training to find a hidden platform and a fifth day of reversal learning, in which the platform was moved to a new location.
RESULTS: The TFA+MSG combination caused a central adiposity that was accompanied by impairment in locating the hidden platform in the MWM. Females in the TFA+MSG group showed a greater impairment compared to the other diet groups, and also showed elevated levels of fasting serum LDL-C and T-CHOL:HDL-C ratio, together with the lowest levels of HDL-C. Similarly, males in the TFA+MSG diet group were less successful than control mice at locating the hidden platform and had the highest level of abdominal adiposity and elevated levels of fasting serum LDL-C.
CONCLUSION: Dietary trans-fat combined with MSG increased central adiposity, promoted dyslipidemia and impaired spatial learning.
http://www.ncbi.nlm.nih.gov/pubmed/19945473View this and related abstracts via PubMed here
1404Duncan & Bazinet 2010 - Brain arachidonic acid uptake and turnover: implications for signaling and bipolar disorder.Brain arachidonic acid uptake and turnover: implications for signaling and bipolar disorder. Brain arachidonic acid uptake and turnover: implications for signaling and bipolar disorder.Duncan RE, Bazinet RP.01/03/2010Curr Opin Clin Nutr Metab Care. 2010 Mar;13(2):130-8.13(2)130-8.
PURPOSE OF REVIEW: Arachidonic acid was first detected in the brain in 1922. Although earlier work examined the role of arachidonic acid in growth and development, more recent advancements have elucidated roles for arachidonic acid in brain health and disease.
RECENT FINDINGS: In this review, we summarize evidence demonstrating that unesterified arachidonic acid in the plasma pool, which is supplied in part from adipose, is readily taken up and incorporated into brain phospholipids. By labeling plasma unesterified arachidonic acid, it is possible to trace the subsequent release of arachidonic acid from brain phospholipids upon neuroreceptor-mediated release by phospholipase A2 in response to drugs and neuroinflammation in rodents. With the synthesis of C labeled fatty acids, brain arachidonic acid signaling can now be measured in humans with position emission tomography. Arachidonic acid signals are known to regulate important biological functions, including neuroinflammation and excitotoxicity, and we focus on how the brain arachidonic acid cascade is a common target of drugs used to treat bipolar disorder (e.g. lithium, carbamazepine and valproate).
SUMMARY: A better understanding of the regulation of arachidonic acid uptake into the brain and the brain arachidonic acid cascade could lead to new imaging techniques and the identification of novel therapeutic targets in excitotoxicity, neuroinflammation and bipolar disorder.
fatty acids, omega-6, arachidonic acid, AA, metabolism, bipolar disorder, metabolism, pharmacology, inflammation, neurotransmitter function, cell signalling, review http://www.ncbi.nlm.nih.gov/pubmed/20145439?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3View this and related abstracts via PubMed here
1458Gracious et al 2010 - Randomized, placebo-controlled trial of flax oil in pediatric bipolar disorder.Randomized, placebo-controlled trial of flax oil in pediatric bipolar disorder. Randomized, placebo-controlled trial of flax oil in pediatric bipolar disorder.Gracious BL, Chirieac MC, Costescu S, Finucane TL, Youngstrom EA, Hibbeln JR.01/03/2010Bipolar Disord.12(2)142-54
OBJECTIVES: This clinical trial evaluated whether supplementation with flax oil, containing the omega-3 fatty acid alpha-linolenic acid (alpha-LNA), safely reduced symptom severity in youth with bipolar disorder.
METHODS: Children and adolescents aged 6-17 years with symptomatic bipolar I or bipolar II disorder (n = 51), manic, hypomanic, mixed, or depressed, were randomized to either flax oil capsules containing 550 mg alpha-LNA per 1 gram or an olive oil placebo adjunctively or as monotherapy. Doses were titrated to 12 capsules per day as tolerated over 16 weeks. Primary outcomes included changes in the Young Mania Rating Scale, Child Depression Rating Scale-Revised, and Clinical Global Impressions-Bipolar ratings using Kaplan-Meier survival analyses.
RESULTS: There were no significant differences in primary outcome measures when compared by treatment assignment. However, clinician-rated Global Symptom Severity was negatively correlated with final serum omega-3 fatty acid compositions: %alpha-LNA (r = -0.45, p < 0.007), % eicosapentaenoic acid (EPA) (r = -0.47, p < 0.005); and positively correlated with final arachidonic acid (AA) (r = 0.36, p < 0.05) and docosapentaenoic acid (DPA) n-6 (r = 0.48, p < 0.004). The mean duration of treatment for alpha-LNA was 11.8 weeks versus 8 weeks for placebo; however, the longer treatment duration for alpha-LNA was not significant after controlling for baseline variables. Subjects discontinued the study for continued depressive symptoms.
CONCLUSIONS: Studies of essential fatty acid supplementation are feasible and well tolerated in the pediatric population. Although flax oil may decrease severity of illness in children and adolescents with bipolar disorder who have meaningful increases in serum EPA percent levels and/or decreased AA and DPA n-6 levels, individual variations in conversion of alpha-LNA to EPA and docosahexaenoic acid as well as dosing burden favor the use of fish oil both for clinical trials and clinical practice. Additionally, future research should focus on adherence and analysis of outcome based on changes in essential fatty acid tissue compositions, as opposed to group randomization alone.
bipolar disorder, children, omega-3, flax oil, alpha-linolenic acid, treatment, RCThttp://www.ncbi.nlm.nih.gov/pubmed/20402707View this and related abstacts via PubMed here
1620Kulkarni & Dhir 2010 - An overview of curcumin in neurological disordersAn overview of curcumin in neurological disorders An overview of curcumin in neurological disorders Kulkarni SK, Dhir A.01/03/2010Indian J Pharm Sci. 72(2)149-54
Curcumin, the principal curcuminoid found in spice turmeric, has recently been studied for its active role in the treatment of various central nervous system disorders.
Curcumin demonstrates neuroprotective action in Alzheimer's disease, tardive dyskinesia, major depression, epilepsy, and other related neurodegenerative and neuropsychiatric disorders.
The mechanism of its neuroprotective action is not completely understood. However, it has been hypothesized to act majorly through its anti-inflammatory and antioxidant properties. Also, it is a potent inhibitor of reactive astrocyte expression and thus prevents cell death. Curcumin also modulates various neurotransmitter levels in the brain.
The present review attempts to discuss some of the potential protective role of curcumin in animal models of major depression, tardive dyskinesia and diabetic neuropathy. These studies call for well planned clinical studies on curcumin for its potential use in neurological disorders.
curcumin, turmeric, neurological disorders, psychiatric disorders, motor control, depression, dementia, Alzheimer's disease, inflammation, anti-inflammatory, anti-oxidant, neuroprotector, animal studies, human studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20838516View this and related abstracts via PubMed here
1453Sawada & Yokoi 2010 - Effect of zinc supplementation on mood states in young women: a pilot study.Effect of zinc supplementation on mood states in young women: a pilot study. Effect of zinc supplementation on mood states in young women: a pilot study.
Sawada T, Yokoi K.01/03/2010Eur J Clin Nutr. 64(3) 331-3. Epub 2010 Jan 20.
The relation of zinc (Zn) nutriture to brain development and function has been elucidated. The purpose of this study is to examine whether Zn supplementation improves mood states in young women.
The study used a double-blind, randomized and placebo-controlled procedure. The major outcomes were psychological measures, somatic symptoms and serum Zn. Thirty women were placed randomly and in equal numbers into two groups, and they ingested one capsule containing multivitamins (MVs) or MV and 7 mg Zn daily for 10 weeks. Women who took MV and Zn showed a significant reduction in anger-hostility score (P=0.009) and depression-dejection score (P=0.011) in the Profile of Moods State (POMS) and a significant increase in serum Zn concentration (P=0.008), whereas women who took only MV did not.
Our results suggest that Zn supplementation may be effective in reducing anger and depression.
zinc, mood, anger, depression, treatment trial, RCT, human study http://www.ncbi.nlm.nih.gov/pubmed/20087376View this and related abstracts via PubMed here
1593Zhuo & Praticò 2010 - Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient dietAcceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient dietAcceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet Zhuo JM, Praticò D.01/03/2010Exp Gerontol. 45(3)195-201. Epub 2009 Dec 11.
Epidemiological and clinical studies indicate that elevated circulating level of homocysteine (Hcy) is a risk factor for developing Alzheimer's disease (AD). Dietary deficiency of folate, vitamin B6 and B12 results in a significant increase of Hcy levels, a condition also known as hyperhomocysteinemia (HHcy). In the present study we tested the hypothesis that a diet deficient for these three important factors when administered to a mouse model of AD, i.e. Tg2576, will result in HHcy and in an acceleration of their amylodotic phenotype. Compared with Tg2576 mice on regular chow, the ones receiving the diet deficient for folate, B6 and B12 developed HHcy. This condition was associated with a significant increase in Abeta levels in the cortex and hippocampus, and an elevation of Abeta deposits in the same regions. No significant changes were observed for steady-state levels of total APP, BACE-1, ADAM-10, PS1 and nicastrin in the brains of mice with HHcy. No differences were observed for the main Abeta catabolic pathways, i.e. IDE and neprilysin proteins, or the Abeta chaperone apolipoprotein E. Our findings demonstrate that a dietary condition which leads to HHcy may also result in increased Abeta levels and deposition in a transgenic mouse model of AD-like amylodosis. They further support the concept that dietary factors can contribute to the development of AD neuropathology.
Alzheimer's disease, neuropathology, beta-amyloid, mouse model, diet, B vitamins, Vit_B, folate, B6, B12, homocysteine, animal studyhttp://www.ncbi.nlm.nih.gov/pubmed/20005283View this and related abstracts via PubMed here
1444Zhuo & Praticò 2010 - Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet.Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet. Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet.
Zhuo JM, Praticò D.01/03/2010Exp Gerontol. 45(3)195-201. Epub 2009 Dec 11.
Epidemiological and clinical studies indicate that elevated circulating level of homocysteine (Hcy) is a risk factor for developing Alzheimer's disease (AD). Dietary deficiency of folate, vitamin B6 and B12 results in a significant increase of Hcy levels, a condition also known as hyperhomocysteinemia (HHcy).
In the present study we tested the hypothesis that a diet deficient for these three important factors when administered to a mouse model of AD, i.e. Tg2576, will result in HHcy and in an acceleration of their amylodotic phenotype.
Compared with Tg2576 mice on regular chow, the ones receiving the diet deficient for folate, B6 and B12 developed HHcy. This condition was associated with a significant increase in Abeta levels in the cortex and hippocampus, and an elevation of Abeta deposits in the same regions. No significant changes were observed for steady-state levels of total APP, BACE-1, ADAM-10, PS1 and nicastrin in the brains of mice with HHcy. No differences were observed for the main Abeta catabolic pathways, i.e. IDE and neprilysin proteins, or the Abeta chaperone apolipoprotein E.
Our findings demonstrate that a dietary condition which leads to HHcy may also result in increased Abeta levels and deposition in a transgenic mouse model of AD-like amylodosis. They further support the concept that dietary factors can contribute to the development of AD neuropathology.
Copyright 2009 Elsevier Inc. All rights reserved.
diet, Vitamin B6, Vitamin B12, folate, Alzheimer's disease, animal studyhttp://www.ncbi.nlm.nih.gov/pubmed/20005283View this and related abstracts via PubMed here
1924Koetzko et al 2010 - Dietary intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in children - a workshop reportDietary intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in children - a workshop reportDietary intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in children - a workshop reportKoletzko B, Uauy R, Palou A, Kok F, Hornstra G, Eilander A, Moretti D, Osendarp S, Zock P, Innis S.26/02/2010Br J Nutr. 2010 103(6):923-8. Epub 2010 Feb 26.
There is controversy whether children should have a dietary supply of preformed long-chain polyunsaturated n-3 fatty acids EPA and DHA. The aims of the workshop were to review evidence for a possible benefit of a preformed EPA and/or DHA supply, of data required to set desirable intakes for children aged 2-12 years, and of research priorities.
The authors concluded that EPA and DHA intakes per kg body weight may often be low in 2- to 12-year-old children, relative to intakes per kg body weight of breast-fed infants and adult intakes, but reliable data are scarce.
Little information is available that increasing dietary intakes of EPA or DHA in children has benefits to physical or mental function or other health endpoints. Studies addressing EPA and DHA intakes and tissue status among groups of children with different dietary habits, and measures of relevant development and health endpoints, are needed for developing potential advice on desirable intakes of EPA and/or DHA in children.
At this time it appears prudent to advise that dietary intakes in childhood are consistent with future eating patterns supporting adult health, such as prevention of metabolic disorders and CVD, supporting immune function, and reproductive health.
In conclusion, the available information relating dietary EPA and DHA intakes in children aged 2-12 years to growth, development and health is insufficient to derive dietary intake recommendations for EPA and DHA. Adequately designed studies addressing dietary intakes, measures of status and relevant functional or health effects across this age group are needed.
fatty acids, omega-3, EFA, HUFA, EPA, DHA, dietary intakes, recommended daily intakes, RNI, EAR, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20187993View this and related abstracts via PubMed here
1799Kenny 2010 - Reward mechanisms in obesity: new insights and future directionsReward mechanisms in obesity: new insights and future directionsReward mechanisms in obesity: new insights and future directionsKenny PJ.24/02/2010Neuron. 69(4):664-79.
Food is consumed in order to maintain energy balance at homeostatic levels. In addition, palatable food is also consumed for its hedonic properties independent of energy status. Such reward-related consumption can result in caloric intake exceeding requirements and is considered a major culprit in the rapidly increasing rates of obesity in developed countries.
Compared with homeostatic mechanisms of feeding, much less is known about how hedonic systems in brain influence food intake. Intriguingly, excessive consumption of palatable food can trigger neuroadaptive responses in brain reward circuitries similar to drugs of abuse. Furthermore, similar genetic vulnerabilities in brain reward systems can increase predisposition to drug addiction and obesity.
Here, recent advances in our understanding of the brain circuitries that regulate hedonic aspects of feeding behavior will be reviewed. Also, emerging evidence suggesting that obesity and drug addiction may share common hedonic mechanisms will also be considered.
obesity, food addiction, substance use, neural mechanisms, review http://www.ncbi.nlm.nih.gov/pubmed/21338878View this and related abstracts via PubMed here
1448Ryan et al 2010 - Effects of long-chain polyunsaturated fatty acid supplementation on neurodevelopment in childhood: A review of human studies.Effects of long-chain polyunsaturated fatty acid supplementation on neurodevelopment in childhood: A review of human studies.Effects of long-chain polyunsaturated fatty acid supplementation on neurodevelopment in childhood: A review of human studies.
Ryan AS, Astwood JD, Gautier S, Kuratko CN, Nelson EB, Salem N Jr.24/02/2010Prostaglandins Leukot Essent Fatty Acids. Feb 24. [Epub ahead of print]
1430Zaalberg et al 2010 - Effects of nutritional supplements on aggression, rule-breaking, and psychopathology among young adult prisonersEffects of nutritional supplements on aggression, rule-breaking, and psychopathology among young adult prisonersDiet, antisocial behaviour, aggression, prisoners, nutrition, controlled trialZaalberg A, Nijman H, Bulten E, Stroosma L, van der Staak C24/02/2010Aggressive BehaviorVolume 36, Issue 2117 - 126Wiley InterScience
Objective: In an earlier study, improvement of dietary status with food supplements led to a reduction in antisocial behavior among prisoners. Based on these earlier findings, a study of the effects of food supplements on aggression, rule-breaking, and psychopathology was conducted among young Dutch prisoners.
Methods: Two hundred and twenty-one young adult prisoners (mean age=21.0, range 18-25 years) received nutritional supplements containing vitamins, minerals, and essential fatty acids or placebos, over a period of 1-3 months.
Results: As in the earlier (British) study, reported incidents were significantly reduced (P=.017, one-tailed) in the active condition (n=115), as compared with placebo (n=106). Other assessments, however, revealed no significant reductions in aggressiveness or psychiatric symptoms.
Conclusion: As the incidents reported concerned aggressive and rule-breaking behavior as observed by the prison staff, the results are considered to be promising. However, as no significant improvements were found in a number of other (self-reported) outcome measures, the results should be interpreted with caution.
Diet, antisocial behaviour, aggression, prisoners, nutrition, randomised controlled trial, RCT, dietary supplements, MVM, fatty acidshttp://www3.interscience.wiley.com/journal/123213582/abstractView this extract via Wiley Interscience here
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