1427McNamara et al 2010 - DHA supplementation increases prefrontal cortex activation during sustained attention in healthy boys: a placebo-controlled, dose-ranging, functional magnetic resonance imaging studyDocosahexaenoic acid supplementation increases prefrontal cortex activation during sustained attention in healthy boys: a placebo-controlled, dose-ranging, functional magnetic resonance imaging studyADHD and omega-3 Robert K McNamara, Jessica Able, Ronald Jandacek, Therese Rider, Patrick Tso, James C Eliassen, David Alfieri, Wade Weber, Kelly Jarvis, Melissa P DelBello, Stephen M Strakowski, and Caleb M Adler19/02/2010Am J Clin Nutr doi: 10.3945/ajcn.2009.28549
Background: Emerging evidence suggests that docosahexaenoic acid (DHA, 22:6n23), the principal omega-3 (n23) fatty acid in brain gray matter, positively regulates cortical metabolic function and cognitive development. However, the effects of DHA supplementation on functional cortical activity in human subjects are unknown. Objective: The objective was to determine the effects of DHA supplementation on functional cortical activity during sustained attention in human subjects. Design: Healthy boys aged 8–10 y (n = 33) were randomly assigned to receive placebo or 1 of 2 doses of DHA (400 or 1200 mg/d) for 8 wk. Relative changes in cortical activation patterns during sustained attention at baseline and endpoint were determined by functional magnetic resonance imaging. Results: At 8 wk, erythrocyte membrane DHA composition increased significantly from baseline in subjects who received lowdose (by 47%) or high-dose (by 70%) DHA but not in those who received placebo (211%). During sustained attention, both DHA dose groups had significantly greater changes from baseline in activation of the dorsolateral prefrontal cortex than did the placebo group, and the low-dose and high-dose DHA groups had greater decreases in the occipital cortex and cerebellar cortex, respectively. Relative to low-dose DHA, high-dose DHA resulted in greater decreases in activation of bilateral cerebellum. The erythrocyte DHA composition was positively correlated with dorsolateral prefrontal cortex activation and was inversely correlated with reaction time, at baseline and endpoint. Conclusion: Dietary DHA intake and associated elevations in erythrocyte DHA composition are associated with alterations in functional activity in cortical attention networks during sustained attention in healthy boys. This trial was registered at clinicaltrials.gov as NCT00662142. Am J Clin Nutr doi: 10.3945/ajcn.2009.28549.
http://www.ncbi.nlm.nih.gov/pubmed/20130094?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2View this and related abstracts at PUBMED here
1649Kirby et al 2010 - A double-blind, placebo-controlled study investigating the effects of omega-3 supplementation in children aged 8-10 years from a mainstream school populationA double-blind, placebo-controlled study investigating the effects of omega-3 supplementation in children aged 8-10 years from a mainstream school population A double-blind, placebo-controlled study investigating the effects of omega-3 supplementation in children aged 8-10 years from a mainstream school population Kirby A, Woodward A, Jackson S, Wang Y, Crawford MA.18/02/2010Res Dev Disabil. 31(3):718-30. Epub 2010 Feb 18.
Despite the increased interest in the effects of omega-3 supplementation on children's learning and behaviour, there are a lack of controlled studies of this kind that have utilised a typically developing population.
This study investigated the effects of omega-3 supplementation in 450 children aged 8-10 years old from a mainstream school population, using a randomised, double-blind, placebo-controlled design. Participants were supplemented with either active supplements (containing docosahexaenoic acid, DHA and eicosapentaenoic acid, EPA) or a placebo for 16 weeks. Cheek cell fatty acid levels were recorded pre- and post-supplementation and a range of cognitive tests and parent and teacher questionnaires were used as outcome measures.
After supplementation, changes in the relationship between omega-6 and omega-3 were significant in the active group. Despite the wide range of cognitive and behavioural outcome measures employed, only three significant differences between groups were found after 16 weeks, one of which was in favour of the placebo condition. Exploring the associations between changes in fatty acid levels and changes in test and questionnaire scores also produced equivocal results. These findings are discussed in relation to previous findings with clinical populations and future implications for research.
fatty acids, omega-3, dietary supplementation, RCT, childrenhttp://www.ncbi.nlm.nih.gov/pubmed/20171055View this and related abstracts via PubMed here
1595D'Asti et al 2010 - Maternal dietary fat determines metabolic profile and endocannabinoid inhibition of the stress response in neonatal rat offspringMaternal dietary fat determines metabolic profile and the magnitude of endocannabinoid inhibition of the stress response in neonatal rat offspring Maternal dietary fat determines metabolic profile and the magnitude of endocannabinoid inhibition of the stress response in neonatal rat offspring D'Asti E, Long H, Tremblay-Mercier J, Grajzer M, Cunnane SC, Di Marzo V, Walker CD.16/02/2010Endocrinology. 151(4)1685-94. Epub 2010 Feb 16
Endocannabinoids (eCBs) are products of phospholipid (PL)-derived arachidonic acid (AA) that regulate hypothalamus-pituitary-adrenal axis activity. We hypothesized that differences in the quality and quantity of maternal dietary fat would modulate the PL AA content in the neonatal brain affecting stress responsiveness via differences in eCB production and activity in stress-activated brain areas.
Pregnant rats were fed a 5% (control (C)) or 30% fat (high fat (HF)) diet rich in either n-6 (HF-n-6) or n-3 (HF-n-3) fat during the last week of gestation and lactation. Postnatal d 10 offspring were tested for metabolic hormones, AA (n-6) and eCB brain content, and hormonal effects of eCB receptor antagonism (AM251, 1 or 3 mg/kg ip) on stress responses.
Like maternal diet, milk from HF-n-3 mothers had a reduced n-6/n-3 fat ratio compared with that of C and HF-n-6 mothers. Hypothalamic and hippocampal levels of PL AA were diet specific, reflecting the maternal milk and dietary n-6/n-3 ratio, with HF-n-3 offspring displaying reduced AA content relative to C and HF-n-6 offspring. Plasma corticosterone and insulin were elevated in HF-fed pups, whereas leptin was increased only in HF-n-6 pups. Basal eCB concentrations were also diet and brain region specific. In C pups, eCB receptor antagonist pretreatment increased stress-induced ACTH secretion, but not in the HF groups. Stress-induced corticosterone secretion was not sensitive to AM251 treatment in HF-n-3 pups. Thus, the nature of preweaning dietary fat differentially influences neonatal metabolic hormones, brain PL AA levels, and eCB, with functional consequences on hypothalamus-pituitary-adrenal axis modulation in developing rat pups.
endocannabinoid, fatty acid, diet, maternal diet, pregnancy, omega-3, omega-6, high-fat diet, stress, anxiety, animal study http://www.ncbi.nlm.nih.gov/pubmed/20160134View this and related abstracts via PubMed here
1400Suphioglu et al 2010 - The omega-3 DHA decreases neuronal cell death in association with altered zinc transport The omega-3 fatty acid, DHA, decreases neuronal cell death in association with altered zinc transport The omega-3 fatty acid, DHA, decreases neuronal cell death in association with altered zinc transport Suphioglu C, De Mel D, Kumar L, Sadli N, Freestone D, Michalczyk A, Sinclair A, Ackland ML.05/02/2010FEBS Lett. 584(3)612-8. Epub 2009 Dec 17.
Docosahexaenoic acid (DHA) is the major polyunsaturated fatty acid in neuronal cell membranes. We hypothesize that DHA induces a decrease in neuronal cell death through reduced ZnT3 expression and zinc uptake. Exposure of M17 cells to DHA-deficient medium increased the levels of active caspase-3, relative to levels in DHA-replete cells, confirming the adverse effects of DHA deficiency in promoting neuronal cell death. In DHA-treated M17 cells, zinc uptake was 65% less and ZnT3 mRNA and protein levels were reduced in comparison with DHA-depleted cells. We propose that the neuroprotective function of DHA is exerted through a reduction in cellular zinc levels that in turn inhibits apoptosis.
omega-3, DHA, zinc, brain, neurodegenerative disorders, alzheimer's disease, apoptosis, neuroprotectins http://www.ncbi.nlm.nih.gov/pubmed/20006607?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4View this and related abstracts via PubMed here
1433Bilbo & Tsang 2010 - Enduring consequences of maternal obesity for brain inflammation and behavior of offspring.Enduring consequences of maternal obesity for brain inflammation and behavior of offspring. Enduring consequences of maternal obesity for brain inflammation and behavior of offspring.Bilbo SD, Tsang V.02/02/2010FASEB J. 242104-2115. Epub Feb 2
Obesity is well characterized as a systemic inflammatory condition, and is also associated with cognitive disruption, suggesting a link between the two. We assessed whether peripheral inflammation in maternal obesity may be transferred to the offspring brain, in particular, the hippocampus, and thereby result in cognitive dysfunction. Rat dams were fed a high-saturated-fat diet (SFD), a high-trans-fat diet (TFD), or a low-fat diet (LFD) for 4 wk prior to mating, and remained on the diet throughout pregnancy and lactation.
SFD/TFD exposure significantly increased body weight in both dams and pups compared to controls. Microglial activation markers were increased in the hippocampus of SFD/TFD pups at birth. At weaning and in adulthood, proinflammatory cytokine expression was strikingly increased in the periphery and hippocampus following a bacterial challenge (lipopolysaccharide (LPS)) in the SFD/TFD groups compared to controls. Microglial activation within the hippocampus was also increased basally in SFD rats, suggesting a chronic priming of the cells. Finally, there were marked changes in anxiety and spatial learning in SFD/TFD groups.
These effects were all observed in adulthood, even after the pups were placed on standard chow at weaning, suggesting these outcomes were programmed early in life.
dietary fat, obesity, pregnancy, nutritional programming, inflammation, behaviour, experimental study, biochemical study, animal studyhttp://www.ncbi.nlm.nih.gov/pubmed/20124437View this and related abstracts via PubMed here
1401Amminger et al 2010 - Long-chain omega-3 for prevention of psychosis: RCTLong-chain omega-3 fatty acids for indicated prevention of psychotic disorders: a randomized, placebo-controlled trial. Long-chain omega-3 fatty acids for indicated prevention of psychotic disorders: a randomized, placebo-controlled trial.Amminger GP, Schäfer MR, Papageorgiou K, Klier CM, Cotton SM, Harrigan SM, Mackinnon A, McGorry PD, Berger GE.01/02/2010Arch Gen Psychiat67(2)146-54
CONTEXT: The use of antipsychotic medication for the prevention of psychotic disorders is controversial. Long-chain omega-3 (omega-3) polyunsaturated fatty acids (PUFAs) may be beneficial in a range of psychiatric conditions, including schizophrenia. Given that omega-3 PUFAs are generally beneficial to health and without clinically relevant adverse effects, their preventive use in psychosis merits investigation.
OBJECTIVE: To determine whether omega-3 PUFAs reduce the rate of progression to first-episode psychotic disorder in adolescents and young adults aged 13 to 25 years with subthreshold psychosis. DESIGN: Randomized, double-blind, placebo-controlled trial conducted between 2004 and 2007.
SETTING: Psychosis detection unit of a large public hospital in Vienna, Austria.
PARTICIPANTS: Eighty-one individuals at ultra-high risk of psychotic disorder.
INTERVENTIONS: A 12-week intervention period of 1.2-g/d omega-3 PUFA or placebo was followed by a 40-week monitoring period; the total study period was 12 months.
MAIN OUTCOME MEASURES: The primary outcome measure was transition to psychotic disorder. Secondary outcomes included symptomatic and functional changes. The ratio of omega-6 to omega-3 fatty acids in erythrocytes was used to index pretreatment vs posttreatment fatty acid composition.
RESULTS: Seventy-six of 81 participants (93.8%) completed the intervention. By study's end (12 months), 2 of 41 individuals (4.9%) in the omega-3 group and 11 of 40 (27.5%) in the placebo group had transitioned to psychotic disorder (P = .007). The difference between the groups in the cumulative risk of progression to full-threshold psychosis was 22.6% (95% confidence interval, 4.8-40.4). omega-3 Polyunsaturated fatty acids also significantly reduced positive symptoms (P = .01), negative symptoms (P = .02), and general symptoms (P = .01) and improved functioning (P = .002) compared with placebo. The incidence of adverse effects did not differ between the treatment groups.
CONCLUSIONS: Long-chain omega-3 PUFAs reduce the risk of progression to psychotic disorder and may offer a safe and efficacious strategy for indicated prevention in young people with subthreshold psychotic states.
omega-3, LC-PUFA, EPA, DHA, RCT, psychosis, treatment, prevention, psychosis-proneness, schizotypy, human study, clinical trial, free full texthttp://www.ncbi.nlm.nih.gov/pubmed/20124114?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1View this and related abstracts via PubMed here. Free full text of this article is available online.
1405Borja-Hart & Marino 2010 - Role of omega-3 Fatty acids for prevention or treatment of perinatal depressionRole of omega-3 Fatty acids for prevention or treatment of perinatal depression Role of omega-3 Fatty acids for prevention or treatment of perinatal depressionBorja-Hart NL, Marino J.01/02/2010Pharmacotherapy30(2)210-6
Perinatal depression is a complex mental health disorder that can manifest during pregnancy or after childbirth. Women with perinatal depression may not receive proper medical treatment because of concerns over teratogenic effects related to drug therapy. Evidence suggests that low levels of omega-3 fatty acids are correlated with depressive symptoms during pregnancy and after delivery. Omega-3 fatty acids may produce antidepressant effects due to their role in serotonin functioning.
A literature search identified seven clinical trials of omega-3 fatty acids for the prevention or treatment of perinatal depression. Depression rating scale scores used in the studies improved, but results were statistically significant in only three trials. Four studies were randomized and placebo controlled, and three were open label. One study evaluating the prevention of postpartum depression in women with a history of depression was discontinued early due to relapse of depressive symptoms.
In the trials we evaluated, the most common adverse effects were foul breath and/or unpleasant taste, and gastrointestinal complaints; no serious adverse events were reported. The seven studies were limited by small sample sizes and variable dosing and study durations. In the studies that demonstrated statistical significance, improvement in depression rating scale scores for omega-3 fatty acids was comparable to placebo. Overall, results have been inconclusive, but further investigation of omega-3 fatty acids is warranted because they did improve depression scores and appeared to be safe during pregnancy.
depression, pregnancy, perinatal, fatty acids, omega-3, treatment, RCTs, open trials, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20099994?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2View this and related abstracts via PubMed here
1625Craddock & Owen 2010 - The Kraepelinian dichotomy - going, going... but still not gone.The Kraepelinian dichotomy - going, going... but still not gone.The Kraepelinian dichotomy - going, going... but still not gone.
Craddock N, Owen MJ.01/02/2010Br J Psychiatry. 196(2):92-5.
Recent genetic studies reinforce the view that current approaches to the diagnosis and classification of major psychiatric illness are inadequate. These findings challenge the distinction between schizophrenia and bipolar disorder, and suggest that more attention should be given to the relationship between the functional psychoses and neurodevelopmental disorders such as autism. We are entering a transitional period of several years during which psychiatry will need to move from using traditional descriptive diagnoses to clinical entities (categories and/or dimensions) that relate more closely to the underlying workings of the brain.
schizophrenia, bipolar disorder, diagnosis, psychiatry, aetiology, biology, genetics, review http://www.ncbi.nlm.nih.gov/pubmed/20118450View this and related abstracts via PubMed here. Free full text of this paper is available online.
1727Lattka et al 2010 - Genetic variants of the FADS1 FADS2 gene cluster as related to essential fatty acid metabolismGenetic variants of the FADS1 FADS2 gene cluster as related to essential fatty acid metabolismGenetic variants of the FADS1 FADS2 gene cluster as related to essential fatty acid metabolismLattka E, Illig T, Koletzko B, Heinrich J.01/02/2010Curr Opin Lipidol.21(1):64-9.
PURPOSE OF REVIEW:The delta-5 and delta-6 desaturases have long been known to be important enzymes in the endogenous formation of long-chain polyunsaturated fatty acids (LC-PUFAs). Cloning of the coding sequences and chromosomal localization of the desaturase encoding genes fatty acid desaturase 1 and 2 (FADS1 and FADS2) opened the way for analyses of genetic factors as regulators of desaturase activity and LC-PUFA homeostasis. The present review summarizes the recent association studies on FADS genotypes and LC-PUFA levels and suggests ideas how FADS genotypes can be integrated in future research.
RECENT FINDINGS:An initial candidate gene study reported highly significant associations between FADS gene cluster polymorphisms and fatty acid levels in serum phospholipids with an extraordinary high genetically explained variance for arachidonic acid levels of 28.5%. Carriers of the minor alleles had enhanced levels of desaturase substrates and decreased levels of desaturase products, suggesting a decline in desaturase expression or activity because of the polymorphisms. These results were replicated in several association studies additionally showing an effect in different human tissues as well as in a recent genome-wide association study on LC-PUFA levels.
SUMMARY:The validated strong association between FADS genotypes and fatty acid levels in diverse human tissues shows that FADS gene cluster polymorphisms are, in addition to nutritional regulation of fatty acid synthesis, a very important regulator of LC-PUFA synthesis.
genetics, FADS genes, fatty acids, EFA-HUFA conversion, LC-PUFA, RBCFA, human studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/19809313View this and related abstracts via PubMed here
1583Makrides et al 2010 - Role of LC-PUFA in neurodevelopment and growthRole of long-chain polyunsaturated fatty acids in neurodevelopment and growthRole of long-chain polyunsaturated fatty acids in neurodevelopment and growth Makrides M, Smithers LG, Gibson RA.01/02/2010Nestle Nutr Workshop Ser Pediatr Program. 65123-33; discussion 133-6. Epub 2010 Feb 1.
There has been intense interest in the role of the n-3 long-chain polyunsaturated fatty acid (LCPUFA) docosahexaenoic acid (DHA, 22:6n-3), in growth and development of infants.
In 2009, there are at least twelve published randomized controlled trials (RCT) assessing the effects of LCPUFA supplementation of infant formula for preterm infants and seventeen RCTs involving formula-fed term infants. In addition, at least five RCTs have investigated the effect of DHA supplementation during pregnancy and/or lactation on infant and early child development.
Collectively, the published literature has demonstrated no harm of dietary LCPUFA for infants regardless of whether they are born preterm or at term. However, developmental benefit is more consistently observed in infants born preterm. This may be explained by the fact that DHA accretion to neural tissues peaks during the fetal brain growth spurt in the last trimester of pregnancy. Infants born preterm are denied the full gestation period to accumulate DHA and are at risk of incomplete DHA accumulation. New research is focused on the timing and dose of DHA supplementation needed to optimize developmental outcomes.
LC-PUFA, omega-3, omega-6, DHA, AA, pregnancy, lactation, child development, brain development, prematurity, infant feeding, RCTs, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20139678View this and related abstracts via PubMed here
1758Melse-Boonstra & Jaiswal 2010 - Iodine deficiency in pregnancy, infancy and childhood and its consequences for brain developmentIodine deficiency in pregnancy, infancy and childhood and its consequences for brain developmentIodine deficiency in pregnancy, infancy and childhood and its consequences for brain developmentMelse-Boonstra A, Jaiswal N.01/02/2010Best Pract Res Clin Endocrinol Metab. 24(1):29-38.
Iodine deficiency during foetal development and early childhood is associated with cognitive impairment.
Randomised clinical studies in school-aged children encountered in the literature indicate that cognitive performance can be improved by iodine supplementation, but most studies suffer from methodological constraints. Tests to assess cognitive performance in the domains that are potentially affected by iodine deficiency need to be refined.
Maternal iodine supplementation in areas of mild-to-moderate iodine deficiency may improve cognitive performance of the offspring, but randomised controlled studies with long-term outcomes are lacking. Studies in infants or young children have not been conducted.
The best indicators for iodine deficiency in children are thyroid-stimulating hormone (TSH) in newborns and thyroglobulin (Tg) in older children. Urinary iodine may also be useful but only at the population level. Adequate salt iodisation will cover the requirements of infants and children as well as pregnant women. However, close monitoring remains essential.
iodine, thyroid, hpothyroxinemia, pregnancy, child development, cognition, human studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20172468View this and related abstracts via PubMed here
1604Rodriguez 2010 - Maternal pre-pregnancy obesity and risk for inattention and negative emotionality in childrenMaternal pre-pregnancy obesity and risk for inattention and negative emotionality in childrenMaternal pre-pregnancy obesity and risk for inattention and negative emotionality in children Rodriguez A.01/02/2010J Child Psychol Psychiatry. 51(2)134-43. Epub 2009 Aug 6.
OBJECTIVE:This study aimed to replicate and extend previous work showing an association between maternal pre-pregnancy adiposity and risk for attention deficit hyperactivity disorder (ADHD) symptoms in children.
METHODS: A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714). Mothers and kindergarten teachers rated children's ADHD symptoms, presence and duration of problems, and emotionality. Dichotomized outcomes examined difficulties of clinical relevance (top 15% of the distribution). Analyses adjusted for pregnancy (maternal smoking, depressive symptoms, life events, education, age, family structure), birth outcomes (birth weight, gestational age, infant sex) and concurrent variables (family structure, maternal depressive symptoms, parental ADHD symptoms, and child overweight) in an attempt to rule out confounding.
RESULTS: Maternal pre-pregnancy overweight and obesity predicted high inattention symptom scores and obesity was associated with a two-fold increase in risk of difficulties with emotion intensity and emotion regulation according to teacher reports. Means of maternal ratings were unrelated to pre-pregnancy body mass index (BMI). Presence and duration of problems were associated with both maternal over and underweight according to teachers.
CONCLUSIONS: Despite discrepancies between maternal and teacher reports, these results provide further evidence that maternal pre-pregnancy overweight and obesity are associated with child inattention symptoms and extend previous work by establishing a link between obesity and emotional difficulties. Maternal adiposity at the time of conception may be instrumental in programming child mental health, as prenatal brain development depends on maternal energy supply. Possible mechanisms include disturbed maternal metabolic function. If maternal pre-pregnancy obesity is a causal risk factor, the potential for prevention is great.
obesity, pregnancy, ADHD, mood disorders, epidemiologyhttp://www.ncbi.nlm.nih.gov/pubmed/19674195View this and related abstracts via PubMed here
1607Kale et al 2010 - Reduced folic acid, vitamin B12 and DHA and increased homocysteine and cortisol in never-medicated schizophrenia patientsReduced folic acid, vitamin B12 and docosahexaenoic acid and increased homocysteine and cortisol in never-medicated schizophrenia patients: implications for altered one-carbon metabolism Reduced folic acid, vitamin B12 and docosahexaenoic acid and increased homocysteine and cortisol in never-medicated schizophrenia patients: implications for altered one-carbon metabolismKale A, Naphade N, Sapkale S, Kamaraju M, Pillai A, Joshi S, Mahadik S.30/01/2010Psychiatry Res. 175(1-2)47-53. Epub 2009 Dec 6.
Abnormal one-carbon metabolism has long been suggested as one of the mechanisms for neuropathology and psychopathology of schizophrenia. Variable levels of components of one-carbon metabolism (folic acid and vitamin B12) and consequent altered levels of homocysteine and phospholipid docosahexaenoic acid (DHA) have been independently reported, mostly in medicated patients. This study examined the simultaneous levels of these key components of one-carbon metabolism and its consequences in unique, medication-naïve first-episode psychotic patients (FEP, n=31) and healthy controls (HC, n=48) matched for confounds such as race, diet and lifestyle to reduce the variability. Significantly lower levels of folate and vitamin B12 in plasma and folate in red blood cells were observed in FEP compared to HC. These reductions paralleled the significant increase in plasma homocysteine and cortisol levels. Significantly reduced levels of membrane DHA were also observed in FEP compared to HC. This study, using a unique cohort, provided a broader mechanism (disturbed folic acid-vitamin B12-DHA balance) of altered one-carbon metabolism and one of its key consequential components, an increased homocysteine level that together with cortisol, can contribute to the neuropathology of psychosis. These data may have important implications for the amelioration of psychopathology in schizophrenia.
schizophrenia, first-episode schizophrenia, one-carbon metabolism, homocysteine, Vitamin B, Vit_B, folate, B6, B12, fatty acids, omega-3, DHA, human study, biochemical study, case-control study http://www.ncbi.nlm.nih.gov/pubmed/19969375View this and related abstracts via PubMed here
1435Xu et al 2010 - Lactational zinc deficiency-induced hippocampal neuronal apoptosis by a BDNF-independent TrkB signaling pathway.Lactational zinc deficiency-induced hippocampal neuronal apoptosis by a BDNF-independent TrkB signaling pathway.Lactational zinc deficiency-induced hippocampal neuronal apoptosis by a BDNF-independent TrkB signaling pathway.
Xu H, Gao HL, Zheng W, Xin N, Chi ZH, Bai SL, Wang ZY.25/01/2010HippocampusJan 25. [Epub ahead of print]
It is well-known that zinc deficiency leads to neuronal death in the brain. Here we tested the hypothesis that changes in the TrkB signaling pathway are involved in hippocampal neuronal apoptosis of suckling offspring with maternal zinc deficiency.
Postpartum mice were fed a zinc-deficient (0.85 ppm) diet and their offspring were used as a lactational zinc deficiency mouse model. At P7, P14, and P21, changes in hippocampal neuronal apoptosis were assessed by Nissl and TUNEL staining. BDNF levels and TrkB neurotrophic signaling were examined using immunoblotting assay.
Lactational zinc deficiency resulted in lower levels of p-TrkB and p-ERK, and higher levels of Bax/Bcl-2 and caspase-3 in the hippocampus, suggesting that zinc deficiency-induced low levels of TrkB phosphorylation would abrogate the downstream ERK signaling pathway, leading to hippocampal neuronal apoptosis. Most interestingly, our data showed that the activity of Src, a key molecule for zinc-induced TrkB activation through the BDNF-independent pathway, was inhibited significantly, and the expression levels of BDNF were significantly increased in the hippocampus of suckling mice.
The present data indicate that zinc depletion-induced hippocampal neuronal apoptosis is likely through modulation of the TrkB neurotrophic signaling pathway by a BDNF-independent and Src-dependent mechanism, whereas higher expression of BDNF is considered as a protective response, which cannot fully compensate for the injury caused by maternal zinc deficiency. (c) 2010 Wiley-Liss, Inc.
diet, zinc deficiency, pregancy, lactation, neuronal cell death, hippocampus, apoptosis, animal studyhttp://www.ncbi.nlm.nih.gov/pubmed/20101602View this and related abstracts via PubMed here
1735Sørensen et al 2010 - Association Between Prepartum Maternal Iron Deficiency and Offspring Risk of Schizophrenia: Population-Based Cohort Study With Linkage of Danish National RegistersAssociation Between Prepartum Maternal Iron Deficiency and Offspring Risk of Schizophrenia: Population-Based Cohort Study With Linkage of Danish National RegistersAssociation Between Prepartum Maternal Iron Deficiency and Offspring Risk of Schizophrenia: Population-Based Cohort Study With Linkage of Danish National RegistersSørensen HJ, Nielsen PR, Pedersen CB, Mortensen PB.21/01/2010Schizophr Bull. Jan 21. [Epub ahead of print]
Recent findings suggest that maternal iron deficiency may increase the risk of schizophrenia-spectrum disorder in offspring. We initiated this study to determine whether maternal prepartum anemia influences offspring risk of schizophrenia.
We conducted a population-based study with individual record linkage of the Danish Civil Registration System, the Danish Psychiatric Central Register, and the Danish National Hospital Register. In a cohort of 1 115 752 Danish singleton births from 1978 to 1998, cohort members were considered as having a maternal history of anemia if the mother had received a diagnosis of anemia at any time during the pregnancy. Cohort members were followed from their 10th birthday until onset of schizophrenia, death, or December 31, 2008, whichever came first.
Adjusted for relevant confounders, cohort members whose mothers had received a diagnosis of anemia during pregnancy had a 1.60-fold (95% confidence interval = 1.16-2.15) increased risk of schizophrenia. Although the underlying mechanisms are unknown and independent replication is needed, our findings suggest that maternal iron deficiency increases offspring risk of schizophrenia.
schizophrenia, risk factors, pregnancy, iron, maternal iron deficiency, anaemia, human study, observational study, birth cohort studyhttp://www.ncbi.nlm.nih.gov/pubmed/20093425View this and related abstracts via PubMed here
588Welsh et al 2010 - Caffeine for asthma.Caffeine for asthma.Caffeine for asthma.Welsh EJ, Bara A, Barley E, Cates CJ.20/01/2010Cochrane Database Syst Rev.Jan 20;(1):CD001112.
This systematic review is an update of: Bara & Barley 2001. Caffeine for asthma. Cochrane Database Syst Rev. 2001;(4):CD001112.
BACKGROUND:Caffeine has a variety of pharmacological effects; it is a weak bronchodilator and it also reduces respiratory muscle fatigue. It is chemically related to the drug theophylline which is used to treat asthma. It has been suggested that caffeine may reduce asthma symptoms and interest has been expressed in its potential role as an asthma treatment. A number of studies have explored the effects of caffeine in asthma, this is the first review to systematically examine and summarise the evidence.
OBJECTIVES:To assess the effects of caffeine on lung function and identify whether there is a need to control for caffeine consumption prior to either lung function or exhaled nitric oxide testing.
SEARCH STRATEGY:We searched the Cochrane Airways Group trials register and the reference lists of articles (August 2009). We also contacted study authors.
SELECTION CRITERIA:Randomised clinical trials of oral caffeine compared to placebo or coffee compared to decaffeinated coffee in adults with asthma.
DATA COLLECTION AND ANALYSIS: Trial selection, quality assessment and data extraction were done independently by two reviewers.
MAIN RESULTS: Seven trials involving a total of 75 people with mild to moderate asthma were included. The studies were all of cross-over design .Six trials involving 55 people showed that in comparison with placebo, caffeine, even at a 'low dose' (< 5mg/kg body weight), appears to improve lung function for up to two hours after consumption. Forced expiratory volume in one minute showed a small improvement up to two hours after caffeine ingestion (SMD 0.72; 95% CI 0.25 to 1.20), which translates into a 5% mean difference in FEV1. However in two studies the mean differences in FEV1 were 12% and 18% after caffeine. Mid-expiratory flow rates also showed a small improvement with caffeine and this was sustained up to four hours.One trial involving 20 people examined the effect of drinking coffee versus a decaffeinated variety on the exhaled nitric oxide levels in patients with asthma and concluded that there was no significant effect on this outcome.
AUTHORS' CONCLUSIONS: Caffeine appears to improve airways function modestly, for up to four hours, in people with asthma . People may need to avoid caffeine for at least four hours prior to lung function testing, as caffeine ingestion could cause misinterpretation of the results. Drinking caffeinated coffee before taking exhaled nitric oxide measurements does not appear to affect the results of the test, but more studies are needed to confirm this.
asthma, caffeine, theophylline, treatment, RCT, human studies, systematic reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20091514View this and related abstracts via PubMed here.
1408Fernandes de Abreu et al 2010 - Developmental vitamin D deficiency alters learningDevelopmental vitamin D deficiency alters learning in C57Bl/6J mice Developmental vitamin D deficiency alters learning in C57Bl/6J miceFernandes de Abreu DA, Nivet E, Baril N, Khrestchatisky M, Roman F, Féron F15/01/2010Behav Brain Res. 2010 Jan 15. [Epub ahead of print]
Epidemiological studies have highlighted a season of birth effect in multiple sclerosis and schizophrenia. As a result, low prenatal vitamin D has been proposed as a candidate risk factor for these brain diseases, with cognitive impairments.
In order to further investigate the long-term consequences of a transient gestational hypovitaminosis D, we used a mouse developmental vitamin D (DVD) deficiency model. Female C57Bl/6J mice were fed a vitamin D-free diet for 6 weeks prior to conception and during gestation. At birth, dams and their offspring were fed a normal vitamin D-containing diet. The adult offspring underwent a learning test based on olfactory cues, at 30 weeks and 60 weeks of age. In addition, using magnetic resonance imaging (MRI), volumes of cerebrum, hippocampus and lateral ventricles were measured at 30 weeks and 70 weeks of age.
We found that DVD-deficient mice, when compared to control animals at Week 30, displayed impaired learning and smaller lateral ventricles. At Weeks 60-70, both groups deteriorated when compared to young mice and no significant difference was observed between groups.
This study confirms that transient prenatal vitamin D deficiency alters brain development and functioning and induces cognitive impairments in the young adult offspring.
Vit-D, brain, learning, animal studieshttp://www.ncbi.nlm.nih.gov/pubmed/20079764?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmedView this and related abstracts via PubMed here
1446Pitozzi et al 2010 - Effects of dietary extra-virgin olive oil on behaviour and brain biochemical parameters in ageing ratsEffects of dietary extra-virgin olive oil on behaviour and brain biochemical parameters in ageing ratsEffects of dietary extra-virgin olive oil on behaviour and brain biochemical parameters in ageing ratsPitozzi V, Jacomelli M, Zaid M, Luceri C, Bigagli E, Lodovici M, Ghelardini C, Vivoli E, Norcini M, Gianfriddo M, Esposto S, Servili M, Morozzi G, Baldi E, Bucherelli C, Dolara P, Giovannelli L.14/01/2010Br J Nutr.Jan 14:1-10. [Epub ahead of print]
The aim of the present study was to verify whether extra-virgin olive oil, a dietary component naturally containing phenolic antioxidants, has the potential to protect the brain from the deleterious effects of ageing. To accomplish this goal, we used male rats fed a high-energy diet containing either maize oil, or extra-virgin olive oil with high or low phenol content (720 or 10 mg total phenols/kg oil, corresponding to a daily dose of 4 or 0.05 mg total phenols/kg body weight, respectively) from age 12 months to senescence. The measured endpoints were biochemical parameters related to oxidative stress and functional tests to evaluate motor, cognitive and emotional behaviour. Olive oil phenols did not exert major protective actions on motor and cognitive function, as we observed only a tendency to improved motor coordination on the rotarod in the old animals treated with the oil rich in phenols (40 % average increase in the time to first fall; P = 0.18). However, an interesting finding of the present study was a reduced step-through latency in the light-dark box test, found in the older animals upon treatment with the oil rich in antioxidant phenols, possibly indicating an anxiety-lowering effect. This effect was associated with decreased glutathione reductase activity and expression in the brain, a phenomenon previously associated with decreased anxiety in rodents. These results indicate a previously undetected effect of a diet containing an olive oil rich in phenols. Further studies are warranted to verify whether specific food antioxidants might also have an effect on emotional behaviour.
diet, olive oil, monounsaturates, oleic acid, ARCD, behaviour, animal studyhttp://www.ncbi.nlm.nih.gov/pubmed/20070918View this and related abstracts via PubMed here
1676Yoshida et al 2010 - Endocannabinoids selectively enhance sweet tasteEndocannabinoids selectively enhance sweet taste Endocannabinoids selectively enhance sweet tasteYoshida R, Ohkuri T, Jyotaki M, Yasuo T, Horio N, Yasumatsu K, Sanematsu K, Shigemura N, Yamamoto T, Margolskee RF, Ninomiya Y.12/01/2010Proc Natl Acad Sci U S A. 107(2):935-9. Epub 2009 Dec 22.
Endocannabinoids such as anandamide (N-arachidonoylethanolamine (AEA)) and 2-arachidonoyl glycerol (2-AG) are known orexigenic mediators that act via CB(1) receptors in hypothalamus and limbic forebrain to induce appetite and stimulate food intake.
Circulating endocannabinoid levels inversely correlate with plasma levels of leptin, an anorexigenic mediator that reduces food intake by acting on hypothalamic receptors. Recently, taste has been found to be a peripheral target of leptin. Leptin selectively suppresses sweet taste responses in wild-type mice but not in leptin receptor-deficient db/db mice.
Here, we show that endocannabinoids oppose the action of leptin to act as enhancers of sweet taste. We found that administration of AEA or 2-AG increases gustatory nerve responses to sweeteners in a concentration-dependent manner without affecting responses to salty, sour, bitter, and umami compounds.
The cannabinoids increase behavioral responses to sweet-bitter mixtures and electrophysiological responses of taste receptor cells to sweet compounds. Mice genetically lacking CB(1) receptors show no enhancement by endocannnabinoids of sweet taste responses at cellular, nerve, or behavioral levels. In addition, the effects of endocannabinoids on sweet taste responses of taste cells are diminished by AM251, a CB(1) receptor antagonist, but not by AM630, a CB(2) receptor antagonist. Immunohistochemistry shows that CB(1) receptors are expressed in type II taste cells that also express the T1r3 sweet taste receptor component.
Taken together, these observations suggest that the taste organ is a peripheral target of endocannabinoids. Reciprocal regulation of peripheral sweet taste reception by endocannabinoids and leptin may contribute to their opposing actions on food intake and play an important role in regulating energy homeostasis.
endocannabinoid, anandamide, 2-AG, appetite, taste, sweetness, animal studyhttp://www.ncbi.nlm.nih.gov/pubmed/20080779View this and related abstracts via PubMed here
1447Frisardi et al 2010 - Aluminum in the Diet and Alzheimer's Disease: From Current Epidemiology to Possible Disease-Modifying TreatmentAluminum in the Diet and Alzheimer's Disease: From Current Epidemiology to Possible Disease-Modifying TreatmentAluminum in the Diet and Alzheimer's Disease: From Current Epidemiology to Possible Disease-Modifying TreatmentFrisardi V, Solfrizzi V, Capurso C, Kehoe PG, Imbimbo BP, Santamato A, Dellegrazie F, Seripa D, Pilotto A, Capurso A, Panza F.07/01/2010J Alzheimers Dis. 2010 Jan 7. [Epub ahead of print]
In recent years, interest in the potential role of metals in the pathogenesis of Alzheimer's disease (AD) has grown considerably. In particular, aluminum (Al) neurotoxicity was suggested after its discovery in the senile plaques and neurofibrillary tangles that represent the principal neuropathological hallmarks of AD. Al is omnipresent in everyday life and can enter the human body from several sources, most notably from drinking water and food consumption. The evidence supporting association from ingestion of Al from drinking water is somewhat stronger than for its ingestion from food. However, other elements present in drinking water, such as fluoride, copper, zinc, or iron could also have an effect on cognitive impairment or modify any Al neurotoxicity. Some epidemiological studies, but not all, suggested that silica could be protective against Al damage, because it reduced oral absorption of Al and/or enhanced Al excretion. Some epidemiological investigations suggested an association between chronic exposure to Al and risk of AD, although this relationship falls short of all the criteria generally attributed to causation. Future studies need to be more rigorous to truly test the validity of previous findings and in doing so attempt to identify dose-response relationships between Al and AD risk which may provide new routes to disease-modifying treatment of AD or possibly some lifestyle modification, to supplement existing symptomatic approaches.
aluminium, Alzheimer's disease, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/20061616View this and related abstracts via PubMed here
To read pdf documents on this site you may need to download
Adobe Acrobat Reader. Get it here.
Website Glossary If you hover your mouse over words that appear underlined
with a blue, dashed line, a definition of that word will appear as a 'tooltip'. You may find further information about the term in our
Food and Behaviour Research is a registered charity (No SC034604) and a company limited by guarantee (Co No SC 253448).
FAB Research | The Green House | Beechwood Business Park | Inverness | Scotland
| IV2 3BL | Telephone: 01463 667318 Website by Calligrafix
Medical opinion and guidance should always be sought for any symptoms that might
possibly reflect a known or suspected disease, disorder or medical condition. Information
provided on this website (or by FAB Research via any other means) does not in any
way constitute advice on the treatment of any medical condition formally diagnosed