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1315Whelan 2008 - (n-6) and (n-3) Polyunsaturated fatty acids and the aging brain: food for thought.(n-6) and (n-3) Polyunsaturated fatty acids and the aging brain: food for thought.(n-6) and (n-3) Polyunsaturated fatty acids and the aging brain: food for thought.Whelan J01/12/2008J Nutr. 138(12)2521-2
Over the last decade, the role of dietary PUFA in growth, development, and cognitive function in the infant has been a topic at numerous national and international meetings. Only recently has the role of PUFA been more seriously examined as they relate to the aging brain. In fact, a search of the literature reveals very few randomized control trials exploring this research area. However, the literature reveals growing mechanistic evidence that cognitive function of the aging brain can be preserved, or loss of function can be diminished with docosahexaenoic acid, a long-chain (n-3) PUFA. Furthermore, no symposia have taken a serious look at the impact of (n-6) PUFA on the brain, in particular arachidonic acid (AA), the most highly concentrated (n-6) PUFA in the brain. This symposium explores the role of AA metabolism in the brain as it relates to neurological mood disorders. To that end, this symposium was designed to highlight the potential effects of dietary PUFA on the adult brain, an important issue given the growing elderly population in this country and the growing problems with neurological disorders (dementia, Alzheimer disease, Parkinson disease, bipolar disorders, etc.)
fatty acids, omega-3, omega-6, brain, ageing, diethttp://www.ncbi.nlm.nih.gov/pubmed/19022982?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this and rleated abstracts via PubMed here
1737Brown & Susser 2008 - Prenatal nutritional deficiency and risk of adult schizophreniaPrenatal nutritional deficiency and risk of adult schizophreniaPrenatal nutritional deficiency and risk of adult schizophreniaBrown AS, Susser ES.01/11/2008Schizophr Bull. 34(6):1054-63. Epub 2008 Aug 4.
Converging evidence suggests that a neurodevelopmental disruption plays a role in the vulnerability to schizophrenia. The authors review evidence supporting in utero exposure to nutritional deficiency as a determinant of schizophrenia.
We first describe studies demonstrating that early gestational exposure to the Dutch Hunger Winter of 1944--1945 and to a severe famine in China are each associated with an increased risk of schizophrenia in offspring. The plausibility of several candidate micronutrients as potential risk factors for schizophrenia and the biological mechanisms that may underlie these associations are then reviewed. These nutrients include folate, essential fatty acids, retinoids, vitamin D, and iron.
Following this discussion, we describe the methodology and results of an epidemiologic study based on a large birth cohort that has tested the association between prenatal homocysteine, an indicator of serum folate, and schizophrenia risk. The study capitalized on the use of archived prenatal serum specimens that make it possible to obtain direct, prospective biomarkers of prenatal insults, including levels of various nutrients during pregnancy.
Finally, we discuss several strategies for subjecting the prenatal nutritional hypothesis of schizophrenia to further testing. These approaches include direct assessment of additional prenatal nutritional biomarkers in relation to schizophrenia in large birth cohorts, studies of epigenetic effects of prenatal starvation, association studies of genes relevant to folate and other micronutrient deficiencies, and animal models.
Given the relatively high prevalence of nutritional deficiencies during pregnancy, this work has the potential to offer substantial benefits for the prevention of schizophrenia in the population.
schizophrenia, risk factors, nutrition, nutritional programming, famine, iron, zinc, fatty acids, Vit_D, folic acid, Vit_A, retinoids, human studies, research, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/18682377View this and related abstracts via PubMed here. Free full text of this article is available online
1311Clayton et al 2008 - Long-chain omega-3 PUFA in the blood of children and adolescents with juvenile bipolar disorder.Long-chain omega-3 polyunsaturated fatty acids in the blood of children and adolescents with juvenile bipolar disorder.Long-chain omega-3 polyunsaturated fatty acids in the blood of children and adolescents with juvenile bipolar disorder.Clayton EH, Hanstock TL, Hirneth SJ, Kable CJ, Garg ML, Hazell PL.01/11/2008Lipids. 43(11)1031-8. Epub 2008 Sep 10
Reduced long-chain omega-3 polyunsaturated fatty acids (LCn-3PUFA), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been reported in adult patients suffering from depression and bipolar disorder (BD). LCn-3PUFA status has not previously been examined in children and adolescents with BD compared with healthy controls. Fifteen children and adolescents (9-18 years, M +/- SD = 14.4 +/- 3.48) diagnosed with juvenile bipolar disorder (JBD) and fifteen healthy age and sex-matched controls were assessed for dietary intake and fasting red blood cell (RBC) membrane concentrations of LCn-3PUFA. Fatty acid concentrations were compared between participants diagnosed with JBD and controls after controlling for dietary intake. RBC membrane concentrations of EPA and DHA were not significantly lower in participants diagnosed with JBD compared with healthy controls (M +/- sem EPA = 3.37 +/- 0.26 vs. 3.69 +/- 0.27 microg/mL, P = 0.458; M +/- sem DHA = 22.08 +/- 2.23 vs. 24.61 +/- 2.38 microg/mL, P = 0.528) after controlling for intake. Red blood cell DHA was negatively (r = -0.55; P = 0.044) related to clinician ratings of depression. Although lower RBC concentrations of LCn-3PUFA were explained by lower intakes in the current study, previous evidence has linked reduced LCn-3PUFA to the aetiology of BD. As RBC DHA was also negatively related to symptoms of depression, a randomised placebo-controlled study examining supplementation with LCn-3PUFA as an adjunct to standard pharmacotherapy appears warranted in this patient population.
omega-3, LC-PUFA, DHA, EPA, bipolar disorder, children, RBCFA, dietary intake, case-control studyhttp://www.ncbi.nlm.nih.gov/pubmed/18781353?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this and related abstracts via PubMed here
1247Xie & Innis 2008 - Genetic variants of the FADS1 FADS2 gene cluster are associated with altered (n-6) and (n-3) essential fatty acids in plasma and erythrocyte phospholipids in women during pregnancy and in breast milk during lactation.Genetic variants of the FADS1 FADS2 gene cluster are associated with altered (n-6) and (n-3) essential fatty acids in plasma and erythrocyte phospholipids in women during pregnancy and in breast milk during lactation.Genetics, fatty acids, desaturase enzymes, desaturase genes, FADS, pregnancy, breastfeeding, omega-3, omega-6Xie L, Innis SM.01/11/2008J Nutr. 138(11)2222-8
The enzymes encoded by fatty acid desaturase (FADS) 1 and FADS2 are rate-limiting enzymes in the desaturation of linoleic acid
to arachidonic acid
, and alpha-linolenic acid
to eicosapentaenoic acid
and docosahexaenoic acid
. ARA, EPA, and DHA play central roles in infant growth, neural development, and immune function. The maternal ARA, EPA, and DHA status in gestation influences maternal-to-infant transfer and breast milk provides fatty acids for infants after birth. We determined if single nucleotide polymorphisms in FADS1 and FADS2 influence plasma phospholipid and erythrocyte ethanolamine phosphoglyceride (EPG) (n-6) and (n-3) fatty acids of women in pregnancy or their breast milk during lactation. We genotyped rs174553, rs99780, rs174575, and rs174583 in the FADS1 FADS2 gene cluster and analyzed plasma and erythrocyte fatty acids and dietary intake for 69 pregnant women and breast milk for a subset of 54 women exclusively breast-feeding at 1 mo postpartum. Minor allele homozygotes of rs174553(GG), rs99780(TT), and rs174583(TT) had lower ARA but higher LA in plasma phospholipids and erythrocyte EPG and decreased (n-6) and (n-3) fatty acid product:precursor ratios at 16 and 36 wk of gestation. Breast milk fatty acids were influenced by genotype, with significantly lower 14:0, ARA, and EPA but higher 20:2(n-6) in the minor allele homozygotes of rs174553(GG), rs99780(TT), and rs174583(TT) and lower ARA, EPA, 22:5(n-3), and DHA in the minor allele homozygotes G/G of rs174575. We showed that genetic variants of FADS1 and FADS2 influence blood lipid and breast milk essential fatty acids in pregnancy and lactation.
Genetics, fatty acids, desaturase enzymes, desaturase genes, FADS, pregnancy, breastfeeding, omega-3, omega-6, EFA-HUFA conversionhttp://www.ncbi.nlm.nih.gov/pubmed/18936223?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this abstract via PubMed here
3241Cha et al 2008 - Differential effects of central fructose and glucose on hypothalamic malonyl-CoA and food intake.Differential effects of central fructose and glucose on hypothalamic malonyl-CoA and food intake.Differential effects of central fructose and glucose on hypothalamic malonyl-CoA and food intake.Cha SH, Wolfgang M, Tokutake Y, Chohnan S, Lane MD.29/10/2008Proc Natl Acad Sci U S A.105(44):16871-5. Epub 2008 Oct 29.
The American diet, especially that of adolescents, contains highly palatable foods of high-energy content and large amounts of high-fructose sweeteners. These factors are believed to contribute to the obesity epidemic and insulin resistance.
Previous investigations revealed that the central metabolism of glucose suppresses food intake mediated by the hypothalamic AMP-kinase/malonyl-CoA signaling system. Unlike glucose, centrally administered fructose increases food intake.
Evidence presented herein indicates that the more rapid initial steps of central fructose metabolism deplete hypothalamic ATP level, whereas the slower regulated steps of glucose metabolism elevate hypothalamic ATP level.
Consistent with effects on the
ratio, fructose increases phosphorylation/activation of hypothalamic AMP kinase causing phosphorylation/inactivation of acetyl-CoA carboxylase, whereas glucose has the inverse effects.
The changes provoked by central fructose administration reduce hypothalamic malonyl-CoA level and thereby increase food intake. These findings explain the paradoxical fructose effect on food intake and lend credence to the malonyl-CoA hypothesis.
fructose, glucose, sugar, energy-regulation, appetite, satiety, food intake, obesity, eating disorders, metabolic syndrome, metabolism, animal studies, Free Full Texthttp://www.ncbi.nlm.nih.gov/pubmed/18971329View this and related articles via PubMed here. Free full text of this article is available online.
1257Tassabehji et al 2008 - Zinc deficiency induces depression-like symptoms in adult rats.Zinc deficiency induces depression-like symptoms in adult rats.Zinc deficiency induces depression-like symptoms in adult rats.Tassabehji NM, Corniola RS, Alshingiti A, Levenson CW.20/10/2008Physiol Behav. 95(3)365-9. Epub 2008 Jul 3
There is mounting evidence suggesting a link between serum zinc levels and clinical depression. Not only is serum zinc negatively correlated with the severity of symptoms, but zinc levels appear to be lowest in patients who do not respond to antidepressant drug therapy. It is not known if reduced zinc levels are contributing to depression, or the result of dietary or other factors associated with major depression. Thus, we designed this study to test the hypothesis that dietary zinc deficiency would induce depression-like behaviors in rats. Two-month-old male rats were fed zinc adequate (ZA, 30 ppm), deficient (ZD, 1 ppm), or supplemented (ZS, 180 ppm) diets for 3 weeks. Consistent with the development of depression, ZD rats displayed anorexia (p<0.001), anhedonia (reduced saccharin:water intake, p< 0.001), and increased anxiety-like behaviors in a light-dark box test (p<0.05). Furthermore, the antidepressant drug fluoxetine (10 mg/kg body wt) reduced behavioral despair, as measured by the forced swim test, in rats fed the ZA and ZS rats (p<0.05), but was ineffective in ZD rats. Together these studies suggest that zinc deficiency leads to the development of depression-like behaviors that may be refractory to antidepressant treatment.
zinc, depression, treatment http://www.ncbi.nlm.nih.gov/pubmed/18655800?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this and related abstracts via PubMed here
1269Aisen et al 2008 - High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial.High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial.High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial.Aisen PS, Schneider LS, Sano M, Diaz-Arrastia R, van Dyck CH, Weiner MF, Bottiglieri T, Jin S, Stokes KT, Thomas RG, Thal LJ; Alzheimer Disease Cooperative Study.15/10/2008JAMA300(15)1774-83
CONTEXT: Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B(6) and B(12). Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.
OBJECTIVE: To determine the efficacy and safety of B vitamin supplementation in the treatment of AD.
DESIGN, SETTING, AND PATIENTS: A multicenter, randomized, double-blind controlled clinical trial of high-dose folate, vitamin B(6), and vitamin B(12) supplementation in 409 (of 601 screened) individuals with mild to moderate AD (Mini-Mental State Examination scores between 14 and 26, inclusive) and normal folic acid, vitamin B(12), and homocysteine levels. The study was conducted between February 20, 2003, and December 15, 2006, at clinical research sites of the Alzheimer Disease Cooperative Study located throughout the United States.
INTERVENTION: Participants were randomly assigned to 2 groups of unequal size to increase enrollment (60% treated with high-dose supplements (5 mg/d of folate, 25 mg/d of vitamin B(6), 1 mg/d of vitamin B(12)) and 40% treated with identical placebo); duration of treatment was 18 months.
MAIN OUTCOME MEASURE: Change in the cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog).
RESULTS: A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Although the vitamin supplement regimen was effective in reducing homocysteine levels (mean (SD), -2.42 (3.35)) in active treatment group vs -0.86 (2.59) in placebo group; P < .001), it had no beneficial effect on the primary cognitive measure, rate of change in ADAS-cog score during 18 months (0.372 points per month for placebo group vs 0.401 points per month for active treatment group, P = .52; 95% confidence interval of rate difference, -0.06 to 0.12; based on the intention-to-treat generalized estimating equations model), or on any secondary measures. A higher quantity of adverse events involving depression was observed in the group treated with vitamin supplements.
CONCLUSION: This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD.
Vitamin B, Vit_B, folate, B6, B12, homocysteine, Alzheimer's disease, dietary supplementation, RCT, human clinical trialhttp://www.ncbi.nlm.nih.gov/pubmed/18854539?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmedView this and related abstracts via PubMed here. Free full text of this paper is available online.
11998 October 2008 - Nutraingredients - Don't ignore omega-3 for mood and behaviour, say UK expertsFAB Research conference, omega-3, mood disorders, child behaviour and learning08/10/2008by Lorraine Heller who attended the 'Feeding Young Minds' event in Oxford on 3 October 2008.
Academic and nutrition experts in the UK are calling for an increased focus on the benefits of omega-3 in mood and behaviour, especially in children, as a lack of consistent research is stunting potential in the field.
The resounding message that came out of a Food and Behaviour (FAB) research conference held in Oxford last week was the need for more funding for additional scientific studies.
"Omega-3s are precious nutrients that have never reached such historically low levels in our diets. We cannot ignore the physical health risks to children from a poor nutritional diet as they are all too visible. What's less visible is the damage to their brains," said Dr Alex Richardson, a research scientist at the University of Oxford and founder and director of FAB.
Dr Richardson and other speakers highlighted the studies that have so far indicated the crucial role of omega-3 in improving behaviour, learning and mood disorders.
Potential benefits of the fatty acids include a reduction in violent or impulsive behaviour, improvements in neurodevelopmental disorders in children (such as ADHD, dyslexia, dyspraxia and autism), as well as improvements or even prevention of adult psychiatric disorders (such as schizophrenia, bipolar disorder, anxiety disorders and depression).
A number of randomized controlled trials - the gold standard in the scientific world - have demonstrated some of these benefits, explained the speakers. However, the results cannot be compared and confirmed through systematic reviews or meta-analyses because the studies are too differing - conducted in different populations and using different measures.
Ultimately, this means that regulatory authorities require more studies before the benefits can be recognised, but funds for these remain limited.
"Omega-3s do not work in the same way for everyone - we all agree that we need more studies. The department of education wants to see the results, but they don't want to contribute anything," said Dr Richardson.
"Stop setting the bar so high that there will never be enough evidence for us to do something about it," she said.
Other speakers at the event - entitled Feeding Young Minds - included:
1270Malouf et al 2008 - Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people.Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people. Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people.Malouf R, Grimley Evans J.08/10/2008Cochrane Database Syst Rev. (4):CD004514
BACKGROUND: Folate deficiency can result in congenital neural tube defects and megaloblastic anaemia. Low folate levels may be due to insufficient dietary intake or inefficient absorption, but impaired metabolic utilization also occurs.Because B12 deficiency can produce a similar anaemia to folate deficiency, there is a risk that folate supplementation can delay the diagnosis of B12 deficiency, which can cause irreversible neurological damage. Folic acid supplements may sometimes therefore include vitamin B12 supplements with simultaneous administration of vitamin B12.Lesser degrees of folate inadequacy are associated with high blood levels of the amino acid homocysteine which has been linked with the risk of arterial disease, dementia and Alzheimer's disease. There is therefore interest in whether dietary supplementation can improve cognitive function in the elderly.However, any apparent benefit from folic acid which was given in combination with B12 needs to be "corrected" for any effect of vitamin B12 alone. A separate Cochrane review of vitamin B12 and cognitive function has therefore been published.
OBJECTIVES: To examine the effects of folic acid supplementation, with or without vitamin B12, on elderly healthy or demented people, in preventing cognitive impairment or retarding its progress.
SEARCH STRATEGY: Trials were identified from a search of the Cochrane Dementia and Cognitive Improvement Group's Specialized Register on 10 October 2007 using the terms: folic acid, folate, vitamin B9, leucovorin, methyltetrahydrofolate, vitamin B12, cobalamin and cyanocobalamin. This Register contains references from all major health care databases and many ongoing trials databases. In addition MEDLINE, EMBASE, CINAHL, PsychINFO and LILACS were searched (years 2003-2007) for additional trials of folate with or without vitamin B12 on healthy elderly people.
SELECTION CRITERIA: All double-blind, placebo-controlled, randomized trials, in which supplements of folic acid with or without vitamin B12 were compared with placebo for elderly healthy people or people with any type of dementia or cognitive impairment.
DATA COLLECTION AND ANALYSIS: The reviewers independently applied the selection criteria and assessed study quality. One reviewer extracted and analysed the data. In comparing intervention with placebo, weighted mean differences and standardized mean difference or odds ratios were estimated.
MAIN RESULTS: Eight randomized controlled trials fulfilled the inclusion criteria for this review. Four trials enrolled healthy older people, and four recruited participants with mild to moderate cognitive impairment or dementia with or without diagnosed folate deficiency. Pooling the data was not possible owing to heterogeneity in sample selections, outcomes, trial duration, and dosage. Two studies involved a combination of folic acid and vitamin B12.There is no adequate evidence of benefit from folic acid supplementation with or without vitamin B12 on cognitive function and mood of unselected healthy elderly people. However, in one trial enrolling a selected group of healthy elderly people with high homocysteine levels, 800 mcg/day folic acid supplementation over three years was associated with significant benefit in terms of global functioning (WMD 0.05, 95% CI 0.004 to 0.096, P = 0.033); memory storage (WMD 0.14, 95% CI 0.04 to 0.24, P = 0.006) and information-processing speed (WMD 0.09, 95% CI 0.02 to 0.16, P = 0.016).Four trials involved people with cognitive impairment. In one pilot trial enrolling people with Alzheimer's disease, the overall response to cholinesterase inhibitors significantly improved with folic acid at a dose of 1mg/day (odds ratio: 4.06, 95% CI 1.22 to 13.53; P = 0.02) and there was a significant improvement in scores on the Instrumental Activities of Daily Living and the Social Behaviour subscale of the Nurse's Observation Scale for Geriatric Patients (WMD 4.01, 95% CI 0.50 to 7.52, P = 0.02). Other trials involving people with cognitive impairment did not show any benefit in measures of cognitive function from folic acid, with or without vitamin B12.Folic acid plus vitamin B12 was effective in reducing serum homocysteine concentrations (WMD -5.90, 95% CI -8.43 to -3.37, P < 0.00001). Folic acid was well tolerated and no adverse effects were reported.
AUTHORS' CONCLUSIONS: The small number of studies which have been done provide no consistent evidence either way that folic acid, with or without vitamin B12, has a beneficial effect on cognitive function of unselected healthy or cognitively impaired older people. In a preliminary study, folic acid was associated with improvement in the response of people with Alzheimer's disease to cholinesterase inhibitors. In another, long-term use appeared to improve the cognitive function of healthy older people with high homocysteine levels. More studies are needed on this important issue.
Folic acid, B12, ageing, age-related cognitive decline, ARCD, dementiahttp://www.ncbi.nlm.nih.gov/pubmed/18843658?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmedView this and related abstracts via PubMed here
1839Anton et al 2008 - Effects of chromium picolinate on food intake and satiety.Effects of chromium picolinate on food intake and satiety.Effects of chromium picolinate on food intake and satiety.
Anton SD, Morrison CD, Cefalu WT, Martin CK, Coulon S, Geiselman P, Han H, White CL, Williamson DA.01/10/2008Diabetes Technol Ther.10(5):405-12.
BACKGROUND: Chromium picolinate (CrPic) has been shown to attenuate weight gain, but the mechanism underlying this effect is unknown.
METHODS: We assessed the effect of CrPic in modulating food intake in healthy, overweight, adult women who reported craving carbohydrates (Study 1) and performed confirmatory studies in Sprague-Dawley rats (Study 2). Study 1 utilized a double-blind placebo-controlled design and randomly assigned 42 overweight adult women with carbohydrate cravings to receive 1,000 mg of CrPic or placebo for 8 weeks. Food intake at breakfast, lunch, and dinner was directly measured at baseline, week 1, and week 8. For Study 2, Sprague-Dawley rats were fasted for 24 h and subsequently injected intraperitoneally with 0, 1, 10, or 50 microg/kg CrPic. Subsequently, rats were implanted with an indwelling third ventricular cannula. Following recovery, 0, 0.4, 4, or 40 ng of CrPic was injected directly into the brain via the intracerebroventricular cannula, and spontaneous 24-h food intake was measured.
RESULTS: Study 1 demonstrated that CrPic, as compared to placebo, reduced food intake (P<0.0001), hunger levels (P<0.05), and fat cravings (P<0.0001) and tended to decrease body weight (P=0.08). In study 2, intraperitoneal administration resulted in a subtle decrease in food intake at only the highest dose (P=0.03). However, when administered centrally, CrPic dose-dependently decreased food intake (P<0.05).
CONCLUSIONS: These data suggest CrPic has a role in food intake regulation, which may be mediated by a direct effect on the brain.
chromium, dietary supplementation, appetite, satiety, food intake, human study, intervention study, RCT, Free Full Texthttp://www.ncbi.nlm.nih.gov/pubmed/18715218View this and related abstracts via PubMed here. Free full text of this article is available online.
1555Banks 2008 - The blood-brain barrier as a cause of obesityThe blood-brain barrier as a cause of obesity The blood-brain barrier as a cause of obesity Banks WA01/10/2008Curr Pharm Des. 14(16)1606-14
The dramatic increase in the number of obese and overweight persons has spurred interest in control of appetite, body weight, and adiposity. Leptin is the humoral component of a negative feedback loop between adipose tissue and brain. Leptin is secreted from fat in proportion to the degree of adiposity, is transported across the blood-brain barrier (BBB), and acts in the brain to decrease appetite and increase thermogenesis, actions that ultimately decrease adiposity. However, leptin fails as an adipostat because leptin resistance arises in obesity. The BBB transporter is the first part of the feedback loop to fail, producing the so called "peripheral resistance" to leptin. In this sense, obesity is a disease of the BBB. Failure of leptin as an adipostat raises the question of what its primary role is as does its effects on reproduction, bone, immunity, breathing, cognition, and neurogenesis. Kinetics analysis shows that the BBB transporter performs most efficiently at low serum levels of leptin, suggesting that the feedback loop evolved to operate at lower leptin levels than those seen in ideal body weight. We suggest that low levels of serum leptin inform the brain that adipose reserves are adequate to expend calories on functions other than feeding, such as reproduction and the immune system. This feedback loop is short-circuited when an animal enters starvation. Hallmarks of starvation include decreased secretion of leptin by adipose tissue and hypertriglyceridemia. Triglycerides inhibit the transport of leptin across the BBB, thus attenuating the leptin signal across the BBB and providing a mechanism for peripheral leptin resistance. Triglycerides are elevated in both starvation and obesity. We postulate that hypertriglyceridemia evolved as a starvation signal to the brain that acts in part to inhibit the transport of the leptin across the BBB. The hypertriglyceridemia of obesity invokes this aspect of the starvation response, inducing leptin resistance at the BBB. Thus, the BBB plays important roles in both obesity and starvation.
obesity, adiposity, starvation, blood-brain barrier, leptin, leptin resistance, triglycerideshttp://www.ncbi.nlm.nih.gov/pubmed/18673202View this and related abstracts via Pubmed here
1303Berk et al 2008 - Is this D vitamin to worry about? Vitamin D insufficiency in an inpatient sample.Is this D vitamin to worry about? Vitamin D insufficiency in an inpatient sample. Vitamin D, psychiatric disorders, mental healthBerk M, Jacka FN, Williams LJ, Ng F, Dodd S, Pasco JA01/10/2008Aust N Z J Psychiatry. 42(10)874-8
OBJECTIVE: The aim of the present study was to investigate the relationship between reduced serum vitamin D levels and psychiatric illness.
METHOD: This study was an audit of serum 25-hydroxyvitamin D (25-OHD) levels measured routinely in a sample of 53 inpatients in a private psychiatric clinic. These levels were compared with those of controls without psychiatric illness.
RESULTS: The median levels of serum 25-OHD were 43.0 nmol L(-1) (range 20-102 nmol L(-1)) in the patient population, 46.0 nmol L(-1) (range 20-102 nmol L(-1)) in female patients (n =33) and 41.5 nmol L(-1) (range 22-97 nmol L(-1)) in male patients (n =20). The proportion of vitamin D insufficiency (serum 25-OHD < or =50 nmol L(-1)) in this patient population was 58%. Furthermore, 11% had moderate deficiency (serum 25-OHD < or =25 nmol L(-1)). There was a 29% difference between mean levels in the patient population and control sample (geometric mean age- and season-adjusted levels: 46.4 nmol L(-1) (95% confidence interval (CI) =38.6-54.9 nmol L(-1)) vs 65.3 nmol L(-1) (95%CI =63.2-67.4 nmol L(-1)), p <0 .001).
CONCLUSION: Low levels of serum 25-OHD were found in this patient population. These data add to the literature suggesting an association between vitamin D insufficiency and psychiatric illness, and suggest that routine monitoring of vitamin D levels may be of benefit given the high yield of clinically relevant findings.
Vitamin D, Vit-D, mental health, psychiatric disorder, case-control studyhttp://www.ncbi.nlm.nih.gov/pubmed/18777231?ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this and related abstracts via PubMed here
1736Insel et al 2008 - Maternal iron deficiency and the risk of schizophrenia in offspring.Maternal iron deficiency and the risk of schizophrenia in offspring.Maternal iron deficiency and the risk of schizophrenia in offspring.
Insel BJ, Schaefer CA, McKeague IW, Susser ES, Brown AS.01/10/2008Arch Gen Psychiatry. 65(10):1136-44.
CONTEXT:Iron is essential for brain development and functioning. Emerging evidence suggests that iron deficiency in early life leads to long-lasting neural and behavioral deficits in infants and children. Adopting a life course perspective, we examined the effects of early iron deficiency on the risk of schizophrenia in adulthood.
OBJECTIVE:To determine whether maternal iron deficiency, assessed by maternal hemoglobin concentration during pregnancy, increases the susceptibility to schizophrenia spectrum disorders (SSDs) among offspring.
DESIGN: Data were drawn from a population-based cohort born from 1959 through 1967 and followed up for development of SSD from 1981 through 1997.
PARTICIPANTS: Of 6872 offspring for whom maternal hemoglobin concentration was available, 57 had SSDs (0.8%) and 6815 did not (99.2%).
MAIN OUTCOME MEASURE: Prospectively assayed, the mean value of maternal hemoglobin concentration was the primary exposure. Hemoglobin concentration was analyzed as a continuous and a categorical variable.
RESULTS:A mean maternal hemoglobin concentration of 10.0 g/dL or less was associated with a nearly 4-fold statistically significant increased rate of SSDs (adjusted rate ratio, 3.73; 95% confidence interval, 1.41-9.81; P = .008) compared with a mean maternal hemoglobin concentration of 12.0 g/dL or higher, adjusting for maternal education and ethnicity. For every 1-g/dL increase in mean maternal hemoglobin concentration, a 27% decrease in the rate of SSDs was observed (95% confidence interval, 0.55-0.96; P = .02).
CONCLUSIONS: The findings suggest that maternal iron deficiency may be a risk factor for SSDs among offspring. Given that this hypothesis offers the potential for reducing the risk for SSDs, further investigation in independent samples is warranted.
schizophrenia, risk factors, nutrition, pregnancy, iron, maternal iron deficiency, human study, birth cohort study, Free Full Text http://www.ncbi.nlm.nih.gov/pubmed/18838630View this and related abstracts via PubMed here. Free full text of this article is available online
1326Rubin et al 2008 - Acne vulgaris, mental health and omega-3 fatty acids: a report of casesAcne vulgaris, mental health and omega-3 fatty acids: a report of casesAcne vulgaris, mental health and omega-3 fatty acids: a report of casesRubin MG, Kim K, Logan AC01/10/2008Lipids Health Dis. 13;7:36
Acne vulgaris is a common skin condition, one that is associated with significant psychological disability. The psychological impairments in acne include higher rates of depression, anxiety, anger and suicidal thoughts. Despite a paucity of clinical research, patients with skin conditions and/or mental health disorders are frequent consumers of dietary supplements. An overlap may exist between nutrients that potentially have both anti-acne and mood regulating properties; examples include omega-3 fatty acids from fish oil, chromium, zinc and selenium. Here we report on five cases of acne treated with eicosapentaenoic acid and antioxidant nutrients. Self-administration of these nutrients may have improved inflammatory acne lesions and global aspects of well-being; the observations suggest a need for controlled trials.
acne, skin, fatty acids, omega-3, vitamins, mineralshttp://www.ncbi.nlm.nih.gov/pubmed/18851733?ordinalpos=30&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this and related abstracts via PubMed here. Free Full Text of this paper is available on the Journal website
1586Smithers et al 2008 - Higher dose of DHA in the neonatal period improves visual acuity of preterm infants: results of a randomized controlled trial.Higher dose of docosahexaenoic acid in the neonatal period improves visual acuity of preterm infants: results of a randomized controlled trial. Higher dose of docosahexaenoic acid in the neonatal period improves visual acuity of preterm infants: results of a randomized controlled trial.
Smithers LG, Gibson RA, McPhee A, Makrides M.01/10/2008Am J Clin Nutr. 88(4)1049-56.
BACKGROUND: Preterm infants have improved visual outcomes when fed a formula containing 0.2-0.4% docosahexaenoic acid (DHA) compared with infants fed no DHA, but the optimal DHA dose is unknown.
OBJECTIVE: We assessed visual responses of preterm infants fed human milk (HM) and formula with a DHA concentration estimated to match the intrauterine accretion rate (high-DHA group) compared with infants fed HM and formula containing DHA at current concentrations.
DESIGN: A double-blind randomized controlled trial studied preterm infants born at <33 wk gestation and fed HM or formula containing 1% DHA (high-DHA group) or approximately 0.3% DHA (current practice; control group) until reaching their estimated due date (EDD). Both groups received the same concentration of arachidonic acid. Sweep visual evoked potential (VEP) acuity and latency were assessed at 2 and 4 mo corrected age (CA). Weight, length, and head circumference were assessed at EDD and at 2 and 4 mo CA.
RESULTS: At 2 mo CA, acuity of the high-DHA group did not differ from the control group (high-DHA group (x +/- SD): 5.6 +/- 2.4 cycles per degree (cpd), n = 54; control group: 5.6 +/- 2.4 cpd, n = 61; P = 0.96). By 4 mo CA, the high-DHA group exhibited an acuity that was 1.4 cpd higher than the control group (high-DHA: 9.6 +/- 3.7 cpd, n = 44; control: 8.2 +/- 1.8 cpd; n = 51; P = 0.025). VEP latencies and anthropometric measurements were not different between the high-DHA and control groups.
CONCLUSION: The DHA requirement of preterm infants may be higher than currently provided by preterm formula or HM of Australian women.
omega-3, DHA, prematurity, infant feeding, dose-response, RCT, vision, visual acuity, FFThttp://www.ncbi.nlm.nih.gov/pubmed/18842793View Free Full Text of this paper and related abstracts via PubMed here
1310McNamara et al 2008 - Deficits in DHA and associated elevations in the metabolism of AA and saturated fatty acids in postmortem orbitofrontal cortex of patients with bipolar disorder.Deficits in docosahexaenoic acid and associated elevations in the metabolism of arachidonic acid and saturated fatty acids in the postmortem orbitofrontal cortex of patients with bipolar disorder.Deficits in docosahexaenoic acid and associated elevations in the metabolism of arachidonic acid and saturated fatty acids in the postmortem orbitofrontal cortex of patients with bipolar disorder.McNamara RK, Jandacek R, Rider T, Tso P, Stanford KE, Hahn CG, Richtand NM.30/09/2008Psychiatry Res.160(3)285-99. Epub 2008 Aug 20
Previous antemortem and postmortem tissue fatty acid composition studies have observed significant deficits in the omega-3 fatty acid docosahexaenoic acid (DHA, 22:6n-3) in red blood cell (RBC) and postmortem cortical membranes of patients with unipolar depression. In the present study, we determined the fatty acid composition of postmortem orbitofrontal cortex (OFC, Brodmann area 10) of patients with bipolar disorder (n=18) and age-matched normal controls (n=19) by gas chromatography. After correction for multiple comparisons, DHA (-24%), arachidonic acid (-14%), and stearic acid (C18:0) (-4.5%) compositions were significantly lower, and cis-vaccenic acid (18:1n-7) (+12.5%) composition significantly higher, in the OFC of bipolar patients relative to normal controls. Based on metabolite:precursor ratios, significant elevations in arachidonic acid, stearic acid, and palmitic acid conversion/metabolism were observed in the OFC of bipolar patients, and were inversely correlated with DHA composition. Deficits in OFC DHA and arachidonic acid composition, and elevations in arachidonic acid metabolism, were numerically (but not significantly) greater in drug-free bipolar patients relative to patients treated with mood-stabilizer or antipsychotic medications. OFC DHA and arachidonic acid deficits were greater in patients plus normal controls with high vs. low alcohol abuse severity. These results add to a growing body of evidence implicating omega-3 fatty acid deficiency as well as the OFC in the pathoaetiology of bipolar disorder.
fatty acids, omega-3, omega-6, DHA, AA, bipolar disorder, post-mortem studyhttp://www.ncbi.nlm.nih.gov/pubmed/18715653?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this and related abstracts via PubMed here
1248Innis SM 2008 - Dietary omega 3 fatty acids and the developing brain.Dietary omega 3 fatty acids and the developing brain.omega-3, brain developmentInnis SM.09/09/2008Brain Research1237 35-43.
The omega-3 fatty acids are essential dietary nutrients and one of their important roles is providing the fatty acid with 22 carbons and 6 double bonds known as docosahexaenoic acid (DHA) for nervous tissue growth and function. Inadequate intakes of omega-3 fatty acids decrease DHA and increase omega-6 fatty acids in the brain. Decreased DHA in the developing brain leads to deficits in neurogenesis, neurotransmitter metabolism, and altered learning and visual function in animals. Western diets are low in omega-3 fatty acids, including the 18 carbon omega-3 fatty acid alpha linolenic acid found mainly in plant oils, and DHA, which is found mainly in fish. The DHA status of the newborn and breast-fed infant depends on the maternal intake of DHA and varies widely. Epidemiological studies have linked low maternal DHA to increased risk of poor child neural development. Intervention studies have shown improving maternal DHA nutrition decreases the risk of poor infant and child visual and neural development. Thus, sufficient evidence is available to conclude that maternal fatty acid nutrition is important to DHA transfer to the infant before and after birth, with short and long-term implications for neural function. However, genetic variation in genes encoding fatty acid desaturases also influence essential fatty acid metabolism, and may increase requirements in some individuals. Consideration of omega-3 fatty acid to include brain development, optimizing omega-3 and omega-6 fatty acids in gestation and lactation, and in fatty acid nutrition support for intravenous and formula-fed neonates is important.
omega-3, diet, brain developmenthttp://www.ncbi.nlm.nih.gov/pubmed/18789910?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSumView this abstract via PubMed here
Nutri People maintains a UK database of qualified nutritional practitioners working one on one in private practice with the general public. These practitioners include dietitians, nutritionists and nutritional therapists all of which have successfully qualified in their respective fields of nutrition.
Nutri People can help connect you with your local fully qualified nutritional practitioner. They also have lots of nutritional information and a listing of nutritional events across the UK.
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1195Nutrition Policy Unit - London Metropolitan University Nutrition Policy Unit - London Metropolitan University; Jack WinklerUntil recently, London Metropolitan University was one of the UK's leading centres for research and teaching on food, nutrition and dietetics. 06/09/2008
The Nutrition Policy Unit was created to bring this expertise together in the formulation of research-based policy, and to disseminate London Metropolitan's research findings to people who can make practical use of them.
The Unit was set up to make the university's skills and knowledge available to diverse groups in the community who are dealing with contemporary dietary problems, including:
Another function of the Unit was to train London Metropolitian's postgraduate students to see policy development as an essential component of their work, through teaching on Nutrition Politics & Policy. This included sessions with a diverse array of "frontline practitioners" active in varied forms of nutrition policy.
Professor Jack T Winkler was the Director of the Unit, which operated for several years until major changes at London Metropolitan University prevented its continuation there.
1238Age-Related Eye Disease Study Research Group 2008 - The relationship of dietary carotenoid and vitamin A, E, and C intake with age-related macular degeneration: a case-control study The relationship of dietary carotenoid and vitamin A, E, and C intake with age-related macular degeneration in a case-control study: AREDS Report No. 22.dietary carotenoids, vitamin A, alpha-tocopherol, vitamin C, age-related macular degeneration, AMD, visionAge-Related Eye Disease Study Research Group, SanGiovanni JP, Chew EY, Clemons TE, Ferris FL 3rd, Gensler G, Lindblad AS, Milton RC, Seddon JM, Sperduto RD.01/09/2008Archives of Ophthalmology125(9)1225-32
OBJECTIVE: To evaluate the relationship of dietary carotenoids, vitamin A, alpha-tocopherol, and vitamin C with prevalent age-related macular degeneration (AMD) in the Age-Related Eye Disease Study (AREDS).
METHODS: Demographic, lifestyle, and medical characteristics were ascertained on 4519 AREDS participants aged 60 to 80 years at enrollment. Stereoscopic color fundus photographs were used to categorize participants into 4 AMD severity groups and a control group (participants with < 15 small drusen). Nutrient intake was estimated from a self-administered semiquantitative food frequency questionnaire at enrollment. Intake values were energy adjusted and classified by quintiles. The relationship between diet and AMD status was assessed using logistic regression analyses.
RESULTS: Dietary lutein/zeaxanthin intake was inversely associated with neovascular AMD (odds ratio (OR), 0.65; 95% confidence interval (CI), 0.45-0.93), geographic atrophy (OR, 0.45; 95% CI, 0.24-0.86), and large or extensive intermediate drusen (OR, 0.73; 95% CI, 0.56-0.96), comparing the highest vs lowest quintiles of intake, after adjustment for total energy intake and nonnutrient-based covariates. Other nutrients were not independently related to AMD.
CONCLUSION: Higher dietary intake of lutein/zeaxanthin was independently associated with decreased likelihood of having neovascular AMD, geographic atrophy, and large or extensive intermediate drusen.
diet, dietary carotenoids, vitamin A, alpha-tocopherol, vitamin C, age-related macular degeneration, AMD, vision, case-control studyhttp://www.ncbi.nlm.nih.gov/pubmed/17846363?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmedView this abstract via PubMed here
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