1869Oddy et al 2011 - Dietary intake of omega-3 fatty acids and risk of depressive symptoms in adolescentsDietary intake of omega-3 fatty acids and risk of depressive symptoms in adolescentsDietary intake of omega-3 fatty acids and risk of depressive symptoms in adolescentsOddy WH, Hickling S, Smith MA, A O'Sullivan T, Robinson M, H de Klerk N, Beilin LJ, A Mori T, Syrette J, R Zubrick S, R Silburn S.29/06/2011Depress Anxiety.Apr 27. [Epub ahead of print]
Background: Previous randomized controlled trials have demonstrated that omega-3 polyunsaturated fatty acids (n-3 PUFA) are beneficial in reducing symptoms of depression. However, there is limited evidence regarding the influence of dietary n-3 PUFA intake on mood in adolescents drawn from population studies.
Objective: In the present investigation, we examined the relationship between dietary n-3 PUFA intake on depression symptomatology in a large prospective pregnancy cohort followed for 17 years.
Methods: Adolescents enrolled in the Western Australian Pregnancy Cohort (Raine) Study completed a Food Frequency Questionnaire to assess dietary fatty acid intake, as well as other dietary factors at age 14 and a fasting blood sample was taken. Participants also completed the Beck Depression Inventory for Youth (BDI-Y) at age 14 (N = 1,407) and at age 17 (N = 995).
Results: An inverse relationship was observed between intake of both saturated fat and of n-3 PUFA at age 14 and BDI-Y scores at both 14 and 17 years of age. However, after adjusting for energy (kJ) intake and other lifestyle confounders, the relationships were no longer significant. Conclusions: Associations previously reported between n3 PUFA and depressive symptoms may be due to collinearity with other dietary and lifestyle factors.
diet, omega-3, depression, adolescents, human study, observational cohort studyhttp://www.ncbi.nlm.nih.gov/pubmed/21538725View this and related abstracts via Pubmed here
1858Bell et al 2011 - Using a fingertip whole blood sample for rapid fatty acid measurementUsing a fingertip whole blood sample for rapid fatty acid measurement: method validation and correlation with erythrocyte polar lipid compositionsUsing a fingertip whole blood sample for rapid fatty acid measurement:
method validation and correlation with erythrocyte polar lipid compositions
in UK subjectsBell JG, Mackinlay EE, Dick JR, Younger I, Lands B23/06/2011Br J Nutritionin press
It is well accepted that n-3 long-chain PUFA intake is positively associated with a range of health benefits. However, while benefits have been clearly shown, especially for CVD, the mechanisms for prevention/benefit are less understood.
Analysis of plasma and erythrocyte phospholipids (PL) have been used to measure the status of the highly unsaturated fatty acids (HUFA), especially EPA (20:5 n-3) and DHA (22:6 n-3), although the time and complexity of the process places limitations on the sample numbers analysed.
An assay has been developed using whole blood, collected by finger prick, and stored on absorbant paper, subjected to direct methylation and fatty acids quantified by automated GC. Tests on fatty acid stability show that blood samples are stable when stored at -20 degrees C for 1 month although some loss of HUFA was seen at 4 degrees C. A total of fifty-one patients, including twenty-seven who consumed no fatty acid supplements, provided a blood sample for analysis.
Concentrations of all major fatty acids were measured in erythrocyte PL and whole blood. The major HUFA, including EPA, DHA and arachidonic acid (ARA; 20:4 n-6), as well as the ARA:EPA ratio and the percentage n-3 HUFA/total HUFA all showed good correlations, between erythrocyte PL and whole blood. Values of r 2 ranged from 0.48 for ARA to 0.95 for the percentage of n-3 HUFA/total HUFA.
This assay provides a non-invasive, rapid and reliable method of HUFA quantification with the percentage of n-3 HUFA value providing a potential blood biomarker for large-scale nutritional trials.
1861Rett & Whelan 2011 - Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic reviewIncreasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic reviewIncreasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review
Rett BS, Whelan J.23/06/2011Nutr Metab (Lond). 10;8(1):36. [Epub ahead of print]
BACKGROUND: Linoleic acid, with a DRI of 12-17g/d, is the most highly consumed polyunsaturated fatty acid in the Western diet and is found in virtually all commonly consumed foods. The concern with dietary linoleic acid, being the metabolic precursor of arachidonic acid, is its consumption may enrich tissues with arachidonic acid and contribute to chronic and overproduction of bioactive eicosanoids. However, no systematic review of human trials regarding linoleic acid consumption and subsequent changes in tissue levels of arachidonic acid has been undertaken.
OBJECTIVE: In this study, we reviewed the human literature that reported changes in dietary linoleic acid and its subsequent impact on changing tissue arachidonic acid in erythrocytes and plasma/serum phospholipids.
DESIGN: We identified, reviewed, and evaluated all peer-reviewed published literature presenting data outlining changes in dietary linoleic acid in adult human clinical trials that reported changes in phospholipid fatty acid composition (specifically arachidonic acid) in plasma/serum and erythrocytes within the parameters of our inclusion/exclusion criteria.
RESULTS: Decreasing dietary linoleic acid by up to 90% was not significantly correlated with changes in arachidonic acid levels in the phospholipid pool of plasma/serum (p=0.39). Similarly, when dietary linoleic acid levels were increased up to six fold, no significant correlations with arachidonic acid levels were observed (p=0.72). However, there was a positive relationship between dietary gamma-linolenic acid and dietary arachidonic acid on changes in arachidonic levels in plasma/serum phospholipids.
CONCLUSIONS: Our results do not support the concept that modifying current intakes of dietary linoleic acid has an effect on changing levels of arachidonic acid in plasma/serum or erythrocytes in adults consuming Western-type diets.
omega-6 PUFA, EFA-HUFA conversion, linoleic acid, LA, arachidonic acid, AA, human study, systematic review, free full texthttp://www.ncbi.nlm.nih.gov/pubmed/21663641View this and related abstracts via PubMed here. Free full text of this article is available online
1883Xu et al 2011 - Curcumin prevents corticosterone-induced neurotoxicity and abnormalities of neuroplasticity via 5-HT receptor pathwayCurcumin prevents corticosterone-induced neurotoxicity and abnormalities of neuroplasticity via 5-HT receptor pathwayCurcumin prevents corticosterone-induced neurotoxicity and abnormalities of neuroplasticity via 5-HT receptor pathwayXu Y, Li S, Vernon MM, Pan J, Chen L, Barish PA, Zhang Y, Acharya AP, Yu J, Govindarajan SS, Boykin E, Pan X, O'Donnell JM, Ogle WO.20/06/2011J Neurochem. 2011 Jun 20. [Epub ahead of print]
Curcumin, a major active component of Curcuma longa, possesses antioxidant and neuroprotective activities. The present study explores the mechanisms underlying the neuroprotective effect of curcumin against corticosterone and its relation to 5-hydroxy tryptamine (5-HT) receptors.
Exposure of cortical neurons to corticosterone results in decreased mRNA levels for three 5-HT receptor subtypes, 5-HT(1A) , 5-HT(2A) and 5-HT(4) , but 5-HT(1B,) 5-HT(2B) , 5-HT(2C) , 5-HT(6) and 5-HT(7) receptors remain unchanged.
Pretreatment with curcumin reversed this effect on mRNA for the 5-HT(1A) and 5-HT(4) receptors, but not for the 5-HT(2A) receptor. Moreover, curcumin exerted a neuroprotective effect against corticosterone-induced neuronal death.
This observed effect of curcumin was partially blocked by either 5-HT(1A) receptor antagonist p-MPPI or 5-HT(4) receptor antagonist RS 39604 alone; whereas, the simultaneous application of both antagonists completely reversed the effect.
Curcumin was also found to regulate corticosterone-induced morphological changes such as increases in soma size, dendritic branching and dendritic spine density, as well as elevate synaptophysin expression in cortical neurons. p-MPPI and RS 39604 reversed the effect of curcumin-induced change in neuronal morphology and synaptophysin expression of corticosterone-treated neurons.
In addition, an increase in cyclic adenosine monophosphate (cAMP) level was observed after curcumin treatment, which was further prevented by RS 39604, but not by p-MPPI. However, curcumin-induced elevation in protein kinase A (PKA) activity and phosphorylation of cAMP response element-binding protein (pCREB) levels were inhibited by both p-MPPI and RS 39604.
These findings suggest that the neuroprotection and modulation of neuroplasticity exhibited by curcumin might be mediated, at least in part, via the 5-HT receptor-cAMP-PKA-CREB signal pathway.
curcumin, antioxidant, neuroplasticity, neuroprotection, serotonin, 5-HT, animal study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/21689105View this and related abstracts via Pubmed here
3466Katz et al 2011 - Cocoa and chocolate in human health and disease.Cocoa and chocolate in human health and disease.Cocoa and chocolate in human health and disease.Katz DL, Doughty K, Ali A.13/06/2011Antioxid Redox Signal.15(10)2779-811. doi: 10.1089/ars.2010.3697. Epub 2011 Jun 13.
Cocoa contains more phenolic antioxidants than most foods. Flavonoids, including catechin, epicatechin, and procyanidins predominate in antioxidant activity.
The tricyclic structure of the flavonoids determines antioxidant effects that scavenge reactive oxygen species, chelate Fe2+ and Cu+, inhibit enzymes, and upregulate antioxidant defenses.
The epicatechin content of cocoa is primarily responsible for its favorable impact on vascular endothelium via its effect on both acute and chronic upregulation of nitric oxide production.
Other cardiovascular effects are mediated through anti-inflammatory effects of cocoapolyphenols, and modulated through the activity of NF-κB.
Antioxidant effects of cocoa may directly influence insulin resistance and, in turn, reduce risk for diabetes. Further, cocoa consumption may stimulate changes in redox-sensitive signaling pathways involved in gene expression and the immune response.
Cocoa can protect nerves from injury and inflammation, protect the skin from oxidative damage from UV radiation in topical preparations, and have beneficial effects on satiety, cognitive function, and mood.
As cocoa is predominantly consumed as energy-dense chocolate, potential detrimental effects of overconsumption exist, including increased risk of weight gain. Overall, research to date suggests that the benefits of moderate cocoa or dark chocolate consumption likely outweigh the risks.
Chocolate, cocoa flavanols, cardiovascular health, inflammation, insulin regulation, human studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/21470061View this and related abstracts via PubMed here
1841Howard et al 2011 - ADHD is associated with a 'Western' dietary pattern in adolescentsADHD is associated with a 'Western' dietary pattern in adolescentsADHD is associated with a "western" dietary pattern in adolescentsHoward AL, Robinson M, Smith GJ, Ambrosini GL, Piek JP, Oddy WH.12/06/2011J Atten Disord.Jul;15(5):403-11. Epub 2010 Jul 14.
Objective: To examine the relationship between dietary patterns and ADHD in a population-based cohort of adolescents.
Method: The Raine Study is a prospective study following 2,868 live births. At the 14-year follow-up, the authors collected detailed adolescent dietary data, allowing for the determination of major dietary patterns using factor analysis. ADHD diagnoses were recorded according to International Classification of Diseases, 9th Revision coding conventions. Logistic regression was used to assess the relationship between scores for major dietary pattern and ADHD diagnoses.
Results: Data were available for 1,799 adolescents, and a total of 115 adolescents had an ADHD diagnosis. Two major dietary patterns were identified: "Western" and "Healthy." A higher score for the Western dietary pattern was associated with ADHD diagnosis (odds ratio = 2.21, 95% confidence interval = 1.18, 4.13) after adjusting for known confounding factors from pregnancy to 14 years. ADHD diagnosis was not associated with the "Healthy" dietary pattern.
Conclusion: A Western-style diet may be associated with ADHD.
diet, ADHD, western diet, human study, observational study, adolescents http://www.ncbi.nlm.nih.gov/pubmed/20631199View this and related abstracts via PubMed here
2015Buydens-Branchey et al 2011 - Higher n-3 fatty acids are associated with more intense fenfluramine-induced ACTH and cortisol responses among cocaine-abusing menHigher n-3 fatty acids are associated with more intense fenfluramine-induced ACTH and cortisol responses among cocaine-abusing menHigher n-3 fatty acids are associated with more intense fenfluramine-induced ACTH and cortisol responses among cocaine-abusing menBuydens-Branchey L, Branchey M, Hibbeln JR11/06/2011Psychiatry Res. 2011 Aug 15;188(3):422-7. Epub 2011 Jun 11
Preclinical studies have shown that diets supplemented with or deficient in n-3 polyunsaturated fatty acids (PUFAs) could influence serotonergic neurotransmission, but information about their effects on the serotonergic function of humans is scant. Therefore, simultaneous assessments of n-3 PUFAs and of the adrenocorticotropic hormone (ACTH) and cortisol responses to challenges with the serotonin (5-HT) probe d,l-fenfluramine (FEN) were performed in 25 cocaine-abusing men and 12 control subjects. Cocaine abusers were tested 18 days after their admission to a closed ward. ACTH and cortisol were measured in plasma samples collected on two testing days separated by 48 h following the random administration of 60 mg of FEN or placebo. Fatty acids were measured in the first test day samples. Patients' FEN-induced ACTH rises were significantly and positively correlated with docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). Patients' cortisol rises were positively and significantly correlated with EPA but not with DHA. There were no significant correlations between hormonal responses and pre-hospitalization cocaine use parameters. Control subjects' responses to FEN were not correlated with any PUFA. In conclusion, higher EPA and DHA levels were associated with a more intense FEN-induced ACTH response and higher EPA levels with a more intense cortisol response in cocaine-abusing men withdrawn from cocaine but not in control subjects. These findings support and expand existing evidence that EPA and DHA could influence 5-HT function in some human subgroups.
http://www.ncbi.nlm.nih.gov/pubmed/21658782View this and related abstracts via PubMed here.
1882Sood et al 2011 - Curcumin Attenuates Aluminum-Induced Oxidative Stress and Mitochondrial Dysfunction in Rat BrainCurcumin Attenuates Aluminum-Induced Oxidative Stress and Mitochondrial Dysfunction in Rat BrainCurcumin Attenuates Aluminum-Induced Oxidative Stress and Mitochondrial Dysfunction in Rat BrainSood PK, Nahar U, Nehru B.09/06/2011Neurotox Res. Jun 9. [Epub ahead of print]
Aluminum is neurotoxic both in animals and human beings primarily because of its interference with biological enzymes in key mechanisms of metabolic pathways. Mitochondrial dysfunction is one such mechanism that has been implicated in the pathogenesis of neurodegenerative diseases like Alzheimer's disease.
Aluminum toxicity is very closely related to Alzheimer's disease. We evaluated the potentials of curcumin, a known cytoprotectant, against neurotoxic consequences of aluminum that acts through a wide range of mechanisms. Curcumin has been reported to be an antioxidant, and it is this property that is widely held to be responsible for its protective effects in tissue.
Aluminum was administered by oral gavage at a dose level of 100 mg/kg body wt/day for a period of 8 weeks. Curcumin was administered in conjunction with aluminum at a dose of 50 mg/kg of body wt i.p. for a period of 8 weeks on alternate days. The effects of different treatments were studied on oxidative phosphorylation and reduced glutathione of different regions of rat brain.
The study indicates reduced activity of NADH dehydrogenase (complex I), succinic dehydrogenase (complex II), and cytochrome oxidize (Complex IV) in all the three regions of rat brain, i.e., cerebral cortex, mid brain, and cerebellum. Curcumin supplementation to aluminum-treated rats was able to normalize significantly the activities of all the three mitochondrial complexes as well as reduced glutathione content in all the three regions of brain which were altered following aluminum treatment.
We conclude that curcumin, by attenuating oxidative stress, as evident by hypoxia in histological observations and mitochondrial dysfunction holds a promise as an agent that can potentially reduce aluminum-induced adverse effects in brain.
curcumin, aluminium, neurotoxicity, antioxidant, mitochondria, animal study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/21656326View this and related abstracts via Pubmed here
1859Adams et al 2011 - Nutritional and Metabolic Status of Children with Autism vs. Neurotypical Children, and the Association with Autism SeverityNutritional and Metabolic Status of Children with Autism vs. Neurotypical Children, and the Association with Autism SeverityNutritional and Metabolic Status of Children with Autism vs. Neurotypical Children, and the Association with Autism SeverityAdams JB, Audhya T, McDonough-Means S, Rubin RA, Quig D, Geis E, Gehn E, Loresto M, Mitchell J, Atwood S, Barnhouse S, Lee W.08/06/2011Nutr Metab (Lond). 8(1):34. [Epub ahead of print]
BACKGROUND: The relationship between relative metabolic disturbances and developmental disorders is an emerging research focus. This study compares the nutritional and metabolic status of children with autism with that of neurotypical children and investigates the possible association of autism severity with biomarkers.
METHOD: Participants were children ages 5-16 years in Arizona with Autistic Spectrum Disorder (n=55) compared with non-sibling, neurotypical controls (n=44) of similar age, gender and geographical distribution. Neither group had taken any vitamin/mineral supplements in the two months prior to sample collection. Autism severity was assessed using the Pervasive Development Disorder Behavior Inventory (PDD-BI), Autism Treatment Evaluation Checklist (ATEC), and Severity of Autism Scale (SAS). Study measurements included: vitamins, biomarkers of vitamin status, minerals, plasma amino acids, plasma glutathione, and biomarkers of oxidative stress, methylation, sulfation and energy production.
RESULTS: Biomarkers of children with autism compared to those of controls using a t-test or Wilcoxon test found the following statistically significant differences (p<0.001): Low levels of biotin, plasma glutathione, RBC SAM, plasma uridine, plasma ATP, RBC NADH, RBC NADPH, plasma sulfate (free and total), and plasma tryptophan; also high levels of oxidative stress markers and plasma glutamate. Levels of biomarkers for the neurotypical controls were in good agreement with accessed published reference ranges. In the Autism group, mean levels of vitamins, minerals, and most amino acids commonly measured in clinical care were within published reference ranges. A stepwise, multiple linear regression analysis demonstrated significant associations between several groups of biomarkers with all three autism severity scales, including vitamins (adjusted R2 of 0.25-0.57), minerals (adj. R2 of 0.22-0.38), and plasma amino acids (adj. R2 of 0.22-0.39).
CONCLUSION: The autism group had many statistically significant differences in their nutritional and metabolic status, including biomarkers indicative of vitamin insufficiency, increased oxidative stress, reduced capacity for energy transport, sulfation and detoxification. Several of the biomarker groups were significantly associated with variations in the severity of autism. These nutritional and metabolic differences are generally in agreement with other published results and are likely amenable to nutritional supplementation. Research investigating treatment and its relationship to the co-morbidities and etiology of autism is warranted.
nutrition, metabolism, vitamins, minerals, oxidative stress, autism, ASD, human study, case-control study, free full texthttp://www.ncbi.nlm.nih.gov/pubmed/21651783View this and related abstracts via PubMed here. Free full text of this article is available online
3462Field et al 2011 - Consumption of cocoa flavanols results in an acute improvement in visual and cognitive functions.Consumption of cocoa flavanols results in an acute improvement in visual and cognitive functions.Cocoa flavanols found in dark Chocolate improve visual and cognitive functionField DT, Williams CM, Butler LT.01/06/2011Physiol Behav. 103(3-4):255-60. doi: 10.1016/j.physbeh.2011.02.013. Epub 2011 Feb 12.
Cocoa flavanols (CF) influence physiological processes in ways that suggest their consumption may improve aspects of neural function, and previous studies have found positive influences of CF on cognitive performance.
In this preliminary study we investigated whether visual, as well as cognitive, function is influenced by an acute dose of CF in young adults. We employed a randomized, single-blinded, order counterbalanced, crossover design in which 30 healthy adults consumed both dark chocolate containing 720mg CF and a matched quantity of white chocolate, with a one week interval between testing sessions.
Visual contrast sensitivity was assessed by reading numbers that became progressively more similar in luminance to their background. Motion sensitivity was assessed firstly by measuring the threshold proportion of coherently moving signal dots that could be detected against a background of random motion, and secondly by determining the minimum time required to detect motion direction in a display containing a high proportion of coherent motion. Cognitive performance was assessed using a visual spatial working memory for location task and a choice reaction time task designed to engage processes of sustained attention and inhibition.
Relative to the control condition, CF improved visual contrast sensitivity and reduced the time required to detect motion direction, but had no statistically reliable effect on the minimum proportion of coherent motion that could be detected. In terms of cognitive performance, CF improved spatial memory and performance on some aspects of the choice reaction time task.
As well as extending the range of cognitive tasks that are known to be influenced by CF consumption, this is the first report of acute effects of CF on the efficiency of visual function. These acute effects can be explained by increased cerebral blood flow caused by CF, although in the case of contrast sensitivity there may be an additional contribution from CF induced retinal blood flow changes.
Chocolate, cocoa flavanols, vision, cognition, mental performance, human study, RCThttp://www.ncbi.nlm.nih.gov/pubmed/21324330View this and related abstracts via PubMed here
3577McCann & Ames 2011 - Adaptive dysfunction of selenoproteins from the perspective of the triage theory: why modest selenium deficiency may increase risk of diseases of agingAdaptive dysfunction of selenoproteins from the perspective of the triage theory: why modest selenium deficiency may increase risk of diseases of agingselenium and diseases of agingMcCann JC, Ames BN.01/06/2011FASEB J.25(6)1793-814. doi: 10.1096/fj.11-180885. Epub 2011 Mar 14.
The triage theory proposes that modest deficiency of any vitamin or mineral (V/M) could increase age-related diseases. V/M-dependent proteins required for short-term survival and/or reproduction (i.e., "essential") are predicted to be protected on V/M deficiency over other "nonessential" V/M-dependent proteins needed only for long-term health. The result is accumulation of insidious damage, increasing disease risk. We successfully tested the theory against published evidence on vitamin K.
Here, we review about half of the 25 known mammalian selenoproteins; all of those with mouse knockout or human mutant phenotypes that could be used as criteria for a classification of essential or nonessential. Five selenoproteins (Gpx4, Txnrd1, Txnrd2, Dio3, and Sepp1) were classified as essential and 7 (Gpx1, Gpx 2, Gpx 3, Dio1, Dio2, Msrb1, and SelN) nonessential. On modest selenium (Se) deficiency, nonessential selenoprotein activities and concentrations are preferentially lost, with one exception (Dio1 in the thyroid, which we predict is conditionally essential). Mechanisms include the requirement of a special form of tRNA sensitive to Se deficiency for translation of nonessential selenoprotein mRNAs except Dio1.
The same set of age-related diseases and conditions, including cancer, heart disease, and immune dysfunction, are prospectively associated with modest Se deficiency and also with genetic dysfunction of nonessential selenoproteins, suggesting that Se deficiency could be a causal factor, a possibility strengthened by mechanistic evidence. Modest Se deficiency is common in many parts of the world; optimal intake could prevent future disease.
triage theory, nutrition, micronutrients, vitamins and minerals, selenium, diseases of aging, cardiovascular disease, cancer, immune disorders, dementiahttp://www.ncbi.nlm.nih.gov/pubmed/21402715View this and related abstracts via PubMed here. Free full text of this article is available online.
1870Milte et al 2011 - Erythrocyte polyunsaturated fatty acid status, memory, cognition and mood in older adults with mild cognitive impairment and healthy controlsErythrocyte polyunsaturated fatty acid status, memory, cognition and mood in older adults with mild cognitive impairment and healthy controlsErythrocyte polyunsaturated fatty acid status, memory, cognition and mood in older adults with mild cognitive impairment and healthy controlsMilte CM, Sinn N, Street SJ, Buckley JD, Coates AM, Howe PR.30/05/2011Prostaglandins Leukot Essent Fatty Acids. 84(5-6):153-61. Epub 2011 Mar 9.
Polyunsaturated fatty acid (PUFA) levels are altered in adults with cognitive decline and also depression. Depression facilitates progression from mild cognitive impairment (MCI) to dementia.
We investigated associations between omega-3 (n-3) and omega-6 (n-6) PUFAs and cognition, memory and depression in 50 adults ≥65 years with MCI and 29 controls. Memory, depressive symptoms and erythrocyte PUFAs (% total fatty acids) were assessed.
Eicosapentaenoic acid (EPA) was lower in MCI vs controls (.94% vs 1.26%, p<.01); n-6 PUFAs were higher: dihomo-gamma-linolenic acid (1.51% vs 1.32%, p<.01), arachidonic acid (11.54% vs 10.70%, p<.01), n-6 docosapentaenoic acid (DPA:.46% vs.34%, p<.01), and total n-6 PUFA (24.14% vs 23.37%, p<.05). Higher n-6 DPA predicted poorer mental health. Lower n-3 DPA was associated with higher self-reported bodily pain. Adults with MCI had higher depression scores (3.05±.39 vs 1.33±.24, p<.01).
Depressive symptoms associated with elevated n-6 PUFA may contribute to cognitive decline in this population.
fatty acids, PUFA, omega-6, omega-3, RBCFA, ageing, cognitive decline, depression, mood, cognition, human studyhttp://www.ncbi.nlm.nih.gov/pubmed/21392955View this and related abstracts via PubMed here
1894Moghe et al 2011 - Histone modifications and alcohol-induced liver disease: Are altered nutrients the missing link?Histone modifications and alcohol-induced liver disease: Are altered nutrients the missing link?Histone modifications and alcohol-induced liver disease: Are altered nutrients the missing link?
Moghe A, Joshi-Barve S, Ghare S, Gobejishvili L, Kirpich I, McClain CJ, Barve S.28/05/2011World J Gastroenterol. 17(20):2465-72.
Alcoholism is a major health problem in the United States and worldwide, and alcohol remains the single most significant cause of liver-related diseases and deaths.
Alcohol is known to influence nutritional status at many levels including nutrient intake, absorption, utilization, and excretion, and can lead to many nutritional disturbances and deficiencies. Nutrients can dramatically affect gene expression and alcohol-induced nutrient imbalance may be a major contributor to pathogenic gene expression in alcohol-induced liver disease (ALD).
There is growing interest regarding epigenetic changes, including histone modifications that regulate gene expression during disease pathogenesis. Notably, modifications of core histones in the nucleosome regulate chromatin structure and DNA methylation, and control gene transcription.
This review highlights the role of nutrient disturbances brought about during alcohol metabolism and their impact on epigenetic histone modifications that may contribute to ALD. The review is focused on four critical metabolites, namely, acetate, S-adenosylmethionine, nicotinamide adenine dinucleotide and zinc that are particularly relevant to alcohol metabolism and ALD.
alcoholism, nutrition, epigenetics, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/21633651View this and related abstracts via Pubmed here. Free full text of this article is available online
1868Pascoe et al 2011 - What you eat is what you are - A role for PUFA in neuroinflammation induced depression?What you eat is what you are - A role for polyunsaturated fatty acids in neuroinflammation induced depression?What you eat is what you are - A role for polyunsaturated fatty acids in neuroinflammation induced depression?
Pascoe MC, Crewther SG, Carey LM, Crewther DP.27/05/2011Clin Nutr. May 27. [Epub ahead of print]
As essential polyunsaturated fatty acids (PUFAs) influence both inflammatory and depressive disorders, nutrition related treatment methods deserve great research interest. However, currently biological mechanisms underlying the depression modulating effects of the PUFA Omega-3 (ω-3) and Omega-6 (ω-6) derived eicosanoids (central nervous system messengers) are not fully established. Depression related naturally occurring cell death (apoptosis) is thought to be mediated by excitotoxicity and free radicals that appear in the brain immediately following any inflammatory or ischemic damage, and increases the likelihood of clinically defined depression. This review explores the hypothesis that the interaction between ω-6 and ω-3 derived eicosanoids plays a central role in control over apoptosis linked with inflammation and inflammation-driven depression, via regulation of apoptosis inducing factors including excitotoxicity and free radicals.
fatty acids, PUFA, depression, inflammation, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/21621887View this and related abstracts via PubMed here
1848Mathias et al 2011 - The impact of FADS genetic variants on omega-6 PUFA metabolism in African AmericansThe impact of FADS genetic variants on n-6 polyunsaturated fatty acid metabolism in African AmericansThe impact of FADS genetic variants on ?6 polyunsaturated fatty acid metabolism in African Americans
Mathias RA, Sergeant S, Ruczinski I, Torgerson DG, Hugenschmidt CE, Kubala M, Vaidya D, Suktitipat B, Ziegler JT, Ivester P, Case D, Yanek LR, Freedman BI, Rudock ME, Barnes KC, Langefeld CD, Becker LC, Bowden DW, Becker DM, Chilton FH20/05/2011BMC Genet. 12(1)50. [Epub ahead of print]
BACKGROUND: Arachidonic acid (AA) is a long-chain omega-6 polyunsaturated fatty acid (PUFA) synthesized from the precursor dihomo-gamma-linolenic acid (DGLA) that plays a vital role in immunity and inflammation. Variants in the Fatty Acid Desaturase (FADS) family of genes on chromosome 11q have been shown to play a role in PUFA metabolism in populations of European and Asian ancestry; no work has been done in populations of African ancestry to date.
RESULTS: In this study, we report that African Americans have significantly higher circulating levels of plasma AA (p=1.35x10-48) and lower DGLA levels (p=9.80x10-11) than European Americans. Tests for association in N=329 individuals across 80 nucleotide polymorphisms (SNPs) in the Fatty Acid Desaturase (FADS) locus revealed significant association with AA, DGLA and the AA/DGLA ratio, a measure of enzymatic efficiency, in both racial groups (peak signal p= 2.85x10-16 in African Americans, 2.68x10-23 in European Americans). Ancestry-related differences were observed at an upstream marker previously associated with AA levels (rs174537), wherein, 79-82% of African Americans carry two copies of the G allele compared to only 42-45% of European Americans. Importantly, the allelic effect of the G allele, which is associated with enhanced conversion of DGLA to AA, on enzymatic efficiency was similar in both groups.
CONCLUSIONS: We conclude that the impact of FADS genetic variants on PUFA metabolism, specifically AA levels, is likely more pronounced in African Americans due to the larger proportion of individuals carrying the genotype associated with increased FADS1 enzymatic conversion of DGLA to AA.
The huge excess of omega-6 over omega-3 fats in modern western-type diets is now thought to underlie a very wide range of physical and mental health disorders. These new findings show that people of African ancestry may be at particularly high risk for such health problems when consuming such a diet, owing to interactions between normal genetic variation and dietary fat intake.
Humans have only a limited ability to convert the simplest forms of omega-3 and omega-6 polyunstaurated fats (found in vegetable oils, nuts and seeds) into the highly unsaturated forms on which brain and body health depend.
This new research shows that on average, Americans of African descent are better at this conversion than Americans of European descent, owing to normal genetic variations affecting the enzymes involved.
Unfortunately, this can be disadvantageous to health when consuming a modern, western-type diet, which provides a huge excess of the simplest omega-6 fats, and very little omega-3. In brief, 'good converters' are more likely to accumulate a correspondong excess of the longer-chain omega-6 than 'poor converters'. This in turn increases their risks of inflammatory disorders, heart disease and stroke, and many other degenerative conditions.
genetics, fatty acid metabolism, EFA, HUFA, EFA-HUFA conversion, omega-6, DGLA, AA, inflammation, racial ancestry, African-American, Caucasian, disease risk, free full texthttp://www.ncbi.nlm.nih.gov/pubmed/21599946View this and related abstracts via PubMed here. Free full text of this article is available online.
1921Yehuda et al 2011 - Effects of essential fatty acids in iron deficient and sleep-disturbed attention deficit hyperactivity disorder (ADHD) childrenEffects of essential fatty acids in iron deficient and sleep-disturbed attention deficit hyperactivity disorder (ADHD) childrenEffects of essential fatty acids in iron deficient and sleep-disturbed attention deficit hyperactivity disorder (ADHD) childrenYehuda S, Rabinovitz-Shenkar S, Carasso RL.18/05/2011Eur J Clin Nutr. May 18. [Epub ahead of print]
Inattention, hyperactivity and impulsivity constitute the core diagnostic criteria for attention deficit hyperactivity disorder (ADHD) children. Patients generally suffer from sleep disturbance and malnutrition that can account for tiredness during the day, poor concentration, poor eating and depressed mood, along with anemia and an n-3 polyunsaturated acid deficiency.
The change of ADHD behavior in children (9-12) was studied, following 10 weeks of treatment with a polyunsaturated acid mixture on six variables: cooperation, mood, concentration, homework preparation, fatigue and sleep quality. Iron status was also examined. Polyunsaturated acid administration was associated with significant improvement in quality of life, ability to concentrate, sleep quality and hemoglobin levels.
ADHD, sleep, iron, fatty acids, omega-3, omega-6, EFA, RCTFAhttp://www.ncbi.nlm.nih.gov/pubmed/21587279View this and related abstracts via PubMed here
1922Cortese et al 2011 - Brain iron levels in ADHD: A pilot MRI studyBrain iron levels in attention-deficit/hyperactivity disorder: A pilot MRI studyIron and ADHDCortese S, Azoulay R, Castellanos FX, Chalard F, Lecendreux M, Chechin D, Delorme R, Sebag G, Sbarbati A, Mouren MC, Bernardina BD, Konofal E.17/05/2011World J Biol Psychiatry. May 17. [Epub ahead of print]
Objective. Brain iron deficiency has been supposed to be involved in the pathophysiology of ADHD. Available studies assessing iron in ADHD are based on serum ferritin, a peripheral marker of iron status. To what extent serum ferritin correlates with brain iron (BI) is unclear. The main aim of this study was to compare BI, estimated with magnetic resonance imaging (MRI) in the putamen, pallidum, caudate, and thalamus, between children with and without ADHD. The secondary aim was to assess the correlation between serum ferritin and BI levels.
Methods. Thirty-six children (18 with and 18 without ADHD, the latter including nine healthy controls and nine psychiatric controls) completed MRI and blood sampling. Brain iron levels were estimated by imaging T2*.
Results. Children with ADHD showed significantly lower estimated BI in right and left thalamus compared to healthy controls. Estimated BI did not differ significantly between children with ADHD and psychiatric controls. Children with ADHD had significantly lower levels of serum ferritin than healthy as well as psychiatric controls. Serum ferritin and T2* values did not correlate significantly in most regions.
Conclusions. Low iron in the thalamus may contribute to ADHD pathophysiology.
iron, ferritin, ADHD, brain imaging, children, human study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/21585274View this and related abstracts via PubMed here
1888Schrag et al 2011 - Iron, zinc and copper in the Alzheimer's disease brain: A quantitative meta-analysis. Some insight on the influence of citation bias on scientific opinionIron, zinc and copper in the Alzheimer's disease brain: A quantitative meta-analysis. Some insight on the influence of citation bias on scientific opinionIron, zinc and copper in the Alzheimer's disease brain: A quantitative meta-analysis. Some insight on the influence of citation bias on scientific opinionSchrag M, Mueller C, Oyoyo U, Smith MA, Kirsch WM.11/05/2011Prog Neurobiol. 94(3):296-306. [Epub ahead of print]
Dysfunctional homeostasis of transition metals is believed to play a role in the pathogenesis of Alzheimer's disease (AD). Although questioned by some, brain copper, zinc, and particularly iron overload are widely accepted features of AD which have led to the hypothesis that oxidative stress generated from aberrant homeostasis of these transition metals might be a pathogenic mechanism behind AD.
This meta-analysis compiled and critically assessed available quantitative data on brain iron, zinc and copper levels in AD patients compared to aged controls. The results were very heterogeneous. A series of heavily cited articles from one laboratory reported a large increase in iron in AD neocortex compared to age-matched controls (p<0.0001) while seven laboratories failed to reproduce these findings reporting no significant difference between the groups (p=0.76).
A more than three-fold citation bias was found to favor outlier studies reporting increases in iron and this bias was particularly prominent among narrative review articles. Additionally, while zinc was not significantly changed in the neocortex (p=0.29), copper was significantly depleted in AD (p=0.0003). In light of these findings, it will be important to re-evaluate the hypothesis that transition metal overload accounts for oxidative injury noted in AD.
zinc, iron, copper, brain, Alzheimer's disease, systematic review, meta-analysis, citation biashttp://www.ncbi.nlm.nih.gov/pubmed/21600264View this and related abstracts via Pubmed here
1827W L Xu et al - 2011 - Midlife overweight and obesity increase late-life dementia risk: A population-based twin studyMidlife overweight and obesity increase late-life dementia riskobesity and dementia; overweight and dementia; dementia; Alzheimer disease; AlzheimersW.L. Xu, MD, PhD, A.R. Atti, MD, PhD, M. Gatz, PhD, N.L. Pedersen, PhD, B. Johansson, PhD and L. Fratiglioni, MD, PhD06/05/2011Neurology. 2011 May 3;76(18):1568-74.
Objective: The relation of overweight to dementia is controversial. We aimed to examine the association of midlife overweight and obesity with dementia, Alzheimer disease (AD), and vascular dementia (VaD) in late life, and to verify the hypothesis that genetic and early-life environmental factors contribute to the observed association.
Methods: From the Swedish Twin Registry, 8,534 twin individuals aged ≥65 (mean age 74.4) were assessed to detect dementia cases (DSM-IV criteria). Height and weight at midlife (mean age 43.4) were available in the Registry. Data were analyzed as follows: 1) unmatched case-control analysis for all twins using generalized estimating equation (GEE) models and 2) cotwin matched case-control approach for dementia-discordant twin pairs by conditional logistic regression taking into account lifespan vascular disorders and diabetes.
Results: Among all participants, dementia was diagnosed in 350 subjects, and 114 persons had questionable dementia. Overweight (body mass index (BMI) >25–30) and obesity (BMI >30) at midlife were present in 2,541 (29.8%) individuals. In fully adjusted GEE models, compared with normal BMI (20–25), overweight and obesity at midlife were related to dementia with odds ratios (ORs) (95% CIs) of 1.71 (1.30–2.25) and 3.88 (2.12–7.11), respectively. Conditional logistic regression analysis in 137 dementia-discordant twin pairs led to an attenuated midlife BMI-dementia association. The difference in ORs from the GEE and the matched case-control analysis was statistically significant (p = 0.019).
Conclusions: Both overweight and obesity at midlife independently increase the risk of dementia, AD, and VaD. Genetic and early-life environmental factors may contribute to the midlife high adiposity–dementia association.
obesity and dementia; overweight and dementia; dementia; Alzheimer disease; Alzheimershttp://www.ncbi.nlm.nih.gov/pubmed/21536637View this and related abstracts via Pubmed here
3261Corwin et al 2011 - Feeding and reward: perspectives from three rat models of binge eating.Feeding and reward: perspectives from three rat models of binge eating.Feeding and reward: perspectives from three rat models of binge eating, food addictionCorwin RL, Avena NM, Boggiano MM.01/05/2011Physiol Behav.104(1)87-97. doi: 10.1016/j.physbeh.2011.04.041. Epub 2011 May 1.
Research has focused on understanding how overeating can affect brain reward mechanisms and subsequent behaviors, both preclinically and in clinical research settings. This work is partly driven by the need to uncover the etiology and possible treatments for the ongoing obesity epidemic.
However, overeating, or non-homeostatic feeding behavior, can occur independent of obesity. Isolating the variable of overeating from the consequence of increased body weight is of great utility, as it is well known that increased body weight or obesity can impart its own deleterious effects on physiology, neural processes, and behavior.
In this review, we present data from three selected animal models of normal-weight non-homeostatic feeding behavior that have been significantly influenced by Bart Hoebel's 40+-yr career studying motivation, feeding, reinforcement, and the neural mechanisms that participate in the regulation of these processes.
First, a model of sugar bingeing is described (Avena/Hoebel), in which animals with repeated, intermittent access to a sugar solution develop behaviors and brain changes that are similar to the effects of some drugs of abuse, serving as the first animal model of food addiction.
Second, another model is described (Boggiano) in which a history of dieting and stress can perpetuate further binge eating of palatable and non-palatable food. In addition, a model (Boggiano) is described that allows animals to be classified as having a binge-prone vs. binge-resistant behavioral profile.
Lastly, a limited access model is described (Corwin) in which non-food deprived rats with sporadic limited access to a high-fat food develop binge-type behaviors.
These models are considered within the context of their effects on brain reward systems, including dopamine, the opioids, cholinergic systems, serotonin, and GABA. Collectively, the data derived from the use of these models clearly show that behavioral and neuronal consequences of bingeing on a palatable food, even when at a normal body weight, are different from those that result from simply consuming the palatable food in a non-binge manner.
These findings may be important in understanding how overeating can influence behavior and brain chemistry.
food addiction, binge eating, eating disorders, substance use disorders, mechanisms, obesity, animal studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/21549136View this and related articles via PubMed here. Free full text of this article is available online.
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