The prevalence of obesity is growing and now includes at least one-third of the adult population in the United States. As obesity and dementia rates reach epidemic proportions, an even greater interest in the effects of nutrition on the brain have become evident. This review discusses various mechanisms by which a high fat diet and/or obesity can alter the brain and cognition. It is well known that a poor diet and obesity can lead to certain disorders such as type II diabetes, metabolic syndrome, and heart disease. However, long-term effects of obesity on the brain need to be further examined. The contribution of insulin resistance and oxidative stress is briefly reviewed from studies in the current literature. The role of inflammation and vascular alterations are described in more detail due to our laboratory’s experience in evaluating these specific factors. It is very likely that each of these factors plays a role in diet-induced and/or obesity-induced cognitive decline.
Cognition; Brain Health; Obesity; Inflammation; Cerebrovascularization
To determine whether externalizing behaviors are more prevalent in youth who
have experienced an episode of malnutrition in the first year of life than in healthy
Parents of previously malnourished youth and a matched healthy comparison group
completed a behavior rating scale when the youth were 9–15 years of age and
again, 2 years later, when they were 11–17 years of age. Longitudinal multiple
regression analysis was applied to evaluate group differences adjusted for baseline age,
sex, household standard of living, and maternal depressive symptoms.
Early childhood malnutrition was associated with problems in executive
functioning at both occasions. Malnutrition also predicted discernibly higher
parent-reported levels of aggression toward peers at 9–15 years than at
11–17 years. These findings were independent of baseline age, sex, household
standard of living, and maternal depressive symptoms. Problem behaviors in general
decreased during follow-up.
Parents report persisting problems with executive functioning through
adolescence in youth who suffered an episode of moderate-to-severe protein-energy
malnutrition in the first year of life, while reports of aggression, although more
common when this cohort were younger, did not persist at follow-up.
Executive function; Aggression; Malnutrition; Youth; Cross-cultural; Longitudinal study
Prenatal protein malnutrition alters the structure and function of the
adult rat hippocampal formation. The current study examines the effect of
prenatal protein malnutrition on numbers of parvalbumin-immunoreactive (PV-IR)
GABAergic interneurons, which are important for perisomatic inhibition of
hippocampal pyramidal neurons. Brain sections from prenatally protein
malnourished and normally nourished rats were stained for parvalbumin and PV-IR
neurons were quantified using stereology in the dentate gyrus, CA3/2 and CA1
subfields, and the subiculum for both cerebral hemispheres. Results demonstrated
that prenatal malnutrition did not affect the number of PV-IR interneurons in
the hippocampus. Since prenatal protein malnutrition reduces total neuron
numbers in the CA1 subfield (1), this results in an altered ratio of PV-IR
interneurons to total neuronal numbers (from 1:22.9 in controls to 1:20.5 in
malnourished rats). Additionally, there was no hemispheric asymmetry of either
PV-IR neuron numbers or ratio of PV-IR:total neuron numbers.
Undernutrition; Hemispheric asymmetry; Inhibition; CA1 subfield; CA3 subfield; Stereology
Docosahexaenoic acid (DHA, 22:6n-3) is the principal omega-3 fatty acid in mammalian brain gray matter, and emerging preclinical evidence suggests that DHA has neurotrophic and neuroprotective properties. This study investigated relationships among DHA status, neurocognitive performance, and cortical metabolism measured with proton magnetic resonance spectroscopy (1H MRS) in healthy developing male children (aged 8–10 years, n = 38). Subjects were segregated into low-DHA (n = 19) and high-DHA (n = 19) status groups by a median split of erythrocyte DHA levels. Group differences in 1H MRS indices of cortical metabolism, including choline (Cho), creatine (Cr), glutamine + glutamate + γ-aminobutyric acid (Glx), myo-inositol (mI), and N-acetyl aspartate (NAA), were determined in the right and left dorsolateral prefrontal cortex (R/L-DLPFC, BA9) and bilateral anterior cingulate cortex (ACC, BA32/33). Group differences in neurocognitive performance were evaluated with the Kaufman Brief Intelligence Test and identical-pairs version of the continuous performance task (CPT-IP). Subjects in the low-DHA group consumed fish less frequently (P = 0.02), had slower reaction times on the CPT-IP (P = 0.007), and exhibited lower mI (P = 0.007), NAA (P = 0.007), Cho (P = 0.009), and Cr (P = 0.01) concentrations in the ACC compared with the high-DHA group. There were no group differences in ACC Glx or any metabolite in the L-DLPFC and R-DLPFC. These data indicate that low-DHA status is associated with reduced indices of metabolic function in the ACC and slower reaction time during sustained attention in developing male children.
Docosahexaenoic acid; myo-inositol; dorsolateral prefrontal cortex; Anterior cingulate cortex; Proton magnetic resonance spectroscopy; omega-3 fatty acid; omega-6 fatty acid
Proliferating adult stem cells in the subgranular zone of the dentate gyrus have the capacity not only to divide, but also to differentiate into neurons and integrate into the hippocampal circuitry. The present study identifies several hippocampal genes putatively regulated by zinc and tests the hypothesis that zinc deficiency impairs neuronal stem cell differentiation.
Genes that regulate neurogenic processes were identified using microarray analysis of hippocampal mRNA isolated from adult rats fed zinc-adequate or zinc-deficient (ZD) diets. We directly tested our hypothesis with cultured human neuronal precursor cells (NT2), stimulated to differentiate into post-mitotic neurons by retinoic acid (RA), along with immunocytochemistry and western analysis.
Microarray analysis revealed the regulation of genes involved in cellular proliferation. This analysis also identified a number of genes known to be involved in neuronal differentiation, including the nuclear RA receptor, retinoid X receptor (RXR), doublecortin, and a transforming growth factor-beta (TGF-β) binding protein (P < 0.05). Zinc deficiency significantly reduced RA-induced expression of the neuronal marker proteins doublecortin and β-tubulin type III (TuJ1) to 40% of control levels (P < 0.01). This impairment of differentiation may be partially mediated by alterations in TGF-β signaling. The TGF-β type II receptor, responsible for binding TGF-β during neuronal differentiation, was increased 14-fold in NT2 cells treated with RA (P < 0.001). However, this increase was decreased by 60% in ZD RA-treated cells (P < 0.001).
This research identifies target genes that are involved in governing neurogenesis under ZD conditions and suggests an important role for TGF-β and the trace metal zinc in regulating neuronal differentiation.
Hippocampus; Neurogenesis; NT2; RXR; TGF-β
Key antioxidants, vitamins C and E, are necessary for normal brain development and neuronal function. In this study, we depleted both of these vitamins in two mouse models to determine if oxidative stress due to combined vitamin C and E dietary deficiency altered their neurological phenotype. The first model lacked both alleles for the Gulonolactone oxidase gene (Gulo−/−) and therefore was unable synthesize vitamin C. To obtain an additional cellular deficiency of vitamin C, the second model also lacked one allele for the cellular vitamin C transporter gene (Gulo−/−/SVCT2+/−).
The experimental treatment was 16 weeks of vitamin E deprivation followed by 3 weeks of vitamin C deprivation. Mice were assessed for motor coordination deficits, vitamin levels, and oxidative stress biomarkers.
In the first model, defects in motor performance were more apparent in both vitamin C-deficient groups (VE+VC−, VE−VC−) compared to vitamin C-supplemented groups (VE+VC+, VE−VC+) regardless of vitamin E level. Analysis of brain cortex and liver confirmed decreases of at least 80% for each vitamin in mice on deficient diets. Vitamin E deficiency doubled oxidative stress biomarkers (F2-isoprostanes and malondialdehyde). In the second model, Gulo−/−/SVCT2+/− mice on the doubly deficient diets showed deficits in locomotor activity, Rota-rod performance, and other motor tasks, with no concomitant change in anxiety or spatial memory.
Vitamin E deficiency alone caused a modest oxidative stress in brain that did not affect motor performance. Adding a cellular deficit in vitamin C to dietary deprivation of both vitamins significantly impaired motor performance.
Ascorbic acid; Brain; Mouse behavior; Oxidative stress; SVCT2; Vitamin C deficiency; Vitamin E deficiency
Consumption of a high-fat and/or high-cholesterol diet can have detrimental effects on the brain. In the present study, dietary treatment with saturated fats, trans fats, or cholesterol to middle-aged Fischer 344 rats resulted in alterations to serum triglyceride and cholesterol levels, organ weights, and hippocampal morphology. Previously, we demonstrated that a 10% hydrogenated coconut oil and 2% cholesterol diet resulted in worse performance on the 12-day water radial arm maze, increased cholesterol and triglyceride levels, and decreased dendritic microtubule associated protein 2 (MAP2) staining in the hippocampus. The diets administered herein were used to examine components from the previous diet and further examine their effects on hippocampal morphology. Specifically, neuronal morphology, dendritic integrity, fatty acid metabolism, microgliosis, and blood vessel structure in the hippocampus and/or adjacent structures were explored. Our results indicate alterations to peripheral and neural systems following each of the diets.
Saturated fat; Trans fat; Morphology; Aging; Dietary effects
Our laboratory is investigating the effects of protein–energy malnutrition (PEM) on cognitive outcome following global ischemia. Here, we investigated whether PEM independently impairs working memory in the T-maze and if the associated food reward reverses PEM. Gerbils were fed 12.5% (control diet) or 2% protein. A loss of body weight (20.1%) in the 2% protein group and decreased food intake and serum albumin concentration compared to controls (17.5% and 18.2%, respectively) indicated that PEM was achieved. Based on T-maze criterion frequently used in ischemia studies, no difference was observed in the mean (±SEM) number of trials required (control 5.2 ± 0.7; PEM 4.9 ± 0.4; p = 0.758) or the number of animals reaching criterion (control 10/12; PEM 12/12; p = 0.140). Using more stringent criterion, PEM animals required fewer trials (control 7.3 ± 0.7; PEM 5.4 ± 0.4; p = 0.035), and more reached criterion (control 8/12; PEM 12/12; p = 0.028). PEM may increase motivation to obtain a food reward.
PMID: 18019396 CAMSID: cams3783
Protein–energy malnutrition; gerbil; T-maze; reward; nutrition; global ischemia
Xanthophyll pigments lutein and zeaxanthin cross the blood-retina barrier to preferentially accumulate in the macular region of the neural retina. There they form macular pigment, protecting the retina from blue light damage and oxidative stress. Lutein and zeaxanthin also accumulate in brain tissue. The objective of the study was to evaluate the relationship between retinal and brain levels of these xanthophylls in non-human primates.
Study animals included rhesus monkeys reared on diets devoid of xanthophylls that were subsequently fed pure lutein or pure zeaxanthin (both at 3.9 μmol/kg*d, n=6/group) and normal rhesus monkeys fed a stock diet (0.26 μmol/kg*d lutein and 0.24 μmol/kg*d zeaxanthin, n=5). Retina (4 mm macular punch, 4-8 mm annulus and periphery) and brain tissue (cerebellum, frontal cortex, occipital cortex and pons) from the same animals were analyzed by reverse phase HPLC.
Lutein in the macula and annulus were significantly related to lutein levels in the cerebellum, occipital cortex and pons, both in bivariate analysis and after adjusting for age, sex and n–3 fatty acid status. In the frontal cortex the relationship was marginally significant. Macular zeaxanthin was significantly related to zeaxanthin in the cerebellum and frontal cortex, while the relationship was marginally significant in the occipital cortex and pons in a bivariate model.
An integrated measure of total macular pigment optical density, which can be measured noninvasively, has the potential to be used as a biomarker to assess brain lutein and zeaxanthin status.
brain; cognition; lutein; macula; zeaxanthin
The purpose of this study was to compare the prevalence of conduct
problems in a well-documented sample of Barbadian adolescents malnourished
as infants and a demographic comparison group and to determine the extent to
which cognitive impairment and environmental factors account for this
Behavioral symptoms were assessed using a 76-item self-report scale
in 56 Barbadian youth (11–17 years of age) with histories of
protein–energy malnutrition (PEM) limited to the first year of life
and 60 healthy classmates. Group comparisons were carried out by
longitudinal and cross-sectional multiple regression analyses at 3 time
points in childhood and adolescence.
Self-reported conduct problems were more prevalent among previously
malnourished youth (P < 0.01). Childhood IQ and
home environmental circumstances partially mediated the association with
malnutrition. Teacher-reported classroom behaviors at earlier ages were
significantly correlated with youth conduct problems, confirming the
continuity of conduct problems through childhood and adolescence.
Self-reported conduct problems are elevated in children and
adolescents with histories of early childhood malnutrition. Later
vulnerability to increased conduct problems appears to be mediated by the
more proximal neurobehavioral effects of the malnutrition on cognitive
function and by adverse conditions in the early home environment.
Conduct problem; Malnutrition; Adolescence; Cross-cultural; Longitudinal study
Phenolics are important phytochemicals which have positive effects on chronic diseases, including neurodegenerative ailments. The oil palm (Elaeis guineensis) is a rich source of water-soluble phenolics. This study was carried out to discover the effects of administering oil palm phenolics (OPP) to mice, with the aim of identifying whether these compounds possess significant neuroprotective properties.
OPP was given to BALB/c mice on a normal diet as fluids for 6 weeks while the controls were given distilled water. These animals were tested in a water maze and on a rotarod weekly to assess the effects of OPP on cognitive and motor functions, respectively. Using Illumina microarrays, we further explored the brain gene expression changes caused by OPP in order to determine the molecular mechanisms involved. Real-time quantitative reverse transcription-polymerase chain reaction experiments were then carried out to validate the microarray data.
We found that mice given OPP showed better cognitive function and spatial learning when tested in a water maze, and their performance also improved when tested on a rotarod, possibly due to better motor function and balance. Microarray gene expression analysis showed that these compounds up-regulated genes involved in brain development and activity, such as those under the regulation of the brain-derived neurotrophic factor. OPP also down-regulated genes involved in inflammation.
These results suggest that the improvement of mouse cognitive and motor functions by OPP is caused by the neuroprotective and anti-inflammatory effects of the extract.
Antioxidants; Gene expression; Microarray; Neurodegeneration; Oil palm phenolics
The present study investigated the relationships among oxidative stress, β-amyloid and cognitive abilities in the APP/PSEN1 double-transgenic mouse model of Alzheimer’s disease. In two experiments, long-term dietary supplements were given to aged APP/PSEN1 mice containing vitamin C alone (1g/kg diet, Expt. 1) or in combination with a high (750 IU/kg diet, Expts. 1 and 2) or lower (400 IU/kg diet, Expt. 2) dose of vitamin E. Oxidative stress, measured by F4-neuroprostanes or malondialdehyde, was elevated in cortex of control-fed APP/PSEN1 mice and reduced to wild-type levels by vitamin supplementation. High dose vitamin E with C was less effective at reducing oxidative stress than vitamin C alone or the low EC diet combination. The high-dose combination also impaired water maze performance in mice of both genotypes. In Experiment 2 the lower vitamin EC treatment attenuated spatial memory deficits in APP/PSEN1 mice and improved performance in wild-type mice in the water maze. Amyloid deposition was not reduced by antioxidant supplementation in either experiment.
Vitamin C; Vitamin E; oxidative stress; Alzheimer’s disease; cognition
Epidemiological studies have demonstrated that the consumption of fruits and vegetables is associated with reduced risk for cardiovascular disease and stroke. Detailed investigations into the specific dietary components of these foods have revealed that many polyphenolic constituents exert anti-oxidant effects on key substrates involved in the pathogenesis and progression of ischemic injury. These data have perpetuated the belief that the protective effects of flavonoids result from direct anti-oxidant actions at the levels of the cerebral vasculature and brain parenchyma. While many in vitro studies using purified extracts support this contention, first-pass metabolism alters the bioavailability of flavonoids such that the achievable concentrations after oral consumption are not consistent with this mechanism. Importantly, oral consumption of flavonoids may promote neural protection by facilitating the expression of gene products responsible for detoxifying the ischemic microenvironment through both anti-oxidative and anti-inflammatory actions. In particular, the transcriptional factor nuclear factor erythroid 2-related factor 2 has emerged as a critical regulator of flavonoid-mediated protection through the induction of various cytoprotective genes. The pleiotropic effects associated with potent transcriptional regulation likely represent the primary mechanisms of neural protection, as the flavonoid concentrations reaching ischemic tissues in vivo are sufficient to alter intracellular signal transduction but likely preclude the one-to-one stoichiometry necessary to confer protection by direct anti-oxidation. These data reflect an exciting new direction in the study of complementary and alternative medicine that may lead to the development of novel therapies for ischemic/hemorrhagic stroke, traumatic brain injury, and other neurological disorders.
Ischemia; Nuclear factor (erythroid-derived 2)-like 2; Polyphenol; Stroke; Therapy; Complementary and alternative medicine
Polyphenols, natural compounds found in plant-based foods, possess special properties that can battle oxidative stress and stimulate the activation of molecules that aid in synaptic plasticity, a process that underlies cognitive function. Unlike many traditional treatments, polyphenols affect a broad range of mechanisms in the brain that can assist in the maintenance of cognitive and mental health, as well as the recovery from neurodegenerative diseases. Examining the molecular basis underlying the link between food intake and brain function has presented the exciting possibility of using diet as a viable method to battle cognitive and psychiatric disorders.
We will discuss the molecular systems that link polyphenols, the gut, and the brain, as well as introduce published human and animal studies demonstrating the effects of polyphenol consumption on brain plasticity and cognition.
By influencing cellular energy metabolism and modulating the signaling pathways of molecules involved with brain plasticity, dietary factors – formerly recognized for just their effects on bodily systems – have emerged as affecters of the brain.
Thus, the consumption of diets enriched with polyphenols may present the potential of dietary manipulation as a non-invasive, natural, and inexpensive therapeutic means to support a healthy brain.
BDNF; Cognition; Metabolism; Polyphenol; Psychiatric disorder; Synaptic plasticity
Perinatal iron deficiency results in persistent hippocampus-based cognitive deficits in adulthood despite iron supplementation. The objective of the present study was to determine the long-term effects of perinatal iron deficiency and its treatment on hippocampal anatomy and neurochemistry in formerly iron-deficient young adult rats.
Perinatal iron deficiency was induced using a low-iron diet during gestation and the first postnatal week in male rats. Hippocampal size was determined using volumetric magnetic resonance imaging at 8 weeks of age. Hippocampal neurochemical profile, consisting of 17 metabolites indexing neuronal and glial integrity, energy reserves, amino acids, and myelination, was quantified using high-field in vivo 1H NMR spectroscopy at 9.4 T (N = 11) and compared with iron-sufficient control group (N = 10).
The brain iron concentration was 56% lower than the control group at 7 days of age in the iron-deficient group, but had recovered completely at 8 weeks. The cross-sectional area of the hippocampus was decreased by 12% in the formerly iron-deficient group (P = 0.0002). The hippocampal neurochemical profile was altered: relative to the control group, creatine, lactate, N-acetylaspartylglutamate, and taurine concentrations were 6–29% lower, and glutamine concentration 18% higher in the formerly iron-deficient hippocampus (P < 0.05).
Perinatal iron deficiency was associated with reduced hippocampal size and altered neurochemistry in adulthood, despite correction of brain iron deficiency. The neurochemical changes suggest suppressed energy metabolism, neuronal activity, and plasticity in the formerly iron-deficient hippocampus. These anatomic and neurochemical changes are consistent with previous structural and behavioral studies demonstrating long-term hippocampal dysfunction following perinatal iron deficiency.
Hippocampus; 1H NMR spectroscopy; Iron; Newborn; Perinatal iron deficiency
Iron deficiency in infancy negatively impacts a variety of neurodevelopmental processes at the time of nutrient insufficiency, with persistent central nervous system alterations and deficits in behavioral functioning, despite iron therapy. In rodent models, early iron deficiency impairs the hippocampus and the dopamine system. We examined the possibility that young adults who had experienced chronic, severe iron deficiency as infants would exhibit deficits on neurocognitive tests with documented frontostriatal (Trail Making Test, Intra-/Extra-dimensional Shift, Stockings of Cambridge, Spatial Working Memory, Rapid Visual Information Processing) and hippocampal specificity (Pattern Recognition Memory, Spatial Recognition Memory). Participants with chronic, severe iron deficiency in infancy performed less well on frontostriatal-mediated executive functions, including inhibitory control, set-shifting, and planning. There was also evidence of impairment on a hippocampus-based recognition memory task. We suggest that these deficits may result from the long-term effects of early iron deficiency on the dopamine system, the hippocampus, and their interaction.
Iron deficiency; development; memory; executive functioning
Studies have shown that modifying dietary cholesterol may improve learning and that serum cholesterol levels can be positively correlated with cognitive performance. Rabbits fed a 0, 0.5, 1 or 2% cholesterol diet for eight weeks and 0.12ppm copper added to their drinking water received trace and then delay classical conditioning pairing tone with corneal air puff during which movement of the nictitating membrane (NM) across the eye was monitored. We found that the level of classical conditioning and conditioning-specific reflex modification (CRM) as well as the number of beta amyloid-labeled neurons in the cortex and hippocampus were a function of the concentration of cholesterol in the diet. The data provide support for the idea that dietary cholesterol may facilitate learning and memory.
Beta amyloid; cholesterol; classical conditioning; nictitating membrane response; learning; rabbit
Modifying dietary cholesterol may improve learning and memory but very high cholesterol can cause pathophysiology and death. Rabbits fed 2% cholesterol for 8, 10 or 12 weeks with 0.12 ppm copper added to distilled water and rabbits fed a normal diet without copper added to distilled water (0 weeks) were given a difficult trace classical conditioning task and an easy delay conditioning task pairing tone with corneal air puff. The majority of cholesterol-fed rabbits survived the deleterious effects of the diet but survival was an inverse function of the diet duration. Compared to controls, the level of classical conditioning and conditioning-specific reflex modification were an inverted “U”-shaped function of diet duration. Highest levels of responding occurred in rabbits on cholesterol for 10 weeks and trace conditioning was negatively correlated with the number of hippocampal β-amyloid-positive neurons. Rabbits on the diet for 12 weeks responded at levels comparable to controls. The data provide support for the idea that dietary cholesterol may facilitate learning and memory but there is an eventual trade off with pathophysiological consequences of the diet.
β-Amyloid; cholesterol; classical conditioning; nictitating membrane response; learning; rabbit
The pre-school years (i.e., 1–5 years of age) is a time of rapid and dramatic postnatal brain development, i.e., neural plasticity, and of fundamental acquisition of cognitive development i.e., working memory, attention and inhibitory control. Also, it is a time of transition from a direct maternal mediation/selection of diet-based nutrition to food selection that is more based on self-selection and self-gratification. However, there have been fewer published studies in pre-school children than in infants or school-aged children that examined the role of nutrition in brain/mental development (i.e., 125 studies vs. 232 and 303 studies, respectively during the last 28 years, Figure 1). This may arise because of age-related variability, in terms of individual differences in temperament, linguistic ability, and patterns of neural activity that may affect assessment of neural and cognitive development in pre-school children. In this review, we suggest several approaches for assessing brain function in children that can be refined. It would be desirable if the discipline developed some common elements to be included in future studies of diet and brain function, with the idea that they would complement more targeted measures based on time of exposure and understanding of data from animal models. Underlining this approach is the concepts of “window of sensitivity” during which nutrients may affect postnatal neural development: investigators and expert panels need to specifically look for region-specific changes and do so with understanding of the likely time window during which the nutrient was, or was not available. (244 words)
Brain plasticity; children; nutrition; cognition; memory; neurogenesis; synaptogenesis
Copper deficiency is associated with impaired brain development and mitochondrial dysfunction. Perinatal copper deficiency was produced in Holtzman rats. In vivo proton NMR spectroscopy was used to quantify 18 cerebellar and hippocampal metabolites on postnatal day 21 (P21). Copper status was evaluated in male copper-adequate (CuA) and copper-deficient (CuD) brothers at P19 and at P23, 2 days following NMR experiments, by metal and in vitro metabolite data. Compared to CuA pups, CuD pups had lower ascorbate concentration in both brain regions, confirming prior HPLC data. Both regions of CuD rats also had lower N-acetylaspartate levels consistent with delayed development or impaired mitochondrial function similar to prior work demonstrating elevated lactate and citrate. For other metabolites, the P21 neurochemical profile of CuD rats was remarkably similar to CuA rats but uniquely different from iron-deficient or chronic hypoxia models. Further research is needed to determine the neurochemical consequences of copper deficiency.
copper deficient; rat; cerebellum; hippocampus; NMR; metabolites
Dietary copper (Cu) deficiency was induced perinatally in Swiss Albino mice and postnatally in male Holtzman rats to investigate the effect of L-threo 3,4-dihydroxyphenylserine (DOPS) on pup survival and catecholamine levels in a 2 × 2 factorial design. Mouse dams were placed on one of four treatments 14 days after mating and rats at postnatal day 19 (P19). Treatments were Cu-adequate (Cu +) and Cu-deficient (Cu −) diets with or without DOPS (1 mg/ml) in the drinking water. Mouse pups were killed at P14 and rats at P49. Mortality in Cu − pups was 46% and not significantly improved by DOPS, 39%. A repeat study with mice adding ascorbic acid in the water with DOPS showed no improvement. Compared to Cu + animals, Cu − animals were smaller, anemic and had a 92% reduction in liver Cu. DOPS treatment made no improvement to and in some cases exacerbated the Cu deficiency. Catecholamine levels measured in heart and brain by LCEC showed decreased NE levels and increased DA levels in Cu − animals compared to controls. DOPS treatment did not alter this pattern. Although DOPS was present in treated animal’s tissues, survival in mice and catecholamine levels in mice and rats were not altered by the 1 mg/ml dose of DOPS.
L-threo 3,4-dihydroxyphenylserine; catecholamines; copper deficiency; development; mice; rats
This symposium examined current trends in neuroscience and developmental psychology as they apply to assessing the effects of nutrients on brain and behavioral development of 0-6 year olds. Although the spectrum of nutrients with brain effects has not changed much in the last 25 years, there has been an explosion in new knowledge about the genetics, structure, and function of the brain. This has helped to link brain mechanistic pathway by which these nutrients act with cognitive functions. Clear examples of this are linking of brain structural changes due to hypoglycemia vs. hyperglycemia with cognitive functions by using Magnetic Resonance Imaging (MRI) to assess changes in brain-region volumes in combination with cognitive test of intelligence, memory and processing speed. Another example is the use of Event Related Potential (ERP) studies to show that infants of diabetic mothers have impairments in memory from birth through 8 months of age that are consistent with alterations in mechanistic pathways of memory observed in animal models of perinatal iron deficiency. However, gaps remain in the understanding of how nutrients and neurotrophic factors interact with each other in optimizing brain development and function.
Brain; behavior; event related potentials; magnetic resonance imaging; nutrition; nutrients
To establish whether a diet based on the usage of low-protein products for renal patients (LPP) is associated with higher energy expenditure (EE) than a free low-protein diet (NO-LPP) by calculating 24 h EE by indirect calorimetry using an electronic armband monitor.
Randomized, cross-over, single-blind, pilot clinical trial performed comparing two different low-protein dietary regimens.
Forty-two days with LPP and 42 days with NO-LPP regimen in six patients with Parkinson's disease with levodopa.
Monitoring patient response to two different nutritional schemes through indirect calorimetry (armband), BMI, Patient Global Improvement Scale.
Mean total EE was 1731 ± 265 kcal/day with NO-LPP vs. 1903 ± 265 kcal/day with LPP (p = 0.02).
The usage of LPP increases EE and improves motor function in PD patients to a greater extent than NO-LPP dietary regimen. Calorie intake should be increased to prevent malnutrition in the long-term.
Fondazione Grigioni per il Morbo di Parkinson.
Parkinson's disease; diet; energy expenditure; levodopa
Decreased tissue levels of n-3 (omega-3) fatty acids, particularly docosahexaenoic acid (DHA), are implicated in the etiologies of non-puerperal and postpartum depression. This study examined the effects of a diet-induced loss of brain DHA content and concurrent reproductive status on dopaminergic parameters in adult female Long–Evans rats. An α-linolenic acid-deficient diet and breeding protocols were used to produce virgin and parous female rats with cortical phospholipid DHA levels 20–22% lower than those fed a control diet containing adequate α-linolenic acid. Decreased brain DHA produced a significant main effect of decreased density of ventral striatal D2-like receptors. Virgin females with decreased DHA also exhibited higher density of D1-like receptors in the caudate nucleus than virgin females with normal DHA. These receptor alterations are similar to those found in several rodent models of depression, and are consistent with the proposed hypodopaminergic basis for anhedonia and motivational deficits in depression.
omega-3; polyunsaturated fatty acid; dopamine receptor; postpartum; docosahexaenoic acid; rat