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, , Merve Altın, Özge Hacıraifoğlu, Burak Yıldız
Published: 27 October 2017
Nutritional Neuroscience, Volume 22, pp 392-400; https://doi.org/10.1080/1028415x.2017.1392429

Abstract:
Obesity is one of today's most important public health problems. It is suggested that overeating and substance addiction show similarities, and addiction to food may be an important factor in the obesity epidemic. This study aimed to determine the prevalence of food addiction among schizophrenic patients and to examine the relationship between food addiction and anthropometric measurements and dietary nutrient intake.Study participants included a total of 104 schizophrenic outpatients, 62 females and 42 males. Food addiction was assessed by using the Yale Food Addiction Scale, and the anthropometric measurements of participants and their three-day food consumption were recorded.This study found that more than half of the schizophrenic patients (60.6%) had food addiction, and that female schizophrenic patients had a higher prevalence (62.9%) of food addiction than male patients (57.1%). More than one-third of the schizophrenic patients with food addiction (41.3%) were found to be obese and their BMI, body weight, waist circumference, and body-fat ratio were higher than those of schizophrenic patients who did not have food addiction (P > 0.05). Moreover, the schizophrenic patients with food addiction were found to take significantly more energy, carbohydrate, and fat in their diet (P < 0.05).It was observed that the development of food addiction in schizophrenic patients increased the risk of obesity and cardiovascular diseases, which were found to be at higher levels in these patients. Educational programs should be planned for these patients to acquire health dietary habits and to increase their physical activity levels, and an additional psychosocial support should be provided for patients with food addiction.
Shahabeddin Rezaei, Ahmed Abdulahi Abdurahman, Amene Saghazadeh, Reza Shervin Badv,
Published: 23 October 2017
Nutritional Neuroscience, Volume 22, pp 317-334; https://doi.org/10.1080/1028415x.2017.1387721

Abstract:
Objectives: Classical ketogenic diet (KD) and modified Atkins diet (MAD) are two types of KD commonly used for the treatment of intractable epilepsy throughout the world. Studies have shown the efficacy of these diets. However, no systematic review and meta-analysis study has to date compared the efficacy of KD and MAD in a time trend. Therefore, the objectives of the present study were to compare the short-term and long-term efficacy of classical KD and MAD in children and adolescents with epilepsy and to determine the efficacy of classical KD and MAD at multiple time points and in a time trend. Methods: Main electronic literature databases, including MEDLINE/PubMed, Web of Science, Scopus, and EMBASE, were searched in November 2016. Rate difference and random effects model were used to compare the efficacy of the classical KD and MAD. Results: Overall, 70 studies were eligible for inclusion. Meta-analysis revealed a non-significant trend toward a higher efficacy of MAD at month-3 and month-6 (P > 0.05). In the classical KD group, the percentage of responder patients achieving ≥50% seizure reduction was 62, 60, 52, 42, and 46% at month-1, 3, 6, 12 and 24 and for the MAD group was 55, 47, 42, and 29% at month-1, 3, 6, and 12, respectively. Discussion: Classical KD does not differ substantially from MAD in ≥50% and ≥90% reduction of seizure frequency at month-3 and month-6. Overall, the number of patients achieving seizure freedom increases over time.
, , F. Bernardo Pliego-Rivero, Gustavo G. Mendieta
Published: 23 October 2017
Nutritional Neuroscience, Volume 22, pp 363-372; https://doi.org/10.1080/1028415x.2017.1391529

Abstract:
Objective: To use quantitative electroencephalography (qEEG) to assess the impact of iron-deficiency anemia on central nervous system maturation in the first year of life. Method: Twenty-five infants (3–12 months old) presenting ferropenic anemia (IDA) and 25 healthy controls (CTL1), matched by age/gender with the former, were studied in two stages. Electroencephalogram during spontaneous sleep was recorded from all participants; the fast Fourier transform was calculated to obtain absolute power (AP) and relative power (RP) qEEG measures. In the first stage, a qEEG comparison between CTL1 and IDA was performed. Second stage consisted in comparing qEEG of the IDA infants before and after supplementation with iron (IDA-IS group), and comparing qEEG of the IDA-IS group with another control age-matched group (CTL2). Non-parametric multivariate permutation tests (NPT) were applied to assess differences between CTL1 and IDA groups, as well as IDA vs. IDA-IS, and IDA-IS vs. CTL2. Results: More power in slow frequency bands and less power in fast frequency bands in 64% of IDA babies were observed. NPT evinced higher alpha AP and RP (P < 0.001), less theta AP, and less delta and theta RP in CTL1 than in IDA. After iron-restoration therapy, alpha AP and RP increased while theta AP and theta and delta RP decreased, reaching almost normal values. Discussion: This work reveals CNS developmental delay through the study of qEEG (less rapid and more slow frequencies) which recovered significantly with iron supplementation. It is concluded that IDA constitutes a high risk factor for a lag of CNS maturation.
, Anthony Oppong-Gyebi
Published: 24 October 2017
Nutritional Neuroscience, Volume 22, pp 375-391; https://doi.org/10.1080/1028415x.2017.1391933

Abstract:
Genistein is a plant estrogen promoted as an alternative to post-menopausal hormone therapy because of a good safety profile and its promotion as a natural product. Several preclinical studies of cerebral ischemia and other models of brain injury support a beneficial role for genistein in protecting the brain from injury whether administered chronically or acutely. Like estrogen, genistein is a pleiotropic molecule that engages several different mechanisms to enhance brain health, including reduction of oxidative stress, promotion of growth factor signaling, and immune suppression. These actions occur in endothelial, glial, and neuronal cells to provide a coordinated beneficial action to ischemic challenge. Though many of these protective actions are associated with estrogen-like actions of genistein, additional activities on other receptors and intracellular targets suggest that genistein is more than a mere estrogen-mimic. Importantly, genistein lacks some of the detrimental effects associated with post-menopausal estrogen treatment and may provide an alternative to hormone therapy in those patients at risk for ischemic events.
Published: 23 October 2017
Nutritional Neuroscience, Volume 22, pp 373-374; https://doi.org/10.1080/1028415x.2017.1391934

Abstract:
Children with cerebral palsy commonly present with feeding difficulties that result from multiple orofacial sequelae, especially deficits in mastication. A previous study demonstrated that perinatal protein undernutrition accentuated the chewing impact in an experimental model of cerebral palsy. Therefore, the present study investigated whether nutritional manipulation reversed or minimized the chewing sequelae in cerebral palsy. We emphasized the relevance of evaluating the therapeutic potential of nutrients, especially tryptophan supplementation, to reduce the chewing deficits that are typical of this syndrome. Clarification of the role of nutrients may help in the development of new treatment strategies for these children.
, Yen-Wen Chen, , Andre F. Carvalho, Paul Whiteley, Chia-Hung Tang, , Tien-Yu Chen, , Che-Sheng Chu, et al.
Published: 18 October 2017
Nutritional Neuroscience, Volume 22, pp 354-362; https://doi.org/10.1080/1028415x.2017.1388598

Abstract:
Objectives: Autism spectrum disorder (ASD) refers to a group of conditions variably affecting communicative and social interactive abilities presenting alongside behaviors with various restricted and repetitive patterns. In addition to genetic factors that influence the onset of the symptoms, there is growing interest in the potential involvement of non-genetic environmental factors. Some aspects of breastfeeding practices, including rates, timing, or optimality, have been put forward as environmental risk factors for autism. However, previous studies showed a controversial relationship between ASD and breastfeeding. Methods: A meta-analysis on the association between maternal breastfeeding and ASD in children was conducted. We also explored potential moderating factors which might influence this association. Articles reporting the association between breastfeeding and a diagnosis of ASD were included. Results: Seven articles were included in the meta-analysis. Cumulatively, children with ASD (n = 1463), either in the form of clinical diagnosis or self-report, were significantly less likely to have been breastfed than children without ASD (n = 1180) (OR = 0.61, 95% CI = 0.45–0.83, P = 0.002). Subgroup analyses revealed that results remained significant for children who were breastfed with additional supplementation. Discussion: This meta-analysis provides evidence that breastfeeding (exclusively or including additional supplements) may protect against ASD. Prospective longitudinal research is required to disentangle the complex relationships and to explore potential pathophysiological mechanisms.
Kathryn S. Sarfert, Melina L. Knabe, Nicole S. Gunawansa,
Published: 17 October 2017
Nutritional Neuroscience, Volume 22, pp 344-353; https://doi.org/10.1080/1028415x.2017.1388557

Abstract:
Research demonstrates a link between diet-induced obesity and cognitive impairments; however, no studies have utilized the Sholl analysis to assess changes in dendritic arborization as a possible cause of obesity-induced memory deficits. Therefore, the purpose of this study was to examine the effect of a Western-style diet (WSD) on memory and dendritic complexity of male Sprague-Dawley rats.Male Sprague-Dawley rats (n = 18) were fed either a control or WSD. Spatial memory and episodic memory were assessed using the Morris Water Maze and novel object recognition (NOR) tasks, respectively. At termination, brains were removed and prepared with the Golgi-Cox method. Stained neurons in both the hippocampus and entorhinal cortex (EC) were imaged and digitally reconstructed.Results indicated significant differences in percent body fat and TNFα levels between dietary conditions. WSD males also experienced reduced NOR exploration ratios, but no deficits in spatial memory were observed. Analysis of dendritic length and number of branch points revealed no significant differences in either the EC or the hippocampus; however, the Sholl analysis indicated that a WSD increased neuronal complexity in the EC.Sholl analysis of the EC suggests a possible diet-induced dysfunction of pruning, which may contribute to reduced performance on the NOR task. Elevated TNFα levels indicate a putative role of inflammation in neuronal remodeling. The results demonstrate the importance of investigating mechanisms underlying obesity-related cognitive impairments.
Jian Han, Justin Plummer, , Aria Byrd, Michael Aschner,
Published: 16 October 2017
Nutritional Neuroscience, Volume 22, pp 335-343; https://doi.org/10.1080/1028415x.2017.1387720

Abstract:
Background: The importance of iron homeostasis is particularly apparent in the brain, where iron deficiency results in impaired cognition and iron accumulation is associated with neurodegenerative diseases. Obesity is linked to iron deficiency systemically, but the effects of obesity on brain iron and its associated consequences, including neurodegenerative processes remain unexplored. This preliminary study examined the effect of dietary-induced obesity on brain regional iron, α-synuclein expression, and F2-isoprostane (oxidative stress marker) concentrations in selected brain regions. Objective: The objective of the study was to elucidate the vulnerability of selected brain regions (e.g. midbrain, hippocampus) to the possible process of neurodegeneration due to the altered iron content associated with obesity. Methods: Twenty-one-day-old male C57BL/6J mice were fed with a high-fat diet (60% kcal from fat) or a control-fat diet (10% kcal from fat) for 20 weeks. Brain samples were collected and dissected into hippocampus, midbrain, striatum, and thalamus regions. Iron content, ferritin H (FtH) and α-synuclein protein and mRNA expressions, and F2-isoprostane were measured in selected regions. Results: The results indicated that obesity caused significant differences in iron levels in the midbrain and thalamus, but not in the hippocampus or striatum, compared to control mice. Furthermore, markers of neurodegeneration (α-synuclein mRNA expression and F2-isoprostanes) were increased in the midbrain. Discussion: These results support previous findings that brain iron metabolism responds to environmental stress in a regionally distinct manner and suggests that alterations in brain iron metabolism due to obesity may be relevant in neurodegeneration.
Farshad Arsalandeh, , Shahin Ahmadian, , Hamed Mohammadi Kamsorkh, ,
Published: 29 September 2017
Nutritional Neuroscience, Volume 22, pp 295-301; https://doi.org/10.1080/1028415x.2017.1384173

Abstract:
Growing evidence sheds light on the use of flavonoids as the promising alternatives for the treatment of chronic conditions, including cancer and neurodegenerative disorders. Accordingly, in the present study, we aimed at evaluating the effects of oral intake of two structurally different flavonoids 5-hydroxy-6,7,4'-trimethoxyflavone (flavone 1) and 5,7,4'-trihydroxyflavone (flavone 2) on recognition memory, hippocampal protein level of immediate early gene cFos and mitochondrial dynamic markers in Amyloid β (Aβ)-injected rats. Recognition aspect of memory and level of proteins were measured using novel object recognition test and Western blot, respectively. Our data indicated that even though flavone 1 was more effective than flavone 2 to prevent memory impairment, feeding with both flavones alleviated memory in Aβ-injected rats. Furthermore, in flavones-administered rats, mitochondrial dynamic balancing returned to the control level by the decline in Dynamin-related protein-1 protein level, a known marker for mitochondrial fission, and elevation in protein level of mitochondrial fusion factors Mitofusins 1 and 2. In parallel with behavior results, flavone 1 was more effectual on mitochondrial dynamic moderating. The more neuroprotective effects of flavone 1 could be attributed to its methylated structure leading to crossing of the blood-brain barrier with ease and metabolic stability and bioactivity.
Mithu Storoni, Matthieu P. Robert,
Published: 10 September 2017
Nutritional Neuroscience, Volume 22, pp 156-164; https://doi.org/10.1080/1028415x.2017.1368170

Abstract:
Leber hereditary optic neuropathy (LHON) is a maternally inherited, bilateral, sequential optic neuropathy that usually affects young males. LHON arises from a defect in complex I of the oxidative phosphorylation chain that generates increased reactive oxygen species and causes a decline in cellular ATP production. There exists no cure at present for LHON. Asymptomatic LHON mutation carriers show signs of increased mitochondrial biogenesis that may compensate for the compromise in complex I activity. Partial recovery in LHON is associated with a wider optic disc diameter and a younger age at disease onset, which may allow for greater mitochondrial bioenergetic capacity. Rescuing a mitochondrial bioenergetic deficit soon after disease onset may improve the chances of recovery and reduce visual loss in the second eye. We here propose that a calorie-restricted ketogenic diet has the potential to enhance mitochondrial bioenergetic capacity and should be explored as a potential therapeutic option for treating LHON.
Published: 3 October 2017
Nutritional Neuroscience, Volume 22, pp 302-305; https://doi.org/10.1080/1028415x.2017.1385176

Abstract:
Arginine-glycine amidinotransferase (AGAT) deficiency is a rare inherited metabolic disorder that severely affects brain bioenergetics. Characterized by mental retardation, language impairment, and behavioral disorders, AGAT deficiency is a treatable condition, where long-term creatine supplementation usually restores brain creatine levels and improves its clinical features. In some cases of AGAT deficiency, creatine treatment might be somewhat limited due to possible shortcomings in performance and transport of creatine to the brain. Guanidinoacetic acid (GAA), a direct metabolic precursor of creatine, has recently been suggested as a possible alternative to creatine to tackle brain creatine levels in experimental medicine. AGAT patients might benefit from oral GAA due to upgraded bioavailability and convenient utilization of the compound, while possible drawbacks (e.g. brain methylation issues, neurotoxicity, and hyperhomocysteinemia) should be accounted as well.
Deborah Teixeira, Ana Lucia Cecconello, Wania Aparecida Partata, , Maria Flávia Marques Ribeiro,
Published: 29 September 2017
Nutritional Neuroscience, Volume 22, pp 284-294; https://doi.org/10.1080/1028415x.2017.1380892

Abstract:
Objectives: To compare the effects of a palatable cafeteria diet on serum parameters and neuroinflammatory markers of young and aged female Wistar rats. Methods: Three-month-old (young) and 18-month-old (aged) female Wistar rats had access to a cafeteria diet (Caf-Young, Caf-Aged) or a standard chow diet (Std-Young, Std-Aged). Results: The Caf-Young group showed a higher food consumption, weight gain, visceral fat depot, serum insulin and leptin levels, and the insulin resistance index (HOMA-IR) than the Std-Young group. The Caf-Aged group exhibited an increase in interleukin-1 levels in the cerebral cortex and hippocampus. The number of GFAP-positive cells did not differ between the groups, but there was a diet effect in the cerebral cortex and an age effect in the hippocampus. Phospho-tau expression did not differ between the groups. Discussion: The 3- and 18-month-old rats responded differently to a cafeteria diet. Insulin and leptin levels are elevated in young animals fed a cafeteria diet, whereas aged animals are prone to neuroinflammation (indicated by an increase in interleukin-1β levels). A combination of hypercaloric diet and senescence have detrimental effects on the inflammatory response in the brain, which may predispose to neurological diseases.
Published: 26 September 2017
Nutritional Neuroscience, Volume 22, pp 264-272; https://doi.org/10.1080/1028415x.2017.1376928

Abstract:
Coenzyme Q10 (CoQ10, ubiquinone) stands among the safest supplements in the elderly to protect against cardiovascular disorders. Noteworthy, CoQ10 deficiency is common in many surviving stroke patients as they are mostly prescribed statins for the secondary prevention of stroke incidence lifelong. Accordingly, the current study aims to experimentally examine whether CoQ10 supplementation in animals receiving atorvastatin may affect acute stroke-induced injury.
, Ted M. Hsu, Joanna Liang, Scott E. Kanoski
Published: 25 September 2017
Nutritional Neuroscience, Volume 22, pp 273-283; https://doi.org/10.1080/1028415x.2017.1378851

Abstract:
Added dietary sugars contribute substantially to the diet of children and adolescents in the USA, and recent evidence suggests that consuming sugar-sweetened beverages (SSBs) during early life has deleterious effects on hippocampal-dependent memory function. Here, we test whether the effects of early-life sugar consumption on hippocampal function persist into adulthood when access to sugar is restricted to the juvenile/adolescent phase of development. Male rats were given ad libitum access to an 11% weight-by-volume sugar solution (made with high fructose corn syrup-55) throughout the adolescent phase of development (post-natal day (PN) 26-56). The control group received a second bottle of water instead, and both groups received ad libitum standard laboratory chow and water access throughout the study. At PN 56 sugar solutions were removed and at PN 175 rats were subjected to behavioral testing for hippocampal-dependent episodic contextual memory in the novel object in context (NOIC) task, for anxiety-like behavior in the Zero maze, and were given an intraperitoneal glucose tolerance test. Early-life exposure to SSBs conferred long-lasting impairments in hippocampal-dependent memory function later in life- yet had no effect on body weight, anxiety-like behavior, or glucose tolerance. A second experiment demonstrated that NOIC performance was impaired at PN 175 even when SSB access was limited to 2 hours daily from PN 26-56. Our data suggest that even modest SSB consumption throughout early life may have long-term negative consequences on memory function during adulthood.
Amanda N. Carey, Kelsea R. Gildawie, Abigail Rovnak, Nopporn Thangthaeng, Derek R. Fisher,
Published: 21 September 2017
Nutritional Neuroscience, Volume 22, pp 253-263; https://doi.org/10.1080/1028415x.2017.1376472

Abstract:
This study demonstrated that supplementation of a HFD with blueberry reduced indices of microglia activation and increased neuroplasticity, and these changes may underlie the protection against memory deficits in HFD-fed mice supplemented with blueberry.
Liming Dong, Yi Wang, Jingwei Lv, Hongxia Zhang, Ning Jiang, Cong Lu, Pan Xu,
Published: 15 September 2017
Nutritional Neuroscience, Volume 22, pp 235-242; https://doi.org/10.1080/1028415x.2017.1373928

Abstract:
Chronic stress exposure can disrupt the balance of organisms, result in learning and memory impairments and induce oxidative stress. However, there is a lack of safe and effective long-term therapeutic agents for stress-related injuries. Fresh ginseng (FG), an unprocessed raw root of ginseng, has antioxidant and neuroprotective activities and has been used as functional health food in Asian countries for many years. The aim of this study was to verify the protective effects of FG on chronic restraint stress (CRS)-induced learning and memory impairments as well as oxidative stress damage in mice.
Işınsu Alkan, , Gamze Altun, Erkan Erener
Published: 15 September 2017
Nutritional Neuroscience, Volume 22, pp 243-252; https://doi.org/10.1080/1028415x.2017.1374033

Abstract:
Objective: The aim of the present study is to investigate the effects of topiramate on the fat mass/obesity-associated protein (FTO) and on the neuropeptide Y (NPY) level in the hypothalamus depending on the recently increased prevalence of obesity. Method: In this study, twenty-four female rats were divided into four equal groups: Non-obese control, obese control, non-obese topiramate, and obese topiramate. Obese groups were fed with a 40% high-fat diet. At the end of the 9th week, the drug treatment started and the subjects were treated with topiramate once a day for 6 weeks. All animals underwent cardiac perfusion under high-dose anesthesia on the 15th week. Tissues were analyzed using biochemical, histological, and stereological methods. Results: In terms of neuron number in the arcuate nucleus area, a significant difference was observed among all groups (P < 0.01). The neuron number of the non-obese topiramate group was found to be significantly higher than that of the non-obese control group (P < 0.01). In the examination of the ventromedial nucleus of the entire group, it was observed that the neuron number of the non-obese control group was significantly lower than those of the other groups (P < 0.01). A significant increase in the NPY levels of the obese groups compared to the groups treated with topiramate was observed. Furthermore, the amount of the FTO protein increased in obese rats, while FTO and NPY levels decreased in the groups treated with topiramate. Discussion: In conclusion, the mechanism of the effect of topiramate to create a state of obesity is thought to involve the decrease in the levels of NPY and FTO.
Shoug M. Alashmali, Alex P. Kitson, Lin Lin, ,
Published: 13 September 2017
Nutritional Neuroscience, Volume 22, pp 223-234; https://doi.org/10.1080/1028415x.2017.1372160

Abstract:
The present study examines how lowering maternal dietary n-6 polyunsaturated fatty acids (PUFA) (starting from pregnancy) compared to offspring (starting from post-weaning) affect the levels of n-6 and n-3 fatty acids in phospholipids (PL) and lipid mediators in the hippocampus of mice.
, Iman Farahani, , , , Mohsen Ebrahimimonfared, Mana Shojapour,
Published: 10 September 2017
Nutritional Neuroscience, Volume 22, pp 215-222; https://doi.org/10.1080/1028415x.2017.1371389

Abstract:
Objectives: Therapeutic approaches for multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), are accompanied by various undesirable side effects. Owing to the anti-inflammatory and antioxidant effects of walnut, we investigated its effects on the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. Methods: After EAE induction in mice, the treated group was gavaged daily with walnut oil. The weights and clinical symptoms were monitored daily for 21 days following the onset of symptoms. The spleens and brains of the mouse were removed and used for ELISA and histological studies. Results: The average disease severity and plaque formation in the brains of the walnut oil-treated group were significantly lower (P< 0.05) than those of the untreated group. Stimulated splenocytes of the treated group expressed significantly less INF-γ and interleukin (IL)-17 than the untreated group with no significant differences in IL-10 or IL-5 production. In serum from the treated group, IL-17 expression was also significantly less than in the untreated group, while IL-10 was greater (P< 0.05). Conclusion: Walnut oil significantly reduced disease severity, inhibited plaque formation, and altered cytokine production. More studies are required to identify the mechanism of action of walnut oil as a valuable supplement in the treatment of MS.
Published: 10 September 2017
Nutritional Neuroscience, Volume 22, pp 174-184; https://doi.org/10.1080/1028415x.2017.1358472

Abstract:
Objectives: Ovarian hormones (OH) and early malnutrition may affect the developing brain, with repercussions on behavioral and excitability-dependent processes. However, the possible synergistic effects of both factors have not been analyzed. In this study, we investigated the effect of treatment in early life with OH and suckling among distinct litter sizes on recognition memory, anxiety behavior, and the excitability-dependent phenomenon known as cortical spreading depression (CSD). Methods: Female Wistar rats were suckled under favorable and unfavorable lactation, corresponding to litters with 9 and 15 pups (L9 and L15 groups, respectively). From postnatal days (P) 7 to 21, the animals received 50 µg/kg of β-estradiol or progesterone. From P80 to P84, we tested behavioral reactions. From P90 to P120, we analyzed CSD parameters. Results: Compared with the corresponding L9 groups, the OH-treated L15 groups performed worse in recognition memory tasks. No intergroup difference in the anxiety parameters was observed. Compared with naive and vehicle-treated controls, OH-treated groups displayed higher CSD velocities and amplitudes and shorter CSD durations. Discussion: Early treatment with OH facilitates recognition memory and CSD, and in association with unfavorable lactation (L15) impaired recognition memory, but not anxiety behavior, in the adult brain. OH treatment and L15 lactation condition seem to interact regarding OH action on memory, but not on CSD. Data suggest a long-lasting differential effect that might be related to the lasting hormonal action on brain excitability. We postulate and discuss the possibility that these findings may be implicated in human neurological diseases.
Francesca Saba, Annarita Sirigu, Rita Pillai, Paola Caria, Lina Cordeddu, , , ,
Published: 29 August 2017
Nutritional Neuroscience, Volume 22, pp 207-214; https://doi.org/10.1080/1028415x.2017.1367130

Abstract:
Conjugated linoleic acid (CLA) isomers have been shown to possess anti-inflammatory activity in the central nervous system. In this study, we aimed to evaluate whether modulation of the fatty acid profile by the CLA isomers c9,t11 or t10,c12CLA was associated with changes in the expression of pro-inflammatory molecules in human astrocytes.Cultured astrocytes were treated for 6 days with 100 µM fatty acids (c9,t11CLA or t10,c12CLA or oleic acid). Following the treatment, the fatty acid profile of the cell and pro-inflammatory molecule expression were assessed.Only the t10,c12CLA isomer induced a significant decrease in arachidonic acid and increased the ratio of docosahexaenoic acid/eicosapentaenoic acid, which constitutes indirect evidence of peroxisome proliferator-activated receptor alpha activation. Inhibition of tumour necrosis factor-α, interleukin-1β, and RANTES expression was observed in astrocytes treated with c9,t11CLA and t10,c12CLA.Current data demonstrate that CLA isomers, particularly t10,c12, may affect neuroinflammation by reducing the pro-inflammatory molecules in cultured astrocytes, suggesting a potential nutritional role of CLA isomers in modulating the astrocyte inflammatory response.
Mohammad Gol, Davoud Ghorbanian, , ,
Published: 31 July 2017
Nutritional Neuroscience, Volume 22, pp 110-118; https://doi.org/10.1080/1028415x.2017.1354959

Abstract:
Objectives: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive pathological changes of the brain. A number of studies demonstrated compelling evidence of the importance of oxidative processes in AD pathogenesis. Raisin contains polyphenol, phenolic acid, and tannin compounds, which have antioxidant and anti-inflammatory properties. The present study was aimed to evaluate the protective effect of raisin on neurobehavioral and histological changes in rats with Alzheimer. Methods: Animal model of AD was induced by intraperitoneal injection of aluminium chloride for 60 days (100 mg/kg body weight). During these 60 days both Alzheimer’s and control rats were given 6 g of raisin per rat. At the end of the treatment, blood was collected for biochemical assessment. We used a Morris water task and passive avoidance test to assess spatial memory. Results: Our results showed that aluminium exposure significantly decreased the memory in the MWT and passive avoidance test, but in the raisin + AlCl3 group, it significantly increased spatial memory in both tests. Also, Aluminium exposure significantly increased malondialdehyde (MDA) and decreased ferric reducing ability of plasma (ferric reducing/antioxidant power (FRAP)), while treatment with raisin significantly decreased MDA and increased FRAP in plasma of blood. Discussion: Our findings showed that raisin has a neuroprotective effect and improves the spatial memory in AD animal models.
, Carlo Brera, , Sabina Soricelli, Francesca Ciceri, , Francesca Debegnach, , Laura Villa, Massimo Molteni, et al.
Published: 31 July 2017
Nutritional Neuroscience, Volume 22, pp 132-144; https://doi.org/10.1080/1028415x.2017.1357793

Abstract:
Objectives: Gene–environment interaction is an emerging hypothesis to expound not only the autism pathogenesis but also the increased incidence of neurodevelopmental disorders (such as autistic spectrum disorder, attention-deficit, hyperactivity disorder). Among xenobiotics, mycotoxins are worldwide contaminants of food that provoke toxicological effects, crucially resembling several symptoms associated with autism such as oxidative stress, intestinal permeability, and inflammation. Here, we focused on a group of mycotoxins to test their role in the manifestation of autism, try to explain their mechanism of action, and discuss possible preventive and therapeutic interventions. Methods: Autistic children (n = 52) and healthy children [n = 58 (31 siblings and 27 unrelated subjects)] were recruited and body fluids and clinical data collected. The diagnosis of autism was made according to DSM V criteria, then with GMDS 0-2, WPPSI, and ADOS. Ochratoxin A (OTA), gliotoxin, zearalenone, and sphingosine/sphinganine ratio were determined by LC analysis in sera and urines. Statistical analysis was performed by the Wilcoxon Rank Sum (Mann–Whitney) test and Spearman test. Results: By comparing the results of autistic patients with those of unrelated controls, a significant association was found for OTA levels in urines (P = 0.0002) and sera (P = 0.0017), and also comparing patients with siblings and unrelated controls together (P = 0.0081). Discussion: Our results are the first describing a possible role of OTA in the pathobiology of autism. Recalling the male prevalence of ASD (male/female = 4–5/1), it is noted that, in animal models, OTA exerts its neurotoxicity especially in males. Moreover, in vitro, OTA increases microRNA-132 that is dysregulated in autistic patients and involved in reciprocal regulation of the autism-related genes MeCP2 and PTEN. A personalized diet coupled with probiotic administration, especially OTA adsorbing Lactobacillus, could ameliorate autistic symptoms in OTA-positive patients.
Rosângela Figueiredo Mendes-Da-Silva, Diorginis José Soares Ferreira, Andréia Albuquerque Cunha Lopes-De-Morais, , Cláudia J. Lagranha,
Published: 7 July 2017
Nutritional Neuroscience, Volume 21, pp 753-760; https://doi.org/10.1080/1028415x.2017.1360549

Abstract:
Objectives: To evaluate how safflower oil (SFO) influences brain electrophysiology and cortical oxidative status in the offspring, mothers received a diet with SFO during brain development period. Methods: Beginning on the 14th day of gestation and throughout lactation, rats received safflower (safflower group – SG) or soybean oil (control group – CG) in their diet. At 65 days old, cortical spreading depression (CSD) and cortex oxidative status were analyzed in the offspring. Results: SG presented reduction of the CSD velocity as compared to the CG (SG: 3.24 ± 0.09; CG: 3.37 ± 0.07 mm/min). SFO reduced levels of lipid peroxidation by 39.4%. SG showed the following increases: glutathione-S-transferase, 40.8% and reduced glutathione, 34.3%. However, SFO decreased superoxide dismutase by 40.4% and catalase by 64.1%. To control for interhemispheric effects, since CSD was recorded only in the right cortex, we evaluated the oxidative status in both sides of the cortex; no differences were observed. Discussion: Data show that when SFO is consumed by the female rats during pregnancy and lactation, the offspring present long-term effects on brain electrophysiology and cortical oxidative state. The present study highlights the relevance of understanding the SFO intake of pregnant and lactating mammals.
Published: 7 August 2017
Nutritional Neuroscience, Volume 22, pp 196-206; https://doi.org/10.1080/1028415x.2017.1360559

Abstract:
Objectives: Iron deficiency (ID) – the highly prevalent nutritional deficiency – has been shown to have deleterious effects on measures of cognitive performance and brain activity. Many of these results are suggestive of the impact of ID on neurotransmitter regulation and myelination. A third critical potential effect of ID on brain function is at the level of brain energy expenditure; however, to date there has not been any method for indirectly estimating the impact of ID on energy expenditure in humans in the context of cognitive work. Methods: We report here a study comparing ID and iron sufficient (IS) college students in which simultaneous behavioral, encephelographic (EEG), and metabolic data were collected in a task designed as a cognitive analog to standard physical exertion tasks. Results: We show that increases in cognitive demands produced decrements in behavioral measures of performance, and increases in EEG and metabolic measures of work. Critically, we found that the magnitudes of those changes were directly related to iron levels. Discussion: We find support for the idea that brain activity mediates the relationship between cognitive demands and energy expenditure, with ferritin and hemoglobin moderating those relationships in distinct ways. Finally, we show that levels of energy expenditure can be indirectly estimated by measures of EEG spectral power.
, Pragati P. Nahar, , Aseel Eid, Zhengxi Wei, Susan Meschwitz, Nasser H. Zawia, Angela L. Slitt,
Published: 7 August 2017
Nutritional Neuroscience, Volume 22, pp 185-195; https://doi.org/10.1080/1028415x.2017.1360558

Abstract:
The attenuation of neuroinflammation by urolithins may contribute, in part, toward pomegranate's neuroprotective effects against AD.
Azam Mesdaghinia, Marziye Alinejad, Alireza Abed, Azhdar Heydari,
Published: 2 August 2017
Nutritional Neuroscience, Volume 22, pp 165-173; https://doi.org/10.1080/1028415x.2017.1357919

Abstract:
Objectives: Thiamine serves as a cofactor for several enzymes involved in brain function and neurotransmitters biosynthesis. Thiamine-dependent enzymes are important for oxidant stress defenses. Several studies have reported that thiamine deficiency in the central nervous system reduces seizure threshold. The present study was designed to investigate the effect of acute and chronic administration of thiamine alone and in combination with sub-effective dose of diazepam on pentylenetetrazole (PTZ)-induced tonic–clonic seizures in mice. Methods: Animals were randomly divided into control and experimental groups. In experimental groups, thiamine (50, 100, and 200 mg/kg i.p.) was administered acutely or chronically (once a day, for 14 days). Slow intravenous infusion of PTZ (5 mg/ml) by infusion pump with a constant rate (0.3 ml/min) was used to induce clonic and tonic seizures. Results: Acute injection of thiamine (50, 100, and 200 mg/kg i.p.) did not increase seizure threshold significantly, but chronic treatment with thiamine (200 mg/kg i.p.) increases the clonic and tonic seizure threshold. Moreover, the combination of sub-effective dose of thiamine (100 mg/kg) and diazepam (0.1 mg/kg) significantly increased seizure threshold and enhanced the anticonvulsant effect of diazepam at ineffective dose (0.1 mg/kg). Discussion: Our results suggest that thiamine can be considered as a potential add-on treatment in deficient and non-deficient thiamine epileptic patients. Co-administration of this vitamin with classic antiepileptics to decrease the required doses of regular drugs may be recommended. Nevertheless, more well-designed studies may be executed to provide further accurate information.
Pramod Kumar Singh, Manish Kumar Singh, , , Anju Mehrotra, Akash Rawat, Rakesh Kumar Dixit
Published: 31 July 2017
Nutritional Neuroscience, Volume 22, pp 83-97; https://doi.org/10.1080/1028415x.2017.1354542

Abstract:
Objectives: In view of the increasing risk of lead on human health, the present study has been carried out to investigate the neuroprotective effect of omega-3 fatty acid on chronic lead-induced neurotoxicity and behavioral impairment in rats. Methods: Different neurobehavioral parameters, biochemical assays, and histopathological analyses in brain regions of rats were conducted. Results: Rats exposed to different doses of lead (lead acetate 2.5, 5.0, 7.5 mg/kg body weight p.o. for 90 days) caused a significant decrease in body weight, brain weight, and behavioral changes as compared to controls. Abnormal histopathological and increased levels of lead in blood and brain regions increased the levels of ROS, LPO, PCC and decreased the levels of GSH with concomitant reduction in SOD, CAT, and GPx activities in the brain region of rats treated with different doses of lead as compared to controls. Co-treatment of lead with omega-3 fatty acid (500 mg/kg body weight p.o. for 90 days) decreased the levels of ROS, LPO, PCC, and increased the level of GSH, also increased SOD, CAT, and GPx activity and showed improvements in behavioral as well as histopathological changes as compared to lead-treated groups. Discussion: Our results proved that omega-3 fatty acid improved behavioral deficits, altered histopathological and oxidative stress in lead-intoxicated rats. Among three different doses, 2.5 mg/kg b.wt. of lead along with omega-3 fatty acid was the most preventive dose for the neurotoxicity. This work reveals the potential of omega-fatty acid as a protective drug for lead neurotoxicity.
Rita Cassia Macedo, Eduardo Fernandes Bondan,
Published: 31 July 2017
Nutritional Neuroscience, Volume 22, pp 119-131; https://doi.org/10.1080/1028415x.2017.1356030

Abstract:
Objectives: The purpose of this study was to evaluate some indicators of redox status, and inflammation on different regions of the central nervous system (CNS) of obese rats treated with green tea (GT). We hypothesized that obesity could affect the redox balance in different brain regions due to the diverse nature of the cells as well as the selective neuronal vulnerability to oxidative stress, and GT could triggers benefits effects restoring the redox status. Methods: Male Wistar rats were treated with GT by gavage (12 weeks/5 days/week; 500 mg/kg of body weight) and obesity was induced by cafeteria diet (8 weeks). After this period, the animals were killed and brain tissue (cerebral cortex, cerebellum, and brainstem) was removed to evaluate oxidative stress and inflammation (cytokine release). Results: We showed that the cafeteria diet had little effect on redox balance in the cerebral cortex and cerebellum; however, the brainstem was the region of the CNS most sensitive to cafeteria diet-induced redox unbalance. GFAP expression was increased in the cerebral cortex of obese rats and reduced by GT. It was also evident that GT treatment had numerous beneficial effects against oxidative damage to biomolecules in all brain regions analyzed. Discussion: Our study established that different CNS regions show selective neuronal vulnerability when exposed to a diet enriched with fats and sugars, and the beneficial effect of GT was similar among these regions. We conclude that GT could be a good strategy for improving and maintaining brain function under healthy and pathological conditions.
Hande Cekici,
Published: 1 August 2017
Nutritional Neuroscience, Volume 22, pp 145-155; https://doi.org/10.1080/1028415x.2017.1358481

Abstract:
Summary: The link between nutrition and autism spectrum disorder (ASD), which is a complex developmental disorder manifesting itself in significant delays or deviation in interaction and communication, has provided a fresh point of view and signals that nutrition may have a role in the aetiology of ASD, as well as play an active role in treatment by alleviating symptoms. Objective: In this review study aimed at evaluating, with scientific and concrete proof, the current medical nutrition implementations on ASD, existing medical nutrition therapies have been addressed and their effects on ASD symptoms have been discussed in light of current research. Methods: We reviewed articles regarding the medical nutritional therapy of autism on current nutritional approaches selected from PubMed, Science Direct, EBSCO, and databases about autism and nutrition. Results: The research put forward that in individuals with ASD, while gluten-free/casein-free and ketogenic diets, camel milk, curcumin, probiotics, and fermentable foods can play a role in alleviating ASD symptoms, consumption of sugar, additives, pesticides, genetically modified organisms, inorganic processed foods, and hard-to-digest starches may aggravate symptoms. Discussion: Further prospective controlled trials with large sample sizes are needed before recommendations can be made regarding the ideal ASD diet. This review emphasizes the value of identifying current nutritional approaches specific to individuals with ASD and integrating their effects on symptoms to the conversation and presents suggestions for future research designed to identify medical nutrition therapies targeting this population to better understand the link between ASD and nutrition.
, , , Raquel De Arruda Campos Benjamim, Thaynan Raquel Dos Prazeres Oliveira, Jacqueline Maria Silva, ,
Published: 28 July 2017
Nutritional Neuroscience, Volume 22, pp 98-109; https://doi.org/10.1080/1028415x.2017.1354958

Abstract:
Objective: The main goal of the present study was to investigate the effects of two maternal high-fat diets with different energy densities on the somatic growth, reflex ontogeny, and locomotor activity of offspring. Methods: Twenty-nine female Wistar rats (220–250 g) were mated and grouped into three different dietary conditions: control (n = 11, AIN-93G diet, 3.6 kcal/g), high-fat/high-caloric (HH, n = 9, 51% of the calories from fat, 4.62 kcal/g), and high-fat/isocaloric (HI, n = 9, 51% of the calories from fat, 3.64 kcal/g). The fat source was mainly lard. The dietary groups were maintained during gestation and lactation. From postnatal day 1 (PND1) until weaning, the somatic growth, maturation of physical features, and reflex ontogeny of the male pups were evaluated. The locomotor activity was evaluated in an open field at PND8, PND14, PND17, PND21, PND30, PND45, and PND60. Results: HH dams had a lower food intake but no difference in caloric intake or body weight gain. The HH pups had higher body weights, greater tail and body lengths, and an increased axis of the head at weaning. The prediction of ear unfolding, delayed palmar grasp, and cliff avoidance maturation were also observed in the HH offspring. At PND60, the HH pups showed an increased average speed as well as an average potency and kinetic energy in the open field. Conclusion: A high-fat/high-caloric maternal diet increases somatic growth, predicts the maturation of physical features, and delays reflex ontogeny during lactation, and it enhances motor performance during late adolescence. A maternal HI diet does not elicit the same influences on offspring development compared with the HH diet.
, , Kentaro Usuda, , Yi-Ju Jill Chiang, Tai-Wei Guu, , , , , et al.
Published: 11 July 2017
Nutritional Neuroscience, Volume 22, pp 63-71; https://doi.org/10.1080/1028415x.2017.1354540

Abstract:
Objectives: Although safe approaches for improving depression in pregnancy are required and the efficacy of omega-3 polyunsaturated fatty acids (PUFAs) has been suggested, the amount of supplemental omega-3 PUFAs has varied among previous studies and adequate amount might be different among countries. The aim of this pilot study is to explore the feasibility of using 1800 mg of omega-3 PUFAs supplementation for our future double-blind, placebo-control trial, and to clarify the clinical difference and the similarity between two sites of Japan and Taiwan. Methods: Pregnant women between 12 and 24 weeks’ gestation with depressive symptoms were recruited. Participants were supplemented daily with omega-3 PUFAs capsules containing 1206 mg eicosapentaenoic acid and 609 mg docosahexaenoic acid for 12 weeks. The primary outcome was change in total score on the 17-item Hamilton Rating Scale for Depression (HAMD) at 12 weeks after supplementation. Results: Eight pregnant women in Japan and five in Taiwan participated in the study. A substantial proportion of pregnant women reported high consumption of omega-3 supplements and dietary fish were excluded in Taiwan rather than in Japan sites. The decrease in HAMD score from baseline to 12 weeks after the start of the intervention was significantly larger in Japanese participants than in Taiwanese participants (Wilcoxon rank sum test; P = 0.045). Discussion: The improvement of depressive symptoms was smaller at the Taiwan site than at the Japan site. Differences in psychopathology of recruited participants identified by self-rating scales might affect the degree of population heterogeneity and the treatment efficacy. A randomized-controlled trial is needed to confirm these findings. Trial Registration: ClinicalTrials.gov Identifier: NCT01948596.
, Dagmara Mirowska-Guzel,
Published: 26 July 2017
Nutritional Neuroscience, Volume 22, pp 72-82; https://doi.org/10.1080/1028415x.2017.1354543

Abstract:
Protocatechuic acid has very promising properties potentially useful in the inhibition of neurodegenerative diseases progression. It is the main metabolite of the complex polyphenolic compounds and is believed to be responsible for beneficial effects associated with consumption of the food products rich in polyphenols. Protocatechuic acid is present in the circulation significantly longer and at higher concentrations than parent compounds and easily crosses the blood brain barrier. The aim of the following paper is to provide an extensive and actual report on protocatechuic acid and its pharmacological potential in prevention and/or treatment of neurodegenerative diseases in humans based on existing data from both in vitro and in vivo studies. Experimental studies strongly support the role of protocatechuic acid in the prevention of neurodegenerative processes, including Alzheimer’s and Parkinson’s diseases, due to its favorable influence on processes underlying cognitive and behavioral impairment, namely accumulation of the β-amyloid plaques in brain tissues, hyperphosphorylation of tau protein in neurons, excessive formation of reactive oxygen species and neuroinflammation. There is a growing evidence that protocatechuic acid may become in the future efficacious and safe substance that protects against neurodegenerative disorders.
Dsouza Serena Stephen,
Published: 11 July 2017
Nutritional Neuroscience, Volume 22, pp 51-62; https://doi.org/10.1080/1028415x.2017.1354511

Abstract:
Objectives: To study the effect of specially formulated high-fat simple carbohydrate diet (HFSC) on the serotonin metabolic pathway in male C57BL/6J mice. Methods: Previous studies from our laboratory have shown that specially formulated HFSC induces metabolic syndrome in C57BL/6J mice. In the present investigation, 5-hydroxytryptophan, serotonin and 5-hydroxyindoleacetic acid were analyzed in two brain regions (hypothalamus, corpus striatum), urine and plasma of HFSC-fed mice on a monthly basis up to 5 months using high-performance liquid chromatography fitted with electrochemical detector. The data were analyzed using Graph pad Prism v7.3 by two-way ANOVA and post hoc Tukey’s test (to assess the effect of time on the serotonergic metabolic pathway). Results: HFSC feed was observed to lower the hypothalamic serotonergic tone as compared to the age-matched control-fed C57BL/6J mice. Although the hypothalamic serotonergic tone was unaltered over time due to consumption of diet per se, hypothalamic 5-HTP levels were observed to be lower on consumption of HFSC feed over duration of 5 months as compared to 1st month of consumption of HFSC feed. The striatal 5-HTP levels were lowered in the HFSC-fed mice after 4 months of feeding as compared to the age-matched control-fed mice. The striatal 5-HTP levels were also lower in both control and HFSC-fed mice due to consumption of the respective diet over a duration of 5 months. Increased plasma 5-HTP levels were observed due to consumption of HFSC feed over duration of 5 months in the HFSC-fed group. However, higher breakdown of serotonin was observed in both the plasma and urine of HFSC-fed C57BL/6J mice as per the turnover studies. Discussion: The central and peripheral serotonergic pathway is affected differentially by both the type of diet consumed and the duration for which the diet is consumed. The hypothalamic, striatal and plasma serotonergic pathway were altered both by the type of feed consumed and the duration of feeding. The urine serotonergic pathway was affected by mainly the duration for which a particular diet was consumed. These findings may have implications in the feeding behavior, cognitive decline and depression associated with metabolic syndrome patients.
Published: 11 July 2017
Nutritional Neuroscience, Volume 22, pp 40-50; https://doi.org/10.1080/1028415x.2017.1352121

Abstract:
Gastrointestinal disturbances, nutritional deficiencies, and food intolerances are frequently observed in children with neurodevelopmental disorders (NDD). To reveal possible association of celiac disease risk variants (HLA-DQ), lactose intolerance associated variant (LCT-13910C>T) as well as variant associated with vitamin D function (VDR FokI) with NDD, polymerase chain reaction-based methodology was used. Additionally, intestinal peptide permeability was estimated in NDD patients and healthy children by measuring the level of peptides in urine using high-performance liquid chromatography. Levels of opioid peptides, casomorphin 8, and gluten exorphin C were significantly elevated in urine samples of NDD patients (P = 0.004 and P = 0.005, respectively), but no association of genetic risk variants for celiac disease and lactose intolerance with NDD was found. Our results indicate that increased intestinal peptide permeability observed in analyzed NDD patients is not associated with genetic predictors of celiac disease or lactose intolerance. We have also found that FF genotype of VDR FokI and lower serum levels of vitamin D (25-OH) showed association with childhood autism (CHA), a subgroup of NDD. We hypothesize that vitamin D might be important for the development of CHA.
Published: 11 July 2017
Nutritional Neuroscience, Volume 22, pp 19-28; https://doi.org/10.1080/1028415x.2017.1349359

Abstract:
Background: Differences in the composition of control diets may confound outcomes in studies investigating dietary effects. Objective: We compared the effects of two control diets commonly used in mice studies, chow (SD) and a purified low-fat diet (LFD), in relation to a chronic high-fat diet (HFD). We hypothesized that SD and LFD will have similar effects on phenotypic, metabolic, and behavioral outcomes. Methods: Fifty-four 5-week-old male C57BL/6J mice were randomly assigned to one of the three dietary interventions (SD, LFD, or HFD) for 18 weeks. At week 16, mice were tested for behavioral changes. Glucose tolerance testing was conducted at week 17 and terminal blood collection at week 18. Results: SD and LFD mice exhibited no differences in cognitive performance on the Y-maze test and comparable anxiety-like behavior in the open-field and elevated zero maze tests. Significant declines in cognitive function and greater anxiety-like behavior were observed in the HFD group compared to both SD and LFD. Areas under the glucose tolerance curve were similar for SD and LFD, as were levels of high-density lipoprotein, triglycerides, cytokines, and adipocytokines. Only total cholesterol was significantly higher in LFD mice compared to SD mice. All measures were significantly higher in the HFD group. Discussion: Our data demonstrate that young mice develop similar phenotypic, metabolic, and behavioral profiles when fed SD vs. LFD. The two diets may thus be equally appropriate as controls for an HFD, although some studies may want to consider differences in effects on cholesterol levels.
Sasha M. Barnett, , Anne M. Walk, , Christopher Moulton, Neal J. Cohen, , , ,
Published: 23 May 2017
Nutritional Neuroscience, Volume 21, pp 632-640; https://doi.org/10.1080/1028415x.2017.1329976

Abstract:
Objective: Macular pigment optical density (MPOD) – a non-invasive indicator of retinal xanthophylls and correlate of brain lutein – has been associated with superior cognitive function among adult populations. Given that lutein accumulation in the brain occurs in early life, it is possible that the cognitive implications of greater MPOD may be evident in childhood. Methods: Participants aged 8–9 years (n = 56) completed MPOD measurements via heterochromatic flicker photometry. Academic performance was assessed using the Kaufman Test of Academic and Educational Achievement II (KTEA). Habitual dietary intake of L and Z was measured among a subsample of participants (n = 35) using averaged 3-day food records. Stepwise hierarchical regression models were developed to determine the relationship between MPOD and academic achievement tests, following the adjustment of key covariates including sex, aerobic fitness, body composition, and intelligence quotient (IQ). Results: The regression analyses revealed that MPOD improved the model, beyond the covariates, for overall academic achievement (ΔR2 = 0.10, P < 0.01), mathematics (ΔR2 = 0.07, P = 0.02), and written language composite standard scores (ΔR2 = 0.15, P < 0.01). Discussion: This is the first study to demonstrate that retinal L and Z, measured as MPOD, is positively related to academic achievement in children, even after accounting for the robust effects of IQ and other demographic factors. These findings extend the positive associations observed between MPOD and cognitive abilities to a pediatric population. Trail registration: The Fitness Improves Thinking in Kids 2 (FITKids2) trial was registered at www.clinicaltrials.gov as NCT01619826.
Tommy J. Wilson, , Jan-Willem Van Klinken, Melissa Kaczmarczyk,
Published: 7 July 2017
Nutritional Neuroscience, Volume 21, pp 729-743; https://doi.org/10.1080/1028415x.2017.1347998

Abstract:
Background: At present, the impact of macronutrient composition and nutrient intake on sustained attention in adults is unclear, although some prior work suggests that nutritive interventions that engender slow, steady glucose availability support sustained attention after consumption. A separate line of evidence suggests that nutrient consumption may alter electroencephalographic markers of neurophysiological activity, including neural oscillations in the alpha-band (8–14 Hz), which are known to be richly interconnected with the allocation of attention. It is here investigated whether morning ingestion of foodstuffs with differing macronutrient compositions might differentially impact the allocation of sustained attention throughout the day as indexed by both behavior and the deployment of attention-related alpha-band activity. Methods: Twenty-four adult participants were recruited into a three-day study with a cross-over design that employed a previously validated sustained attention task (the Spatial CTET). On each experimental day, subjects consumed one of three breakfasts with differing carbohydrate availabilities (oatmeal, cornflakes, and water) and completed blocks of the Spatial CTET throughout the morning while behavioral performance, subjective metrics of hunger/fullness, and electroencephalographic (EEG) measurements of alpha oscillatory activity were recorded. Results: Although behavior and electrophysiological metrics changed over the course of the day, no differences in their trajectories were observed as a function of breakfast condition. However, subjective metrics of hunger/fullness revealed that caloric interventions (oatmeal and cornflakes) reduced hunger across the experimental day with respect to the non-caloric, volume-matched control (water). Yet, no differences in hunger/fullness were observed between the oatmeal and cornflakes interventions. Conclusion: Observation of a relationship between macronutrient intervention and sustained attention (if one exists) will require further standardization of empirical investigations to aid in the synthesis and replicability of results. In addition, continued implementation of neurophysiological markers in this domain is encouraged, as they often produce nuanced insight into cognition even in the absence of overt behavioral changes. ClinicalTrials.gov Identifier: NCT03169283
, , Francisca Díaz, , Mª Ángeles Pérez-Izquierdo,
Published: 11 July 2017
Nutritional Neuroscience, Volume 22, pp 29-39; https://doi.org/10.1080/1028415x.2017.1349574

Abstract:
Background: Overnutrition due to a high-fat diet (HFD) can increase the vulnerability of the metabolic system to maladjustments. Estradiol has an inhibitory role on food intake and this hormone has demonstrated to be a crucial organizer during brain development. Objective: Our aim was to determine whether increased levels of estradiol in the early postnatal period modulate the alterations in metabolism and brain metabolic circuits produced by overnutrition. Methods: Twenty-four male and 24 female Wistar rats were submitted to a HFD (34.9% fat) or a control diet (5% fat) from gestational day 6. From postnatal (P) 6 to P13, both control and HFD groups were administered a s.c. injection of vehicle or estradiol benzoate (0.4 mg/kg), resulting in eight experimental groups (n = 6 in each group). Body weight, food intake and subcutaneous, visceral, and brown fat pads were measured. Agouti-related peptide, neuropeptide Y, orexin, and proopiomelanocortin (POMC) were analyzed by quantitative real-time polymerase chain reaction assay and plasma estradiol levels were measured by ELISA. Results: Males fed a HFD showed an increase in body weight and the amount of visceral and subcutaneous fat, which was coincident with an increase in the number of kilocalories ingested. Neonatal estradiol treatment restored the body weight and subcutaneous fat of HFD males to control levels. Hypothalamic POMC mRNA levels in HFD females were increased with respect to control females. This increase was reverted with estradiol treatment during development. Discussion: HFD and estradiol treatment have different effects on males and females. Overnutrition affects physiological parameters, such as body weight, visceral, and subcutaneous fat content, in males, while females present alterations in hypothalamic POMC mRNA levels. Hence, the increase in estradiol levels during a period that is critical for the programing of the feeding system can modulate some of the alterations produced by the continuous intake of high-fat content food.
, , Demosthenes B. Panagiotakos, Ekavi N. Georgousopoulou, , ,
Published: 11 July 2017
Nutritional Neuroscience, Volume 22, pp 1-18; https://doi.org/10.1080/1028415x.2017.1349032

Abstract:
There is a significant body of research undertaken in order to elucidate the mechanisms underlying the pathology of Alzheimer’s disease (AD), as well as to discover early detection biomarkers and potential therapeutic strategies. One such proposed biomarker is the calcium binding protein S100β, which, depending on its local concentration, is known to exhibit both neurotrophic and neuroinflammatory properties in the central nervous system. At present, relatively little is known regarding the effect of chronic S100β disruption in AD. Dietary intake has been identified as a modifiable risk factor for AD. Preliminary in vitro and animal studies have demonstrated an association between S100β expression and dietary intake which links to AD pathophysiology. This review describes the association of S100β to fatty acids, ketone bodies, insulin, and botanicals as well as the potential impact of physical activity as a lifestyle factor. We also discuss the prospective implications of these findings, including support of the use of a Mediterranean dietary pattern and/or the ketogenic diet as an approach to modify AD risk. GRAPHICAL ABSTRACT
Ghazaleh Hajiluian, , Ghazaleh Nameni, , Mehran Megari-Abbasi
Published: 6 July 2017
Nutritional Neuroscience, Volume 21, pp 744-752; https://doi.org/10.1080/1028415x.2017.1348436

Abstract:
Background: There is evidence that obesity leads to cognitive impairments via several markers of oxidative stress including glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase and malondialdehyde (MDA) in the hippocampus. Increased inflammatory markers in the brain have obesity triggering effects. In the current study we aimed to investigate the effects of vitamin D on cognitive function, nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α concentration and markers of oxidative stress in the hippocampus of high-fat diet-induced obese rats. Methods and materials: Forty male Wistar rats were divided into two groups: control diet (CD) and high-fat diet (HFD) for 16 weeks; then each group subdivided into two groups including: CD, CD + vitamin D, HFD and HFD + vitamin D. Vitamin D was administered at 500 IU/kg dosage for 5 weeks. Four weeks after supplementation, Morris water maze test was performed. NF-κB and TNF-α concentration in the hippocampus were determined using ELISA kits. Moreover, oxidative stress markers in the hippocampus including GPx, SOD, MDA and CAT concentrations were measured by spectrophotometry methods. Results: HFD significantly increased TNF-α (P = 0.04) and NF-κB (P = 0.01) concentrations in the hippocampus compared with CD. Vitamin D treatment led to a significant reduction in hippocampus NF-κB concentrations in HFD + vitamin D group (P = 0.001); however, vitamin D had no effect on TNF-α concentrations. Moreover, HFD significantly induced oxidative stress by reducing GPx, SOD and increasing MDA concentrations in the hippocampus. Vitamin D supplementation in HFD group also significantly increased GPx, SOD and reduced MDA concentrations. Conclusion: Vitamin D improved hippocampus oxidative stress and inflammatory markers in HFD-induced obese rats and improved cognitive performance. Further studies are needed to better clarify the underlying mechanisms.
Published: 6 July 2017
Nutritional Neuroscience, Volume 21, pp 682-694; https://doi.org/10.1080/1028415x.2017.1345425

Abstract:
The formation of β amyloid plaques is one of the pathological hallmarks of Alzheimer’s disease (AD). The process of accumulation of extracellular deposits of amyloid plaques occurs by the abnormal proteolysis of amyloid precursor protein, resulting in the formation of β amyloid peptides which further aggregates and results in the formation of oligomers, protofibrils, fibrils, and plaques. The complexity in understanding the aggregation process has provided avenues for identifying potential targets against amyloid toxicity in the treatment of AD. The therapeutic approach mainly focuses on reducing the toxicity by halting the β amyloid fibril formation. Besides conventional medicine, several naturally available compounds were shown to reduce the toxicity of amyloid plaques in the current scenario. This review provides a comprehensive account on recent updates of FDA-approved and naturally available compounds against toxicity of amyloid peptides and plaques both in vitro and in vivo.
, Michelle R. Hernandez, Nicholas Margolies, Ali Yasrebi,
Published: 7 July 2017
Nutritional Neuroscience, Volume 21, pp 715-728; https://doi.org/10.1080/1028415x.2017.1347374

Abstract:
Fatty acid-induced hypothalamic inflammation (HI) is a potential cause of the obesity epidemic. It is unclear whether saturated or n-6 polyunsaturated fat is the primary driver of these effects. Premenopausal women are protected, in part, from obesity and associated comorbidities by circulating 17β-estradiol (E2). It is unknown how HI interacts with E2, because most studies of HI do not examine females despite the involvement of E2 in hypothalamic energy homeostasis. Our objective is to determine the effects of high-fat diets with varying levels of linoleic acid (LA) and saturated fat on the energy and glucose homeostasis in female mice with and without E2. Female C57BL/6J mice were fed either a control diet or a 45% kilocalories from fat diet with varying levels of LA (1, 15, or 22.5% kilocalories from LA) with or without E2 (300 μg/kg/day orally). After 8 weeks, the oil-treated high-fat groups gained more weight than control groups regardless of fat type. E2 reduced body fat accumulation in all high-fat groups. Glucose clearance from glucose challenge was impaired by LA. Nighttime O2 consumption was increased by E2, regardless of diet and independent of activity. Neuropeptides and HI genes were not affected by LA or SFA content. These data show that fatty acid type does not affect body weight, but does affect glucose metabolism in females, and these effects are not associated with an induction in HI gene expression.
Sanaa Y. Shaaban, , , , Howaida S. A. El-Feki, ,
Published: 30 June 2017
Nutritional Neuroscience, Volume 21, pp 676-681; https://doi.org/10.1080/1028415x.2017.1347746

Abstract:
Objective: There are limited data on the efficacy of probiotics in children with ASD, therefore, this study aims to evaluate the efficacy and tolerability of probiotics in an Egyptian cohort of children with ASD. Methods: Gastrointestinal (GI) flora were assessed by quantitative real-time PCR of stool samples of 30 autistic children from 5 to 9 years old. GI symptoms of autistic children were assessed with a modified six-item Gastrointestinal Severity Index (6-GSI) questionnaire, and autistic symptoms were assessed with Autism Treatment Evaluation Checklist (ATEC) before and after 3 months of supplementation of probiotics nutritional supplement formula (each gram contains 100 × 106 colony forming units of three probiotic strains; Lactobacillus acidophilus, Lactobacillus rhamnosus and Bifidobacteria longum). Results: After probiotic supplementation, the stool PCR of autistic children showed increases in the colony counts of Bifidobacteria and Lactobacilli levels, with a significant reduction in their body weight as well as significant improvements in the severity of autism (assessed by the ATEC), and gastrointestinal symptoms (assessed by the 6-GSI) compared to the baseline evaluated at the start of the study. Conclusions: We concluded that probiotics have beneficial effects on both behavioral and GI manifestations of ASD. Probiotics (a non-pharmacological and relatively risk-free option) could be recommended for children with ASD as an adjuvant therapy. At this stage, this study is a single center with a small number of patients and a great deal of additional wide-scale randomized controlled trials are needed to critically confirm the efficacy of probiotics in ASD. Trial registration number: UMIN-CTR Study Design: Trial Number UMIN000026157
Published: 7 July 2017
Nutritional Neuroscience, Volume 21, pp 695-714; https://doi.org/10.1080/1028415x.2017.1347373

Abstract:
Polyunsaturated fatty acids (PUFAs) are lipid derivatives of omega-3 (docosahexaenoic acid, DHA, and eicosapentaenoic acid, EPA) or of omega-6 (arachidonic acid, ARA) synthesized from membrane phospholipids and used as a precursor for endocannabinoids (ECs). They mediate significant effects in the fine-tune adjustment of body homeostasis. Phyto- and synthetic cannabinoids also rule the daily life of billions worldwide, as they are involved in obesity, depression and drug addiction. Consequently, there is growing interest to reveal novel active compounds in this field. Cloning of cannabinoid receptors in the 90s and the identification of the endogenous mediators arachidonylethanolamide (anandamide, AEA) and 2-arachidonyglycerol (2-AG), led to the characterization of the endocannabinoid system (ECS), together with their metabolizing enzymes and membrane transporters. Today, the ECS is known to be involved in diverse functions such as appetite control, food intake, energy balance, neuroprotection, neurodegenerative diseases, stroke, mood disorders, emesis, modulation of pain, inflammatory responses, as well as in cancer therapy. Western diet as well as restriction of micronutrients and fatty acids, such as DHA, could be related to altered production of pro-inflammatory mediators (e.g. eicosanoids) and ECs, contributing to the progression of cardiovascular diseases, diabetes, obesity, depression or impairing conditions, such as Alzheimer’ s disease. Here we review how diets based in PUFAs might be linked to ECS and to the maintenance of central and peripheral metabolism, brain plasticity, memory and learning, blood flow, and genesis of neural cells.
Leila Maghsoumi-Norouzabad, , Reza Abed, Farideh Shishehbor
Published: 30 June 2017
Nutritional Neuroscience, Volume 21, pp 614-623; https://doi.org/10.1080/1028415x.2017.1344371

Abstract:
The present systematic review with meta-analysis of randomized controlled trials (RCTs) aimed to analyze the effectiveness of omega-3 fatty acids on the frequency, severity, and duration of migraine. This systematic review was performed by searching several databases for controlled clinical trials. Of the 13 trials, five, two, and three RCTs met the eligibility criteria to evaluate the efficacy of omega-3 on the frequency, duration, and severity of migraine attacks, respectively. The Jadad scale was used to evaluate the risk of bias analysis. Overall estimates of the intervention effect were obtained from random-effect meta-analysis. The studies' heterogeneity was evaluated using the chi-squared test (χ(2)) (Cochran's test (Q test)) and I(2) Index. Potential sources of heterogeneity among the trials were investigated by meta-regression analyses. The results showed that omega-3 intake had no effect on frequency (WMD = -0.20; 95%CI -0.67, 0.27; P = 0.401, and I(2) = 4.6%; P = 0.380) and severity (SMD = -0.59; 95%CI -1.85, 0.66; P = 0.35, and I(2) = 88.8%; P = 0.000) of migraine but had a reduction effect on the duration of migraine attacks (WMD = -3.44; 95%CI -5.70, -1.19; P = 0.003, and I(2) = 0.0%; P = 0.926). In conclusion, omega-3 intake leads to a significant reduction of approximately 3.44 hours in the duration of migraine. Further randomized controlled trials of high methodological quality with adequate sample sizes are required to confirm the results of the meta-analyses.
Dinesh Dhingra, Shikha Goswami, Nidhi Gahalain
Published: 22 June 2017
Nutritional Neuroscience, Volume 21, pp 667-675; https://doi.org/10.1080/1028415x.2017.1338549

Abstract:
Objectives: The present study was designed to evaluate the effect of hesperetin on haloperidol-induced orofacial dyskinesia and catalepsy in Wistar male albino rats. Methods: Haloperidol (1 mg/kg, ip) was administered for 21 successive days to induce orofacial dyskinesia and catalepsy. Hesperetin (50 and 100 mg/kg, po) was administered 10 min prior to the injection of haloperidol for 21 successive days. Vacuous chewing movements (VCMs), tongue protrusions, catalepsy, and locomotor activity scores were recorded on 7th, 14th, and 22nd day of drug treatment. After behavioral testing, animals were sacrificed and various biochemical parameters such as brain levels of dopamine, serotonin, malondialdehyde, and reduced glutathione (GSH); and superoxide dismutase (SOD) and catalase activities were estimated. Results: Chronic administration of haloperidol significantly increased VCMs, tongue protrusions, and catalepsy in rats. It also produced hypolocomotion in rats. Hesperetin significantly inhibited haloperidol-induced VCMs, tongue protrusions, and catalepsy. Haloperidol significantly increased brain levels of malondialdehyde, decreased brain GSH, SOD, and catalase activities; and also decreased brain dopamine and serotonin levels. Hesperetin significantly reversed haloperidol-induced increase in brain oxidative stress and decrease in brain dopamine and serotonin levels. Discussion: Hesperetin significantly ameliorated haloperidol-induced orofacial dyskinesia and catalepsy possibly through alleviation of oxidative stress and increase in brain dopamine and serotonin levels. Thus, hesperetin may be explored further as a possible therapeutic agent for clinical management of neuroleptic drug-induced tardive dyskinesia.
Veerappan Venkatesh Gobi, , Muthu Ramkumar, Chinnasamy Dhanalakshmi, , , , Ranganathan Chidambaram, Ameer Kalandar
Published: 19 June 2017
Nutritional Neuroscience, Volume 21, pp 657-666; https://doi.org/10.1080/1028415x.2017.1337290

Abstract:
Neuroinflammation and oxidative damage are the two main malfactors that play an important role in the pathogenesis of experimental and clinical Parkinson’s disease (PD). The current study was aimed to study the possible anti-oxidant and anti-inflammatory effects of the methanolic extract of Agaricus blazei (A. blazei) against rotenone-induced PD in mice. Male Albino mice were randomized and divided into the following groups: control, treated with rotenone (1 mg/kg/day), co-treated with rotenone and A. blazei (50, 100, and 200 mg/kg b.w.), and treated with A. blazei alone (200 mg/kg b.w.). After the end of the experimental period, behavioral studies, biochemical estimations, and protein expression patterns of inflammatory markers were studied. Rotenone treatment exhibited enhanced motor impairments, neurochemical deficits, oxidative stress, and inflammation, whereas oral administration of A. blazei extract attenuated the above-said indices. Even though further research is needed to prove its efficacy in clinical studies, the results of our study concluded that A. blazei extract offers a promising and new therapeutic lead for treatment of PD.
, , Elena Garicano Vilar, Manuela Echeverry López, Marta García Bernat, Yaiza Quevedo Santos, Marta Blanco López, Paloma Elortegui Pascual, Elena Borregon Rivilla, Mario Rincón Barrado
Published: 11 June 2017
Nutritional Neuroscience, Volume 21, pp 641-647; https://doi.org/10.1080/1028415x.2017.1331952

Abstract:
Attention-deficit hyperactivity disorder (ADHD) has been related to nutrient deficiencies and 'unhealthy' diets, and to date there is only one study that examined the relationship between the Mediterranean diet and ADHD. The aim was to determine the association between those environmental, nutritional, and body composition factors that may affect the pathogenesis and symptomatology of patients with ADHD in Spain. A total of 89 children and adolescents (41 with diagnosed ADHD and 48 controls) were studied in an observation case-control study. Anthropometry, nutritional status, adherence to a Mediterranean diet, sedentary behaviour, and sleep were measured. Lower adherence to a Mediterranean diet was associated with ADHD diagnosis. Individuals with ADHD more often missed having a second serving of vegetables daily and showed reduced intakes of fish, pulses, and pasta or rice almost every day when compared with controls. Statistically significant differences (P < 0.05) were found for fish, cereal, no breakfast and commercially baked goods consumption. There were also statistically significant differences between ADHD individuals and controls when analysing sedentary behaviours and BMI (P < 0.05). Low adherence to a Mediterranean diet might play a role in ADHD development. Not only specific nutrients but also the whole diet should be considered in ADHD. No clear association was found for anthropometry and sedentary behaviours.
Aruna Potukuchi, Uma Addepally, Kirankumar Sindhu,
Published: 30 June 2017
Nutritional Neuroscience, Volume 21, pp 648-656; https://doi.org/10.1080/1028415x.2017.1332509

Abstract:
Background: Obesity and Type 2 Diabetes (T2D) are chronic nutrient-related disorders that occur together and pose a grave burden to society. They are among the most common causes of ageing and death. Obesity and T2D per se accelerate ageing albeit the underlying mechanisms are unclear yet. Also, it is not clear whether or not superimposing T2D on obesity accelerates ageing. Present study validated the hypothesis, ‘super-imposing T2D on obesity accelerates ageing’ in WNIN/Gr-Ob, the impaired glucose tolerant, obese rat as the model and evaluated probable underlying mechanisms. Objectives: To estimate the survival analysis of WNIN/Gr-Ob rats induced with T2D. To determine the extent of DNA damage and oxidative stress in the brain, the master controller of the body, in WNIN/Gr-Ob rats with/without high sucrose induced T2D/aggravation of insulin resistance (IR) after 3 and 6 months of feeding. Methods: T2D was induced/IR was aggravated by feeding high sucrose diet (HSD) to 9–10 weeks old, male WNIN/Gr-Ob rats. Survival percentage was determined statistically by Kaplan–Meier estimator. Neuronal DNA damage was quantified by the Comet assay while the oxidative stress and antioxidant status were evaluated from the levels of malonaldialdehyde, reduced glutathione, and superoxide dismutase (SOD) activity. Results and Discussion: HSD feeding decreased longevity of WNIN/Gr-Ob rats and was associated with significantly higher total neuronal DNA damage after three months of feeding but not later. In line with this was the increased neuronal oxidative stress (lipid peroxidation) and decreased antioxidant status (reduced glutathione and SOD activity) in HSD than Starch-based diet (SBD) fed rats. The results suggest that HSD feeding decreased the longevity of WNIN/Gr-Ob obese rats probably by increasing oxidative stress and aggravating IR, a condition that precedes T2D.
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