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Mood and Food

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Abstract

The relationship between mood and food is complex. Mood can influence the foods we choose to eat. Sometimes we hear friends or family saying that they were so stressed by events in their lives that their eating was out of control – either they overate or, less frequently, that they could not eat. Overeating when stressed is a common reaction. More than a third of the participants in a national survey conducted by National Public Radio, the Robert Wood Johnson Foundation and the Harvard School of Public Health (2014) said they change their diets during stressful times. The term ‘comfort food’ has entered our lexicon and refers to traditional foods that we feel provide a relief from negative emotions and an increase in positive feelings; eating comfort food is seen as a response to emotional stress. Comfort food is specific to culture and frequently has a high carbohydrate level and a simple preparation. When we feel stressed, we reach for foods that will comfort us immediately, but one theory proposes that this can lead to a vicious cycle: foods high in carbohydrates may lead to surges and crashes in blood sugar accompanied by a surge in adrenaline, or epinephrine, often called ‘the stress hormone’ (Aubrey, 2014). According to this explanation, eating lots of refined carbohydrates and sugar may exacerbate our responses to stress. The relationship between food and mood can also go the other way: the food we choose to eat may affect our mood. There may be types of food that make us more resilient to stress. Over the last two decades, researchers have been investigating the links between the omega-3 fatty acids found in fish (eggs, dark leafy greens, etc.) and emotional health and wellbeing (Aubrey, 2014). Others have shown a strong day-today relationship between more positive mood and higher fruit and vegetable consumption (Hopf, 2013; White, Horwath, & Conner, 2013). And others have demonstrated a link between

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... Bunun aksine, karbonhidrattan zengin bir diyetin ise insülin salınımını daha fazla stimüle ederek daha fazla aminoasidin kas hücrelerine girişini sağlar. Böylece, kan ve beyin bariyerlerinde triptofan oranı artacağından serotonin sentezinde de bir artış meydana gelmektedir (Flaskerud, 2015). Diyette antioksidan kaynağı besinlerin yüksek miktarlarda alımının zaman içerisinde daha düşük inflamasyon ve daha düşük triptofan yıkım oranıyla ilişkili olduğu bildirilmiştir. ...
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Duygu durumları birçok faktörden etkilenir. Besinler ve beslenmenin duygu ve davranışları etkilediği günümüzde daha iyi anlaşılmıştır. Çalışmalar, bitkilerde bulunan polifenol bileşiklerinin antioksidan, antimikrobiyal ve prebiotik özelliklerinin duygu durumunda aktif rol oynayan çeşitli mekanizmalar üzerinde olumlu etkileri olabileceğini göstermektedir. Polifenollerin, özellikle mikrobiyota, beyin-bağırsak aksı ve merkezi sinir sistem sağlığı üzerinde olumlu etkileri ile duygu durumu ve bilişsel fonksiyonlar açısından yararlı etkiler sağlayabileceği düşünülmektedir.
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Emotional eating is commonly defined as the tendency to (over)eat in response to emotion. Insofar as it involves the (over)consumption of high-calorie palatable foods, emotional eating is a maladaptive behavior that can lead to eating disorders, and ultimately to metabolic disorders and obesity. Emotional eating is associated with eating disorder subtypes and with abnormalities in emotion processing at a behavioral level. However, not enough is known about the neural pathways involved in both emotion processing and food intake. In this review, we provide an overview of recent neuroimaging studies, highlighting the brain correlates between emotions and eating behavior that may be involved in emotional eating. Interaction between neural and neuro-endocrine pathways (HPA axis) may be involved. In addition to behavioral interventions, there is a need for a holistic approach encompassing both neural and physiological levels to prevent emotional eating. Based on recent imaging, this review indicates that more attention should be paid to prefrontal areas, the insular and orbitofrontal cortices, and reward pathways, in addition to regions that play a major role in both the cognitive control of emotions and eating behavior. Identifying these brain regions could allow for neuromodulation interventions, including neurofeedback training, which deserves further investigation.
Article
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Optimal nutrition can improve well-being and might mitigate the risk and morbidity associated with coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This review summarizes nutritional guidelines to support dietary counseling provided by dietitians and health-related professionals. The majority of documents encouraged the consumption of fruits, vegetables, and whole grain foods. Thirty-one percent of the guidelines highlighted the importance of minerals and vitamins such as zinc and vitamins C, A, and D to maintain a well-functioning immune system. Dietary supplementation has not been linked to COVID-19 prevention. However, supplementation with vitamins C and D, as well as with zinc and selenium, was highlighted as potentially beneficial for individuals with, or at risk of, respiratory viral infections or for those in whom nutrient deficiency is detected. There was no convincing evidence that food or food packaging is associated with the transmission of COVID-19, but good hygiene practices for handling and preparing foods were recommended. No changes to breastfeeding recommendations have been made, even in women diagnosed with COVID-19.
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Despite omega-3 polyunsaturated fatty acids (PUFA) supplementation in depressed patients have been suggested to improve depressive symptomatology, previous findings are not univocal. To conduct an updated meta-analysis of randomized controlled trials (RCTs) of omega-3 PUFA treatment of depressive disorders, taking into account the clinical differences among patients included in the studies. A search on MEDLINE, EMBASE, PsycInfo, and the Cochrane Database of RCTs using omega-3 PUFA on patients with depressive symptoms published up to August 2013 was performed. Standardized mean difference in clinical measure of depression severity was primary outcome. Type of omega-3 used (particularly eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) and omega-3 as mono- or adjuvant therapy was also examined. Meta-regression analyses assessed the effects of study size, baseline depression severity, trial duration, dose of omega-3, and age of patients. Meta-analysis of 11 and 8 trials conducted respectively on patients with a DSM-defined diagnosis of major depressive disorder (MDD) and patients with depressive symptomatology but no diagnosis of MDD demonstrated significant clinical benefit of omega-3 PUFA treatment compared to placebo (standardized difference in random-effects model 0.56 SD [95% CI: 0.20, 0.92] and 0.22 SD [95% CI: 0.01, 0.43], respectively; pooled analysis was 0.38 SD [95% CI: 0.18, 0.59]). Use of mainly EPA within the preparation, rather than DHA, influenced final clinical efficacy. Significant clinical efficacy had the use of omega-3 PUFA as adjuvant rather than mono-therapy. No relation between efficacy and study size, baseline depression severity, trial duration, age of patients, and study quality was found. Omega-3 PUFA resulted effective in RCTs on patients with bipolar disorder, whereas no evidence was found for those exploring their efficacy on depressive symptoms in young populations, perinatal depression, primary disease other than depression and healthy subjects. The use of omega-3 PUFA is effective in patients with diagnosis of MDD and on depressive patients without diagnosis of MDD.
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The recent escalation of US military suicide deaths to record numbers has been a sentinel for impaired force efficacy and has accelerated the search for reversible risk factors. To determine whether deficiencies of neuroactive, highly unsaturated omega-3 essential fatty acids (n-3 HUFAs), in particular docosahexaenoic acid (DHA), are associated with increased risk of suicide death among a large random sample of active-duty US military. In this retrospective case-control study, serum fatty acids were quantified as a percentage of total fatty acids among US military suicide deaths (n = 800) and controls (n = 800) matched for age, date of collection of sera, sex, rank, and year of incident. Participants were active-duty US military personnel (2002-2008). For cases, age at death ranged from 17-59 years (mean = 27.3 years, SD = 7.3 years). Outcome measures included death by suicide, postdeployment health assessment questionnaire (Department of Defense Form 2796), and ICD-9 mental health diagnosis data. Risk of suicide death was 14% higher per SD of lower DHA percentage (OR = 1.14; 95% CI, 1.02-1.27; P < .03) in adjusted logistic regressions. Among men, risk of suicide death was 62% greater with low serum DHA status (adjusted OR = 1.62; 95% CI, 1.12-2.34; P < .01, comparing DHA below 1.75% [n = 1,389] to DHA of 1.75% and above [n = 141]). Risk of suicide death was 52% greater in those who reported having seen wounded, dead, or killed coalition personnel (OR = 1.52; 95% CI, 1.11-2.09; P < .01). This US military population had a very low and narrow range of n-3 HUFA status. Although these data suggest that low serum DHA may be a risk factor for suicide, well-designed intervention trials are needed to evaluate causality.
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Hippocrates was the first to suggest the healing power of food; however, it was not until the medieval ages that food was considered a tool to modify temperament and mood, although scientific methods as we know them today were not in use at the time. Modern scientific methods in neuroscience began to emerge much later, leading investigators to examine the role of diet in health, including mental wellbeing, with greater precision. This review shows how short- and long-term forced dietary interventions bring about changes in brain structure, chemistry, and physiology, leading to altered animal behavior. Examples will be presented to show how diets alter brain chemistry, behavior, and the action of neuroactive drugs. Most humans and most animal species examined in a controlled setting exhibit a fairly reproducible pattern of what and how they eat. Recent data suggest that these patterns may be under the neurochemical and hormonal control of the organisms themselves. Other data show that in many instances food may be used unconsciously to regulate mood by seemingly normal subjects as well as those undergoing drug withdrawal or experiencing seasonal affective disorders and obesity-related social withdrawal. We will discuss specific examples that illustrate that manipulation of dietary preference is actually an attempt to correct neurochemical make-up.
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Chronic stress causes the release of glucocorticoids, which greatly influence cerebral function, especially glutamatergic transmission. These stress-induced changes in neurotransmission could be counteracted by increasing the dietary intake of omega-3 polyunsaturated fatty acids (n-3 PUFAs). Numerous studies have described the capacity of n-3 PUFAs to help protect glutamatergic neurotransmission from damage induced by stress and glucocorticoids, possibly preventing the development of stress-related disorders such as depression or anxiety. The hippocampus contains glucocorticoid receptors and is involved in learning and memory. This makes it particularly sensitive to stress, which alters certain aspects of hippocampal function. In this review, the various ways in which n-3 PUFAs may prevent the harmful effects of chronic stress, particularly the alteration of glutamatergic synapses in the hippocampus, are summarized.
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Investigation into the psychotropic efficacy of the omega-3 fatty acids (n-3 FAs) has grown tremendously in the past decade and a half. Since the publication of Stoll et al’s1 study of n-3 for treatment of bipolar disorder, many clinical trials, in adults and children, have examined the n-3s in unipolar major depressive disorder (MDD), postpartum depression, bipolar disorder, attention deficit disorder (ADD), psychotic disorders, obsessive-compulsive disorder (OCD), and borderline personality disorder2–5. Psychiatric clinical trials of n-3 FAs in mood disorders now number in the thirties, and various metaanalyses and systematic reviews have generally, but not unequivocally, suggested benefit2,6–16. These efficacy findings are consistent with what is being learned about antidepressants in general, with the growing availability of unpublished studies and databases17, but interpreting the n-3 data is complicated by several factors:
You are what you eat: How food affects your mood
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