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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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Mood and Food
Jacquelyn H. Flaskerud RN, PhD, FAAN
a
a
University of California—Los Angeles, School of Nursing, Los Angeles, California, USA
Published online: 25 Jul 2015.
To cite this article: Jacquelyn H. Flaskerud RN, PhD, FAAN (2015) Mood and Food, Issues in Mental Health Nursing, 36:4,
307-310
To link to this article: http://dx.doi.org/10.3109/01612840.2014.962677
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Issues in Mental Health Nursing, 36:307–310, 2015
Copyright © 2015 Informa Healthcare USA, Inc.
ISSN: 0161-2840 print / 1096-4673 online
DOI: 10.3109/01612840.2014.962677
CULTURAL COMPETENCE COLUMN
Mood and Food
Jacquelyn H. Flaskerud, RN, PhD, FAAN
University of California—Los Angeles, School of Nursing, Los Angeles, California, USA
Edited by
Jacquelyn H. Flaskerud, RN, PhD, FAAN
University of California—Los Angeles, School of Nursing,
Los Angeles, California, USA
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 over-
ate or, less frequently, that they could not eat. Overeating when
stressed is a common reaction. More than a third of the partici-
pants 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 stress-
ful times. The term ‘comfort food’ has entered our lexicon and
refers to traditional foods that we feel provide a relief from nega-
tive 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 re-
sponses 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 in-
vestigating 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-to-
day relationship between more positive mood and higher fruit
and vegetable consumption (Hopf, 2013; White, Horwath, &
Conner, 2013). And others have demonstrated a link between
Address correspondence to Jacquelyn H. Flaskerud, University of
California—Los Angeles, School of Nursing, 700 Tiverton Ave., Factor
Building, Box 951702, Los Angeles, CA 90095–1702, USA. E-mail:
jflasker@earthlink.net
low levels of specific omega 3 fatty acids and mental illness,
including major depressive disorder and the risk for suicide
(Grosso et al., 2014; Hennebelle, Champeil-Potokar, Lavialle,
Vancassel, & Denis, 2014; Lewis, Hibbeln, Johnson, Lin, Hyun,
& Loewke, 2011; Mischoulon, 2011; Sublette, Ellis, Geant, &
Mann, 2011).
When we speak of nutrition and health, we generally think of
nutrition in relation to the prevention or treatment of heart dis-
ease, diabetes, cancer, or of obesity, hyperlipidemia and related
disorders. Most of us, however, rarely relate diet and nutrition
to mental health. Only recently have we begun to study the
role of certain dietary nutrients in relation to mental health and
performance. However, according to Prasad (1998), the use of
diet to enhance mental function is not a recent phenomenon.
In the medieval holistic view of nature, mood was thought to
be modulated by foods. For medieval man, every food item
was important, since it was associated with good or bad effects
that might be immediate or delayed. Some foods were con-
sidered erotic stimulants (eggs, peacock, beef, pomegranates,
apples); others were used as mood enhancers (quince, dates, el-
derberries) or tranquilizers (lettuce, purslane, chicory) (Prasad,
1998).
The serotonin theory is one explanation of how our food
influences our mood (Hopf, 2013; Prasad, 1998). Neurotrans-
mitters and neuromodulators are basic units of chemical com-
munication within the nervous system. Serotonin is an important
neurotransmitter that the brain produces from tryptophan, con-
tained in foods such as clams, oysters, escargot, octopus, squid,
bananas, pineapple, plums, nuts, milk, turkey, spinach, and eggs
(Prasad, 1998). Functions of serotonin include the regulation of
sleep, appetite, and impulse control; increased levels are related
to mood elevation. The role of dietary protein and carbohydrate
in the synthesis of serotonin is of interest to scientists and lay
persons alike, and is the basis of some of the research into the
influence of food on mood (Prasad, 1998; Hopf, 2013).
The synthesis of serotonin in the brain is limited by the
availability of tryptophan. A protein-rich diet decreases brain
serotonin synthesis. Consumption of a protein-rich meal raises
the blood level of many amino acids. Tryptophan is one of
the least common amino acids in dietary protein. A protein-
rich meal contributes proportionately more competing large
307
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308 J. H. FLASKERUD
neutral amino acids than tryptophan, resulting in reduced en-
try of tryptophan into the brain and reduced serotonin synthesis
(Prasad, 1998). A carbohydrate-rich/protein-poor diet increases
brain serotonin synthesis. Consuming foods high in carbohy-
drates can also change amino acid levels in the blood. As blood
glucose levels rise, insulin is released and enables muscle tis-
sues to take up most amino acids except for tryptophan, which is
bound to albumin in the blood. As a result, the ratio of tryptophan
relative to other amino acids in the blood increases, which en-
ables tryptophan to bind to transporters, enter the brain in large
amounts, and stimulate serotonin synthesis (Hopf, 2013). It has
been observed that many individuals consume large quantities of
carbohydrate-rich food to elevate their mood; these include those
diagnosed with conditions with a significant depressive compo-
nent, such as seasonal affective disorder, premenstrual stress
syndrome, or nicotine withdrawal (Hopf, 2013; Prasad, 1998).
Consumption of carbohydrate-rich food may elevate mood in
such individuals by raising brain serotonin levels.
In a study of carbohydrate consumption in young adults in
New Zealand, researchers found that a diet high in fruits and
vegetables made participants calmer, happier and more ener-
getic in their daily life, according to self-report (White et al.,
2013). For the study, a total of 281 young adults (with a mean
age of 20 years) completed an internet-based daily food diary
for 21 consecutive days. On each of the 21 days, participants
logged into their diary each evening and rated how they felt,
using nine positive and nine negative adjectives. They were also
asked five questions about what they had eaten that day. Specif-
ically, participants were asked to report the number of servings
eaten of fruit and vegetables (considered ‘healthy’ carbohy-
drates by the researchers), and several categories of ‘unhealthy’
high carbohydrate foods like biscuits/cookies, potato crisps, and
cakes/muffins. The results showed a strong day-to-day relation-
ship between more positive mood and higher fruit and vegetable
consumption, but not other foods. To understand which comes
first feeling positive or eating healthier foods, the investigators
ran additional analyses and found that eating fruits and vegeta-
bles predicted improvements in positive mood the next day,
suggesting that healthy foods may improve mood (White et al.,
2013). This study might be seen as providing limited support for
the serotonin theory as fruits and vegetables are carbohydrates
(although the serotonin theory does not distinguish carbohy-
drates as healthy vs unhealthy). Also, the study has several
methodologic limitations self-report, cross-sectional design,
and response bias. Studies with randomized controls evaluating
the influence of high fruit and vegetable intake on mood and
wellbeing are needed before any conclusions can be made.
Another take on the relationship between food and mood
comes from the study of omega-3 fatty acids in the diet and what
might be called an ‘anti-inflammatory explanation. Omega-
3 polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid
(EPA) and docosahexaenoic acid (DHA) have been demon-
strated to be effective in cardiovascular disease prevention due
to their anti-inflammatory and cardio-protective effects (Grosso
et al., 2014). Recently, new therapeutic indications for omega-3
PUFAs have been proposed, such as treatment for certain forms
of mental illness, including depressive disorders (Grosso et al.,
2014; Hennebelle et al., 2014; Lewis et al., 2011; Mischoulon
2011; Sublette et al., 2011). Many of the early studies report-
ing these effects were found in CVD patients experiencing de-
pression, leading to the suggestion that some psychiatric dis-
eases, such as depression may share certain pathophysiolog-
ical mechanisms with CVD, namely increased production of
pro-inflammatory cytokines, endothelial dysfunction, and ele-
vations in plasma homocysteine levels (Grosso et al., 2014). The
positive effects of omega-3 PUFAs on depression may depend
on their abundant presence in the human nervous system and
their anti-inflammatory capacity, which may counteract inflam-
matory processes occurring in depression. Several ecological,
cross-sectional, and prospective studies supported this hypothe-
sis by reporting an inverse association between omega-3 intake
and prevalence of depression. Further clinical studies demon-
strated lower concentrations of omega-3 PUFAs in plasma or red
blood cell membranes of depressed subjects. All together, these
observations suggest a correlation between omega-3 PUFAs and
depressive disorders, justifying the rationale of a number of ran-
domized controlled trials of omega-3 PUFA supplementation for
the treatment of depressive disorders.
Many clinical trials, in adults and children, have examined
the omega-3 PUFAs in major depressive disorder (MDD),
postpartum depression, bipolar disorder, attention deficit
disorder (ADD), psychotic disorders, obsessive-compulsive
disorder (OCD), and borderline personality disorder; and
various meta-analyses and systematic reviews have generally,
but not unequivocally, suggested benefit (Grosso et al., 2014).
It should be noted that the results of these studies differ (and
sometimes contradict one another) for a variety of reasons: the
differing populations studied; the use of dietary serum levels
vs augmentation (supplement) regimens; different doses; the
EPA:DHA ratios; the inability to control for comorbidities; and
differences in outcome measures; among other problems. As
examples: in a review of the various ways in which omega-3
PUFAs may prevent the harmful effects of chronic stress, Hen-
nebelle and colleagues (2014) summarized those studies that
focused particularly on the alteration of glutamatergic synapses
in the hippocampus. Lewis and others (2011) used suicide as an
outcome measure in a study of dietary omega-3 PUFAs in US
military personnel. Sublette and colleagues (2011) conducted
a meta-analysis of 15 placebo-controlled trials involving 916
participants, investigating the effect of PUFAs supplementation
in treatment of depressive disorders. Grosso and associates
(2014) conducted an updated meta-analysis of randomized
controlled trials (RCTs) of omega-3 PUFAs in the treatment of
depressive disorders, taking into account the clinical differences
among patients (MDD diagnosis vs other depressive diagnoses)
included in the studies. Details of some of these studies are
provided below to illustrate the differences that may influence
the ambiguity in findings but despite bold assertions by
Downloaded by [Jacquelyn Flaskerud] at 16:03 08 August 2015
CULTURAL COMPETENCE 309
authors of these studies to the contrary, this is a messy knot to
untangle.
Lewis and colleagues’ (2011) objective was to determine
if deficiencies of neuro-active highly unsaturated omega-3 es-
sential fatty acids, in particular DHA, were associated with in-
creased risk of suicide death among a large random sample of
active duty US military. With increasing death by suicide among
US military, the search for reversible risk factors has intensi-
fied. Reasoning that deficiencies of nutrients critical for brain
function may be a significant contributing risk factor for psychi-
atric pathology, especially suicide and stress-related psychiatric
symptoms, these investigators hypothesized that low DHA sta-
tus would be associated with increased risk of suicide death
among military personnel. Prospectively collected serum and
supporting data were available from the Armed Forces Health
Surveillance Center for a large number of active duty suicide
deaths (n = 800) and controls (n = 800) matched for age, date
of collection, sex, rank, and year of incident. All cases selected
had a serum sample collected within 12 months prior to sui-
cide; matched controls also had serum collected in the same
timeframe. Serum fatty acids were quantified as percentage of
total fatty acids among US military suicide deaths and controls.
Outcome measures included death by suicide, post-deployment
health assessment questionnaire, and ICD-9 mental health diag-
nosis data. Among men, risk of suicide death was 62% greater
with low serum DHA status. EPA appeared to confer no sig-
nificant protective effect. The number of women in the total
sample was small (n = 70) and there was no significant dif-
ference between cases and controls. Only participants with the
highest levels of DHA appeared to be protected. Lower levels
of two other fatty acids not known to be related to mood were
associated with increased risk of suicide: stearic acid and di-
homogamma linoleic acid, while higher levels of palmitoleic
acid and cis-vaccenic acid were associated with lower risks
of suicide. Subjective reports of mental health status available
from post-deployment health assessment were associated with
increased risk for suicide among deployed subjects: risk of sui-
cide death was 54% greater in those who reported having seen
wounded, dead or killed coalition personnel (Lewis et al., 2011).
Sublette and colleagues (2011) conducted a meta-analysis
of 15 placebo-controlled trials (involving 916 participants) of
PUFAs supplementation to test the hypothesis that EPA is the
effective component in PUFAs treatment of major depressive
episodes. Trials were included in the meta-analysis if they met
the following inclusion criteria: (1) prospective, randomized,
double-blinded study design; (2) depressive episode as the pri-
mary complaint (with or without comorbid medical conditions);
(3) administration of omega-3 PUFAs supplements as treatment,
either alone or in conjunction with other treatments; (4) ap-
propriate outcome measures to assess depressed mood; (5) a
placebo comparison group, and (6) published in English (Sub-
lette et al., 2011).
Their findings were that supplements containing EPA 60%
in excess of DHA (dose range 200–2,200 mg EPA) were effec-
tive against primary depression. This finding contradicts that of
Lewis and colleagues (2011) who found no effect of EPA, but
rather a protective effect of DHA. One study says that dietary
DHA is protective against suicide and EPA is not; the other says
that EPA given as a supplement is more effective than DHA
for alleviating depression. However, the differences in these
two investigations are great, making a head-to-head comparison
difficult.
As detailed by Mischoulon (2011), Lewis and colleagues
selected a specific, unambiguous outcome: suicide death and
examined a narrow segment of the population: active duty, pre-
dominantly male military personnel serving during the post-
9/11 era. Sublette and associates (2011) examined depressive
improvement, an outcome more subject to patient and investi-
gator bias and included studies with depressed individuals of
both genders (presumably with a more balanced distribution
than in the Lewis sample), from many walks of life, which
would make their sample more representative of the general
population with depression (Mischoulon, 2011). While Lewis
and colleagues focused on dietary serum levels of omega-3,
Sublette and colleagues examined a wide range of omega-3
supplementation regimens, including monotherapy, augmenta-
tion therapy, different doses and EPA:DHA ratios, and differ-
ent treatment durations. Diagnoses included major depressive
disorder (MDD) of different severities, bipolar disorder, dys-
thymia, depressive episode, Parkinson’s, and coronary heart
disease (Sublette et al., 2011). Both studies reported difficulty
controlling for medical and psychiatric comorbidity, including
substance abuse and PTSD, which may be especially relevant
in a military population. Considering the above, these studies
are difficult to compare and cannot necessarily be viewed as
contradictory. EPA may have benefits for the overall constella-
tion of symptoms known as DSM-IV MDD that exceed those of
DHA. On the other hand, DHA may impact the mechanism(s)
in the brain that regulate suicidal behavior, independently of
MDD status (Mischoulon, 2011). In the Lewis study, four other
fatty acids that are seemingly unrelated to mood also appeared
to have an effect on the risk of suicide. Therefore, it is difficult
to interpret the overall clinical impact of the different fatty acids
and their ratios, in oral preparations and in the blood, within the
limitations of these studies (Mischoulon, 2011).
In an effort to clarify some of these ambiguities, Grosso
and colleagues (2014) conducted an up-dated meta-analysis of
randomized controlled trials (RCTs) of omega-3 PUFAs in the
treatment of depressive disorders. They noted that the analy-
ses previously conducted focused on the effects of omega-3
PUFAs supplementation on depressive symptoms, but features
associated with the specific pathophysiological nature of the de-
pression occurring in the patients and their comorbidity status
were often lacking. They reasoned that the biological effects of
omega-3 PUFAs may be effective in certain sub-types of de-
pressive disorders rather than in others due to the different types
of depression. Their meta-analysis involved 39 RCTs, including
11 RCTs conducted on patients with a DSM-defined diagnosis
Downloaded by [Jacquelyn Flaskerud] at 16:03 08 August 2015
310 J. H. FLASKERUD
of major depressive disorder (MDD); seven trials on patients
with bipolar disorder; eight RCTs on patients with depressive
symptomatology but no diagnosis of MDD; and 13 trials of
patients with other diagnoses. The investigators (Grosso et al.,
2014) demonstrated that the use of omega-3 PUFAs as thera-
peutic agents was effective in patients with diagnosis of MDD
and on depressive patients without a diagnosis of MDD. Incon-
clusive results were found for patients with other pathologic
conditions (namely schizophrenia, CVD, and ADD), and no
beneficial effect was found in healthy subjects with depressive
symptoms, children and adolescence with bipolar disorder, and
women with perinatal depression. The analysis of the studies on
bipolar disorder showed a positive effect of the omega-3 PU-
FAs but the evidence was weak, because four studies conducted
on bipolar patients reporting poor effects of the omega-3 PU-
FAs intervention were dropped from the meta-analysis due to
missing data. The omega-3 supplement preparations that were
composed mainly of EPA, rather than DHA, influenced final
clinical efficacy. Importantly, significant clinical efficacy was
found when omega-3 PUFAs were used as adjuvant rather than
mono-therapy. A major limiting factor was the inability of the
study investigators to control all the many potential sources of
heterogeneity in the studies included in the meta-analysis (e.g.,
how depression was diagnosed and measured, the dose of sup-
plements, the ratio of EPA to DHA, populations studied, and so
forth). In addition, all studies included reported a major placebo
response.
What to make of all this? Many of us may have been sup-
plementing our diets with fish oil (EPA and DHA) prepara-
tions, which were promoted as an easy way to protect the heart,
ease inflammation, improve mental health, and lengthen life.
The studies cited above would support that decision. Then in
2013 came two studies that provided a warning against fish oil
supplementation. A study by scientists at the Fred Hutchinson
Cancer Research Center in Seattle linked eating a lot of oily
fish or taking potent fish oil supplements to a 43% increased
risk for prostate cancer overall, and a 71% increased risk for
aggressive prostate cancer (Brasky et al., 2013). Earlier that
year, Italian researchers reported in the New England Journal
of Medicine that omega-3 fatty acid supplements did nothing
to reduce heart attacks, strokes, or deaths from heart disease
in people with risk factors for heart disease (Risk and Preven-
tion Study Collaborative Group, 2013). The meta-analysis by
Grosso and colleagues (2014) also found no effect of EPA for
CVD. This work followed similar warnings about vitamin E sup-
plements, beta-carotene supplements, and other high-dose di-
etary supplements (LeWine, 2013). According to LeWine, Chief
Medical Editor of Harvard Health Publications (see also Lewis
and colleagues’ findings of other protective fatty acids detailed
above):
if we could absolutely, positively say that the benefits of eating
seafood comes entirely from omega-3 fats, then downing fish oil
pills would be an alternative to eating fish. But it’s more than likely
that we need the entire orchestra of fish fats, vitamins, minerals, and
supporting molecules, rather than the lone contributions of EPA and
DHA.
The same holds true of other foods. Taking even a handful of
supplements is no substitute for the wealth of nutrients we get from
eating fruits, vegetables, and whole grains. (LeWine, 2013, paras 12,
& 13).
Apparently, the research on food and mood still has a long
way to go before any prescriptive advice can be given about the
protective use of foods or supplements.
Declaration of Interest: The author reports no conflicts of
interest. The author alone is responsible for the content and
writing of the paper.
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... Prefrontal areas are involved not only in emotion regulation, but also in executive functioning (including inhibitory and attentional control, as well as cognitive flexibility) and the cognitive control of eating behavior [62], which it does by modulating appetitive regions (i.e., OFC, ventral striatum, insula, and amygdala/hippocampus complex) [51]. Furthermore, there is an interplay between emotion and food intake: emotions can influence food choices and, conversely, food intake can influence emotional state, owing to the impact of nutrients on food choices and mood [63][64][65]. ...
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Background The purpose of this study is to examine the effect of education based on learning modality in diabetic individuals who are incompatible with treatment, on treatment compliance and metabolic goals. Methods This study is a randomized controlled trial. Among the individuals who applied to the outpatient clinic and were eligible for inclusion in the study, the odd numbers were assigned to the intervention group (n:30), and the even numbers to the control group (n:30). The practice group of 30 people and the control group were divided into 3 groups. Three groups in the intervention group was given according to the learning modality. The auditory group in the post-training practice group; calling by phone, to the visual group; by Short Messaging Servis, to the tactile group; reminder alerts were made by phone + Short Messaging Servise. Standard training was given to the control group. Result It was observed that the total scale score of the intervention group decreased significantly after the training, while the total scale score of the control group increased significantly after the training. As a result of the diabetes education given based on learning modality, significant decreases were observed in A1C, fasting blood glucose, post-prandial blood glucose, body mass index, high-density lipoprotein and blood pressure values of the intervention group compared to the control group. Conclusion Study findings show that the diabetes education given to the intervention group according to their learning modality positively affects the diabetes management and treatment compliance of the individuals.
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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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Studies of dietary ω-3 fatty acid intake and prostate cancer risk are inconsistent; however, recent large prospective studies have found increased risk of prostate cancer among men with high blood concentrations of long-chain ω-3 polyunsaturated fatty acids ([LCω-3PUFA] 20:5ω3; 22:5ω3; 22:6ω3]. This case-cohort study examines associations between plasma phospholipid fatty acids and prostate cancer risk among participants in the Selenium and Vitamin E Cancer Prevention Trial. Case subjects were 834 men diagnosed with prostate cancer, of which 156 had high-grade cancer. The subcohort consisted of 1393 men selected randomly at baseline and from within strata frequency matched to case subjects on age and race. Proportional hazards models estimated hazard ratios (HR) and 95% confidence intervals (CI) for associations between fatty acids and prostate cancer risk overall and by grade. All statistical tests were two-sided. Compared with men in the lowest quartiles of LCω-3PUFA, men in the highest quartile had increased risks for low-grade (HR = 1.44, 95% CI = 1.08 to 1.93), high-grade (HR = 1.71, 95% CI = 1.00 to 2.94), and total prostate cancer (HR = 1.43, 95% CI = 1.09 to 1.88). Associations were similar for individual long-chain ω-3 fatty acids. Higher linoleic acid (ω-6) was associated with reduced risks of low-grade (HR = 0.75, 95% CI = 0.56 to 0.99) and total prostate cancer (HR = 0.77, 95% CI = 0.59 to 1.01); however, there was no dose response. This study confirms previous reports of increased prostate cancer risk among men with high blood concentrations of LCω-3PUFA. The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis. Recommendations to increase LCω-3PUFA intake should consider its potential risks.
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Trials have shown a beneficial effect of n-3 polyunsaturated fatty acids in patients with a previous myocardial infarction or heart failure. We evaluated the potential benefit of such therapy in patients with multiple cardiovascular risk factors or atherosclerotic vascular disease who had not had a myocardial infarction. In this double-blind, placebo-controlled clinical trial, we enrolled a cohort of patients who were followed by a network of 860 general practitioners in Italy. Eligible patients were men and women with multiple cardiovascular risk factors or atherosclerotic vascular disease but not myocardial infarction. Patients were randomly assigned to n-3 fatty acids (1 g daily) or placebo (olive oil). The initially specified primary end point was the cumulative rate of death, nonfatal myocardial infarction, and nonfatal stroke. At 1 year, after the event rate was found to be lower than anticipated, the primary end point was revised as time to death from cardiovascular causes or admission to the hospital for cardiovascular causes. Of the 12,513 patients enrolled, 6244 were randomly assigned to n-3 fatty acids and 6269 to placebo. With a median of 5 years of follow-up, the primary end point occurred in 1478 of 12,505 patients included in the analysis (11.8%), of whom 733 of 6239 (11.7%) had received n-3 fatty acids and 745 of 6266 (11.9%) had received placebo (adjusted hazard ratio with n-3 fatty acids, 0.97; 95% confidence interval, 0.88 to 1.08; P=0.58). The same null results were observed for all the secondary end points. In a large general-practice cohort of patients with multiple cardiovascular risk factors, daily treatment with n-3 fatty acids did not reduce cardiovascular mortality and morbidity. (Funded by Società Prodotti Antibiotici and others; ClinicalTrials.gov number, NCT00317707.).
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Objectives Prior research has focused on the association between negative affect and eating behaviour, often utilizing laboratory or cross-sectional study designs. These studies have inherent limitations, and the association between positive affect and eating behaviour remains relatively unexplored. Therefore, the objective of this study was to investigate the bidirectional relationships between daily negative and positive affective experiences and food consumption in a naturalistic setting among healthy young adults. DesignDaily diary study across 21days (microlongitudinal, correlational design). MethodsA total of 281 young adults with a mean age of 19.9 (1.2)years completed an Internet-based daily diary for 21 consecutive days. Each day they reported their negative and positive affect, and their consumption of five specific foods. Hierarchical linear modelling was used to test same-day associations between daily affect and food consumption, and next-day (lagged) associations to determine directionality. Moderating effects of BMI and gender were also examined in exploratory analyses. ResultsAnalyses of same-day within-person associations revealed that on days when young adults experienced greater positive affect, they reported eating more servings of fruit (p=.002) and vegetables (p<.001). Results of lagged analysis showed that fruits and vegetables predicted improvements in positive affect the next day, suggesting that healthy foods were driving affective experiences and not vice versa. Meaningful changes in positive affect were observed with the daily consumption of approximately 7-8 servings of fruit or vegetables. Conclusions Eating fruit and vegetables may promote emotional well-being among healthy young adults.
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Randomized trials of omega-3 polyunsaturated fatty acid (PUFA) treatment for depression have differed in outcome. Recent meta-analyses ascribe discrepancies to differential effects of eicosapentaenoic acid (EPA) versus docosahexaenoic acid (DHA) and to diagnostic heterogeneity. This meta-analysis tests the hypothesis that EPA is the effective component in PUFA treatment of major depressive episodes. PubMed/MeSH was searched for studies published in English from 1960 through June 2010 using the terms fish oils (MeSH) AND (depressive disorder [MeSH] OR bipolar depression) AND randomized controlled trial (publication type). The search was supplemented by manual bibliography review and examination of relevant review articles. The search yielded 15 trials involving 916 participants. Studies were included if they had a prospective, randomized, double-blinded, placebo-controlled study design; if depressive episode was the primary complaint (with or without comorbid medical conditions); if omega-3 PUFA supplements were administered; and if appropriate outcome measures were used to assess depressed mood. Extracted data included study design, sample sizes, doses and percentages of EPA and DHA, mean ages, baseline and endpoint depression ratings and standard deviations for PUFA and placebo groups, and P values. The clinical outcome of interest was the standardized mean difference in the change from baseline to endpoint scores on a depression rating scale in subjects taking PUFA supplements versus subjects taking placebo. In a mixed-effect model, percentage of EPA in the supplements was the fixed-effect predictor, dichotomized into 2 groups: EPA < 60% or EPA ≥ 60% of the total EPA + DHA. Secondary analyses explored the relevance of treatment duration, age, and EPA dose. Supplements with EPA ≥ 60% showed benefit on standardized mean depression scores (effect size = 0.532; 95% CI, 0.277-0.733; t = 4.195; P < .001) versus supplements with EPA < 60% (effect size = -0.026; 95% CI, -0.200 to 0.148; t = -0.316; P = .756), with negligible contribution of random effects or heteroscedasticity and with no effects of treatment duration or age. Supplements with EPA < 60% were ineffective. Exploratory analyses supported a nonlinear model, with improvement determined by the dose of EPA in excess of DHA, within the range of 200 to 2,200 mg/d of EPA. Supplements containing EPA ≥ 60% of total EPA + DHA, in a dose range of 200 to 2,200 mg/d of EPA in excess of DHA, were effective against primary depression. Translational studies are needed to determine the mechanisms of EPA's therapeutic benefit.
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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: