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Issues in Mental Health Nursing
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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
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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
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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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