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BMJ
2020;369:m2440 | doi: 10.1136/bmj.m2440 1
FOOD FOR THOUGHT 2020
Food and mood: how do diet and nutrition affect
mental wellbeing?
Poor nutrition may be a causal factor in the experience of low mood, and improving diet may help
to protect not only the physical health but also the mental health of the population, say Joseph
Firth and colleagues
D
epression and anxiety are the
most common mental health
conditions worldwide, mak-
ing them a leading cause of
disability.
1
Even beyond diag
-
nosed conditions, subclinical symptoms of
depression and anxiety aect the wellbeing
and functioning of a large proportion of the
population.2 Therefore, new approaches to
managing both clinically diagnosed and
subclinical depression and anxiety are
needed.
In recent years, the relationships bet-
ween nutrition and mental health have
gained considerable interest. Indeed,
epidemiological research has observed
that adherence to healthy or Mediterranean
dietary patterns—high consumption of
fruits, vegetables, nuts, and legumes;
moderate consumption of poultry, eggs,
and dairy products; and only occasional
consumption of red meat—is associated
with a reduced risk of depression.3 However,
the nature of these relations is complicated
by the clear potential for reverse causality
between diet and mental health (fig 1). For
example, alterations in food choices or
preferences in response to our temporary
psychological state—such as “comfort
foods” in times of low mood, or changes in
appetite from stress—are common human
experiences. In addition, relationships
between nutrition and longstanding mental
illness are compounded by barriers to
maintaining a healthy diet. These barriers
disproportionality affect people with
mental illness and include the financial
and environmental determinants of health,
and even the appetite inducing eects of
psychiatric medications.4
While acknowledging the complex,
multidirectional nature of the relationships
between diet and mental health (fig 1), in
this article we focus on the ways in which
certain foods and dietary patterns could
aect mental health.
Mood and carbohydrates
Consumption of highly refined carbohy-
drates can increase the risk of obesity and
diabetes.5 Glycaemic index is a relative
ranking of carbohydrate in foods accord-
ing to the speed at which they are digested,
absorbed, metabolised, and ultimately
aect blood glucose and insulin levels. As
well as the physical health risks, diets with
a high glycaemic index and load (eg, diets
containing high amounts of refined carbo-
hydrates and sugars) may also have a det-
rimental eect on psychological wellbeing;
data from longitudinal research show an
association between progressively higher
dietary glycaemic index and the incidence
of depressive symptoms.
6
Clinical studies
have also shown potential causal eects
of refined carbohydrates on mood; experi-
mental exposure to diets with a high gly-
caemic load in controlled settings increases
depressive symptoms in healthy volunteers,
with a moderately large eect.7
Although mood itself can affect our
food choices, plausible mechanisms exist
by which high consumption of processed
carbohydrates could increase the risk of
depression and anxiety—for example,
through repeated and rapid increases
and decreases in blood glucose. Measures
of glycaemic index and glycaemic load
can be used to estimate glycaemia and
insulin demand in healthy individuals
after eating.
8
Thus, high dietary glycaemic
load, and the resultant compensatory
responses, could lower plasma glucose to
concentrations that trigger the secretion of
autonomic counter-regulatory hormones
such as cortisol, adrenaline, growth
hormone, and glucagon.5 9 The potential
eects of this response on mood have been
examined in experimental human research
of stepped reductions in plasma glucose
concentrations conducted under laboratory
conditions through glucose perfusion.
These findings showed that such counter-
regulatory hormones may cause changes
in anxiety, irritability, and hunger.10 In
addition, observational research has found
that recurrent hypoglycaemia (low blood
sugar) is associated with mood disorders.9
The hypothesis that repeated and
rapid increases and decreases in blood
glucose explain how consumption
of refined carbohydrate could affect
psychological state appears to be a good
fit given the relatively fast eect of diets
with a high glycaemic index or load on
depressive symptoms observed in human
studies.7 However, other processes may
explain the observed relationships. For
instance, diets with a high glycaemic
index are a risk factor for diabetes,5
which is often a comorbid condition with
depression.411 While the main models
of disease pathophysiology in diabetes
and mental illness are separate, common
abnormalities in insulin resistance, brain
volume, and neurocognitive performance
in both conditions support the hypothesis
that these conditions have overlapping
pathophysiology.12 Furthermore, the
inflammatory response to foods with a
high glycaemic index13 raises the possibility
that diets with a high glycaemic index are
associated with symptoms of depression
through the broader connections between
mental health and immune activation.
Diet, immune activation, and depression
Studies have found that sustained adher-
ence to Mediterranean dietary patterns
can reduce markers of inflammation in
humans.
14
On the other hand, high calorie
Key Messages
•
Healthy eating patterns, such as
the Mediterranean diet, are associ-
ated with better mental health than
“unhealthy” eating patterns, such as
the Western diet
•
The effects of certain foods or die-
tary patterns on glycaemia, immune
activation, and the gut microbiome
may play a role in the relationships
between food and mood
•
More research is needed to under-
stand the mechanisms that link food
and mental wellbeing and determine
how and when nutrition can be used
to improve mental health
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2020;369:m2440 | thebmj
meals rich in saturated fat appear to stim-
ulate immune activation.13 15 Indeed, the
inflammatory eects of a diet high in calo-
ries and saturated fat have been proposed
as one mechanism through which the West-
ern diet may have detrimental eects on
brain health, including cognitive decline,
hippocampal dysfunction, and damage
to the blood-brain barrier.
15
Since various
mental health conditions, including mood
disorders, have been linked to heightened
inflammation,
16
this mechanism also pre-
sents a pathway through which poor diet
could increase the risk of depression. This
hypothesis is supported by observational
studies which have shown that people
with depression score significantly higher
on measures of “dietary inflammation,”317
characterised by a greater consumption
of foods that are associated with inflam-
mation (eg, trans fats and refined carbo-
hydrates) and lower intakes of nutritional
foods, which are thought to have anti-
inflammatory properties (eg, omega-3 fats).
However, the causal roles of dietary inflam-
mation in mental health have not yet been
established.
Nonetheless, randomised controlled
trials of anti-inflammatory agents (eg,
cytokine inhibitors and non-steroidal
anti-inflammatory drugs) have found
that these agents can significantly
reduce depressive symptoms.18 Specific
nutritional components (eg, polyphenols
and polyunsaturated fats) and general
dietary patterns (eg, consumption of a
Mediterranean diet) may also have anti-
inflammatory eects,
14 19 20
which raises the
possibility that certain foods could relieve
or prevent depressive symptoms associated
with heightened inflammatory status.21 A
recent study provides preliminary support
for this possibility.
20
The study shows that
medications that stimulate inflammation
typically induce depressive states in
people treated, and that giving omega-3
fatty acids, which have anti-inflammatory
properties, before the medication seems
to prevent the onset of cytokine induced
depression.20
However, the complexity of the hypo-
thesised three way relation between
diet, inflammation, and depression
is compounded by several important
modifiers. For example, recent clinical
research has observed that stressors
experienced the previous day, or a personal
history of major depressive disorders,
may cancel out the beneficial effects of
healthy food choices on inflammation
and mood.22 Furthermore, as heightened
inflammation occurs in only some
clinically depressed individuals, anti-
inflammatory interventions may only
benefit certain people characterised by
an “inflammatory phenotype,” or those
with comorbid inflammatory conditions.
18
Further interventional research is needed
to establish if improvements in immune
regulation, induced by diet, can reduce
depressive symptoms in those aected by
inflammatory conditions.
Brain, gut microbiome, and mood
A more recent explanation for the way in
which our food may aect our mental well-
being is the eect of dietary patterns on the
gut microbiome—a broad term that refers to
the trillions of microbial organisms, includ-
ing bacteria, viruses, and archaea, living
in the human gut. The gut microbiome
interacts with the brain in bidirectional
ways using neural, inflammatory, and
hormonal signalling pathways.23 The role
of altered interactions between the brain
and gut microbiome on mental health has
been proposed on the basis of the follow-
ing evidence: emotion-like behaviour in
rodents changes with changes in the gut
microbiome,24 major depressive disorder
in humans is associated with alterations
of the gut microbiome,25 and transfer of
faecal gut microbiota from humans with
depression into rodents appears to induce
animal behaviours that are hypothesised
to indicate depression-like states.25 26 Such
findings suggest a role of altered neuroac-
tive microbial metabolites in depressive
symptoms.
In addition to genetic factors and
exposure to antibiotics, diet is a potentially
modifiable determinant of the diversity,
relative abundance, and functionality of
the gut microbiome throughout life. For
instance, the neurocognitive eects of the
Western diet, and the possible mediating
role of low grade systemic immune
activation (as discussed above) may result
from a compromised mucus layer with or
without increased epithelial permeability.
Such a decrease in the function of the gut
barrier is sometimes referred to as a “leaky
gut” and has been linked to an “unhealthy”
gut microbiome resulting from a diet low
in fibre and high in saturated fats, refined
sugars, and artificial sweeteners.15 23 27
Conversely, the consumption of a diet high
in fibres, polyphenols, and unsaturated
fatty acids (as found in a Mediterranean
diet) can promote gut microbial taxa which
can metabolise these food sources into
anti-inflammatory metabolites,15 28 such
as short chain fatty acids, while lowering
the production of secondary bile acids
and p-cresol. Moreover, a recent study
found that the ingestion of probiotics by
healthy individuals, which theoretically
target the gut microbiome, can alter the
brain’s response to a task that requires
emotional attention
29
and may even reduce
symptoms of depression.30 When viewed
together, these studies provide promising
evidence supporting a role of the gut
microbiome in modulating processes that
regulate emotion in the human brain.
However, no causal relationship between
specific microbes, or their metabolites,
and complex human emotions has been
established so far. Furthermore, whether
changes to the gut microbiome induced
by diet can aect depressive symptoms or
clinical depressive disorders, and the time
in which this could feasibly occur, remains
to be shown.
Priorities and next steps
In moving forward within this active field
of research, it is firstly important not to
lose sight of the wood for the trees—that
is, become too focused on the details and
not pay attention to the bigger questions.
Whereas discovering the anti-inflammatory
Determinants of physical and mental comorbidity
Psychological
and social factors
Multiple
biological
pathways
Hormonal,
inflammatory,
neural pathways
Cravings, habits and
situational factors Good quality diet
For example:
Healthy fats
Limited fast foods
Fruits and vegetables
High fibre foods
Physical health
For example:
Insulin sensitivity
Less cardiovascular risk
Healthy weight
Other health behaviours
Mental health
For example:
Better mood
Less stress
Lower risk of illness
Cognitive function
Fig1 | Hypothesised relationship between diet, physical health, and mental health. The dashed
line is the focus of this article.
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FOOD FOR THOUGHT 2020
thebmj
BMJ
2020;369:m2440 | doi: 10.1136/bmj.m2440 3
properties of a single nutrient or uncover-
ing the subtleties of interactions between
the gut and the brain may shed new
light on how food may influence mood,
it is important not to neglect the existing
knowledge on other ways diet may aect
mental health. For example, the later con-
sequences of a poor diet include obesity
and diabetes, which have already been
shown to be associated with poorer mental
health.
11 31-33
A full discussion of the eect
of these comorbidities is beyond the scope
of our article (see fig 1), but it is important
to acknowledge that developing public
health initiatives that effectively tackle
the established risk factors of physical
and mental comorbidities is a priority for
improving population health.
Further work is needed to improve our
understanding of the complex pathways
through which diet and nutrition can
influence the brain. Such knowledge
could lead to investigations of targeted,
even personalised, interventions to
improve mood, anxiety, or other symptoms
through nutritional approaches. However,
these possibilities are speculative at the
moment, and more interventional research
is needed to establish if, how, and when
dietary interventions can be used to
prevent mental illness or reduce symptoms
in those living with such conditions. Of
note, a recent large clinical trial found
no significant benefits of a behavioural
intervention promoting a Mediterranean
diet for adults with subclinical depressive
symptoms.34 On the other hand, several
recent smaller trials in individuals with
current depression observed moderately
large improvements from interventions
based on the Mediterranean diet.35-37 Such
results, however, must be considered
within the context of the eect of people’s
expectations, particularly given that
individuals’ beliefs about the quality of
their food or diet may also have a marked
eect on their sense of overall health and
wellbeing.
38
Nonetheless, even aside from
psychological effects, consideration of
dietary factors within mental healthcare
may help improve physical health out-
comes, given the higher rates of cardio-
metabolic diseases observed in people with
mental illness.33
At the same time, it is important to
be remember that the causes of mental
illness are many and varied, and they will
often present and persist independently
of nutrition and diet. Thus, the increased
understanding of potential connections
between food and mental wellbeing
should never be used to support automatic
assumptions, or stigmatisation, about
an individual’s dietary choices and their
mental health. Indeed, such stigmatisation
could be itself be a casual pathway to
increasing the risk of poorer mental
health. Nonetheless, a promising message
for public health and clinical settings is
emerging from the ongoing research. This
message supports the idea that creating
environments and developing measures
that promote healthy, nutritious diets,
while decreasing the consumption of
highly processed and refined “junk” foods
may provide benefits even beyond the well
known eects on physical health, including
improved psychological wellbeing.
Contributors and sources: JF has expertise in the
interaction between physical and mental health,
particularly the role of lifestyle and behavioural
health factors in mental health promotion. JEG’s
area of expertise is the study of the relationship
between sleep duration, nutrition, psychiatric
disorders, and cardiometabolic diseases. AB leads
research investigating the molecular mechanisms
underlying the eect of stress and inflammation
on human hippocampal neurogenesis, and how
nutritional components and their metabolites can
prevent changes induced by those conditions. REW
has expertise in genetic epidemiology approaches
to examining casual relations between health
behaviours and mental illness. EAM has expertise
in brain and gut interactions and microbiome
interactions. All authors contributed to, read, and
approved the paper, and all the information was
sourced from articles published in peer reviewed
research journals. JF is the guarantor.
Competing interests: We have read and understood
BMJ policy on declaration of interests and declare
the following: JF is supported by a University of
Manchester Presidential Fellowship and a UK
Research and Innovation Future Leaders Fellowship
and has received support from a NICM-Blackmores
Institute Fellowship. JEG served on the medical
advisory board on insomnia in the cardiovascular
patient population for the drug company Eisai.
AB has received research funding from Johnson
& Johnson for research on depression and
inflammation, the UK Medical Research Council, the
European Commission Horizon 2020, the National
Institute for Health Research (NIHR) Biomedical
Research Centre at South London and Maudsley
NHS Foundation Trust, and King’s College London.
REW receives funding from the National Institute for
Health Research Biomedical Research Centre at the
University Hospitals Bristol NHS Foundation Trust
and the University of Bristol. EAM has served on the
external advisory boards of Danone, Viome, Amare,
Axial Biotherapeutics, Pendulum, Ubiome, Bloom
Science, Mahana Therapeutics, and APC Microbiome
Ireland, and he receives royalties from Harper &
Collins for his book The Mind Gut Connection. He is
supported by grants from the National Institute of
Diabetes and Digestive and KidneyDiseases, and the
US Department of Defense. The views expressed are
those of the authors and not necessarily those of the
organisations above.
Provenance and peer review: Commissioned;
externally peer reviewed.
This article is part of series commissioned by The
BMJ. Open access fees are paid by Swiss Re, which
had no input into the commissioning or peer review
of the articles. The BMJ thanks the series advisers,
Nita Forouhi, Dariush Mozaarian, and Anna Lartey
for valuable advice and guiding selection of topics in
the series.
Joseph Firth, research fellow1,2
James E Gangwisch, assistant professor3,4
Alessandra Borisini, researcher5
Robyn E Wootton, researcher6,7,8
Emeran A Mayer, professor9,10
1Division of Psychology and Mental Health, Faculty of
Biology, Medicine and Health, Oxford Road, University
of Manchester, Manchester M13 9PL, UK
2NICM Health Research Institute, Western Sydney
University, Westmead, Australia
3Department of Psychiatry, Columbia University
Vagelos College of Physicians and Surgeons, New
York, USA
4New York State Psychiatric Institute, New York, NY,
USA
5Section of Stress, Psychiatry and Immunology
Laboratory, Institute of Psychiatry, Psychology and
Neuroscience, Department of Psychological Medicine,
King’s College London, London, UK
6School of Psychological Science, University of Bristol,
Bristol, UK
7MRC Integrative Epidemiology Unit, Oakeld House,
Bristol, UK
8NIHR Biomedical Research Centre, University
Hospitals Bristol NHS Foundation Trust and University
of Bristol, Bristol, UK
9G Oppenheimer Center for Neurobiology of Stress and
Resilience, UCLA Vatche and Tamar Manoukian Division
of Digestive Diseases, UCLA, Los Angeles, CA, USA
10UCLA Microbiome Center, David Geen School of
Medicine, UCLA, Los Angeles, CA, USA
Correspondence to: J Firth
joseph.rth@manchester.ac.
uk
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their derivative works on dierent terms, provided
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