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Food and mood: How do diet and nutrition affect mental wellbeing?

2020;369:m2440 | doi: 10.1136/bmj.m2440 1
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
epression and anxiety are the
most common mental health
conditions worldwide, mak-
ing them a leading cause of
Even beyond diag
nosed conditions, subclinical symptoms of
depression and anxiety aect 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
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 eects 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
aect 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
aect 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 eect on psychological wellbeing;
data from longitudinal research show an
association between progressively higher
dietary glycaemic index and the incidence
of depressive symptoms.
Clinical studies
have also shown potential causal eects
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 eect.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.
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
eects 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 eect 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.411 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
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 | thebmj
meals rich in saturated fat appear to stim-
ulate immune activation.13 15 Indeed, the
inflammatory eects 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 eects on
brain health, including cognitive decline,
hippocampal dysfunction, and damage
to the blood-brain barrier.
Since various
mental health conditions, including mood
disorders, have been linked to heightened
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,”317
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
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 eects,
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.
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
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.
Further interventional research is needed
to establish if improvements in immune
regulation, induced by diet, can reduce
depressive symptoms in those aected by
inflammatory conditions.
Brain, gut microbiome, and mood
A more recent explanation for the way in
which our food may aect our mental well-
being is the eect 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
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 eects 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
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 aect 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
and social factors
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
Fig1 | Hypothesised relationship between diet, physical health, and mental health. The dashed
line is the focus of this article.
on 29 June 2020 by guest. Protected by copyright. first published as 10.1136/bmj.m2382 on 29 June 2020. Downloaded from
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 aect
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
11 31-33
A full discussion of the eect
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 eect of people’s
expectations, particularly given that
individuals’ beliefs about the quality of
their food or diet may also have a marked
eect on their sense of overall health and
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 eects 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 eect 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 KidneyDiseases, 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 Mozaarian, 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,
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, Oakeld 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 Geen School of
Medicine, UCLA, Los Angeles, CA, USA
Correspondence to: J Firth
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non-commercial. See:
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Cite this as: BMJ 2020;369:m2440
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... 42 Firth et al. reported that the sense of low mood may be caused by inadequate nutrition, and the intake of better food could help to maintain both physical and MH. 43 Among the complementary recommendations for a sustainable quality of life, increased MH and vitality, physical activity, and healthy nutrition management are considered to be effective components. [43][44][45] These important components are candidates for essential components of the active treatment process for BC patients, although they are presently deemed to be optional, nonmandatory measures for BC patients. ...
... 43 Among the complementary recommendations for a sustainable quality of life, increased MH and vitality, physical activity, and healthy nutrition management are considered to be effective components. [43][44][45] These important components are candidates for essential components of the active treatment process for BC patients, although they are presently deemed to be optional, nonmandatory measures for BC patients. 46 The results of our present study shed light on potentially targetable risk factors for lifestyle changes in BC survivors. ...
... The rate of telomere shortening can be affected by nutritional practices, either directly, for example through their inflammatory/anti-inflammatory and oxidant/antioxidant properties [41,164], or indirectly by influencing other aspects of health also associated with TL, such as mental health (MH). Indeed, nutrition is associated with MH outcomes, such as a higher risk for developing depression and anxiety [165,166] while, on the other hand, MH may affect nutritional status (e.g., through appetite regulation) [167]. Additionally, evidence shows a link between various types of MH disorders and TL, including stress and anxiety [168][169][170], bipolar disorder [171,172], and psychotic disorders [173,174]. ...
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Preterm birth (PTB), a multi-causal syndrome, is one of the global epidemics. Maternal nutrition, but also neonatal and placental telomere length (TL), are among the factors affecting PTB risk. However, the exact relationship between these factors and the PTB outcome, remains obscure. The aim of this review was to investigate the association between PTB, maternal nutrition, and placental-infant TL. Observational studies were sought with the keywords: maternal nutrition, placental TL, newborn, TL, and PTB. No studies were found that included all of the keywords simultaneously, and thus, the keywords were searched in dyads, to reach assumptive conclusions. The findings show that maternal nutrition affects PTB risk, through its influence on maternal TL. On the other hand, maternal TL independently affects PTB risk, and at the same time PTB is a major determinant of offspring TL regulation. The strength of the associations, and the extent of the influence from covariates, remains to be elucidated in future research. Furthermore, the question of whether maternal TL is simply a biomarker of maternal nutritional status and PTB risk, or a causative factor of PTB, to date, remains to be answered.
... The maintenance of a well-balanced and nourishing dietary routine is intrinsically tied to the enhancement of one's mental well-being. Specific components in our diets have the potential to wield substantial influence over metabolic processes, contributing to the intricate and multifaceted interaction between diet and mood [8]. ...
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Background Depression is on the rise and has become a significant concern for public health. Limited research has explored the connection between dietary patterns and depression. This investigation aimed to examine how dietary behaviours relate to depression among adolescents attending school in Malaysia. Methods The study utilized data from the National School-Based Health Survey 2022, a nationwide survey involving school-going adolescents aged 13–17, with a total of 33,523 participants from 239 schools. To assess depression, the study employed the Patient Health Questionnaire (PHQ-9), considering a score of 10 or higher as indicative of depression. Dietary behaviours were assessed using a validated self-administered questionnaire adapted from the World Health Organization's Global School-based Student Health Survey. Descriptive analysis and complex sample logistic regression were carried out using SPSS version 26.0. Results The study revealed a 26.9% overall prevalence of depression, with higher risks among female adolescents (AOR 2.71, 95% CI 2.51, 2.92) and those in higher grades. Malays (AOR 1.71, 95% CI 1.41, 2.07), Other Bumiputeras (AOR 1.69, 95% CI 1.32, 2.17), and Others (AOR 1.63, 95% CI 1.16, 2.30) had elevated odds of depression compared to Indians. Healthy dietary habits, like consuming less than two servings of fruits daily, correlated with depression (AOR 1.44 95% CI 1.35, 1.54). Additionally, unhealthy dietary behaviours such as fast food consumption (AOR 1.73 [95% CI 1.55, 1.93]) and carbonated soft drink intake (AOR 1.59 [95% CI 1.48, 1.70]) were positively associated with depression. Conclusions One out of every four Malaysian adolescents was identified to experience depression. Depression was linked to several factors, such as being female, belonging to higher grade levels, identifying as Malays, Other Bumiputeras, or belonging to other ethnicities, and participating in the consumption of fast food, carbonated soft drinks, and fruits. To address these observations, it is crucial to formulate effective public health programmes that prioritize adolescent mental health and encourage the adoption of healthy eating habits.
... Generally, the gut microbiome can be modulated by diet and nutritional supplements, like live bacteria (probiotics) and non-digestible food components (prebiotics) [88,89]. There is evidence that regular intake of a probiotic supplement improves depressive symptoms [90,91]. ...
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Research conducted on individuals with depression reveals that major depressive disorders (MDDs) coincide with diminished levels of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the brain, as well as modifications in the subunit composition of the primary receptors (GABAA receptors) responsible for mediating GABAergic inhibition. Furthermore, there is substantial evidence supporting the significant role of GABA in regulating stress within the brain, which is a pivotal vulnerability factor in mood disorders. GABA is readily available and approved as a food supplement in many countries. Although there is substantial evidence indicating that orally ingested GABA may affect GABA receptors in peripheral tissues, there is comparatively less evidence supporting its direct action within the brain. Emerging evidence highlights that oral GABA intake may exert beneficial effects on the brain and psyche through the gut–brain axis. While GABA enjoys wide consumer acceptance in Eastern Asian markets, with many consumers reporting favorable effects on stress regulation, mood, and sleep, rigorous independent research is still largely lacking. Basic research, coupled with initial clinical findings, makes GABA an intriguing neuro-nutritional compound deserving of clinical studies in individuals with depression and other psychological problems.
... A basic necessity to support human life is food. The function of food has transformed due to the Industrial Revolution and the advancement of civilization, expanding from simply meeting physiological requirements to providing health advantages beyond basic nutritional value (Firth et al., 2020). When comparing the data collected in Nigeria in 2018 before the COVID-19 outbreak with the data from 2020, there are noticeable disparities in all four indices: meal skipping, food shortage, going without food for a full day, and food insecurity. ...
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At the beginning of 2020, Nigeria grappled with a severe outbreak of the global COVID-19 pandemic. This deadly disease significantly impacted various aspects of the country's economy, leading to socioeconomic challenges primarily attributed to daily increases in reported cases and the subsequent enforcement of lockdown measures. Gwagwalada Area Council in Abuja, Nigeria, was not exempt from the devastating consequences of this epidemic, particularly concerning income generation and food access for its residents. Although several studies have examined the impact of COVID-19 on Nigerian workers, little information exists regarding the differing effects on formal and informal sector workers. This study aimed to investigate the disparities in the consequences of the COVID-19 pandemic's lockdown on household income generation and food consumption among formal and informal sector workers in Gwagwalada Area Council, Abuja, Nigeria. A descriptive survey design was employed for this study. Three hundred and thirty-two completed questionnaires were collected and analyzed. Data were analyzed using descriptive statistics, which included simple percentages and means and independent sample t-tests.
There is a growing interest in the connection between healthy eating, mental health (MH) and chronic disease prevention. Although people with chronic kidney disease (CKD) are disproportionately affected by poor MH, nutritional guidelines have traditionally focused on non-mental factors, such as physical health, disease progression and biochemical control. Dietary manipulation, through healthy eating, may influence the gut microbiome, as well as mental and kidney health. This can be achieved through the interaction between the gut microbiome, brain and kidney, as well as the body's metabolism of nutrients, such as the amino acid tryptophan. While a wide range of nutrients are implicated in brain function and health, there is little evidence to support supplementation-based treatments–other than to avoid conventional malnutrition and micronutrient deficiencies. Whole diets, such as the Mediterranean diet, may benefit MH, as well as reducing cardiovascular, renal and other chronic disease risk. A supportive and individualised approach to renal dietary restrictions may help to reduce the MH burden of CKD.
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The present study harnessed job demands-resources (JD-R) theory to identify key predictors of psychological strain (feeling overwhelmed by one’s problems) and life satisfaction among a sample of 1,060 adults randomly selected from the Australian electoral roll. The investigation sought to ascertain: (a) the relative contribution of health demands (e.g., inadequate health treatment) and health resources (e.g., access to helpful health-related information) in predicting psychological strain and life satisfaction, (b) the extent to which a recently proposed personal resource—adaptability—explained variance in wellbeing beyond individuals’ health demands and resources, and (c) the role of psychological strain in predicting life satisfaction in the context of these demands and resources. Applying structural equation modeling we found that contextual health demands predicted greater psychological strain, individual health resources and adaptability both predicted lower psychological strain and greater life satisfaction, and psychological strain predicted lower life satisfaction. Notably, the adverse effects of health demands reduced significantly when health resources and adaptability were entered into the modeling. Taken together, the findings offer support for a health demands-resources (HD-R) framework that may be applied to better support individuals to respond to the stressors in their lives and in turn boost their sense of subjective wellbeing.
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Objective Ageing is accompanied by deterioration of multiple bodily functions and inflammation, which collectively contribute to frailty. We and others have shown that frailty co-varies with alterations in the gut microbiota in a manner accelerated by consumption of a restricted diversity diet. The Mediterranean diet (MedDiet) is associated with health. In the NU-AGE project, we investigated if a 1-year MedDiet intervention could alter the gut microbiota and reduce frailty. Design We profiled the gut microbiota in 612 non-frail or pre-frail subjects across five European countries (UK, France, Netherlands, Italy and Poland) before and after the administration of a 12-month long MedDiet intervention tailored to elderly subjects (NU-AGE diet). Results Adherence to the diet was associated with specific microbiome alterations. Taxa enriched by adherence to the diet were positively associated with several markers of lower frailty and improved cognitive function, and negatively associated with inflammatory markers including C-reactive protein and interleukin-17. Analysis of the inferred microbial metabolite profiles indicated that the diet-modulated microbiome change was associated with an increase in short/branch chained fatty acid production and lower production of secondary bile acids, p-cresols, ethanol and carbon dioxide. Microbiome ecosystem network analysis showed that the bacterial taxa that responded positively to the MedDiet intervention occupy keystone interaction positions, whereas frailty-associated taxa are peripheral in the networks. Conclusion Collectively, our findings support the feasibility of improving the habitual diet to modulate the gut microbiota which in turn has the potential to promote healthier ageing.
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There is strong epidemiological evidence that poor diet is associated with depression. The reverse has also been shown, namely that eating a healthy diet rich in fruit, vegetables, fish and lean meat, is associated with reduced risk of depression. To date, only one randomised controlled trial (RCT) has been conducted with elevated depression symptoms being an inclusion criterion, with results showing that a diet intervention can reduce clinical levels of depression. No such RCTs have been performed in young adults. Young adults with elevated levels of depression symptoms and who habitually consume a poor diet were randomly allocated to a brief 3-week diet intervention (Diet Group) or a habitual diet control group (Control Group). The primary and secondary outcome measures assessed at baseline and after the intervention included symptoms of depression (Centre for Epidemiological Studies Depression Scale; CESD-R; and Depression Anxiety and Stress Scale– 21 depression subscale; DASS-21-D), current mood (Profile of Mood States), self-efficacy (New General Self-Efficacy Scale) and memory (Hopkins Verbal Learning Test). Diet compliance was measured via self-report questionnaires and spectrophotometry. One-hundred-and-one individuals were enrolled in the study and randomly assigned to the Diet Group or the Control Group. Upon completion of the study, there was complete data for 38 individuals in each group. There was good compliance with the diet intervention recommendations assessed using self-report and spectrophotometry. The Diet group had significantly lower self-reported depression symptoms than the Control Group on the CESD-R (p = 0.007, Cohen’s d = 0.65) and DASS-21 depression subscale (p = 0.002, Cohen’s d = 0.75) controlling for baseline scores on these scales. Reduced DASS-21 depression subscale scores were maintained on follow up phone call 3 months later (p = .009). These results are the first to show that young adults with elevated depression symptoms can engage in and adhere to a diet intervention, and that this can reduce symptoms of depression. The findings provide justification for future research into the duration of these benefits, the impacts of varying diet composition, and their biological basis.
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Inflammation is a natural defence response of the immune system against environmental insult, stress and injury, but hyper- and hypo-inflammatory responses can trigger diseases. Accumulating evidence suggests that inflammation is involved in multiple psychiatric disorders. Using inflammation-related factors as biomarkers of psychiatric disorders requires the proof of reproducibility and specificity of the changes in different disorders, which remains to be established. We performed a cross-disorder study by systematically evaluating the meta-analysis results of inflammation-related factors in eight major psychiatric disorders, including schizophrenia (SCZ), bipolar disorder (BD), autism spectrum disorder (ASD), major depression disorder (MDD), post-trauma stress disorder (PTSD), sleeping disorder (SD), obsessive–compulsive disorder (OCD) and suicide. A total of 43 meta-analyses involving 704 publications on 44 inflammation-related factors were included in the study. We calculated the effect size and statistical power for every inflammation-related factor in each disorder. Our analyses showed that well-powered case–control studies provided more consistent results than underpowered studies when one factor was meta-analysed by different researchers. After removing underpowered studies, 30 of the 44 inflammation-related factors showed significant alterations in at least one disorder based on well-powered meta-analyses. Eleven of them changed in patients of more than two disorders when compared with the controls. A few inflammation-related factors showed unique changes in specific disorders (e.g., IL-4 increased in BD, decreased in suicide, but had no change in MDD, ASD, PTSD and SCZ). MDD had the largest number of changes while SD has the least. Clustering analysis showed that closely related disorders share similar patterns of inflammatory changes, as genome-wide genetic studies have found. According to the effect size obtained from the meta-analyses, 13 inflammation-related factors would need <50 cases and 50 controls to achieve 80% power to show significant differences (p < 0.0016) between patients and controls. Changes in different states of MDD, SCZ or BD were also observed in various comparisons. Studies comparing first-episode SCZ to controls may have more reproducible findings than those comparing pre- and post-treatment results. Longitudinal, system-wide studies of inflammation regulation that can differentiate trait- and state-specific changes will be needed to establish valuable biomarkers.
Preclinical evidence strongly suggests a role for the gut microbiome in modulating the host central nervous system function and behavior. Several communication channels have been identified that enable microbial signals to reach the brain and that enable the brain to influence gut microbial composition and function. In rodent models, endocrine, neural, and inflammatory signals generated by gut microbes can alter brain structure and function, while autonomic nervous system activity can affect the microbiome by modulating the intestinal environment and by directly regulating microbial behavior. The amount of information that reaches the brain is dynamically regulated by the blood-brain barrier and the intestinal barrier. In humans, associations between gut microbial composition and function and several brain disorders have been reported, and fecal microbial transplants from patient populations into gnotobiotic mice have resulted in the reproduction of homologous features in the recipient mice. However, in contrast to preclinical findings, there is little information about a causal role of the gut microbiome in modulating human central nervous system function and behavior. Longitudinal studies in large patient populations with therapeutic interventions are required to demonstrate such causality, which will provide the basis for future clinical trials. © 2020 American Physiological Society. Compr Physiol 10:57-72, 2020.
Importance Children and adolescents with obesity are at higher risk of developing depression and anxiety, and adolescent dieting is a risk factor for the development of depression. Therefore, determining the psychological effect of obesity treatment interventions is important to consider. Objective To investigate the association between obesity treatment interventions, with a dietary component, and the change in symptoms of depression and anxiety in children and adolescents with overweight/obesity. Data Sources Searches of MEDLINE, Embase, Cochrane Library, and PsychINFO were conducted from inception to August 2018. Hand searching of references was conducted to identify missing studies. Study Selection Obesity treatment interventions, with a dietary component, conducted in children and adolescents (age <18 years) with overweight/obesity, and validated assessment of depression and/or anxiety were included. Data Extraction and Synthesis Data were independently extracted by 1 reviewer and checked for accuracy. Meta-analysis, using a random-effects model, was used to combine outcome data and moderator analysis conducted to identify intervention characteristics that may influence change in depression and anxiety. The meta-analyses were finalized in May 2019. Main Outcomes and Measures Change in symptoms of depression and anxiety postintervention and at the latest follow-up. Results Of 3078 articles screened, 44 studies met inclusion criteria with a combined sample of 3702 participants (age range, 5.6 to 16.6 years) and intervention duration of 2 weeks to 15 months. Studies reported either no change or a statistically significant reduction in symptoms of depression or anxiety. Meta-analyses of 36 studies found a reduction in depressive symptoms postintervention (standardized mean difference [SE], −0.31 [0.04]; P < .001), maintained at follow-up in 11 studies at 6 to 16 months from baseline (standardized mean difference [SE], −0.25 [0.07]; P < .001). Anxiety was reduced postintervention (10 studies; standardized mean difference [SE], −0.38 [0.10]; P < .001) and at follow-up (4 studies; standardized mean difference [SE], −0.32 [0.15]; P = .03). Longer intervention duration was associated with a greater reduction in anxiety (R² = 0.82; P < .001). Higher body mass index z score at baseline was associated with a greater reduction in depression (R² = 0.19; P = .03). Conclusions and Relevance Structured, professionally run pediatric obesity treatment is not associated with an increased risk of depression or anxiety and may result in a mild reduction in symptoms. Treatment of weight concerns should be considered within the treatment plan for young people with depression and obesity.
People with mental illness have an increased risk of physical disease, as well as reduced access to adequate health care. Physical-health disparities are observed across all mental illnesses in all countries. The high rate of physical comorbidity, which often has poor clinical management, reduces life expectancy for people with mental illness, and increases the personal, social, and economic cost of mental illness across the lifespan. This Commission summarises advances in understanding on the topic of physical health in people with mental illness, and presents clear directions for health promotion, clinical care, and future research. It aims to: (1) Establish highly pertinent aspects of physical health-related morbidity and mortality that have transdiagnostic applications; (2) Highlight the common modifiable factors that drive disparities in physical health; (3) Present actions and initiatives for health policy and clinical services to address these issues; and (4) Identify promising areas for future research that could identify novel solutions.
Human-associated microbial communities have adapted to environmental pressures. Doses of antibiotics select for a community with increased antibiotic resistance, inflammation is accompanied by expansion of community members equipped to flourish in the presence of immune effectors and Western diets shift the microbiota away from fibre degraders in favour of species that thrive on mucus. Recent data suggest that the microbiota of industrialized societies differs substantially from the recent ancestral microbiota of humans. Rapid modernization, including medical practices and dietary changes, is causing progressive deterioration of the microbiota, and we hypothesize that this may contribute to various diseases prevalent in industrialized societies. In this Opinion article, we explore whether individuals in the industrialized world may be harbouring a microbial community that, while compatible with our environment, is now incompatible with our human biology. In this Opinion article, Sonnenburg and Sonnenburg explore whether individuals in the industrialized world may be harbouring a microbial community that is now incompatible with human biology, and they hypothesize that the modern, industrial lifestyle has contributed to alterations in the microbiota that may be linked to the deterioration of human health.