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. 2024 May 15:11:1346483.
doi: 10.3389/fnut.2024.1346483. eCollection 2024.

Diet quality and anxiety: a critical overview with focus on the gut microbiome

Melissa Basso  1 , Irene Zorzan  2   3 , Nicola Johnstone  1 , Matteo Barberis  2   3   4 , Kathrin Cohen Kadosh  1
Affiliations

Diet quality and anxiety: a critical overview with focus on the gut microbiome

Melissa Basso et al. Front Nutr. .

Abstract

Anxiety disorders disproportionally affect females and are frequently comorbid with eating disorders. With the emerging field of nutritional psychiatry, focus has been put on the impact of diet quality in anxiety pathophysiology and gut microbiome underlying mechanisms. While the relationship between diet and anxiety is bidirectional, improving dietary habits could better facilitate the actions of pharmacological and psychological therapies, or prevent their use. A better understanding of how gut bacteria mediate and moderate such relationship could further contribute to develop personalized programs and inform probiotics and prebiotics manufacturing. To date, studies that look simultaneously at diet, the gut microbiome, and anxiety are missing as only pairwise relationships among them have been investigated. Therefore, this study aims at summarizing and integrating the existing knowledge on the dietary effects on anxiety with focus on gut microbiome. Findings on the effects of diet on anxiety are critically summarized and reinterpreted in relation to findings on (i) the effects of diet on the gut microbiome composition, and (ii) the associations between the abundance of certain gut bacteria and anxiety. This novel interpretation suggests a theoretical model where the relationship between diet and anxiety is mediated and/or modulated by the gut microbiome through multiple mechanisms. In parallel, this study critically evaluates methodologies employed in the nutritional field to investigate the effects of diet on anxiety highlighting a lack of systematic operationalization and assessment strategies. Therefore, it ultimately proposes a novel evidence-based approach that can enhance studies validity, reliability, systematicity, and translation to clinical and community settings.

Keywords: anxiety; diet; diet quality; gut microbiome; sex stratification.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
Bi-directional relationship for diet and anxiety. (A) Diet and anxiety feed each other in a vicious cycle: processed food increases (+++) anxiety through multiple gut microbiome-mediated mechanisms (see Figure 2 for more details) with individual-specific effects dependent on stable features of one’s microbiome, i.e., temporal microbiome. In turn, anxiety and stress trigger emotional eating behavior perpetuating intake of comfort food as in Western-like diet. Comfort food then acts on the brain as an immediate reward while affecting impulse control and positively reinforcing the cycle. (B) Left: psychopharmacological and cognitive-behavioral therapies have limited effect on anxiety. Their efficacy might be affected by unhealthy eating habits that – when not targeted through nutritional interventions and educational programs – keep triggering (+++) anxiety symptomatology and reinforcing emotional eating. Right: shifting toward a more nutritious and healthy diet tailored on individual’s gut microbiome composition would give the opportunity to break that cycle and would complement cognitive-behavioral therapies aimed at stress and emotional management as well as psychopharmacotherapy when strictly required. Created with and adapted from BioRender.com.
Figure 2
Figure 2
Gut microbiome-brain communication routes. Diet can act on mental health through gut-dependent mechanisms. Pathways of communication between the gut microbiome and the brain include processes happening in the gut (white background, bottom half), brain (pink background, upper half), and systemically (mid-figure), specifically: (1) autonomic and enteric nervous system modulation through, e.g., vagal chemoreceptors stimulation, TLR4-LPS binding, local production of neuromodulatory metabolites that can interact with enteroendocrine cells; (2) up/down-regulation of TPH1 expression in Ecs via direct and indirect mechanisms; (3) metabolic routes, i.e., (i) SCFAs production that can exert vagal stimulation, regulate TPH1 expression in Ecs, regulate the gut lining integrity and inhibit pro-inflammatory genes expression. SCFAs that enter circulation can also cross the blood–brain barrier (BBB) and promote neurogenesis, 5-HT, and other neurotransmitters expression other than increasing expression of BBB tight junction proteins such as occluding; (ii) modulation of TRP availability and TDO/IDO enzymatic activity in Quinolinic and Kynurenic pathways with consequent impact on balance between available TRP for 5-HT manufacturing, QUIN, and KYNA; (4) immune modulation through, e.g., direct activation through PRRs or indirect anti/pro-inflammatory actions of SCFAs and LPS respectively; (5) cyclic communication with the HPA axis where a molecular cascade leads to inflammation, leaky gut, and ultimately microbiome modifications and LPS translocation. LPS can in turn trigger stress-hormone release, whereas microbiome can modulate the HPA axis through the NTS. Stress, SCFAs production, inflammation, and gut microbiome disbalances interact together in promoting/disrupting gut lining integrity. In anxiety pathophysiology, highly processed diets could promote gut microbiome disbalances, e.g., increased Bacteroides and decreased Firmicutes (magnified gut circle), which in turn could be related to changes in production of neurometabolites (in red), decreased SCFAs (in blue) with consequent decrease of their protective functions, increased LPS (in purple) and LPS translocation with consequent neurotoxic and inflammatory actions, disruption of QIN/KYNA balance (in pink), increased inflammation (in turquoise) and leaky gut. Psychological stress and highly processed diets could then perpetuate the cycle and reinforce ongoing pathophysiological processes. TLR4, toll-like receptors; LPS, lipopolysaccharide; TPH1, tryptophan hydroxylase 1; Ecs, enteroendocrine cells; SCFAs, short-chain fatty acids; BBB, blood–brain barrier; 5-HT, serotonin; TDO, tryptophan 2,3-dioxygenase; IDO, indoleamine 2,3-dioxygenase; QUIN, quinolinic acid; KYNA, kynurenic acid; PRRs, patterns recognition receptors; HPA, hypothalamus-pituitary–adrenal; NTS, nucleus tractus solitarii; GABA, gamma-aminobutyric acid; NO, nitric oxide; TRP, tryptophan; IL, interleukin; CRF, corticotropin-releasing factor; ACTH, adrenocorticotropin hormone; BDNF, brain-derived neurotropic factor; TNFα, tumor necrosis factor; NF-κB, nuclear factor kappa B; HDAC, histone deacetylase. Created with and adapted from BioRender.com.
Figure 3
Figure 3
A pyramidal hierarchy of diet classification. Optimal and balanced nutrition is essential for good health. Human nutrition can be conceptualized in hierarchical levels: (1) overall diet quality as measured by several dietary quality indexes (DQIs) derived from distinct frameworks of reference including food and nutrient-derived ones, i.e., the Healthy Eating Index, based on the Dietary Guidelines for Americans, the Alternative HEI, adjusted for food associated to disease risk; nutrients-derived ones (right side) i.e. the Dietary Inflammatory Index assigning literature review-based inflammatory scores to 45 nutrients, the Dietary Antioxidant Index summarizing the total dietary antioxidant capacity, the Glycemic Index/Load indexing carbohydrates quality; food-derived ones (left side), i.e., the Food-derived Dietary Inflammatory Index, the Dietary Diversity Score quantifying diet variety and consumed unique food groups, the Dietary Insulin Index/Load quantifying the postprandial insulin response. (2) Dietary patterns as a complex combination of food and/or nutrients that can be either predefined or empirically derived. (3) Food groups and/or Nutrients groups are the units weighted to compute dietary patterns. (4) Single foods and single nutrients are grouped together to form food and nutrients group. The orange triangles highlight transversal hierarchical relationships: single nutrients synergically interact to form the food matrix conferring to foods their unique properties; nutrients groups are differently clustered across food groups. The bar charts in the four corners of the figure summarize the number of studies (y-axis) that investigate the associations between anxiety and (A) dietary quality indexes, (B) dietary patterns, (C) foods, and (D) nutrients. Sweets include sweet beverages; read meat includes processed meat. Blue, grey, and orange bars indicate that a higher index/score/consumption is associated with a decreased anxiety, an increased anxiety, and no effects on anxiety, respectively. Only the most relevant diet classification methods are included. DII, Dietary Inflammatory Index; HEI-2010, Healthy Eating Index-2010; AHEI-2010, Alternative Healthy Eating Index-2010; DDS, Dietary Diversity Score; MD, Mediterranean Diet; VEG, Vegetarian Diet; VG, Vegan Diet; WD, Western Diet; FI, fruits intake; VI, vegetables intake; FVI, Fruits and vegetables intake; PUFA n-3, omega-3 poly-unsaturated fatty-acids; PUFA n-6, omega-6 poly-unsaturated fatty-acids. Created with and adapted from BioRender.com.
Figure 4
Figure 4
Integration of diet, gut microbiome, anxiety, and translational opportunities. (A) The integration of available evidence on relationships among diet, gut microbiome, and anxiety suggests that some bacterial genera such as Faecalibacterium, Roseburia, and Tyzzerella likely play a mediatory role in the relationship between diet and anxiety. Only more relevant relationships cited in the main text are indicated. ↑ (↓) indicates an increased (decreased) genus abundance; an increased (decreased) adherence to a pro-inflammatory, healthy, and Mediterranean diet; and an increased (decreased) consumption of vegetables, fruit, whole/non-refined grain, fibers, and processed meat. (B) Left: The interconnection among diet, gut microbiome, and anxiety, and the mediatory role we propose for the gut microbiome, suggesting that whole diet interventions may alleviate anxiety symptoms by favoring or inhibiting the growth of definite bacterial species. Right: Probiotics, prebiotics, and synbiotics interventions could reduce anxiety by modifying the gut microbiome composition, for example for Faecalibacterium and Roseburia [in green and blu color, respectively, in panels (A,B)]. In combination with high adherence to a healthy diet, they could foster reciprocal benefits, enhancing overall efficacy. Created with and adapted from BioRender.com.
Figure 5
Figure 5
Example of the proposed method: a multilevel approach for dietary analysis should be adopted based on (A) the main research questions, (B) the hierarchical diet composition, and (C) guided by empirical results. Here, the analysis pipeline starts from the main independent variable of interest – the HEI-2020 – and moves down to added sugars based on DPs analysis and/or, e.g., existing evidence of sugars effects on anxiety. Differences in consumption of sweetened foods and beverages are then compared and driving effects of specific added sugars (e.g., lactose, corn-syrup, sucrose) explored. Although multilevel analyses of fats are not initially performed, downstream results (e.g., differences in consumption of ultra-processed food such as cookies and pastries) prompt exploratory analysis of trans-fatty acids. Note that the pipeline can flow in each direction, start at any hierarchical level, and include variable number of layers based on (i) main objective, (ii) relevant literature, (iii) results, (iv) staff and research resources. However, the rationale behind authors’ choices should always be transparent and outlined. As shown in (D), gut microbiome should be measured and included as a stratification or moderation factor. Created with and adapted from BioRender.com.
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Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the Systems Biology Grant of the University of Surrey to MaB and the PhD studentship of the Faculty of Health and Medical Sciences (FHMS-PL-BM-24) to KC and MaB.

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