Evidence map›Paper›PMID 36973313›Full record

ArticleScientific reports2023

Genetic risk of depression is different in subgroups of dietary ratio of tryptophan to large neutral amino acids.

Bence Bruncsics, Gabor Hullam, Bence Bolgar, Peter Petschner, Andras Millinghoffer, Kinga Gecse, Nora Eszlari, Xenia Gonda, Debra J Jones, Sorrel T Burden and 4 more

Open access · goldFull text read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 3 countries.

Bence Bruncsics *Department of Measurement and Information Systems, Budapest University of Technology and Economics, Muegyetem Rkp. 3., 1111, Budapest, Hungary.
Gabor Hullam *Department of Measurement and Information Systems, Budapest University of Technology and Economics, Muegyetem Rkp. 3., 1111, Budapest, Hungary.
Bence Bolgar *Department of Measurement and Information Systems, Budapest University of Technology and Economics, Muegyetem Rkp. 3., 1111, Budapest, Hungary.
Peter PetschnerDepartment of Pharmacodynamics, Faculty of Pharmacy, Semmelweis University, Nagyvarad ter 4., 1089, Budapest, Hungary.
Andras MillinghofferDepartment of Measurement and Information Systems, Budapest University of Technology and Economics, Muegyetem Rkp. 3., 1111, Budapest, Hungary.
Kinga GecseDepartment of Pharmacodynamics, Faculty of Pharmacy, Semmelweis University, Nagyvarad ter 4., 1089, Budapest, Hungary.
Nora EszlariDepartment of Pharmacodynamics, Faculty of Pharmacy, Semmelweis University, Nagyvarad ter 4., 1089, Budapest, Hungary.
Xenia GondaNAP3.0-SE Neuropsychopharmacology Research Group, Hungarian Brain Research Program, Semmelweis University, Budapest, Hungary.
Debra J JonesSchool of Health Sciences, University of Manchester, Manchester, UK.
Sorrel T BurdenSchool of Health Sciences, University of Manchester, Manchester, UK.
Peter AntalDepartment of Measurement and Information Systems, Budapest University of Technology and Economics, Muegyetem Rkp. 3., 1111, Budapest, Hungary.
Bill DeakinDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Gyorgy BagdyDepartment of Pharmacodynamics, Faculty of Pharmacy, Semmelweis University, Nagyvarad ter 4., 1089, Budapest, Hungary.
Gabriella JuhaszDepartment of Pharmacodynamics, Faculty of Pharmacy, Semmelweis University, Nagyvarad ter 4., 1089, Budapest, Hungary. juhasz.gabriella@pharma.semmelweis-univ.hu.
Semmelweis University · HUBudapest University of Technology and Economics · HUManchester Academic Health Science Centre · GBKyoto University Institute for Chemical ResearchUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Manipulation of intake of serotonin precursor tryptophan has been exploited to rapidly induce and alleviate depression symptoms. While studies show that this latter effect is dependent on genetic vulnerability to depression, the effect of habitual tryptophan intake in the context of predisposing genetic factors has not been explored. Our aim was to investigate the effect of habitual tryptophan intake on mood symptoms and to determine the effect of risk variants on depression in those with high and low tryptophan intake in the whole genome and specifically in serotonin and kynurenine pathways. 63,277 individuals in the UK Biobank with data on depressive symptoms and tryptophan intake were included. We compared two subpopulations defined by their habitual diet of a low versus a high ratio of tryptophan to other large amino acids (TLR). A modest protective effect of high dietary TLR against depression was found. NPBWR1 among serotonin genes and POLI in kynurenine pathway genes were significantly associated with depression in the low but not in the high TLR group. Pathway-level analyses identified significant associations for both serotonin and kynurenine pathways only in the low TLR group. In addition, significant association was found in the low TLR group between depressive symptoms and biological process related to adult neurogenesis. Our findings demonstrate a markedly distinct genetic risk profile for depression in groups with low and high dietary TLR, with association with serotonin and kynurenine pathway variants only in case of habitual food intake leading to low TLR. Our results confirm the relevance of the serotonin hypothesis in understanding the neurobiological background of depression and highlight the importance of understanding its differential role in the context of environmental variables such as complexity of diet in influencing mental health, pointing towards emerging possibilities of personalised prevention and intervention in mood disorders in those who are genetically vulnerable.

Indexed as

Amino Acids, NeutralTryptophanAdultDepressionDietHumansKynurenineSerotoninAmino Acids, NeutralKynurenineSerotoninTryptophan

Identifiers

PMID36973313
PMCPMC10042855
OpenAlexW4361004565

What Socratic holds

Textfull text, public
LicenceCC BY
measurements read22
identifiers read1
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.