Evidence map›Paper›PMID 35383287›Full record

ArticleCommunications biology2022

Excess S-adenosylmethionine inhibits methylation via catabolism to adenine.

Kazuki Fukumoto, Kakeru Ito, Benjamin Saer, George Taylor, Shiqi Ye, Mayu Yamano, Yuki Toriba, Andrew Hayes, Hitoshi Okamura, Jean-Michel Fustin

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 46 citations in OpenAlex.

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  16. Vitamin BCommunications biology · 2025
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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

10 authors at 4 institutions in 3 countries.

Kazuki Fukumoto *Kyoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Metabology, Kyoto, Japan.
Kakeru Ito *Kyoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Metabology, Kyoto, Japan.
Benjamin Saer *The University of Manchester, Centre for Biological Timing, Manchester, UK.
George TaylorThe University of Manchester, BioMS Core Facility, Manchester, UK.
Shiqi YeKyoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Metabology, Kyoto, Japan.
Mayu YamanoKyoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Metabology, Kyoto, Japan.ORCID 0000-0002-0878-4888
Yuki ToribaKyoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Metabology, Kyoto, Japan.ORCID 0000-0002-7634-9845
Andrew HayesThe University of Manchester, Genomics Technologies Core Facility, Manchester, UK.ORCID 0000-0002-9525-0306
Hitoshi OkamuraKyoto University, Graduate School of Medicine, Division of Physiology and Neurobiology, Kyoto, Japan. okamura.hitoshi.4u@kyoto-u.ac.jp.ORCID 0000-0002-3013-4881
Jean-Michel FustinKyoto University, Graduate School of Pharmaceutical Sciences, Department of Molecular Metabology, Kyoto, Japan. jean-michel.fustin@manchester.ac.uk.ORCID 0000-0002-6200-6075
Kyoto University · JPUniversity of Manchester · GBKyoto Pharmaceutical University · JPVrije Universiteit Brussel · BE

Funding

Medical Research Council MR/S031812/1
6 · The paper itself

Abstract

The global dietary supplement market is valued at over USD 100 billion. One popular dietary supplement, S-adenosylmethionine, is marketed to improve joints, liver health and emotional well-being in the US since 1999, and has been a prescription drug in Europe to treat depression and arthritis since 1975, but recent studies questioned its efficacy. In our body, S-adenosylmethionine is critical for the methylation of nucleic acids, proteins and many other targets. The marketing of SAM implies that more S-adenosylmethionine is better since it would stimulate methylations and improve health. Previously, we have shown that methylation reactions regulate biological rhythms in many organisms. Here, using biological rhythms to assess the effects of exogenous S-adenosylmethionine, we reveal that excess S-adenosylmethionine disrupts rhythms and, rather than promoting methylation, is catabolized to adenine and methylthioadenosine, toxic methylation inhibitors. These findings further our understanding of methyl metabolism and question the safety of S-adenosylmethionine as a supplement.

Indexed as

AdenineS-AdenosylmethionineDietary SupplementsLiverMethylationAdenineS-Adenosylmethionine

Identifiers

PMID35383287
PMCPMC8983724
OpenAlexW4226324729

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.