Evidence map›Paper›PMID 27478487›Full record

ArticleAnnals of general psychiatry2016

CT genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism is protector factor of major depressive disorder in the Tunisian population: a case control study.

Mohamed Amine Sayadi, Ons Achour, Asma Ezzaher, Ilham Hellara, Asma Omezzine, Wahiba Douki, Ali Bousslama, Lotfi Gaha, Mohamed Fadhel Najjar

Open access · goldAbstract read
In one paragraph

Article in Annals of general psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Behavioral sciences (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Article
  6. Article
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

9 authors at 2 institutions in 1 country.

Mohamed Amine SayadiLaboratory of Biochemistry-Toxicology, Monastir University Hospital, Monastir, Tunisia ; Research Laboratory "Vulnerability to Psychotic disorders LR 05 ES 10", Department of Psychiatry, Monastir University Hospital, Monastir, Tunisia.
Ons AchourLR 12 SP 11, Biochemistry Department, Sahloul Sousse University Hospital, Sousse, Tunisia.
Asma EzzaherLaboratory of Biochemistry-Toxicology, Monastir University Hospital, Monastir, Tunisia ; Research Laboratory "Vulnerability to Psychotic disorders LR 05 ES 10", Department of Psychiatry, Monastir University Hospital, Monastir, Tunisia.
Ilham HellaraLaboratory of Biochemistry-Toxicology, Monastir University Hospital, Monastir, Tunisia.
Asma OmezzineLR 12 SP 11, Biochemistry Department, Sahloul Sousse University Hospital, Sousse, Tunisia.
Wahiba DoukiLaboratory of Biochemistry-Toxicology, Monastir University Hospital, Monastir, Tunisia.
Ali BousslamaLR 12 SP 11, Biochemistry Department, Sahloul Sousse University Hospital, Sousse, Tunisia.
Lotfi GahaResearch Laboratory "Vulnerability to Psychotic disorders LR 05 ES 10", Department of Psychiatry, Monastir University Hospital, Monastir, Tunisia.
Mohamed Fadhel NajjarLaboratory of Biochemistry-Toxicology, Monastir University Hospital, Monastir, Tunisia.
University of Monastir · TNHôpital Sahloul · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMajor depressive disorder (MDD) is a common psychiatric disorder with considerable mortality. Death from unnatural causes, largely suicidal or quasi-suicidal, has a particularly high risk for the functional disorders, especially depression and schizophrenia. One of the prospective risk factors for this disease is hyperhomocysteinemia and folate deficiency. The methylenetetrahydrofolate reductase (MTHFR) gene encodes for a 5-methylenetetrahydrofolate reductase involved in folate metabolism and neurotransmitter synthesis. The aim of this research is to study the association between the C677T polymorphism of MTHFR gene and depression in Tunisian population, to explore their relationship with clinical and therapeutic characteristics of this disease. And it may lead to discover a novel marker to identify a patient with a higher risk of development of depressive disorder to be. This marker can be used for better therapeutic management and prevent disease installation.

methodsOur study included 208 depressive patients, 187 controls aged between 44.1 ± 13.5 and 38.9 ± 13.2 years, respectively. MTHFR gene polymorphisms were determined by PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism).

resultsNo significant difference was detected in the distribution of the genotype frequencies of MTHFR C677T polymorphisms (χ (2) = 5.443, df = 2, p = 0.066) between patients and controls. But when we study the risk of these genotypes, CT genotype is significantly more frequent in controls compared to patients, it may be a protection from depression (OR = 0.655, CI 95 % = 0.432-0.995, p = 0.047, OR* = 0.638, CI 95 %* = 0.415-0.983, p* = 0.04, before and after adjustment). Women, TT Genotype can increase four times the risk to be depressive. Addictive behavior seems to be associated with CT genotype and there was no significant association between clinical and therapeutic characteristics and this polymorphism.

conclusionThis paper is the first study to prove that CT genotype of MTHFR C677T polymorphism may protect from depression and TT genotype seems to be associated with women's depression. Further studies are required with other polymorphisms and biochemical factors that must be investigated to clarify the implication of MTHFR C677T polymorphism in the pathophysiology of depression.

Identifiers

PMID27478487
PMCPMC4967526
OpenAlexW2490062841

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.