Published

The STREGA checklist is the reporting guideline for genetic association studies. The name stands for STrengthening the REporting of Genetic Association studies, and Little and colleagues published it in 2009 as an extension of the STROBE statement [1]. STROBE has 22 items, and STREGA adds genetics-specific text to 12 of them [1]. The additions deal with problems that rarely arise in other observational designs, such as genotyping error, population stratification, Hardy-Weinberg equilibrium and the large number of variants that can be tested.

Most guides stop at listing the items. This guide goes further. After the checklist itself, we apply every STREGA row to a real open-access case-control study, published in the journal Hormones in 2026, that states it followed STREGA, with the article section beside every verdict [2]. The need is documented. Nedovic and colleagues examined 160 genetics and heredity journals and found that only 29 (18.1%) referenced STREGA in their instructions for authors, and adherence to the checklist was significantly higher in journals that endorsed it [3].

In Simple Words

The STREGA checklist is the STROBE checklist with extra lines for genetics. It keeps all 22 STROBE items and adds genetics text to 12 of them. The extra lines ask how DNA was collected and genotyped, how many samples failed, whether genotype counts fit Hardy-Weinberg equilibrium, how ancestry was handled, how many variants were tested, and whether the study is a first report or a replication. Answer each in a sentence or two in Methods or Results, say plainly when an item does not apply, and check that every count agrees across the abstract, the tables and the text.

What the STREGA Checklist Is and How It Relates to STROBE

STREGA is the genetic counterpart of the STROBE guideline for observational studies, which our STROBE guide explains in full. A multidisciplinary group built it from a literature review, workshop presentations and discussion, and iterative electronic correspondence. Thirty-three of 74 invitees attended a workshop in Ottawa in June 2006, among them epidemiologists, geneticists, statisticians, journal editors and graduate students [1]. The statement appeared in 2009 in several journals, and the PLoS Medicine version is released under a Creative Commons CC0 dedication, so its wording can be reused freely [1].

The authors say their recommendations are not meant to support or oppose any particular study design or method. The aim is transparency and completeness in reporting what was done and found [1]. A checklist of this kind therefore records whether a reader can find the information, and it does not rate how good the study was. The reporting gap it targets was visible early. The authors cite an assessment of a random sample of 315 genetic association studies published from 2001 to 2003, in which only some studies described methods to validate genotyping [1].

STREGA Checklist Items by Manuscript Section

Table 1 paraphrases the 22 items and shows what STREGA adds to each, grouped by the section of the manuscript where the answer belongs. The wording is ours, and the original text sits in Table 1 of the open-access paper [1]. By our count the additions amount to 18 extra or extended lines across 12 items, with the heaviest load on item 12, the statistical methods.

Table 1. The 22 STROBE items and the STREGA additions, paraphrased from Little et al., 2009 (CC0).

ItemTopicCore ask, paraphrasedSTREGA addition, paraphrased
1Title and abstractName the design with a common term in the title or abstract, and give an informative, balanced abstract.None
2Background and rationaleExplain the scientific background and rationale.None (the rationale for the chosen genes and variants is requested under item 7)
3ObjectivesState specific objectives, including any prespecified hypotheses.Say whether the study is a first report of an association, a replication, or both.
4Study designPresent the key elements of the design early.None
5SettingGive setting, locations and relevant dates.None
6ParticipantsGive eligibility criteria, sources and selection methods, and matching details for matched studies.Describe how subsets were chosen when participants come from a larger study.
7VariablesDefine outcomes, exposures, predictors, confounders and effect modifiers.Define genetic variants with a widely used nomenclature, and name variables likely to relate to population stratification.
8Data sources and measurementGive the sources and methods of assessment for each variable, and their comparability across groups.Describe the laboratory work, including DNA source and storage, genotyping method and platform, calling algorithm and version, error and call rates, laboratory, comparability, and whether genotypes were assigned together or in batches.
9BiasDescribe efforts to address potential sources of bias.For quantitative outcomes, say whether bias from drug treatment was examined and how it was handled.
10Study sizeExplain how the study size was arrived at.None
11Quantitative variablesExplain how quantitative variables were handled and grouped.Say how treatment effects were dealt with, if applicable.
12Statistical methodsDescribe all methods, subgroup and interaction analyses, missing data, matching or follow-up handling, and sensitivity analyses.State software version and settings. Add Hardy-Weinberg equilibrium (12f), inference of genotypes or haplotypes (12g), population stratification (12h), multiple comparisons (12i) and relatedness (12j).
13Participants (results)Report numbers at each stage, reasons for non-participation, and consider a flow diagram.Report how many individuals had genotyping attempted and how many succeeded.
14Descriptive dataGive participant characteristics, missing data counts, and follow-up time for cohorts.Consider giving information by genotype.
15Outcome dataReport outcome events or exposure categories by study type.Report outcomes or numbers by genotype category.
16Main resultsGive unadjusted and adjusted estimates with precision, category boundaries, and absolute risk if relevant.Add the results of any adjustment for multiple comparisons (16d).
17Other analysesReport other analyses such as subgroups and sensitivity analyses.Summarise results from all variants examined (17b), and say where detailed results can be accessed (17c).
18Key resultsSummarise key results against the objectives.None
19LimitationsDiscuss limitations, with the direction and magnitude of any bias.None
20InterpretationGive a cautious overall interpretation.None
21GeneralizabilityDiscuss external validity.None
22FundingGive the source of funding and the role of the funders.None

Figure 1 shows the same structure at a glance. Twelve of the 22 boxes carry a genetics addition, and they cluster in Methods and Results, where the laboratory, the statistics and the participant counts live. Introduction and Discussion items, with the exception of item 3, keep their STROBE wording.

STREGA checklist item map showing the 12 of 22 STROBE items with genetic association additions
Figure 1. The 22 STROBE items, with the 12 that carry STREGA additions outlined in thick green. Original Editverse diagram based on Little et al., 2009 (CC0).

The Five Genetic Problems STREGA Targets

The STREGA authors single out five areas of special interest that are specific to, or especially relevant in, genetic association studies [1]. Table 2 sets out each one with the item that handles it and the reason it matters.

Table 2. The five main areas of special interest in STREGA, paraphrased from Little et al., 2009.

AreaWhy it mattersItemsWhat to report
Genotyping errorsNon-differential errors usually bias associations towards the null. Systematic differences in genotyping by outcome status can bias results in any direction.8b, 13aDescribe the laboratory work and report how many genotypings were attempted and succeeded.
Population stratificationConfounding arises when subpopulations differ in allele frequencies and in disease risk and are unevenly spread across the groups compared.7b, 12hReport ethnicity information and the methods used to assess or address stratification, or state that none was used.
Haplotype variationHaplotypes usually have to be inferred, and the methods vary.12gDescribe how genotypes or haplotypes were inferred, including uncertainty, rare haplotypes and software.
Hardy-Weinberg equilibriumDeparture from equilibrium can point to genotyping errors or peculiarities in the data. In one analysis of almost 600 studies, results of studies that violated the model differed significantly from those that fitted it in five of 42 gene-disease associations.12fState whether equilibrium was considered and how, and, for large platforms, any threshold used to exclude variants.
ReplicationReports increasingly present and combine several studies in one paper.3Say whether the study is a first report, a replication or both, and document the criteria for claiming replication.

The authors list seven further issues, namely selection of participants, the rationale for choosing genes and variants, treatment effects in studies of quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data tested [1]. The last of these matters most for genome-wide work, where a search across hundreds of thousands of variants can be expected to produce many false-positive odds ratios by chance alone. Our guide to statistical methods in genomics covers the testing side, and our chi-square guide shows the test that compares genotype counts and checks for equilibrium departures.

Choosing Between the STREGA Checklist, STROBE and STROBE-MR

Use the STREGA checklist when the paper reports an association between a genetic variant and a trait or disease in a cohort, case-control or cross-sectional design, whether the variants were picked as candidates or scanned genome-wide. The STREGA table includes the STROBE wording, so one completed table covers both. A Mendelian randomization paper is different, because it treats genetic variants as instruments to estimate a causal effect, and it has its own 20-item guideline, STROBE-MR [5]. Our STROBE-MR worked example scores a real study item by item in the same way as this guide.

For the method itself, start with our explainer on Mendelian randomization, then read how the F-statistic flags weak instruments, what each of the four estimators protects against in our pleiotropy guide, and why the power calculation so often decides a desk rejection. If you are unsure which guideline fits your design, use the design named in the title as the guide, with STREGA for genetic association studies and STROBE-MR for Mendelian randomization. Reviewers who pool genetic association studies may also rate case-control studies with the Newcastle-Ottawa Scale, which is a quality rating tool and not a reporting guideline, so the two answer different questions.

The Open-Access Example We Scored

The article we scored

We chose Kalesis and colleagues, published in Hormones in 2026 on the genetic background of obesity in a case-control design [2]. The paper was received on 7 October 2025, accepted on 24 April 2026 and published online on 2 June 2026. The abstract states “The study was conducted and reported in accordance with STREGA guidelines.”, and the article cites Little and colleagues as its reference for the guideline. The study compares 257 Greek adults with obesity, 136 without type 2 diabetes and 121 with it, at three variants, TCF7L2 rs7903146, FTO rs9939609 and PPARG rs1801282, and it adds an HbA1c analysis within the non-diabetic group.

The licence is CC BY 4.0, and three independent records agree. The Crossref licence record for the version of record gives the Creative Commons Attribution 4.0 URL with a start date of 2 June 2026, the Europe PMC licence field reads “cc by”, and the licence statement inside the article XML (JATS) names the Creative Commons Attribution 4.0 International License. The PMC open-data record also lists the licence as CC BY and the article as not retracted. Because a PMC copy can differ from the publisher version, we compared the XML body text with the typeset PDF held in the PMC open-data bucket, which carries the journal’s own layout and page numbers 527 to 533, and found no differences in the Methods, Results or Discussion wording. Page pointers below refer to that PDF.

We found no completed STREGA checklist among the article files, which are the text, the figure, the XML and the PDF. The only figure is a forest plot of odds ratios, so we reproduce no figure and the tables are summarised in our own words.

How we scored it

The STREGA table has 22 items, and several have lettered parts, so we scored 49 rows, each with the article section or page beside it. Rows that STREGA adds to STROBE are tagged. Each row carries one of five verdicts. Reported means the information is present and clear. Partly reported means some of it is present, or it is present but inconsistent. Not reported means we found nothing. Not applicable means the row does not fit the design, and we say why. Judgement call means reasonable readers could score the row either way, and we explain our reading.

Two cautions apply. First, STREGA is a reporting guideline, so a row marked Not reported means we could not find the information in the article, and the authors may hold it elsewhere. Second, we score only what the published article shows. Quotations are verbatim, no longer than 25 words, and checked against the typeset PDF.

STREGA Checklist Applied to the Example, Item by Item

Table 3. STREGA applied to Kalesis et al., Hormones 2026 (CC BY 4.0). Page numbers and table references in the third column refer to the article, Hormones 2026, volume 25, issue 2, pages 527 to 533.

Item and rowWhat the article reportsWhere to find itVerdict
1a Design named in title or abstractThe title ends with “a case-control study” and the abstract Methods open with “In this case-control study”.Title; Abstract, p. 527Reported
1b Informative and balanced abstractThe abstract gives the sample (257 adults, 136 without and 121 with type 2 diabetes), the three variants, the analysis plan, odds ratios with 95% CI, and two cautions, namely unadjusted models and Hardy-Weinberg departures in controls.Abstract, p. 527Reported
2 Background and rationaleThe Introduction reviews the genetics of type 2 diabetes, genome-wide findings, and prior evidence for TCF7L2 rs7903146, FTO rs9939609 and PPARG rs1801282.Introduction, p. 528Reported
3a Specific objectives and prespecified hypothesesThe primary aim is to compare the frequency of the three variants between obese adults without and with type 2 diabetes, and a secondary aim covers HbA1c in the non-diabetic group. The additive model is called prespecified, but the article cites no protocol or registration.Introduction, last paragraph; Statistical analysis, p. 528 to 529Reported
3b First report, replication or both
STREGA addition
The article does not say whether it is a first report or a replication. The Discussion remarks that evidence from Greek populations is limited, which implies a replication of known loci in a new population, yet the point is left implicit.Discussion, final paragraph, p. 532Judgement call
4 Key design elements earlyThe case-control design is named in the title, the abstract, the end of the Introduction and the first sentence of Methods.Title; Introduction, p. 528; Study population, p. 528Reported
5 Setting, locations and datesRecruitment ran from 20 May 2023 to 20 May 2024, ethics approval is dated, and the genotyping laboratory is named. The recruitment sites are mentioned but not named, and the HbA1c laboratories are not identified.Study population; Clinical evaluation, p. 528 to 529Partly reported
6a Eligibility, sources and selection of cases and controlsCases are adults with BMI above 30 and established type 2 diabetes, controls are adults with obesity and no diabetes, and monogenic diabetes or severe comorbidity was excluded. The article does not state how diabetes was diagnosed, where participants were approached, or why this control group was chosen.Study population, p. 528Partly reported
6a Selection of subsets from a larger study
STREGA addition
The article does not say whether these participants come from a larger study. A “de-identified analytical dataset” is mentioned without an origin, so the row could be read as not applicable or as a gap.Clinical evaluation, p. 528Judgement call
6b Matching criteria for a matched studyNo matching is described, and the mean ages differ by four years (50 and 54), which fits an unmatched design.Study population; Table 1, p. 528 to 529Not applicable
7a Definitions of outcomes, exposures and confoundersObesity (BMI above 30), diabetes status and the HbA1c categories (American Diabetes Association thresholds) are defined. No diagnostic criteria for diabetes are given, and age, sex and BMI are named as covariates but enter no model.Study population; Clinical evaluation, p. 528 to 529Partly reported
7b Genetic exposures in a standard nomenclature
STREGA addition
Each variant is named by gene and rs number, with genotype labels such as CC, CT and TT for TCF7L2 rs7903146.Clinical evaluation, p. 529; Tables 2 to 4Reported
7b Variables linked to population stratification
STREGA addition
The article says “All participants were of Greek Caucasian ancestry according to the study record.” How ancestry was recorded is not described, and no ancestry-related markers or variables are reported.Study population, p. 528Partly reported
8a Sources and measurement of each variableClinical data came from routine evaluation at the recruitment sites. HbA1c was measured by high-performance liquid chromatography at certified clinical laboratories chosen by participants, and comparability across those laboratories is not described. The Limitations name inter-laboratory heterogeneity.Clinical evaluation, p. 528 to 529; Limitations, p. 532Partly reported
8b Laboratory and genotyping methods
STREGA addition
DNA came from whole blood, genotyping used real-time PCR on the rhAmp SNP Genotyping System at a named accredited laboratory, and the article states “All three assays achieved a 100% call rate, and duplicate genotyping showed 100% concordance.” Not stated are DNA storage, the calling software and version, batch assignment, and whether cases and controls were genotyped under identical conditions.Clinical evaluation, p. 529Partly reported
9a Efforts to address biasQuality control (call rate, duplicate genotyping, Hardy-Weinberg testing in controls) and a single-ancestry sample are described. No effort against selection bias or confounding is described, and the Limitations list selection and survivor bias.Clinical evaluation, p. 529; Limitations, p. 532Partly reported
9b and 11 Treatment effects on quantitative traits
STREGA addition
The article does not say whether glucose-lowering treatment could have affected HbA1c. HbA1c is analysed only in non-diabetic controls and only as two categories, so the item may have little bite here, and readers could score it either way.Clinical evaluation, p. 529Judgement call
10 How the study size was reachedNo explanation or power calculation is given for 257 participants. The Limitations call the sample modest.Not found; Limitations, p. 532Not reported
11 Handling of quantitative variablesAge is given as a mean with range, HbA1c is grouped at the ADA cut-offs (normal glycemia 4.0 to 5.6, prediabetes 5.7 to 6.4), and genotype is coded additively per risk allele.Clinical evaluation; Statistical analysis, p. 529Reported
12a Statistical methods and software version
STREGA addition
Genotype distributions were compared by chi-square test, and unconditional logistic regression was used with an additive primary model and dominant and recessive secondary models, all unadjusted with the reason stated. The article gives “IBM SPSS Statistics version 26”. The tool used for the exact Hardy-Weinberg test is not named.Statistical analysis, p. 529Reported
12b Subgroups and interactionsThe only subgroup analysis is genotype by HbA1c category within controls, and it is described. No interaction analysis is stated.Statistical analysis, p. 529Reported
12c Missing dataGenotype completeness is stated, and the absence of participant-level age, sex and BMI is explained at length. How missing HbA1c values were handled is not stated.Statistical analysis; Results, p. 529Partly reported
12d Matching or sampling strategy in the analysisNot applicable because no matching is described.Not applicableNot applicable
12e Sensitivity analysesDominant and recessive models run alongside the additive model, but no analysis tests how the Hardy-Weinberg departures affect the results. Some readers would count the genetic-model comparison as a sensitivity analysis.Statistical analysis, p. 529; Table 4, p. 530Judgement call
12f Hardy-Weinberg equilibrium
STREGA addition
Equilibrium was tested in controls with an exact test and a citation, and Table 2 reports observed and expected heterozygotes. The Methods state “HWE was evaluated using an exact test”, and no exclusion threshold is stated, because all three variants were kept.Clinical evaluation, p. 529; Table 2, p. 529Reported
12g Inferring genotypes or haplotypes
STREGA addition
Single variants were typed directly by real-time PCR and no haplotype analysis is described, so the row does not apply.Clinical evaluation, p. 529Not applicable
12h Population stratification
STREGA addition
Restriction to Greek Caucasian ancestry is the only measure described. The Discussion names principal components as a standard approach and ancestry-informative analysis as future work, but the article never says that none was applied.Study population, p. 528; Discussion, p. 531Partly reported
12i Multiple comparisons and false positives
STREGA addition
Three variants and three genetic models were each tested at 0.05, and the article gives neither a correction nor a reason for none.Statistical analysis, p. 529Not reported
12j Relatedness among subjects
STREGA addition
The article does not say whether participants were unrelated.Not foundNot reported
13a Numbers at each stage of the studyThe article gives 257 participants (136 controls, 121 cases). The numbers approached, assessed for eligibility or excluded under the stated exclusion criteria are not given.Study population, p. 528Partly reported
13a Genotyping attempted and successful
STREGA addition
The article states “All 257 participants were successfully genotyped for all three loci.”Results, p. 529Reported
13b Reasons for non-participationNo reasons or counts are given.Not foundNot reported
13c Flow diagramThere is no flow diagram. The item says to consider one, and a diagram would first need the stage counts missing from row 13a.Not foundJudgement call
14a Participant characteristics, with genotype information
STREGA addition
Table 1 gives age (mean and range), sex counts, mean BMI and HbA1c (mean and SD) by group, with no spread for BMI. No table of characteristics by genotype is given.Table 1, p. 529Partly reported
14b Missing data for each variableThe article says participant-level age, sex and BMI were unavailable, and it gives no counts of missing HbA1c values.Clinical evaluation, p. 528 to 529Partly reported
14c Follow-up timeNot applicable because the study is not a cohort.Not applicableNot applicable
15 Numbers in each genotype category (case-control)
STREGA addition
Table 3 gives counts and percentages of each genotype in controls and cases. The columns add up to 136 and 121 in our arithmetic, for all three variants.Table 3, p. 530Reported
16a Unadjusted and adjusted estimates with precisionTable 4 gives unadjusted odds ratios with 95% CI for three models at each variant, and no adjusted estimates, with the reason stated. Because the mean ages differ by four years, some readers would want adjusted estimates and others accept the explanation.Table 4, p. 530; Discussion, p. 532Judgement call
16b Category boundaries for continuous variablesThe HbA1c boundaries are given (below 5.7, and 5.7 to 6.4).Clinical evaluation, p. 529; Table 5, p. 531Reported
16c Absolute riskNot applicable. A case-control sample with fixed group sizes does not yield absolute risks without outside incidence data.Not applicableNot applicable
16d Results of adjustments for multiple comparisons
STREGA addition
None are reported, which follows from row 12i.Not foundNot reported
17a Other analysesDominant and recessive models (Table 4) and the HbA1c analysis (Table 5) are reported.Tables 4 and 5, p. 530 to 531Reported
17b Summary of results for all variants examined
STREGA addition
Only three variants were analysed, and all of them appear with every model in Tables 2 to 5.Tables 2 to 5, p. 529 to 531Reported
17c Where detailed results can be accessed
STREGA addition
Not applicable because the article does not point to results held elsewhere, and its tables carry every result.Not applicableNot applicable
18 Key results against objectivesThe first Discussion paragraph restates the associations at all three loci and ranks TCF7L2 rs7903146 as the strongest signal.Discussion, p. 530Reported
19 Limitations, with direction and magnitude of biasFive limitations are listed, including unadjusted models, a modest sample and Hardy-Weinberg departures at all three loci. None says in which direction or by how much the estimates may be biased.Limitations, p. 532Partly reported
20 Cautious overall interpretationThe findings are called “informative and hypothesis-generating”, the PPARG result is set against the HuGE meta-analysis, and the Hardy-Weinberg findings are weighed. The multiplicity of analyses is not discussed.Discussion, p. 530 to 532Partly reported
21 GeneralizabilityThe Discussion notes limited Greek evidence and treats the homogeneous cohort as a strength, but it does not state to whom the results apply, for example obese Greek adults recruited at the study sites.Discussion, p. 532Partly reported
22 Funding and role of fundersThe article states that open access funding came from HEAL-Link Greece and that “This research received no external funding.”Funding, p. 532Reported

What the Tally and the Numbers in the Example Show

Across 49 rows the tally is 17 Reported, 15 Partly reported, 5 Not reported, 6 Not applicable and 6 Judgement call. Of the 18 rows that STREGA adds, 6 are Reported, 4 Partly reported, 3 Not reported, 2 Not applicable and 3 Judgement call. The counts are for this one paper and are not a quality score, and a different reader would move some Judgement call rows.

The strengths sit in the laboratory and in the full reporting of results. The article names the genotyping system and laboratory, gives a 100% call rate and 100% duplicate concordance, reports exact Hardy-Weinberg tests for every variant, and shows every variant with every genetic model. The gaps sit in places where STREGA is most specific, namely the study size, multiple comparisons, relatedness, population stratification, and the stage counts before genotyping.

Arithmetic we checked

We recomputed the main numbers from the printed tables, using the control and case genotype counts as printed. Table 4 below sets the printed values beside our results. The agreement is close on the core results, and it breaks in one place.

Table 4. Numbers in the example recomputed from the printed tables. The arithmetic is ours.

CheckPrinted in the articleOur recomputationResult
Genotype columns of article Table 3136 controls and 121 cases136 and 121 for all three variantsMatch
Chi-square p values, article Table 3Below 0.001; 0.006; below 0.001Below 0.001 (4.3e-9); 0.0058; below 0.001 (5.9e-5)Match
Exact Hardy-Weinberg p values in controls, article Table 2Below 0.001; below 0.001; 0.0194.1e-8; 3.6e-18; 0.019Match
Expected heterozygotes, article Table 240.2 (29.5%); 49.4 (36.3%); 46.0 (33.8%)40.2 (29.5%); 49.5 (36.4%); 45.6 (33.6%)Small differences for FTO and PPARG, immaterial to the exact p values
Additive odds ratios, article Table 42.66 (1.92 to 3.68); 1.52 (1.14 to 2.03); 1.98 (1.41 to 2.77)The same, by logistic regression on the Table 3 countsMatch
Dominant and recessive odds ratios, article Table 4Six estimates, for example 5.88 (3.08 to 11.22) for TCF7L2 recessiveThe same, by 2 by 2 tables on the Table 3 countsMatch
Group totals in article Table 5 (headed n = 47 and n = 89)TCF7L2 47 and 89TCF7L2 47 and 89; FTO 52 and 84; PPARG 49 and 87Does not match for FTO and PPARG
Chi-square p values, article Table 50.786; 0.978; 0.9120.786; 0.978; 0.912, using the printed countsMatch, with the counts as printed

The article Table 5 result needs care. The printed counts reproduce the printed p values, so the discrepancy sits either in the column headings or in the counts for two of the three variants. Genotyping was complete for all 257 participants, so the same people should fill the same two HbA1c groups for every variant, and the article alone does not let us tell which figure is intended. We note it as a point to reconcile and not as an error of method.

Inconsistencies a reader will notice

  • Article Table 4 labels three rows in its Notes column as “Primary model; unadjusted”, namely the TCF7L2 recessive, FTO dominant and PPARG recessive rows, while its footnote says “The additive (per-allele) model is the prespecified primary analysis; dominant and recessive models are secondary”. As printed, the labels contradict the footnote and the Methods.
  • Article Table 5 group totals do not agree across the three variants, as set out above.
  • The Methods sentence “The revised report was prepared in accordance with STREGA guidance” carries reference number 19, which in the reference list is the American Diabetes Association Standards of Care, while the STREGA paper is reference 15.
  • The Discussion says the quality control data “support retaining these loci in an exploratory analysis”, and the Limitations say Hardy-Weinberg departures at all three variants raise “concerns regarding genotyping validity, sampling effects, or population structure”. Both statements are open and honest, and a reader has to weigh them together when reading the odds ratios.

Five Reporting Lessons From the Example

Describe the laboratory the way item 8b asks

The example is strong on quality control, with a named platform, a named laboratory, a 100% call rate and duplicate genotyping of about 10% of samples. It still leaves out the calling software and version, the storage of DNA and any statement on batches or on whether cases and controls were genotyped together. These are short sentences that STREGA asks for because differential misclassification between cases and controls can arise from differences in DNA storage, collection or processing even when the genotyping itself is excellent [1].

Decide what Hardy-Weinberg departures mean before the Discussion

Item 12f asks whether equilibrium was considered and how, and the example answers that clearly with an exact test [4]. The STREGA authors add that any procedure to allow for deviations should also be described, and that for large platforms the threshold used to exclude variants should be stated [1]. In the example all three variants depart from equilibrium in controls, and the heterozygote deficits are marked for two of them. A reader needs to see in Methods what would have been done in that event, for example re-checking the assay or running the analysis with and without the variant, because the Discussion then has to carry the whole interpretation.

Say something about multiplicity and stratification, even if the answer is none

Rows 12h, 12i and 16d are the ones where a one-line statement costs the authors almost nothing. Three variants and three genetic models give nine association estimates, and the article states neither a correction nor a reason for none. Stratification is handled by restricting to one ancestry according to the study record, which is a legitimate choice that the STREGA authors would want stated together with how ancestry was ascertained. A sentence saying that no correction and no stratification method was applied, and why, satisfies the item.

Give the stage counts and the basis for the study size

The article gives final group sizes and the genotyping success rate, and not the numbers approached, eligible or excluded, or how 257 was chosen. Those three facts let a reader judge selection and power, and they are the usual contents of a flow diagram. Our free flow diagram generator, listed below, draws a STROBE diagram from the counts.

Make every label, total and citation number agree

The few real inconsistencies in the example are small ones, namely Notes labels in one table, group totals in another and a citation number that points to the wrong reference. None changes the odds ratios, and each is the kind of detail that editors and reviewers check first. A consistency pass, with every count, label and reference number compared between the abstract, the tables, the text and the reference list, takes under an hour.

How to Complete Your Own STREGA Checklist

Start from the STREGA table in the open-access paper, which the authors also provide as an editable file, Table S1 in the supporting information [1]. Add one row for each item, write the manuscript section or page beside it, and write a reason in every row that does not apply. Then write the genetics paragraphs below, each short enough to sit in Methods or Results.

  • Laboratory paragraph. Source and storage of DNA, genotyping method and platform, calling algorithm and version, laboratory, call and error rates, comparability across groups, and whether genotypes were assigned together or in batches.
  • Hardy-Weinberg sentence. The test used, the group it was applied to, any threshold for excluding variants, the result for each variant, and what you did when a variant departed.
  • Stratification sentence. The ancestry information available, how it was ascertained, and the method used to assess or address stratification, or a statement that none was used.
  • Multiplicity sentence. How many variants and models were tested, and whether and how the threshold was adjusted.
  • Counts. Numbers genotyping was attempted and succeeded, numbers per genotype category for cases and controls, and the stages before them.
  • Replication statement. Whether the study is a first report, a replication or both, with the criteria for replication when relevant.

Authors who need the design guideline first can use our STROBE guide, and the official STREGA page is listed on the EQUATOR Network site. The original STROBE statement is also open access [6], and the STROBE website carries the checklists for each design (STROBE statement site).

Common mistakes with the STREGA checklist

  • Writing that the study “followed STREGA” without supplying the checklist or the item locations.
  • Reporting a call rate without the method, the platform or the laboratory.
  • Testing Hardy-Weinberg equilibrium and then saying nothing about the result or what it meant for the analysis.
  • Testing many variants or models without a statement on multiplicity.
  • Giving only final group sizes and leaving out the numbers approached, excluded and genotyped.
  • Leaving table labels, group totals and citation numbers out of step with the text.

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If your question is a causal one that public GWAS summary statistics can answer, the Mendelian randomization study package includes a STROBE-MR checklist.

Conclusion

The STREGA checklist keeps all 22 STROBE items and adds genetics text to 12 of them, so that a reader can judge how DNA was handled, how many samples were genotyped, whether genotype counts fit equilibrium, how ancestry was treated and how many variants were tested. Applied to a real open-access case-control study, it shows what good reporting looks like, with a named platform and laboratory, a full call rate, duplicate genotyping and every variant shown under every model. It also shows where even a careful paper leaves gaps, namely study size, multiplicity, relatedness, stratification and stage counts, and where small inconsistencies creep in. Complete the table before submission, write a reason in every row that does not apply, and check every count, label and citation number in the final proofs.

Frequently Asked Questions About the STREGA Checklist

How many items does the STREGA checklist have?

It keeps the 22 items of the STROBE checklist and adds genetics-specific text to 12 of them, according to the 2009 statement. By our count the additions run to 18 lines, including the new sub-items 12f to 12j, 16d, 17b and 17c.

Does the STREGA checklist replace STROBE?

No. It is an extension, and the STREGA table contains the STROBE wording alongside the genetics additions, so one completed table covers both.

Does the STREGA checklist apply to genome-wide association studies?

Yes. The authors address genome-wide studies directly, for example by asking for the thresholds used to exclude variants and for a summary of all variants examined when many were tested.

Is the STREGA checklist used for Mendelian randomization?

No. Mendelian randomization studies have their own guideline, STROBE-MR, with 20 items.

Is the STREGA checklist a quality score?

No. It records whether the reporting is complete, and it does not rate the quality of the study. Counts of reported and unreported rows describe one paper and should not be turned into a scale.

Where can the official STREGA checklist be found?

The statement is open access in PLoS Medicine under a CC0 dedication, with an editable version of the table in the supporting information, and it is listed on the EQUATOR Network site.

What did the example paper leave out most often?

In our worked example the clearest gaps were the basis for the study size, multiple comparisons, relatedness, the stage counts before genotyping and the handling of population stratification.

References

  1. Little J, Higgins JPT, Ioannidis JPA, Moher D, Gagnon F, von Elm E, et al. STrengthening the REporting of Genetic Association Studies (STREGA): an extension of the STROBE statement. PLoS Med. 2009;6(2):e1000022. doi:10.1371/journal.pmed.1000022. PMID: 19192942. PMCID: PMC2634792. CC0. Publisher page.
  2. Kalesis K, Roidos P, Nikolopoulos V, Katsiki N, Kotsa K, Koufakis T. Genetic background of obesity: a case-control study. Hormones (Athens). 2026;25(2):527-33. doi:10.1007/s42000-026-00790-3. PMID: 42230483. PMCID: PMC13582106. CC BY 4.0. Publisher page.
  3. Nedovic D, Panic N, Pastorino R, Ricciardi W, Boccia S. Evaluation of the endorsement of the STrengthening the REporting of Genetic Association Studies (STREGA) statement on the reporting quality of published genetic association studies. J Epidemiol. 2016;26(8):399-404. doi:10.2188/jea.JE20150173. PMID: 27349199. PMCID: PMC4967660. Facts only are cited. Publisher page.
  4. Wigginton JE, Cutler DJ, Abecasis GR. A note on exact tests of Hardy-Weinberg equilibrium. Am J Hum Genet. 2005;76(5):887-93. doi:10.1086/429864. Publisher page.
  5. Skrivankova VW, Richmond RC, Woolf BAR, Yarmolinsky J, Davies NM, Swanson SA, et al. Strengthening the reporting of observational studies in epidemiology using Mendelian randomization (STROBE-MR). JAMA. 2021;326(16):1614-21. doi:10.1001/jama.2021.18236.
  6. von Elm E, Altman DG, Egger M, Pocock SJ, Gotzsche PC, Vandenbroucke JP. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. PLoS Med. 2007;4(10):e296. doi:10.1371/journal.pmed.0040296.
  7. International Committee of Medical Journal Editors. Recommendations for the Conduct, Reporting, Editing, and Publication of Scholarly Work in Medical Journals. Available at icmje.org/recommendations.
  8. DeTora LM, Toroser D, Sykes A, Vanderlinden C, Plunkett FJ, Lane T, et al. Good Publication Practice (GPP) guidelines for company-sponsored biomedical research, 2022 update. Ann Intern Med. 2022;175(9):1298-1304. doi:10.7326/M22-1460. PMID: 36037471.