Meta-analysiscited by the Tayebat archiveabstract only checked A-INS-22 standard review

Insulin levels and heart disease: pooled analysis

Insulin and risk of cardiovascular disease: a meta-analysis.

Overview

Ruige JB et al.. Circulation 1998 · PMID 9529268 · DOI 10.1161/01.cir.97.10.996

Higher insulin was only weakly linked to heart disease (18% higher risk).

Does the study support the specific claim? Partly · Methodological quality: moderate

Original publication

Plain-language summary

Study explained simply
What did the researchers want to find out?

Strength of relation between hyperinsulinaemia and CVD

How was the study done?

Meta-analysis of prospective cohorts and nested case-control studies

How many people, animals or samples were studied?

12 studies; General population cohorts

What was actually found?

RR 1.18.

How large was the observed effect?

RR 1.18 (1.08-1.29)

What do the results mean in everyday life?

Weak signal.

What are the study's limitations?

Old assays; Heterogeneity

What does it say about Elawady's specific claim?

Weak association for C-INS-03.

Do the results apply to Germany and Europe?

Includes Dutch data.

What can explicitly not be concluded from this study?

Causation; anything about insulin therapy.

Scientific in-depth review

1. Full reference

Authors
Ruige JB, Assendelft WJ, Dekker JM, Kostense PJ, Heine RJ, Bouter LM
Journal
Circulation
Year
1998
Identifier
PMID 9529268 DOI 10.1161/01.cir.97.10.996
Verification
verified – PubMed E-utilities efetch, 2026-10-25
Retracted
no
Corrections
none
Extent checked
abstract only
Conflicts of interest and funding

not stated in abstract

2. Research question

Strength of relation between hyperinsulinaemia and CVD

3. Study design and population

Study design
Meta-analysis – Meta-analysis of prospective cohorts and nested case-control studies
Population

General population cohorts

Country

International

Period

Studies to 1990s

Sample size

12 studies

Inclusion and exclusion criteria

As described in the abstract; details not available in abstract.

4. Methods and endpoints

Exposure / intervention

Fasting/non-fasting insulin

Comparator

Lower insulin (75th vs 25th percentile)

Endpoints

MI, CHD death, ECG changes

Statistical methods

Meta-regression

5. Actual results

Results

Summary RR 1.18 (1.08-1.29); modified by ethnicity and insulin assay.

Absolute risks

not reported

Authors' conclusion

Hyperinsulinaemia is a weak risk indicator for CVD.

6. Strengths

  • Systematic search

7. Weaknesses

  • Old assays
  • Heterogeneity

8. Risk of bias

Orienting tool
AMSTAR 2
Type of assessment
simplified assessment (abstract only)
Full formal assessment
no
Overall risk of bias
some concerns
Rationale

Older methods.

9. Assessment of the statistical interpretation

Weak association.

10. Relevance to the specific claim

Weak association for C-INS-03.

11. Independent contrary findings

A-INS-07.

12. Transferability to Germany and Europe

Includes Dutch data.

13. Overall methodological judgement

Weak marker.

Multidimensional assessment
Multidimensional assessment
Authenticity of the sourceverified
Methodological qualitymoderate
Risk of biassome concerns
Precision of resultsmoderate
Directnessindirect
Reproducibilitypartly replicated
Consistency with the overall evidencemixed
Regional transferabilityhigh
Adequacy of the interpretation (by the archive)not supported by the study

14. Open questions

None beyond those stated.

15. Linked fact checks

Use by the Tayebat archive

Note: according to the archive, the studies were compiled by the archive operators. Whether Dr. Elawady himself cited this study is not established.

What the archive says about the study

Listed in the archive bibliography for 'insulin-injections' without its own interpretation; used as general support for the claim that insulin intensification harms.

A. What was actually studied?

Strength of relation between hyperinsulinaemia and CVD

B. What did the authors find?

RR 1.18.

C. What conclusions do the authors themselves draw?

Hyperinsulinaemia is a weak risk indicator for CVD.

D. What does the archive derive from it?

Support for insulin-atherosclerosis claim.

E. Is this derivation scientifically justified?

Not justified: the authors call the link weak; endogenous insulin only.

Adequacy of the interpretation (by the archive)
not supported by the study