Insulin (and injected insulin) is a principal driver of atherosclerosis.

Original statement

ويصفه بأنه «المسبب الرئيسي للسمنة» و«من أسباب تصلب الشرايين».

verbatim according to source. Translation by the project; the Arabic wording is authoritative.

Translation

Insulin (and injected insulin) is a principal driver of atherosclerosis.

Origin

Source status

Archive quote (no location given)

Attribution

Elawady (archive paraphrase; source video not given)

Origin

https://eltayebat.com/rule/insulin-injections/

Attribution uncertainty

The archive attributes this text to Dr. Diaa in its 'د. ضياء يقول' box but gives no video reference. Transcript check (the project's research files, keyword search of 307 archive transcripts): similar_idea_only. A passage links insulin use to clots and narrowing of coronary arteries (5H-C06AT55Q); the term 'atherosclerosis' and the claim that insulin is its 'principal driver' were not checked verbatim. The central sentence of the same archive quote ('insulin is the only hormone causing obesity') is found verbatim (3j32fjfYRbU) but belongs to C-INS-01.

Claimed mechanism

High insulin levels damage arteries.

Claimed health effect

Atherosclerosis, cardiovascular disease

Population concerned

People with high insulin / insulin-treated diabetes

Geographic restriction by Elawady

none found

Diverging source versions

Scientific assessment

Mostly false – Essential parts of the statement are not supported by the evidence or are strongly exaggerated.

Certainty of evidence: moderate – Further research may still affect the assessment.

1. What was claimed?

Insulin causes hardening of the arteries.

2. What is demonstrably correct?

Endogenous hyperinsulinaemia (a marker of insulin resistance) is weakly associated with ischaemic heart disease: odds ratio 1.7 per SD in a Quebec case-control study (A-INS-21); summary RR 1.18 in a meta-analysis that called hyperinsulinaemia a 'weak risk indicator' (A-INS-22). UKPDS 33 itself noted the historical concern that high insulin concentrations may enhance atheroma (A-INS-16).

3. What is wrong or exaggerated?

Association with endogenous hyperinsulinaemia is not proof that therapeutic insulin causes atherosclerosis. In ORIGIN (12,537 people, 6.2 years) insulin glargine had a neutral effect on cardiovascular outcomes (HR 1.02) (A-INS-07). In UKPDS 33 intensive therapy with insulin or sulfonylurea did not increase macrovascular disease (A-INS-16), and 10-year post-trial follow-up showed a 15% reduction in myocardial infarction and 13% in all-cause death in the sulfonylurea-insulin group (I-INS-02). Even in the archive's own observational study of insulin added to metformin, myocardial infarction or stroke (aHR 0.88, 0.59-1.30) and MI/stroke/CV death (aHR 0.98, 0.71-1.34) were not increased; the excess deaths were mainly from cancer and other non-cardiovascular causes (cancer death aHR 1.85), which points to confounding rather than atherogenesis (A-INS-13).

4. What remains unclear?

Whether very high doses in severely insulin-resistant patients carry specific vascular risk cannot be separated from confounding in observational data (A-INS-10).

5. Which studies support it?

A-INS-21, A-INS-22 (association of endogenous insulin with CHD).

6. Which studies contradict it?

A-INS-07, A-INS-16, I-INS-02 (RCTs: no excess cardiovascular events; long-term benefit); A-INS-13 (observational: no excess MI/stroke with insulin).

7. What applies to Germany and Europe?

European (EASD) and German (DDG) guidance follow the same evidence base as the ADA/EASD consensus: individualised HbA1c targets, insulin as mandatory therapy in type 1 diabetes, and SGLT2 inhibitors/GLP-1 receptor agonists for people with cardiovascular or kidney disease. No country-specific difference changes the assessment.

8. What is known about Egypt?

Egypt has one of the highest diabetes prevalences in the region; the same drug classes and insulins are used. Access barriers and cost may make advice to stop medication attractive, which increases the practical risk of this claim. No Egypt-specific evidence changes the assessment.

9. What practical conclusion is appropriate?

High insulin levels in the blood are a sign of insulin resistance, which is linked to heart disease. Randomised trials do not show that insulin treatment itself causes heart attacks.

Assessment details

Rationale for certainty of evidence

Cohort data show a weak association of fasting hyperinsulinaemia with heart disease (A-INS-21, A-INS-22), but this reflects insulin resistance/metabolic syndrome. Large RCTs of insulin therapy (ORIGIN, UKPDS) found no increase in cardiovascular events, and UKPDS long-term follow-up showed fewer myocardial infarctions.

Source quality

Archive paraphrase without video reference.

Regional transferability

Universal.

Regional scope of the claim

general (biological/medical)

Last reviewed

25 October 2026 provisional

In plain language

People whose bodies make a lot of insulin because of insulin resistance have slightly more heart disease. But when doctors tested insulin treatment in large randomised trials, it did not increase heart attacks or strokes. In one long British study, people treated early with insulin or tablets had fewer heart attacks years later.

Studies on this claim

Regional context

Germany / EU

European (EASD) and German (DDG) guidance follow the same evidence base as the ADA/EASD consensus: individualised HbA1c targets, insulin as mandatory therapy in type 1 diabetes, and SGLT2 inhibitors/GLP-1 receptor agonists for people with cardiovascular or kidney disease. No country-specific difference changes the assessment.

Egypt

Egypt has one of the highest diabetes prevalences in the region; the same drug classes and insulins are used. Access barriers and cost may make advice to stop medication attractive, which increases the practical risk of this claim. No Egypt-specific evidence changes the assessment.

What applies in my country?

General scientific assessment

Mostly false High natural insulin levels are a weak risk marker, but insulin therapy has not been shown to cause atherosclerosis.

This statement concerns biological or medical relationships. The scientific assessment above applies regardless of the country; country-specific food data do not change it.

References

1. Hyperinsulinemia as an independent risk factor for ischemic heart disease.. Després JP et al.. N Engl J Med 1996 · PMID 8596596 · DOI 10.1056/NEJM199604113341504
2. Insulin and risk of cardiovascular disease: a meta-analysis.. Ruige JB et al.. Circulation 1998 · PMID 9529268 · DOI 10.1161/01.cir.97.10.996
3. Basal insulin and cardiovascular and other outcomes in dysglycemia.. ORIGIN Trial Investigators; Gerstein HC et al.. N Engl J Med 2012 · PMID 22686416 · DOI 10.1056/NEJMoa1203858
4. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group.. UKPDS Group. Lancet 1998 · PMID 9742976
5. 10-year follow-up of intensive glucose control in type 2 diabetes.. Holman RR et al.. N Engl J Med 2008 · PMID 18784090 · DOI 10.1056/NEJMoa0806470
6. Association between intensification of metformin treatment with insulin vs sulfonylureas and cardiovascular events and all-cause mortality among patients with diabetes.. Roumie CL et al.. JAMA 2014 · PMID 24915260 · DOI 10.1001/jama.2014.4312
7. Glucose-lowering with exogenous insulin monotherapy in type 2 diabetes: dose association with all-cause mortality, cardiovascular events and cancer.. Holden SE et al.. Diabetes Obes Metab 2015 · PMID 25399739 · DOI 10.1111/dom.12412