Nezam El-Tayebat Fact CheckA scientific assessment of the “نظام الطيبات” nutrition system
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Mostly false Overinterpreted Certainty of evidence: moderate provisional C-INS-03

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

Safety note: Do not stop or reduce insulin on the basis of this claim. In type 1 diabetes and other insulin-deficient states, stopping insulin leads within hours to days to diabetic ketoacidosis, which is life-threatening. Medically accepted position (ADA Standards of Care 2026): insulin treatment is essential for people with type 1 diabetes; people on intensive insulin therapy should not stop basal insulin even when not eating. Any change of diabetes medication should be made together with the treating physician.
In short: This claim is mostly false. High natural insulin levels, a sign of insulin resistance, are linked to coronary disease, but randomised trials of insulin treatment found no increase in heart attacks, strokes or cardiovascular death, so insulin therapy is not a principal driver of atherosclerosis.
Conclusion: High natural insulin levels are a weak risk marker, but insulin therapy has not been shown to cause atherosclerosis.
  1. Original statement
  2. Scientific assessment
  3. Scientific evidence in detail
  4. In plain language
  5. Studies on this claim
  6. Regional context
  7. What applies in my country?
  8. References

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

مش صدفه مش صدفه اللي بياخد انسولين دايما كل سنه يجي له جلطه في الشران بتاع عينيه ولا جلطه في شيران التاجي بالصدفه بالصدفه يضيق عليك وانت بتاخد

It is not a coincidence that whoever takes insulin gets a clot every year in the artery of his eyes or in the coronary arteries; it narrows on you while you are taking [insulin].

Source status
Video transcript (own words)
Attribution
Elawady (machine transcript)
Video
الذبحة الصدرية ؟! (Open source)
Published
3 February 2025
Timestamp
1:13:35 (location in the original video’s automatic YouTube caption track; confirms where the words occur, not who speaks)
Attribution uncertainty
Archive transcript (YouTube CC or AI-generated); no timestamps; YouTube original not checked; wording may contain recognition errors. Similar idea only (clots/narrowing, not 'atherosclerosis' as a term).

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); I-INS-121 (Mendelian randomisation: genetically higher fasting insulin and CAD, OR 1.79, reflecting insulin resistance).

6. Which studies contradict it?

A-INS-07, A-INS-16, I-INS-02 (RCTs: no excess cardiovascular events; long-term benefit); I-INS-122 (meta-analysis of 20 RCTs: CV mortality RR 0.99); 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
26 October 2026 provisional

Scientific evidence in detail

Overinterpreted – A real finding exists, but the claim draws more from it than the data allow (e.g. association taken as cause, animal data applied to humans, small effect presented as large).

Research question: Does insulin (endogenous or injected) causally drive atherosclerosis?

Research question in detail (PECO)
Population
People with insulin resistance or insulin-treated diabetes
Intervention or exposure
Endogenous hyperinsulinaemia; insulin therapy
Comparison
Lower insulin; non-insulin therapy
Geographic scope
universal biology
Outcomes
  • Coronary artery disease
  • Cardiovascular events and mortality

Study results as reported by the authors. Our assessment follows below.

What speaks for the claim?

What speaks against the claim?

What does the overall evidence say?

Editorial assessment based on the studies above – not itself a study result.

Which position is better supported?

Endogenous hyperinsulinaemia (insulin resistance) is linked to coronary disease, but insulin therapy does not increase cardiovascular events in RCTs.

Why some studies weigh more

RCTs of insulin therapy directly test the claim about injected insulin; MR addresses endogenous insulin with pleiotropy concerns.

Is a causal relationship established? Possible, not established Possible causal role of endogenous hyperinsulinaemia/insulin resistance; no causal effect of therapeutic insulin shown.

Remaining uncertainty

Very high doses in severe insulin resistance.

Justified conclusion

Mostly false for insulin as 'principal driver' and for insulin therapy.

Why do studies seem to disagree?

MR and cohort associations (supporting) concern endogenous insulin as a marker of insulin resistance; RCTs (contradicting) concern injected insulin. They answer different questions.

Does this depend on the country?
General biological effects
Insulin physiology, autoimmune type 1 diabetes and ketoacidosis are universal human biology.
Eating habits
Egyptian and European diets differ, but no dietary pattern replaces insulin in insulin-deficient diabetes.
Origin of the food
Not relevant.
Contaminants
Not relevant.
National production conditions
Not relevant.
Legal rules
Insulin is an essential medicine (WHO list) in Egypt and the EU; prescription rules not relevant to the scientific question.
Actual monitoring data
Egyptian/Middle Eastern data show severe DKA is common at presentation in children (I-INS-115, I-INS-114); no data on outcomes among Tayebat followers.

A regional difference that changes the conclusion is not supported by robust data.

Statistical re-check
  • CI log-symmetry and implied SE – Symmetric; SE(log OR) about 0.149 recalculated
  • Compatibility with harm – CV mortality CI 0.90-1.09 excludes large harm recalculated
Certainty of the overall evidence (GRADE, simplified)
Main outcome
Cardiovascular events with insulin therapy
Starting level
high (randomised trials)
Reasons for downgrading
  • indirectness (mostly T2D populations, early to moderate disease)
Result
moderate

Simplified assessment by a single reviewer, following the GRADE approach; not a formal GRADE panel. GRADE rates the body of evidence for one outcome, not individual studies.

Clinical guidelines and official statements checked
  • ADA: 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes-2026 (I-ODD-16) (2026) · Original publication
    'Insulin treatment is essential for individuals with type 1 diabetes'; insulin to be considered in T2D when A1C >10%, glucose >=300 mg/dL or catabolic features (as recorded for I-ODD-16).
  • ADA: 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes-2026 (2026) · Original publication
    Rec 10.1: measure blood pressure at every routine visit or at least every 6 months; rec 10.2 (A): home BP monitoring for people with hypertension and diabetes.
Search strategy

Documented literature searches for this review (search strings in the original database syntax).

DatabaseDateSearchLooking forHitsIncluded
PubMed26 October 2026"mendelian randomization" AND ("fasting insulin" OR hyperinsulinemia OR "insulin secretion") AND ("coronary artery disease" OR "coronary heart disease" OR atherosclerosis)supporting evidence66
PubMed26 October 2026hyperinsulinemia AND atherosclerosis AND (causal OR "mendelian randomization") AND humansupporting evidence4386
Europe PMC26 October 2026(TITLE:"hyperinsulinemia" OR TITLE:"hyperinsulinaemia") AND (TITLE:"atherosclerosis" OR TITLE:"coronary") AND (cohort OR "mendelian")supporting evidence9
PubMed26 October 2026(insulin therapy OR "insulin treatment") AND "type 2 diabetes" AND (cardiovascular OR mortality) AND meta-analysis[pt] AND (randomized OR randomised)contradicting evidence210
Europe PMC26 October 2026(TITLE:"insulin therapy" OR TITLE:"insulin treatment") AND (TITLE:"atherosclerosis" OR TITLE:"cardiovascular") AND (randomized OR randomised) AND "type 2 diabetes"contradicting evidence25
PubMed26 October 2026Erpeldinger S[au] AND insulincontradicting evidence2

How deeply was this checked?

9 linked studies: 2 checked in full text (2 of them with a structured risk-of-bias assessment), 7 on the basis of the abstract, 0 bibliographically only. No formal assessment with two independent reviewers and no independent human expert review has taken place yet.

Last scientific review: 26 October 2026

History of the verdict
  1. 25 October 2026 · Phase 1 · Initial assessment: Mostly false (moderate)
  2. 26 October 2026 · Phase 4 (systematic evidence review) · Re-examined with extended evidence; verdict unchanged: Mostly false (moderate)
    MR evidence strengthens the kernel about endogenous hyperinsulinaemia; RCT meta-analysis strengthens the absence of harm from insulin therapy. Net conclusion unchanged.
    New sources: I-INS-121 I-INS-122

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

Studies supporting the claim (3)

  • High natural insulin and heart disease

    Després JP et al.. N Engl J Med 1996 · PMID 8596596 · DOI 10.1056/NEJM199604113341504
    Case-control studycited by the Tayebat archiveabstract checked

    Men with higher fasting insulin had more heart disease.

    Does the study support the specific claim? Partly · Methodological quality: moderate · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Is fasting hyperinsulinaemia an independent risk factor for IHD?

    How was the study done?

    Nested case-control within prospective cohort (Quebec)

    How many people, animals or samples were studied?

    2,103 men; 91 cases, 105 controls; Non-diabetic men 45-76

    What was actually found?

    OR 1.7 per SD.

    How large was the observed effect?

    OR 1.6-1.7

    What do the results mean in everyday life?

    Insulin resistance is a heart risk marker.

    What are the study's limitations?

    Small number of cases; Men only; Endogenous insulin, not therapy

    What does it say about Elawady's specific claim?

    Association for C-INS-03.

    Do the results apply to Germany and Europe?

    Canadian men.

    What can explicitly not be concluded from this study?

    That insulin injections cause heart disease.

    Scientific details →

  • Insulin levels and heart disease: pooled analysis

    Ruige JB et al.. Circulation 1998 · PMID 9529268 · DOI 10.1161/01.cir.97.10.996
    Meta-analysiscited by the Tayebat archiveabstract checked

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

    Does the study support the specific claim? Partly · Methodological quality: moderate · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

    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 details →

  • Genes for higher insulin levels and heart disease

    Huang X et al.. BMC Med 2025 · PMID 40442727 · DOI 10.1186/s12916-025-04127-6
    Otherindependent cross-checkabstract checked★ key study

    People genetically inclined to higher fasting insulin had a higher risk of coronary artery disease.

    Genetically higher fasting insulin linked to CAD (OR 1.79); endogenous, not therapeutic insulin.

    Does the study support the specific claim? Partly · Methodological quality: moderate · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Test whether higher fasting insulin causes coronary disease.

    How was the study done?

    Mendelian randomisation.

    How many people, animals or samples were studied?

    Large genetic datasets.

    What was actually found?

    OR 1.79 for CAD.

    How large was the observed effect?

    OR 1.79 (1.34-2.40).

    What do the results mean in everyday life?

    Insulin resistance with high natural insulin is bad for arteries.

    What are the study's limitations?

    Instruments reflect insulin resistance; no data on insulin therapy.

    What does it say about Elawady's specific claim?

    Supports the kernel about natural high insulin, not about insulin injections.

    Do the results apply to Germany and Europe?

    Mostly European data.

    What can explicitly not be concluded from this study?

    Cannot say insulin treatment causes atherosclerosis.

    Scientific details →

Studies contradicting or limiting the claim (5)

  • Long-term insulin glargine in early diabetes (ORIGIN)

    ORIGIN Trial Investigators; Gerstein HC et al.. N Engl J Med 2012 · PMID 22686416 · DOI 10.1056/NEJMoa1203858
    Randomised controlled trialcited by the Tayebat archivefull text, structured risk-of-bias assessment★ key study

    Over six years insulin did not change heart attacks, strokes or cancers, but caused more low-sugar episodes and 2 kg weight difference.

    Does the study support the specific claim? No · Methodological quality: high · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Does basal insulin glargine targeting normal fasting glucose reduce CV events in dysglycaemia?

    How was the study done?

    International multicentre RCT, 2x2 factorial (ORIGIN)

    How many people, animals or samples were studied?

    12,537; CV risk factors plus IFG, IGT or type 2 diabetes; mean age 63.5

    What was actually found?

    Neutral CV and cancer outcomes; more hypoglycaemia, slight weight gain.

    How large was the observed effect?

    HR 1.02 CV; HR 1.00 cancer

    What do the results mean in everyday life?

    Insulin itself did not cause heart disease or cancer in this large trial.

    What are the study's limitations?

    Open-label; funded by the glargine manufacturer; early-diabetes population on moderate doses (~28 units/day for 70 kg).

    What does it say about Elawady's specific claim?

    Key randomised evidence against C-INS-03, C-INS-05, C-INS-06; supports hypoglycaemia/weight side effects.

    Do the results apply to Germany and Europe?

    Multinational/US/UK/European data; directly transferable to Germany/EU clinical practice.

    What can explicitly not be concluded from this study?

    Safety in very high-dose, late-stage type 2 diabetes.

    Scientific details →

  • UKPDS: tablets or insulin for new type 2 diabetes

    UKPDS Group. Lancet 1998 · PMID 9742976
    Randomised controlled trialcited by the Tayebat archiveabstract checked★ key study

    Better sugar control with tablets or insulin cut eye/kidney complications by a quarter; insulin caused more weight gain and low-sugar episodes.

    Does the study support the specific claim? Partly · Methodological quality: high · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Intensive control with sulfonylurea or insulin vs diet on complications

    How was the study done?

    Multicentre RCT (UKPDS 33)

    How many people, animals or samples were studied?

    3,867; Newly diagnosed type 2 diabetes, median age 54

    What was actually found?

    Microvascular -25%; more hypoglycaemia and weight gain with insulin.

    How large was the observed effect?

    RR reduction 25% microvascular

    What do the results mean in everyday life?

    Insulin helps prevent complications but has side effects.

    What are the study's limitations?

    Open-label; Older drug regimens

    What does it say about Elawady's specific claim?

    Supports weight/hypoglycaemia (C-INS-01); contradicts C-INS-03, C-INS-05, C-DIAB-01.

    Do the results apply to Germany and Europe?

    UK; directly relevant.

    What can explicitly not be concluded from this study?

    That insulin is harmful overall.

    Scientific details →

  • UKPDS legacy: 10 years after the trial

    Holman RR et al.. N Engl J Med 2008 · PMID 18784090 · DOI 10.1056/NEJMoa0806470
    Randomised controlled trialindependent cross-checkabstract checked★ key study

    People treated intensively early with sulfonylureas or insulin had 15% fewer heart attacks and 13% fewer deaths years later.

    Does the study support the specific claim? No · Methodological quality: high · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Do UKPDS benefits persist and do macrovascular effects emerge?

    How was the study done?

    Post-trial monitoring of an RCT (UKPDS 80)

    How many people, animals or samples were studied?

    4,209 randomised; 3,277 monitored; Newly diagnosed type 2 diabetes from UKPDS

    What was actually found?

    Legacy reductions in MI and death.

    How large was the observed effect?

    Death -13% (SU/insulin), -27% (metformin)

    What do the results mean in everyday life?

    Early good control pays off for decades.

    What are the study's limitations?

    Post-trial therapy not controlled; Questionnaire follow-up

    What does it say about Elawady's specific claim?

    Contradicts C-INS-03, C-INS-05 and C-DIAB-01: early insulin/SU therapy reduced MI and death long-term.

    Do the results apply to Germany and Europe?

    UK; directly relevant.

    What can explicitly not be concluded from this study?

    Effects of extreme targets in late disease.

    Scientific details →

  • Second drug after metformin: insulin or sulfonylurea

    Roumie CL et al.. JAMA 2014 · PMID 24915260 · DOI 10.1001/jama.2014.4312
    Cohort studycited by the Tayebat archivefull text, structured risk-of-bias assessment★ key study

    Veterans who added insulin died more often than those who added a sulfonylurea, but heart attacks and strokes were not more frequent.

    Does the study support the specific claim? Partly · Methodological quality: moderate · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Adding insulin vs sulfonylurea to metformin: AMI, stroke, death

    How was the study done?

    Retrospective cohort with propensity matching and marginal structural models (VHA, Medicare, NDI)

    How many people, animals or samples were studied?

    178,341 (matched 2,436 insulin vs 12,180 SU); Veterans initially treated with metformin

    What was actually found?

    Composite aHR 1.30; death aHR 1.44; CV events not increased.

    How large was the observed effect?

    aHR 1.30 (1.07-1.58)

    What do the results mean in everyday life?

    Possibly reflects sicker patients getting insulin.

    What are the study's limitations?

    Residual confounding (sicker patients get insulin); median follow-up about 1 year; mostly male veterans; extra deaths were mainly from cancer and other non-heart causes.

    What does it say about Elawady's specific claim?

    Association for C-INS-05; mixed for C-INS-03 (no CV increase).

    Do the results apply to Germany and Europe?

    US veterans.

    What can explicitly not be concluded from this study?

    That insulin causes death.

    Scientific details →

  • Insulin in type 2 diabetes: what randomised trials show

    Erpeldinger S et al.. BMC Endocr Disord 2016 · PMID 27391319 · DOI 10.1186/s12902-016-0120-z
    Meta-analysisindependent cross-checkabstract checked★ key study

    In 20 trials with 18,599 people, insulin did not change the risk of death but caused more severe low blood sugar.

    No increase in CV mortality with insulin.

    Does the study support the specific claim? Partly · Methodological quality: high · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Summarise RCTs of insulin in T2D.

    How was the study done?

    Meta-analysis of 20 RCTs.

    How many people, animals or samples were studied?

    18,599 patients.

    What was actually found?

    Mortality unchanged; severe hypoglycaemia +70%.

    How large was the observed effect?

    RR 0.99 death; 1.70 severe hypoglycaemia.

    What do the results mean in everyday life?

    Insulin does not kill, but low sugar is a real risk; use it carefully.

    What are the study's limitations?

    Older trials; heterogeneity.

    What does it say about Elawady's specific claim?

    Refutes 'insulin doubles mortality'; supports caution.

    Do the results apply to Germany and Europe?

    Applicable.

    What can explicitly not be concluded from this study?

    Cannot address insulin in type 1 diabetes, where it is essential.

    Scientific details →

Studies with mixed or unclear results (1)

  • Higher insulin doses and outcomes

    Holden SE et al.. Diabetes Obes Metab 2015 · PMID 25399739 · DOI 10.1111/dom.12412
    Cohort studycited by the Tayebat archiveabstract checked★ key study

    People on higher insulin doses died more often, but higher doses are needed by sicker, more insulin-resistant people.

    Does the study support the specific claim? Partly · Methodological quality: low · Certainty of evidence: see overall assessment of the claim

    Original publication · Scientific details

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

    Association of insulin dose with mortality, MACE, cancer

    How was the study done?

    Retrospective cohort, UK CPRD, time-dependent dose exposure

    How many people, animals or samples were studied?

    6,484; Type 2 diabetes progressing to insulin monotherapy from 2000

    What was actually found?

    Dose-associated increases in death, MACE, cancer.

    How large was the observed effect?

    aHR 1.54 per IU/kg/day

    What do the results mean in everyday life?

    High doses mark severe disease; cause unclear.

    What are the study's limitations?

    Dose reflects insulin resistance and illness; Reverse causation; Residual confounding

    What does it say about Elawady's specific claim?

    Support (association) for C-INS-05; mixed for C-INS-03.

    Do the results apply to Germany and Europe?

    UK data.

    What can explicitly not be concluded from this study?

    That lowering doses would save lives.

    Scientific details →

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. Exploring the pathways linking fasting insulin to coronary artery disease: a proteome-wide Mendelian randomization study.. Huang X et al.. BMC Med 2025 · PMID 40442727 · DOI 10.1186/s12916-025-04127-6
  4. 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
  5. 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
  6. 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
  7. 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
  8. Efficacy and safety of insulin in type 2 diabetes: meta-analysis of randomised controlled trials.. Erpeldinger S et al.. BMC Endocr Disord 2016 · PMID 27391319 · DOI 10.1186/s12902-016-0120-z
  9. 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

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