Nezam El-Tayebat Fact CheckA scientific assessment of the “نظام الطيبات” nutrition system
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False Scientifically refuted Certainty of evidence: high provisional C-SRC-37

'Insulin resistance' is a wrong term; there is no such thing as insulin resistance.

Safety note: Do not ignore a diagnosis of insulin resistance, prediabetes or type 2 diabetes. Discuss treatment and monitoring with a physician; do not stop prescribed glucose-lowering medication on the basis of this claim.
In short: This claim is false: insulin resistance has been measured directly for decades and predicts type 2 diabetes; scientists debate only what causes it, including whether high insulin levels themselves drive it.
Conclusion: This claim is false: insulin resistance is measurable and predicts type 2 diabetes; only its causes, including the role of high insulin, are debated.
  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

هنتكلم المره الجايه ان شاء الله ليه ليه ليه ا مقاومه الانسولين ده مصطلح غلط اصلا المره الجايه ان هو ما في حاجه اسمها مقاومه انسولين اللي هو اي ار ده

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

Translation

'Insulin resistance' is a wrong term; there is no such thing as insulin resistance.

Origin

Source status
Video transcript (own words)
Attribution
Elawady (machine transcript)
Video
Dr Diaa Al Awady د ضياء العوضي is live! النخاميه (Open source)
Published
25 June 2025
Timestamp
1:12:00 (location in the original video’s automatic YouTube caption track; confirms where the words occur, not who speaks)
Attribution uncertainty
Transcript is YouTube CC or machine-generated (no timestamps); wording may contain speech-recognition errors. Speaker attribution within live streams/podcasts is not marked in the transcript; the excerpt was judged to be Elawady's own speech from context. Recurrence = number of archive transcripts matching the keyword pattern ['مقاومه الانسولين', 'غلط|ما فيش|مافيش|كذب|اكذوب|وهم'] (approximate; includes re-uploads/clips; 8 distinct text passages).
Claimed mechanism

Not stated in this excerpt (other videos: insulin is released repeatedly because the gut is obstructed).

Claimed health effect

Not applicable.

Population concerned

Everyone.

Geographic restriction by Elawady

none found; he does not limit this statement to a country or to a production system

Diverging source versions

Source status
Video transcript (own words)
Attribution
Elawady (machine transcript)
Video
Dr Diaa Al Awady د ضياء العوضي is live! النسيج البيني التعرق التبول ؟!! (Open source)
Published
15 October 2025
Timestamp
not available (transcript has no timings)
Attribution uncertainty
Further video in which the same statement recurs; no excerpt recorded. Archive transcript without timestamps.
Source status
Video transcript (own words)
Attribution
Elawady (machine transcript)
Video
اكذوبه مقاومه الإنسولين (Open source)
Published
1 November 2025
Timestamp
not available (transcript has no timings)
Attribution uncertainty
Further video in which the same statement recurs; no excerpt recorded. Archive transcript without timestamps.
Source status
Video transcript (own words)
Attribution
Elawady (machine transcript)
Video
Dr.D Clinics - Diaa Al Awady is live! الكلي (Open source)
Published
20 May 2025
Timestamp
not available (transcript has no timings)
Attribution uncertainty
Further video in which the same statement recurs; no excerpt recorded. Archive transcript without timestamps.

Scientific assessment

False – The statement contradicts the robust evidence.

Certainty of evidence: high – Further research is very unlikely to change the assessment.

1. What was claimed?

He says 'insulin resistance' is a wrong term and that there is no such thing as insulin resistance.

2. What is demonstrably correct?

A fair point is that hyperinsulinaemia and insulin resistance are closely linked and that high insulin levels can themselves drive insulin resistance: a review in Diabetes Care concluded that 'hyperinsulinemia is often both a result and a driver of insulin resistance' (I-INTB-03). The causal order is genuinely debated. Experimental data support his underlying point: four days of raised insulin levels reduced insulin sensitivity by 20-40% in healthy volunteers (I-SRC-127). This shows that high insulin can drive insulin resistance, and it also confirms that insulin resistance can be measured.

3. What is wrong or exaggerated?

The claim that insulin resistance does not exist is wrong. Insulin resistance means that a given amount of insulin lowers blood glucose less than normal; it can be measured and is a key process in type 2 diabetes (I-INTB-01). In a 13-year prospective study, slow glucose removal with compensatory high insulin preceded type 2 diabetes by one to two decades and independently predicted it (I-INTB-02). Fructose feeding reduced measured insulin sensitivity in a randomised trial (A-SOD-07). In Pima Indians studied with the clamp method, nobody with good insulin action and secretion developed diabetes within six years, compared with 27-39% of those with low insulin action (I-SRC-112); in 6538 British civil servants insulin sensitivity fell steeply in the five years before diabetes was diagnosed (I-SRC-128).

4. What remains unclear?

Which mechanisms (fat in liver and muscle, inflammation, excess insulin) cause insulin resistance in humans is still debated (I-INTB-01, I-INTB-03).

5. Which studies support it?

I-INTB-03, I-SRC-127 (excess insulin can drive insulin resistance).

6. Which studies contradict it?

I-INTB-01, I-INTB-02, A-SOD-07, I-SRC-112, I-SRC-128.

7. What applies to Germany and Europe?

European diabetes guidance treats insulin resistance as a central feature of type 2 diabetes (general knowledge; not separately sourced).

8. What is known about Egypt?

Type 2 diabetes and obesity are common in Egypt; the concept applies equally there.

9. What practical conclusion is appropriate?

Insulin resistance is real and measurable. People told they have insulin resistance or prediabetes should not dismiss it; weight loss and physical activity improve it.

Assessment details

Rationale for certainty of evidence

Insulin resistance has been measured directly (clamp and glucose-tolerance methods) for decades and predicts type 2 diabetes in prospective cohorts (I-INTB-02); it is a core concept of diabetes physiology (I-INTB-01). The debate about causal direction (I-INTB-03) does not affect the existence of the phenomenon.

Source quality

Machine transcript of a live stream; wording may contain recognition errors; meaning checked in context.

Regional transferability

Universal physiology.

Individual exceptions

Degree of insulin resistance varies widely between people (genetics, fat distribution, activity, medications).

Regional scope of the claim
general (biological/medical)
Last reviewed
26 October 2026 provisional

Scientific evidence in detail

Scientifically refuted – High-quality evidence shows the opposite, or the claim contradicts well-established physiology.

Research question: Does insulin resistance (a reduced glucose-lowering response to a given amount of insulin) exist as a measurable physiological state that predicts type 2 diabetes?

Research question in detail (PECO)
Population
Adults without diabetes and people with type 2 diabetes
Intervention or exposure
Measured insulin resistance (clamp, HOMA)
Comparison
Insulin-sensitive people
Geographic scope
universal biology
Outcomes
  • Measurability of insulin resistance
  • Incident type 2 diabetes

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

What speaks for the claim?

  • High insulin levels can make the body resistant to insulin

    Del Prato S et al.. Diabetologia 1994 · PMID 7851681 · DOI 10.1007/BF00400466 Randomised controlled trialabstract checkednewly added

    Experimental infusion study in 15 healthy adults.

    Actual result
    4 days of physiological hyperinsulinaemia reduced whole-body glucose disposal by 20-40%.
    Methodological quality
    moderate (small mechanistic)
    Relevance
    indirect: supports 'high insulin drives insulin resistance'
    Limitations
    Small, short; it measures insulin resistance, so it confirms the phenomenon exists.

    Original publication

  • Does too much insulin cause insulin resistance?

    Shanik MH et al.. Diabetes Care 2008 · PMID 18227495 · DOI 10.2337/dc08-s264 Narrative reviewabstract checked

    Diabetes Care review on hyperinsulinaemia vs insulin resistance.

    Actual result
    Hyperinsulinaemia is often both a result and a driver of insulin resistance.
    Methodological quality
    low (narrative)
    Relevance
    indirect: causal-order debate
    Limitations
    Narrative.

    Original publication

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?

Insulin resistance exists and is measurable; its causes (including hyperinsulinaemia) are debated.

Why some studies weigh more

Direct clamp-based prospective studies and large cohorts outweigh narrative arguments; the hyperinsulinaemia evidence concerns cause, not existence.

Is a causal relationship established? Yes, established Existence is a measurement question, answered by clamp studies; predictive role shown prospectively.

Remaining uncertainty

Relative causal order of hyperinsulinaemia and insulin resistance.

Justified conclusion

Saying that insulin resistance does not exist is wrong; the debatable point is whether excess insulin is a driver of it.

Why do studies seem to disagree?

Del Prato (I-SRC-127) and the hyperinsulinaemia review (I-INTB-03) do not conflict with the cohorts: they address what causes insulin resistance, not whether it exists.

Does this depend on the country?
General biological effects
Universal physiology.
Eating habits
Not applicable.
Origin of the food
Not applicable.
Contaminants
Not applicable.
National production conditions
Not applicable.
Legal rules
Not applicable.
Actual monitoring data
Type 2 diabetes is common in Egypt (general).

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

Statistical re-check
  • Risk differences between insulin-action groups – 26-27 percentage-point difference in 6-y incidence; 38/200 = 19% overall recalculated
Certainty of the overall evidence (GRADE, simplified)
Main outcome
Existence and predictive value of insulin resistance
Starting level
low (observational studies)
Reasons for upgrading
  • consistent direct measurement across cohorts
  • dose-response (gradient across insulin action)
Result
high

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
  • WHO: Diabetes fact sheet (2024) · Original publication
    Type 2 diabetes 'stops the body from using insulin properly'; lifestyle changes are the best way to prevent or delay it.
  • ADA: 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes-2026 (2026) · Original publication could not be retrieved; content not used
Search strategy

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

DatabaseDateSearchLooking forHitsIncluded
Europe PMC26 October 2026(hyperinsulinemia OR hyperinsulinaemia) AND ("cause" OR driver OR primary) AND "insulin resistance" AND (humans OR human) AND (review) AND PUB_YEAR:[2018 TO 2026]supporting evidence18319
PubMed26 October 2026Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes Whitehall IIcontradicting evidence2
PubMed26 October 2026insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus prospective studies of Pima Indianscontradicting evidence1
PubMed26 October 2026glucose clamp technique method for quantifying insulin secretion and resistancecontradicting evidence19
PubMed26 October 2026prolonged physiological hyperinsulinaemia induces insulin resistance in mansupporting evidence5
Europe PMC26 October 2026TITLE:"Standards of Care in Diabetes-2026" AND (classification OR prevention)guidelines18
Europe PMC26 October 2026("insulin resistance") AND ("hyperinsulinemic-euglycemic clamp" OR "euglycaemic clamp") AND ("type 2 diabetes") AND (prospective OR incidence) AND (cohort)contradicting evidence1880
PubMed26 October 2026Del Prato S[Author] hyperinsulinaemia insulin resistance 1994 Diabetologiasupporting evidence1
WHO / ADA websites26 October 2026WHO diabetes fact sheet; ADA Standards of Care 2026 section 2 (full text 403; PMC blocked)guidelines2

Open questions

Causal order of hyperinsulinaemia and insulin resistance in humans.

How deeply was this checked?

7 linked studies: 1 checked in full text (1 of them with a structured risk-of-bias assessment), 6 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: False (high)
  2. 26 October 2026 · Phase 4 (systematic evidence review) · Re-examined with extended evidence; verdict unchanged: False (high)
    Additional prospective clamp and cohort data confirm the verdict; the hyperinsulinaemia-as-driver evidence is acknowledged as the correct part.
    New sources: I-SRC-112 I-SRC-127 I-SRC-128

In plain language

Insulin resistance means the body responds less strongly to its own insulin. Scientists can measure this, and it often appears many years before type 2 diabetes. Dr. Elawady said the term is wrong and the condition does not exist. That is not correct. He has a point that very high insulin levels may make the problem worse, and researchers still debate what comes first. But the condition itself is well documented.

Studies on this claim

Studies supporting the claim (0)

No studies in this group.

Studies contradicting or limiting the claim (5)

  • Review: how insulin works and how insulin resistance arises

    Petersen MC, Shulman GI. Physiol Rev 2018 · PMID 30067154 · DOI 10.1152/physrev.00063.2017
    Narrative reviewindependent cross-checkabstract checked

    Insulin resistance in muscle, liver and fat is a central process in type 2 diabetes; some mechanisms are still debated.

    Insulin resistance is a well-described phenomenon.

    Does the study support the specific claim? No · 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?

    Summarise insulin action and resistance

    How was the study done?

    Narrative review

    How many people, animals or samples were studied?

    Literature

    What was actually found?

    Insulin resistance is a key process in type 2 diabetes

    How large was the observed effect?

    not applicable

    What do the results mean in everyday life?

    Doctors and scientists treat insulin resistance as a real, measurable state.

    What are the study's limitations?

    Narrative; abstract only

    What does it say about Elawady's specific claim?

    Contradicts 'there is no such thing as insulin resistance'.

    Do the results apply to Germany and Europe?

    Universal physiology

    What can explicitly not be concluded from this study?

    Does not settle which mediator causes insulin resistance.

    Scientific details →

  • Insulin resistance appears years before type 2 diabetes

    Warram JH et al.. Ann Intern Med 1990 · PMID 2240915 · DOI 10.7326/0003-4819-113-12-909
    Cohort studyindependent cross-checkabstract checked★ key study

    In high-risk offspring, slow glucose clearance with high insulin levels predicted diabetes one to two decades later.

    Insulin resistance measured and predictive.

    Does the study support the specific claim? No · 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?

    Find the first defect in type 2 diabetes

    How was the study done?

    Prospective cohort with glucose tolerance tests

    How many people, animals or samples were studied?

    155 offspring of diabetic parents, 186 controls

    What was actually found?

    Slow glucose clearance and high insulin preceded diabetes

    How large was the observed effect?

    Kg 1.7 vs 2.2 %/min; second-phase insulin 329 vs 117 pM

    What do the results mean in everyday life?

    The body's reduced response to insulin can be measured long before diabetes appears.

    What are the study's limitations?

    High-risk selected group; indirect measure

    What does it say about Elawady's specific claim?

    Contradicts the claim that insulin resistance does not exist.

    Do the results apply to Germany and Europe?

    Moderate

    What can explicitly not be concluded from this study?

    Does not prove insulin resistance is the only cause of diabetes.

    Scientific details →

  • Fructose vs glucose drinks for 10 weeks

    Stanhope KL et al.. J Clin Invest 2009 · PMID 19381015 · DOI 10.1172/JCI37385
    Othercited by the Tayebat archivefull text, structured risk-of-bias assessment★ key study

    At very high doses, fructose drinks increased belly fat and worsened blood fats more than glucose drinks.

    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?

    Do fructose and glucose differ in metabolic effects during sustained consumption?

    How was the study done?

    Controlled parallel-arm intervention; beverages providing 25% of energy for 10 weeks.

    How many people, animals or samples were studied?

    32 completers (17 fructose, 15 glucose) of 39 enrolled overweight/obese adults aged 40-72

    What was actually found?

    Similar weight gain in both groups; visceral adipose volume increased only with fructose; fasting TG +~10% with glucose but not fructose; DNL, postprandial TG, apoB, LDL, small dense LDL, oxidised LDL increased with fructose; fasting glucose and insulin increased and insulin sensitivity decreased with fructose.

    How large was the observed effect?

    Visceral fat +14.0% (fructose) vs +3.2% (glucose); insulin sensitivity -17.3% vs +1.1%; apoB +27.2% vs +3.0%

    What do the results mean in everyday life?

    Very high fructose intake can harm metabolism.

    What are the study's limitations?

    Very high dose (25% of energy); small, matched (not clearly randomised) groups; completers only; many outcomes; liver fat not measured

    What does it say about Elawady's specific claim?

    Mechanistic support for C-SOD-04.

    Do the results apply to Germany and Europe?

    High (physiology).

    What can explicitly not be concluded from this study?

    That normal soda intake has these effects.

    Scientific details →

  • Insulin resistance measured directly predicts diabetes

    Lillioja S et al.. N Engl J Med 1993 · PMID 8247074 · DOI 10.1056/NEJM199312303292703
    Cohort studyindependent cross-checkabstract checked★ key study

    People whose bodies responded poorly to insulin in a clamp test were much more likely to develop diabetes.

    Clamp-measured insulin resistance predicted type 2 diabetes.

    Does the study support the specific claim? No · 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?

    Find predictors of type 2 diabetes

    How was the study done?

    Prospective cohort with clamp test

    How many people, animals or samples were studied?

    200 Pima Indians

    What was actually found?

    Insulin resistance predicted diabetes

    How large was the observed effect?

    6-y incidence 0% vs 27-39%

    What do the results mean in everyday life?

    Insulin resistance is real and measurable

    What are the study's limitations?

    One high-risk population

    What does it say about Elawady's specific claim?

    Contradicts 'no such thing'

    Do the results apply to Germany and Europe?

    Moderate

    Scientific details →

  • Insulin sensitivity falls years before diabetes

    Tabák AG et al.. Lancet 2009 · PMID 19515410 · DOI 10.1016/S0140-6736(09)60619-X
    Cohort studyindependent cross-checkabstract checked

    In 6538 British adults, those who later got diabetes showed falling insulin sensitivity in the 5 years before diagnosis.

    Insulin sensitivity declines measurably years before diabetes.

    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?

    Track metabolism before diabetes

    How was the study done?

    Cohort

    How many people, animals or samples were studied?

    6538 adults

    What was actually found?

    Insulin sensitivity fell before diagnosis

    How large was the observed effect?

    HOMA-S to 86.7%

    What do the results mean in everyday life?

    Insulin resistance is a measurable early warning sign

    What are the study's limitations?

    HOMA not clamp

    What does it say about Elawady's specific claim?

    Contradicts denial

    Do the results apply to Germany and Europe?

    High

    Scientific details →

Studies with mixed or unclear results (2)

  • Does too much insulin cause insulin resistance?

    Shanik MH et al.. Diabetes Care 2008 · PMID 18227495 · DOI 10.2337/dc08-s264
    Narrative reviewindependent cross-checkabstract checked

    Evidence suggests high insulin can be both a result and a driver of insulin resistance.

    Supports a role of excess insulin; does not deny insulin resistance.

    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?

    Examine whether insulin itself causes insulin resistance

    How was the study done?

    Narrative review

    How many people, animals or samples were studied?

    Animal and human studies

    What was actually found?

    Hyperinsulinaemia often both result and driver

    How large was the observed effect?

    not applicable

    What do the results mean in everyday life?

    Excess insulin may worsen the body's response to insulin, but the response problem is real.

    What are the study's limitations?

    Selective review; abstract only

    What does it say about Elawady's specific claim?

    Partly supports his focus on insulin; contradicts 'no such thing'.

    Do the results apply to Germany and Europe?

    Universal

    What can explicitly not be concluded from this study?

    Cannot show that insulin resistance is a wrong term.

    Scientific details →

  • High insulin levels can make the body resistant to insulin

    Del Prato S et al.. Diabetologia 1994 · PMID 7851681 · DOI 10.1007/BF00400466
    Randomised controlled trialindependent cross-checkabstract checked

    Four days of raised insulin reduced the body's response to insulin by 20-40% in healthy volunteers.

    High insulin can cause insulin resistance - a debated causal point, but the study measures insulin resistance and confirms it exists.

    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 high insulin causes insulin resistance

    How was the study done?

    Infusion experiment with clamp tests

    How many people, animals or samples were studied?

    15 healthy adults

    What was actually found?

    Insulin resistance developed

    How large was the observed effect?

    Glucose disposal -20 to -40%

    What do the results mean in everyday life?

    Too much insulin can feed the problem

    What are the study's limitations?

    Small, short

    What does it say about Elawady's specific claim?

    Supports the causal debate, not the denial of insulin resistance

    Do the results apply to Germany and Europe?

    High

    What can explicitly not be concluded from this study?

    Long-term relevance

    Scientific details →

Regional context

Germany / EU

European diabetes guidance treats insulin resistance as a central feature of type 2 diabetes (general knowledge; not separately sourced).

Egypt

Type 2 diabetes and obesity are common in Egypt; the concept applies equally there.

What applies in my country?

General scientific assessment

False This claim is false: insulin resistance is measurable and predicts type 2 diabetes; only its causes, including the role of high insulin, are debated.

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. Mechanisms of Insulin Action and Insulin Resistance.. Petersen MC, Shulman GI. Physiol Rev 2018 · PMID 30067154 · DOI 10.1152/physrev.00063.2017
  2. Slow glucose removal rate and hyperinsulinemia precede the development of type II diabetes in the offspring of diabetic parents.. Warram JH et al.. Ann Intern Med 1990 · PMID 2240915 · DOI 10.7326/0003-4819-113-12-909
  3. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.. Stanhope KL et al.. J Clin Invest 2009 · PMID 19381015 · DOI 10.1172/JCI37385
  4. Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. Prospective studies of Pima Indians.. Lillioja S et al.. N Engl J Med 1993 · PMID 8247074 · DOI 10.1056/NEJM199312303292703
  5. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study.. Tabák AG et al.. Lancet 2009 · PMID 19515410 · DOI 10.1016/S0140-6736(09)60619-X
  6. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse?. Shanik MH et al.. Diabetes Care 2008 · PMID 18227495 · DOI 10.2337/dc08-s264
  7. Effect of sustained physiologic hyperinsulinaemia and hyperglycaemia on insulin secretion and insulin sensitivity in man.. Del Prato S et al.. Diabetologia 1994 · PMID 7851681 · DOI 10.1007/BF00400466

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