Insulin is the single and only cause of obesity (local or generalised) because it is the only hormone that builds fat and blocks fat breakdown (lipolysis).
Original statement
الانسولين هو السبب الوحيد الاوحد للسمنه موضعيه كانت او الابديمه متحجره متحشره الانسولين يا باشا الهرمون الوحيد الذي يكون الدهون
verbatim according to source. Translation by the project; the Arabic wording is authoritative.
Translation
Insulin is the single and only cause of obesity (local or generalised) because it is the only hormone that builds fat and blocks fat breakdown (lipolysis).
Origin
- Source status
- Video transcript (own words)
- Attribution
- Elawady (machine transcript)
- Video
- المفاهيم المضللة عن الإنسولين ومغالطات شائعه حول الإنسولين #ضياء_العوضي (Open source)
- Published
- 17 April 2026
- Timestamp
- 0:05:21 (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; 'published' is the date listed by the archive and may be the upload date. Live-stream transcripts can contain viewer comments read aloud; the quoted passage was checked in context to be spoken by Elawady.
- Claimed mechanism
Insulin inhibits lipolysis and promotes fat storage; therefore insulin alone causes obesity.
- Claimed health effect
Obesity; also: insulin treatment makes people fat.
- Population concerned
General population; people with diabetes treated with insulin
- Geographic restriction by Elawady
none found
Diverging source versions
- 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's 'د. ضياء يقول' box gives no video reference; wording is the archive's paraphrase.
لك السمنه هي اللي ورا السكر السمنه هي اللي ورا السكر طب اذا كان يروح امك الانسولين هو الهرمون الوحيد المسبب للسمنه ها يعني شوف المفاجاه بقى الصادمه الصادمه اللي هي بتقول
Insulin is the only hormone that causes obesity; obesity is not what causes diabetes.
- Source status
- Video transcript (own words)
- Attribution
- Elawady (machine transcript)
- Video
- بدأت قناة ＂Dr Diaa Al Awady د ضياء العوضي＂ بثًا مباشرًا تصليح مفاهيم (Open source)
- Published
- 31 March 2026
- Timestamp
- 1:05:27 (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; 'published' is the date listed by the archive and may be the upload date. Live-stream transcripts can contain viewer comments read aloud; the quoted passage was checked in context to be spoken by Elawady.
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 is the sole cause of all obesity and the only hormone that forms fat and blocks lipolysis.
2. What is demonstrably correct?
Insulin is the main anabolic hormone of fat tissue: it suppresses lipolysis and promotes fat storage. Starting or intensifying insulin therapy in type 2 diabetes causes weight gain: in UKPDS 33 patients assigned insulin gained 4.0 kg vs 1.7-2.6 kg with sulfonylureas (A-INS-16); weight gain rises with insulin dose and intensity (A-INS-17, A-INS-18).
3. What is wrong or exaggerated?
'Only cause' is not supported. Obesity is multifactorial (energy intake, food environment, ultra-processed foods, genetics, sleep, medications, physical activity). In a metabolic-ward crossover study, cutting dietary fat (which barely changes insulin) produced more body-fat loss (89 g/day) than cutting carbohydrate (53 g/day) even though carbohydrate restriction lowered insulin (I-INS-09). Other hormones (cortisol excess, hypothyroidism, sex hormones, leptin deficiency) and drugs also influence fat mass. People with type 1 diabetes and absent insulin lose weight and fat rapidly, which shows insulin is needed to store fat but does not show it is the only cause of obesity. In a related passage (3j32fjfYRbU) he argues against the view that obesity is behind type 2 diabetes. This is contradicted by randomised evidence: in DiRECT, a weight-management programme led to diabetes remission in 46% vs 4% of controls, and remission rose with the amount of weight lost (86% with >=15 kg) (I-FAST-12).
4. What remains unclear?
The relative weight of insulin-driven mechanisms versus energy intake in long-term human obesity (the 'carbohydrate-insulin model' versus the 'energy balance model') is still debated in the literature; this debate does not support the 'only cause' wording.
5. Which studies support it?
A-INS-16, A-INS-17, A-INS-18 (weight gain with insulin therapy, dose-related); A-INS-19 (metformin reduces insulin dose and weight gain); I-INS-120 (mice with prevented hyperinsulinaemia protected from diet-induced obesity); partly I-INS-118 (low-carbohydrate diet raised energy expenditure during weight maintenance).
6. Which studies contradict it?
I-INS-09 (fat restriction > carbohydrate restriction for fat loss at equal calories); I-INS-117 (meta-analysis of 32 controlled feeding studies); I-INS-119 (higher-insulin low-fat diet reduced intake by about 690 kcal/day); I-SYS-05 (DIETFITS: no effect modification by insulin secretion).
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?
Weight gain is a real side effect of insulin therapy in type 2 diabetes and is a reason to use the lowest effective dose and to prefer weight-neutral or weight-reducing drugs where appropriate. It is not a reason to see insulin as the cause of all obesity or to stop prescribed insulin.
Assessment details
- Rationale for certainty of evidence
Physiology (insulin is anti-lipolytic and lipogenic) and weight gain under insulin therapy are well established in RCTs and meta-analyses (high certainty). The claim that insulin is the only cause of obesity is contradicted by controlled feeding studies showing that body-fat loss depends on energy balance more than on insulin lowering (moderate certainty; few, short metabolic-ward studies).
- Source quality
Own words in a machine transcript (verbatim); archive paraphrase consistent.
- Regional transferability
Physiology is universal.
- Individual exceptions
Some people gain more weight on insulin than others; weight gain depends on dose and regimen (A-INS-17).
- 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: Is insulin the single cause of obesity, and the only hormone that builds fat and blocks lipolysis?
Research question in detail (PECO)
- Population
- Adults with and without diabetes
- Intervention or exposure
- Insulin (endogenous hyperinsulinaemia; dietary carbohydrate; insulin therapy)
- Comparison
- Lower insulin exposure at equal energy intake
- Geographic scope
- universal biology
- Outcomes
- Body fat / weight
- Energy expenditure and intake
Study results as reported by the authors. Our assessment follows below.
What speaks for the claim?
UKPDS: tablets or insulin for new type 2 diabetes
UKPDS 33: weight gain with insulin therapy.
- Actual result
- +4.0 kg with insulin vs 1.7-2.6 kg with sulfonylureas.
- Methodological quality
- high (RCT)
- Relevance
- direct for 'insulin therapy causes weight gain'
- Limitations
- Does not address other causes of obesity.
Low-carbohydrate diets and calories burned after weight loss
Ebbeling CB et al.. BMJ 2018 · PMID 30429127 · DOI 10.1136/bmj.k4583 Randomised controlled trialabstract checkednewly addedLow-carbohydrate diet increased energy expenditure during weight maintenance, most in high insulin secretors.
- Actual result
- +209 kcal/d (91-326) low vs high carbohydrate.
- Methodological quality
- moderate (RCT; analyses debated)
- Relevance
- indirect
- Limitations
- Not replicated; does not show exclusivity.
Mice that cannot overproduce insulin do not get fat on a high-fat diet
Mehran AE et al.. Cell Metab 2012 · PMID 23217255 · DOI 10.1016/j.cmet.2012.10.019 Animal studyabstract checkednewly addedMice with genetically prevented hyperinsulinaemia were protected from diet-induced obesity.
- Actual result
- Complete protection from diet-induced obesity.
- Methodological quality
- moderate (animal genetics)
- Relevance
- very indirect (mice)
- Limitations
- Animal model.
What speaks against the claim?
Calories, carbohydrates and body fat in controlled feeding studies
Hall KD, Guo J. Gastroenterology 2017 · PMID 28193517 · DOI 10.1053/j.gastro.2017.01.052 Meta-analysisabstract checkednewly addedMeta-analysis of 32 controlled feeding studies.
- Actual result
- Lower-fat diets: +26 kcal/d expenditure and +16 g/d fat loss vs lower-carbohydrate at equal calories.
- Methodological quality
- moderate
- Relevance
- direct
- Limitations
- Short studies.
Low-fat plant diet versus ketogenic animal diet: how much people eat
Hall KD et al.. Nat Med 2021 · PMID 33479499 · DOI 10.1038/s41591-020-01209-1 Randomised controlled trialabstract checkednewly addedInpatient crossover: low-fat (higher insulin) vs ketogenic diet.
- Actual result
- 689 kcal/d less intake on low-fat diet.
- Methodological quality
- moderate (RCT, small)
- Relevance
- direct
- Limitations
- 2 weeks per diet.
Low-fat and low-carb diets led to similar weight loss
Gardner CD et al.. JAMA 2018 · PMID 29466592 · DOI 10.1001/jama.2018.0245 Randomised controlled trialabstract checkedDIETFITS: 12-month weight loss did not differ by diet or by insulin secretion.
- Actual result
- -5.3 vs -6.0 kg; no insulin-secretion interaction.
- Methodological quality
- high (RCT, n=609)
- Relevance
- direct test of insulin-secretion effect modification
- Limitations
- Free-living adherence.
What does the overall evidence say?
Editorial assessment based on the studies above – not itself a study result.
Which position is better supported?
Insulin promotes fat storage and insulin therapy causes weight gain, but obesity is multifactorial; insulin is not the only cause.
Why some studies weigh more
Human RCTs and controlled feeding outweigh animal data; supporting human data show a role, not exclusivity.
Is a causal relationship established? Probable Insulin's lipogenic, anti-lipolytic action is established; a contributory causal role in obesity is plausible; 'only cause' is not supported.
Remaining uncertainty
Relative weight of the carbohydrate-insulin model vs energy-balance model in long-term human obesity.
Justified conclusion
Mostly false as stated.
Why do studies seem to disagree?
Ebbeling 2018 (supporting) and Hall 2017/2021 (contradicting) differ in phase (weight maintenance vs controlled feeding/ad libitum intake), duration and analytic choices; neither supports 'only cause'.
Does this depend on the country?
- General biological effects
- Insulin physiology, autoimmune type 1 diabetes and ketoacidosis are universal human biology.
- Eating habits
- Applies to Egyptian and European diets alike.
- 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
- Magnitude of effect – Differences of 26 kcal/d and 16 g/d fat are small; direction opposes the insulin-only hypothesis not recalculable from the published data
Certainty of the overall evidence (GRADE, simplified)
- Main outcome
- Body fat change when insulin is lowered at equal energy intake
- Starting level
- high (randomised trials)
- Reasons for downgrading
- indirectness (short-term feeding studies)
- inconsistency (Ebbeling 2018)
- 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: 8. Obesity and Weight Management: Standards of Care in Diabetes-2026 (2026) · Original publication
Sustained loss of >10% body weight may lead to remission of type 2 diabetes (A); weight loss reduces the need for glucose-lowering drugs, particularly insulin.
Search strategy
Documented literature searches for this review (search strings in the original database syntax).
| Database | Date | Search | Looking for | Hits | Included |
|---|---|---|---|---|---|
| Europe PMC | 26 October 2026 | (TITLE:"insulin") AND (TITLE:"obesity" OR TITLE:"adiposity") AND (TITLE:"cause" OR TITLE:"causal" OR TITLE:"hyperinsulinemia drives") | supporting evidence | 29 | |
| Europe PMC | 26 October 2026 | "carbohydrate-insulin model" AND (TITLE:"obesity") AND PUB_YEAR:[2018 TO 2026] | supporting evidence | 72 | |
| PubMed | 26 October 2026 | Ebbeling CB[au] AND "energy expenditure" AND BMJ[ta] | supporting evidence | 1 | |
| PubMed | 26 October 2026 | "insulin therapy" AND "weight gain" AND "type 2 diabetes" AND meta-analysis[pt] | supporting evidence | 19 | |
| PubMed | 26 October 2026 | "carbohydrate-insulin model" AND (randomized OR meta-analysis) AND (energy expenditure OR body fat) | both directions | 7 | |
| PubMed | 26 October 2026 | Hall KD[au] AND Guo J[au] AND "Obesity Energetics" | contradicting evidence | 1 | |
| PubMed | 26 October 2026 | Hall KD[au] AND (plant-based OR "animal-based") AND ketogenic AND Nat Med[ta] | contradicting evidence | 1 |
How deeply was this checked?
11 linked studies: 1 checked in full text (1 of them with a structured risk-of-bias assessment), 10 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
- 25 October 2026 · Phase 1 · Initial assessment: Mostly false (moderate)
- 26 October 2026 · Phase 4 (systematic evidence review) · Re-examined with extended evidence; verdict unchanged: Mostly false (moderate)
New supporting (Ebbeling 2018, Mehran 2012) and contradicting (Hall 2017, Hall 2021, DIETFITS reused) evidence keeps the balance: insulin has a role, but 'only cause' is not supported.
New sources: I-INS-117 I-INS-118 I-INS-119 I-INS-120
In plain language
Insulin is a storage hormone and it does help the body store fat. People who start insulin for type 2 diabetes often gain a few kilograms. But obesity has many causes, and studies show that eating fewer calories reduces body fat even when insulin hardly changes. So insulin is one factor among many, not the only cause.
Studies on this claim
Studies supporting the claim (5)
-
UKPDS: tablets or insulin for new type 2 diabetes
UKPDS Group. Lancet 1998 · PMID 9742976Randomised controlled trialcited by the Tayebat archiveabstract checked★ key studyBetter 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.
-
Weight gain with insulin
Pontiroli AE et al.. Diabetes Obes Metab 2011 · PMID 21645195 · DOI 10.1111/j.1463-1326.2011.01433.xMeta-analysiscited by the Tayebat archiveabstract checkedThe more intensive the insulin treatment, the more weight people gain in the first year.
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?
Weight increase in first year of insulin treatment and predictors
- How was the study done?
Systematic review and meta-analysis of 46 RCTs
- How many people, animals or samples were studied?
46 RCTs; Type 2 diabetes starting/intensifying insulin
- What was actually found?
Weight gain related to intensity and regimen.
- How large was the observed effect?
not reported in abstract
- What do the results mean in everyday life?
Weight gain is a real insulin side effect.
- What are the study's limitations?
Effect sizes not in abstract; Heterogeneous trials
- What does it say about Elawady's specific claim?
Supports weight-gain kernel of C-INS-01.
- Do the results apply to Germany and Europe?
International.
- What can explicitly not be concluded from this study?
That insulin causes obesity in general.
-
Intensive insulin in 14 patients
Henry RR et al.. Diabetes Care 1993 · PMID 8422777 · DOI 10.2337/diacare.16.1.21Case series / case reportcited by the Tayebat archiveabstract checkedBlood sugar normalised but patients gained almost 9 kg in six months.
Does the study support the specific claim? Partly · Methodological quality: very 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?
Metabolic effects of intensive conventional insulin in type 2 diabetes
- How was the study done?
Uncontrolled 6-month clinical study
- How many people, animals or samples were studied?
14; Type 2 diabetes outpatients
- What was actually found?
Glucose improved; +8.7 kg.
- How large was the observed effect?
+8.7 kg
- What do the results mean in everyday life?
Insulin works but can cause substantial weight gain.
- What are the study's limitations?
n=14; No control; 1993 regimen
- What does it say about Elawady's specific claim?
Kernel of C-INS-01.
- Do the results apply to Germany and Europe?
Old US regimen.
- What can explicitly not be concluded from this study?
General conclusions.
-
Adding metformin to insulin
Wulffelé MG et al.. Diabetes Care 2002 · PMID 12453950 · DOI 10.2337/diacare.25.12.2133Randomised controlled trialcited by the Tayebat archiveabstract checkedMetformin improved sugar control and reduced insulin need and weight gain.
Does the study support the specific claim? Yes · 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?
Metformin added to intensive insulin in type 2 diabetes
- How was the study done?
Double-blind placebo-controlled RCT
- How many people, animals or samples were studied?
390; Insulin-treated type 2 diabetes
- What was actually found?
Better control, less insulin, less weight gain.
- How large was the observed effect?
GHb -0.7%
- What do the results mean in everyday life?
Combination lowers insulin needs.
- What are the study's limitations?
Short duration; Dropouts higher with metformin
- What does it say about Elawady's specific claim?
- Do the results apply to Germany and Europe?
Dutch data.
- What can explicitly not be concluded from this study?
That insulin can be stopped.
-
Mice that cannot overproduce insulin do not get fat on a high-fat diet
Mehran AE et al.. Cell Metab 2012 · PMID 23217255 · DOI 10.1016/j.cmet.2012.10.019Animal studyindependent cross-checkabstract checked★ key studyMice genetically prevented from producing excess insulin were protected from diet-induced obesity.
Animal evidence that high insulin drives diet-induced obesity (role, not exclusivity).
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 obesity in mice.
- How was the study done?
Genetic mouse experiment.
- How many people, animals or samples were studied?
Mice.
- What was actually found?
Less insulin = no diet-induced obesity.
- How large was the observed effect?
Not applicable.
- What do the results mean in everyday life?
Insulin can promote fat gain, at least in mice.
- What are the study's limitations?
Animal study.
- What does it say about Elawady's specific claim?
Partly supports a role of insulin; not 'only cause' in humans.
- Do the results apply to Germany and Europe?
Not directly transferable.
- What can explicitly not be concluded from this study?
Cannot show insulin is the only cause of human obesity.
No study in this group is marked as key.
Studies contradicting or limiting the claim (5)
-
Low-fat vs low-carb in a metabolic ward
Hall KD et al.. Cell Metab 2015 · PMID 26278052 · DOI 10.1016/j.cmet.2015.07.021Randomised controlled trialindependent cross-checkfull text, structured risk-of-bias assessmentCutting fat led to more fat loss than cutting carbs, even though cutting carbs lowered insulin more.
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 carbohydrate restriction (lower insulin) cause more fat loss than fat restriction at equal calories?
- How was the study done?
Randomised crossover metabolic-ward study
- How many people, animals or samples were studied?
19 adults with obesity randomised (17 completed both diets)
- What was actually found?
Fat loss 89 g/day on reduced-fat vs 53 g/day on reduced-carbohydrate (463 g vs 245 g over 6 days), although only the low-carb diet lowered insulin (by 22%).
- How large was the observed effect?
+36 g/day with fat restriction
- What do the results mean in everyday life?
Calories matter; insulin is not the only driver.
- What are the study's limitations?
Only 6 days per diet; small sample; fat loss was a secondary outcome; long-term predictions come from a computer model; moderate (not very-low) carbohydrate restriction.
- What does it say about Elawady's specific claim?
Contradicts C-INS-01 ('insulin the only cause of fat').
- Do the results apply to Germany and Europe?
Physiology transferable.
- What can explicitly not be concluded from this study?
Long-term weight outcomes.
-
DiRECT: weight loss to put type 2 diabetes into remission
Lean ME et al.. Lancet 2018 · PMID 29221645 · DOI 10.1016/S0140-6736(17)33102-1Randomised controlled trialindependent cross-checkabstract checked★ key study46% of people in the programme were free of diabetes and medication after one year.
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?
Can intensive weight management in primary care achieve T2D remission?
- How was the study done?
Open-label cluster-randomised trial (DiRECT)
- How many people, animals or samples were studied?
306 (149 per group ITT); 49 practices; Age 20-65, T2D <6 years, BMI 27-45, not on insulin
- What was actually found?
Remission 46% vs 4%.
- How large was the observed effect?
OR 19.7
- What do the results mean in everyday life?
Losing 10-15 kg can reverse early type 2 diabetes.
- What are the study's limitations?
Open-label; Selected population; Formula diet
- What does it say about Elawady's specific claim?
Supports C-DIAB-03 (with conditions); limited relevance to C-INS-10 (insulin users excluded).
- Do the results apply to Germany and Europe?
UK; directly relevant.
- What can explicitly not be concluded from this study?
Effect of the Tayebat diet; effect in type 1 or insulin-treated diabetes.
-
Low-fat and low-carb diets led to similar weight loss
Gardner CD et al.. JAMA 2018 · PMID 29466592 · DOI 10.1001/jama.2018.0245Randomised controlled trialindependent cross-checkabstract checkedAfter a year, weight loss was 5.3 kg vs 6.0 kg - no real difference.
Does the study support the specific claim? Yes · 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?
Compare diets.
- How was the study done?
RCT.
- How many people, animals or samples were studied?
609.
- What was actually found?
No difference.
- How large was the observed effect?
0.7 kg.
- What do the results mean in everyday life?
Total diet quality and quantity matter more than fat share.
- What are the study's limitations?
Adherence.
- What does it say about Elawady's specific claim?
Supports 'fat is not the origin'.
- Do the results apply to Germany and Europe?
High.
- What can explicitly not be concluded from this study?
Long-term weight maintenance.
-
Calories, carbohydrates and body fat in controlled feeding studies
Hall KD, Guo J. Gastroenterology 2017 · PMID 28193517 · DOI 10.1053/j.gastro.2017.01.052Meta-analysisindependent cross-checkabstract checked★ key studyWhen calories were fixed, cutting fat led to slightly more fat loss than cutting carbohydrate, even though carbohydrate cuts lower insulin.
At equal calories, lower-fat diets gave slightly more fat loss despite higher insulin.
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?
Test whether lowering insulin via low-carbohydrate diets increases fat loss.
- How was the study done?
Meta-analysis of 32 controlled feeding studies.
- How many people, animals or samples were studied?
Adults in metabolic studies.
- What was actually found?
Lower-fat diets: +26 kcal/d expenditure, +16 g/d fat loss.
- How large was the observed effect?
Small effects.
- What do the results mean in everyday life?
Insulin is one factor, but calories matter.
- What are the study's limitations?
Short studies.
- What does it say about Elawady's specific claim?
Contradicts 'insulin is the only cause of obesity'.
- Do the results apply to Germany and Europe?
Applicable.
- What can explicitly not be concluded from this study?
Cannot settle long-term diet debates.
-
Low-fat plant diet versus ketogenic animal diet: how much people eat
Hall KD et al.. Nat Med 2021 · PMID 33479499 · DOI 10.1038/s41591-020-01209-1Randomised controlled trialindependent cross-checkabstract checked★ key studyOn a high-carbohydrate low-fat diet people ate about 690 fewer calories per day than on a ketogenic diet.
Higher-insulin low-fat diet reduced intake by about 690 kcal/day.
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?
Test the carbohydrate-insulin model on food intake.
- How was the study done?
Inpatient crossover trial.
- How many people, animals or samples were studied?
20 adults.
- What was actually found?
Low-fat diet: 689 kcal/d less intake.
- How large was the observed effect?
-689 kcal/d.
- What do the results mean in everyday life?
Insulin is not the only factor in weight gain.
- What are the study's limitations?
Short and small.
- What does it say about Elawady's specific claim?
Contradicts 'insulin is the only cause of obesity'.
- Do the results apply to Germany and Europe?
Applicable.
- What can explicitly not be concluded from this study?
Cannot predict long-term weight change.
No study in this group is marked as key.
Studies with mixed or unclear results (1)
-
Low-carbohydrate diets and calories burned after weight loss
Ebbeling CB et al.. BMJ 2018 · PMID 30429127 · DOI 10.1136/bmj.k4583Randomised controlled trialindependent cross-checkabstract checked★ key studyPeople on a low-carbohydrate diet burned about 200 more calories per day than on a high-carbohydrate diet while keeping weight off.
Supports a role of carbohydrate/insulin in energy expenditure; does not support 'only cause'.
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 diet carbohydrate and energy expenditure.
- How was the study done?
Randomised trial over 20 weeks.
- How many people, animals or samples were studied?
164 adults after weight loss.
- What was actually found?
Low-carb: +209 kcal/d.
- How large was the observed effect?
52 kcal/d per 10% less carbohydrate.
- What do the results mean in everyday life?
Insulin may play some role in weight regulation.
- What are the study's limitations?
Results debated; correction published.
- What does it say about Elawady's specific claim?
Partly supports a role of insulin, not 'only cause'.
- Do the results apply to Germany and Europe?
Applicable.
- What can explicitly not be concluded from this study?
Cannot show insulin is the only cause.
No study in this group is marked as key.
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 Insulin promotes fat storage and insulin therapy causes weight gain, but it is not the only cause of obesity.
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
- 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
- Increase of body weight during the first year of intensive insulin treatment in type 2 diabetes: systematic review and meta-analysis.. Pontiroli AE et al.. Diabetes Obes Metab 2011 · PMID 21645195 · DOI 10.1111/j.1463-1326.2011.01433.x
- Intensive conventional insulin therapy for type II diabetes. Metabolic effects during a 6-mo outpatient trial.. Henry RR et al.. Diabetes Care 1993 · PMID 8422777 · DOI 10.2337/diacare.16.1.21
- Combination of insulin and metformin in the treatment of type 2 diabetes.. Wulffelé MG et al.. Diabetes Care 2002 · PMID 12453950 · DOI 10.2337/diacare.25.12.2133
- Hyperinsulinemia drives diet-induced obesity independently of brain insulin production.. Mehran AE et al.. Cell Metab 2012 · PMID 23217255 · DOI 10.1016/j.cmet.2012.10.019
- Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss than Carbohydrate Restriction in People with Obesity.. Hall KD et al.. Cell Metab 2015 · PMID 26278052 · DOI 10.1016/j.cmet.2015.07.021
- Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial.. Lean ME et al.. Lancet 2018 · PMID 29221645 · DOI 10.1016/S0140-6736(17)33102-1
- Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion: The DIETFITS Randomized Clinical Trial.. Gardner CD et al.. JAMA 2018 · PMID 29466592 · DOI 10.1001/jama.2018.0245
- Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition.. Hall KD, Guo J. Gastroenterology 2017 · PMID 28193517 · DOI 10.1053/j.gastro.2017.01.052
- Effect of a plant-based, low-fat diet versus an animal-based, ketogenic diet on ad libitum energy intake.. Hall KD et al.. Nat Med 2021 · PMID 33479499 · DOI 10.1038/s41591-020-01209-1
- Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial.. Ebbeling CB et al.. BMJ 2018 · PMID 30429127 · DOI 10.1136/bmj.k4583