Cohort studycited by the Tayebat archivefull text checked★ key study A-EGG-11 in-depth review
Eggs and deadly prostate cancer in US men
Egg, red meat, and poultry intake and risk of lethal prostate cancer in the prostate-specific antigen-era: incidence and survival.
Overview
Richman EL et al.. Cancer Prev Res (Phila) 2011 · PMID 21930800 · DOI 10.1158/1940-6207.CAPR-11-0354
Men who ate 2.5+ eggs per week had a higher rate of lethal prostate cancer (199 cases in total), but the link weakened and was not significant in a check for reverse causation.
Does the study support the specific claim? Yes · Methodological quality: moderate
Plain-language summary
Study explained simply
- What did the researchers want to find out?
Are red meat, poultry and egg intakes associated with lethal prostate cancer incidence and progression?
- How was the study done?
Prospective cohort (Health Professionals Follow-up Study) with incidence and case-only survival analyses
- How many people, animals or samples were studied?
27,607 men (incidence; 199 lethal events); 3,127 men with nonmetastatic cancer (survival; 123 events); US male health professionals
- What was actually found?
HR 1.81 (1.13-2.89) for >=2.5 vs <0.5 eggs/week; with a 2-6 year lag HR 1.50 (0.90-2.48, not significant); eggs after diagnosis HR 0.95 (no association).
- How large was the observed effect?
Cox regression; HR, 95% CI, P trend
- What do the results mean in everyday life?
A possible signal, not proof.
- What are the study's limitations?
Only 199 lethal events; low egg intake; association not robust to lagging; eggs not the main hypothesis; many foods tested; possible residual confounding (egg eaters smoked more).
- What does it say about Elawady's specific claim?
Supports the claim as an association.
- Do the results apply to Germany and Europe?
Moderate.
- What can explicitly not be concluded from this study?
Cannot prove that eggs cause prostate cancer.
Scientific in-depth review
1. Full reference
- Authors
- Richman EL, Kenfield SA, Stampfer MJ, Giovannucci EL, Chan JM
- Journal
- Cancer Prev Res (Phila)
- Year
- 2011
- Identifier
- PMID 21930800 DOI 10.1158/1940-6207.CAPR-11-0354 · PMC3232297
- Verification
- verified – PubMed E-utilities efetch, 2026-10-25
- Retracted
- no
- Corrections
- none
- Extent checked
- full text
- Conflicts of interest and funding
NIH grants (R01 CA141298-02, R25 CA098566, R01 CA55075, P01 CA055075-19); no conflicts of interest disclosed.
2. Research question
Are red meat, poultry and egg intakes associated with lethal prostate cancer incidence and progression?
3. Study design and population
- Study design
- Cohort study – Prospective cohort (Health Professionals Follow-up Study) with incidence and case-only survival analyses
- Population
US male health professionals in the Health Professionals Follow-up Study, free of cancer in 1994 and reporting a PSA test (PSA era); case-only analysis of men diagnosed with clinically localised or regional prostate cancer after 1994
- Country
USA
- Period
1994-2008
- Sample size
27,607 men (199 lethal events, 306,715 person-years); 3,127 men with non-metastatic prostate cancer (123 events, 19,354 person-years)
- Inclusion and exclusion criteria
Excluded: inadequate baseline FFQ (<800 or >4200 kcal/d or >70 items missing), cancer (except non-melanoma skin) before 1994, no reported PSA test; case-only analysis additionally excluded stage T3b+ and unknown stage/treatment.
4. Methods and endpoints
- Exposure / intervention
Cumulative average intake of eggs (one egg with yolk), total/processed/unprocessed red meat and poultry from semi-quantitative FFQs (1986 onwards, every 4 years); FFQ validity vs diet records r=0.76 for eggs
- Comparator
<0.5 eggs/week
- Endpoints
Lethal prostate cancer (metastases or prostate cancer death)
- Statistical methods
Cox regression stratified by age, calendar time as time scale; Model 2 adjusted for age, energy, BMI, smoking, vigorous activity, lycopene (meats mutually adjusted and adjusted for eggs); other potential confounders (race, family history, diabetes, PSA screening frequency, statins, dairy, fish, tomato, calcium, coffee) dropped by a <10%-change rule; p-trend by category medians; sensitivity analyses with 2-6 year lag and excluding missing items; no multiplicity correction.
5. Actual results
- Results
Eggs (incidence, Model 2): vs <0.5/week, HR 1.33 (0.85-2.07), 1.49 (0.93-2.37) and 1.81 (1.13-2.89) for successively higher categories up to >=2.5/week; p-trend 0.01 (events 30/64/50/55). Lagged sensitivity analysis: HR 1.50 (0.90-2.48), p-trend 0.14 (not significant). Excluding missing items: HR 1.81 (1.13-2.91). Unprocessed red meat: HR 0.64 (0.38-1.06) for >=5 vs <2 servings/week (p-trend 0.03, inverse, contrary to hypothesis). No other meat or poultry group associated with incidence. Case-only: post-diagnostic eggs HR 0.95 (0.55-1.64); post-diagnostic poultry HR 1.69 (0.96-2.99), p-trend 0.07; processed red meat HR 1.45 (0.73-2.87), p-trend 0.08.
- Absolute risks
Overall 199 lethal events in 306,715 person-years (~0.65 per 1,000 person-years); category-specific absolute rates not reported in full text.
- Authors' conclusion
Consumption of eggs may increase risk of developing lethal prostate cancer among healthy men.
6. Strengths
- Large prospective cohort with repeated FFQs and cumulative-average exposure
- Specific clinically important outcome (metastasis or prostate cancer death), deaths ascertained >98%
- PSA-screened population reduces detection bias
- Sensitivity analyses reported, including unfavourable lagged result
7. Weaknesses
- Few events (199; 55 in the top egg category); low egg consumption limits power, as authors note
- Egg association attenuated and non-significant with 2-6 year lag (HR 1.50, 0.90-2.48), raising reverse-causation/instability concerns
- Eggs were not the a priori hypothesis for incidence (red meat was); several foods and items tested without multiplicity correction
- Higher egg eaters smoked more and had more diabetes and family history; covariates dropped by change-in-estimate rule; residual confounding possible
- Post-diagnostic egg intake not associated with progression (HR 0.95)
- Health professionals, mostly white US men: limited generalisability
8. Risk of bias
- Orienting tool
- ROBINS-E
- Type of assessment
- structured assessment based on the full text by a single reviewer (no formal double review)
- Full formal assessment
- no
- Overall risk of bias
- some concerns
- Rationale
Unchanged (some_concerns); full text adds that the egg association is not robust to lagging. Single-reviewer structured judgement; a formal ROBINS-E needs two independent reviewers and the protocol.
| Domain | Judgement | Rationale |
|---|---|---|
| Confounding | some concerns | Adjusted for age, energy, BMI, smoking, activity, lycopene; egg eaters differed in smoking, diabetes and family history; several covariates omitted by a <10% change rule. |
| Exposure measurement | some concerns | Validated FFQ (r=0.76 for eggs), cumulative averages; missing items assumed not consumed (sensitivity analysis unchanged). |
| Selection of participants | some concerns | Restricted to men reporting PSA testing; health-professional cohort. |
| Post-exposure interventions | not applicable | Not applicable to incidence analysis; treatment adjusted in case-only analysis. |
| Missing data | low | Response >94%; death ascertainment >98%. |
| Outcome measurement | low | Lethal outcome (M1 or prostate cancer death) from records and death certificates reviewed by physicians; 83% of cases medically confirmed, unconfirmed included. |
| Selection of reported result | some concerns | Many foods/items tested without correction; egg-incidence association not the primary hypothesis; lagged analysis attenuated (reported transparently). |
Full-text review (25 October 2026): Added exclusion criteria, covariates and confounder-selection rule, egg category HRs and events, lagged sensitivity HR 1.50 (0.90-2.48, p-trend 0.14), post-diagnostic egg HR 0.95, red meat inverse finding, absolute rate, NIH funding; bias unchanged; archive derivation refined.
9. Assessment of the statistical interpretation
A single-cohort relative association with wide CI and modest trend; it loses significance in the lagged analysis, and absolute risk is low (~0.65 lethal cases per 1,000 person-years overall). The finding is hypothesis-generating rather than confirmatory.
10. Relevance to the specific claim
11. Independent contrary findings
I-EGG-09 (no association with total prostate cancer; small-study effects).
12. Transferability to Germany and Europe
Moderate.
13. Overall methodological judgement
Accurately cited but fragile single-cohort signal: highest egg intake was associated with an 81% higher hazard of lethal prostate cancer, but the association weakened and became non-significant with a lag, egg intake after diagnosis showed no association, and eggs were not the primary hypothesis.
| Multidimensional assessment | |
|---|---|
| Authenticity of the source | verified |
| Methodological quality | moderate |
| Risk of bias | some concerns |
| Precision of results | low |
| Directness | direct |
| Reproducibility | partly replicated |
| Consistency with the overall evidence | mixed |
| Regional transferability | moderate |
| Adequacy of the interpretation (by the archive) | essentially correct but incomplete |
14. Open questions
Replication in larger cohorts.
15. Linked fact checks
- Eating 2.5 or more eggs per week is associated with an 81% higher risk of lethal prostate cancer. – Studies supporting the claim
Use by the Tayebat archive
Note: according to the archive, the studies were compiled by the archive operators. Whether Dr. Elawady himself cited this study is not established.
- What the archive says about the study
In 27,607 men, eating 2.5 or more eggs per week was associated with an 81% higher risk of lethal prostate cancer.
- A. What was actually studied?
Egg/meat intake and lethal prostate cancer.
- B. What did the authors find?
HR 1.81 (1.13-2.89) for >=2.5 vs <0.5 eggs/week (55 events in top category); attenuated to HR 1.50 (0.90-2.48) in a lagged sensitivity analysis; post-diagnostic eggs HR 0.95.
- C. What conclusions do the authors themselves draw?
Eggs may increase risk.
- D. What does the archive derive from it?
Used as epidemiological signal against eggs.
- E. Is this derivation scientifically justified?
Numerically correct, but omits that the result rests on 199 events, became non-significant in the authors' lagged sensitivity analysis, was not seen for post-diagnostic egg intake, and is an association in one cohort.
- Adequacy of the interpretation (by the archive)
- essentially correct but incomplete