Cutoff: 9 October 2026. Consensus supports discovery and checks of specific source aspects; it is not a primary study, a full-paper audit or a causal probability meter.
The original clinical cohort reports the early-gestation association with a small exposed group and wide interval; mid/late groups are not increased. This is a valid natural-experiment lead with a mapped window, not uniform famine proof. Original PMID11083734. Access: abstract_metadata.
The original Dutch Families report includes time and sibling controls and finds no increased CAD or ECG risk. It is a distinct cohort contrast, retained alongside the positive Amsterdam series. Original PMID22895645. Access: abstract_metadata.
The original primary abstract reports higher offspring diabetes/BMI after maternal diagnosis, with paternal-diagnosis comparisons null. This strengthens restricted prenatal human causality beyond a birthweight association, while maternal age and birth order remain. Original PMID11118027. Access: abstract_metadata.
Original Results separates transmission from maternal intrauterine effects: maternal lower-birthweight genetic score does not raise adult offspring SBP after fetal adjustment. Its original GWAS/conditional analyses are examined; genetic birthweight cannot simply be renamed nutritional deprivation. Original PMID31043758. Access: full_text_partial.
The original thirty-year RCT follow-up finds no clinical CVD/diabetes or BP/lipid difference despite altered OGTT markers. Specific regimen, retention and horizon limits remain; a biomarker signal is not clinical disease programming. Original PMID15924982. Access: abstract_metadata.
The original Methods defines the Hyderabad trial as nonrandomized, implemented by administrative block, with maternal supplementation and food through childhood. Adult risk-factor nulls cannot be represented as a prenatal-only randomized clinical trial. Original PMID32692751. Access: full_text_partial.
The original updated primary reports no significant measured BMI-PGI difference. This constrains a specific genetic-selection mechanism, without excluding every non-genetic conception, survival or follow-up selection process. Its earlier preprint is not counted twice. Original PMID39358993. Access: abstract_metadata.
Original abstract reports cohort Cox hazard ratios separately from factorial MR. The quoted5.16diabetes hazard ratio is observational. Birthweight genetics is not a direct prenatal nutrition instrument; HBW is at least2.5kg, not macrosomia. The issue-year2026 differs from the provider's2025dating, so date type must be stated. Original PMID39913677. Access: abstract_metadata.
Original study includes both time and sibling controls, finds women but not men affected, no gestational-window association and no HDL effect. These are lipid markers, not directly observed coronary events; triglycerides attenuate under adiposity adjustment. Original PMID19386743. Access: abstract_metadata.
Consensus was used to identify literature and cross-check specific claims about design, endpoints, scope and research gaps. Those aspects were checked against original primary abstracts/status records and selected original Methods/Results passages. Consensus output was not treated as original full text. Provider search omissions are not evidence that a study does not exist. Source access and examination receipts are retained. Scite use or monthly unavailability is recorded per case; provider citation counts do not change causal grades.