Bibliographic record
Abstract
Peanut allergy is estimated to affect 1% to 3% of the population (1) and its prevalence has substantially increased in the past 10 to 15 years (2). It is the leading cause of anaphylaxis and death related to food allergy (3). Recent studies have explored the relationship between dietary introduction and prevention of peanut allergy. In 2008, the American Academy of Pediatrics retracted previous recommendations, and concluded that there was no convincing evidence for early food avoidance to prevent development of allergy (4). In 2011, the Canadian Paediatric Society issued a joint position statement (5) with the Canadian Society of Allergy and Clinical Immunology (CSACI) with a recommendation to not delay introduction of solid food beyond 6 months while active introduction at 4 to 6 months of age is ‘still under investigation’. A landmark UK study, Learning Early About Peanut Allergy (LEAP) (6), investigated whether early introduction of peanut-based products prevented allergy in high-risk infants. A total of 640 infants (4 to 11 months) with severe eczema, egg allergy or both were stratified to cohorts based on pre-existing sensitization assessed using skin prick test (SPT): 542 non-sensitized (0 mm wheal) and 98 sensitized (1 mm to 4 mm wheal). Seventy-six infants with SPT wheal greater than 4 mm were excluded due to perceived higher likelihood of reactions. This was a key limitation of the study. The two groups were randomized to regularly consume or completely avoid peanut products until 60 months of age, when peanut allergy was determined using an oral challenge with peanut protein. The prevalence of peanut allergy showed a striking difference of 17% in the avoidance group compared with 3% in the consumption group, with a corresponding number needed to treat of 7.1, intention-to-treat analysis. This effect was demonstrated in both the non-sensitized group (primary prevention) as well as the sensitized group (secondary prevention). The LEAP study is the first prospective, randomized trial that clearly demonstrates early introduction reduces the risk of peanut allergy. The LEAP ON study further demonstrates that peanut allergy prevention persists after a 1-year period of regular consumption in the same cohort (7). An interim consensus statement from nine international allergy societies was issued to highlight the potential benefits (8). It supports dietary introduction of peanut products in high-risk infants between 4 and 11 months of age (level 1 evidence). It also recommends health care providers to consider evaluation by allergists, who can offer oral challenges, in infants with early-onset allergic diseases before initiating peanut introduction. In 2017, a National Institute of Allergy and Infectious Diseases-sponsored expert panel published addendum guidelines (9) specifically for peanut allergy prevention incorporating data from emerging studies (6,7,10). For infants with severe eczema, egg allergy or both, it recommends evaluation by SPT, peanut specific IgE (sIgE) or both prior to peanut introduction at 4 to 6 months. The CSACI endorsed these recommendations (11) and emphasized that peanuts can be introduced at home for the majority of infants, including those with mild to moderate eczema. Also, it addressed several concerns including discrepancy in defining ‘severe eczema’, peanut sIgE testing by non-allergist physicians and timely assessment of infants by subspecialty allergists. Changing the culture from ‘not delay’ to ‘active introduction’ for primary prevention is vital in the setting of increasing peanut allergy. However, health care resources must be ready to accommodate these applications, especially the increasing need for evaluation by an allergist in the large number of high-risk infants at an early age. Further research is required to address the optimum dose, frequency and duration of ingestion to prevent allergy; the prevalence of allergy after cessation of regular consumption; and applications to other allergenic foods. For high-risk infants, early feeding at 4 to 6 months after medical assessment can be an effective intervention in primary prevention of peanut allergy. For non-high-risk infants, delayed introduction beyond 6 months is not recommended.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.005 | 0.031 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.002 | 0.002 |
| Bibliometrics | 0.003 | 0.002 |
| Science and technology studies | 0.001 | 0.000 |
| Scholarly communication | 0.002 | 0.002 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.004 | 0.006 |
| Insufficient payload (model declined to judge) | 0.026 | 0.006 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".