New Insights into IBD Epidemiology: Are There Any Lessons for Treatment?
Bibliographic record
Abstract
Changing trends in the epidemiology of IBD provide an opportunity to examine possible etiological hypotheses. Why did IBD emerge in developed nations in the middle of the 20th century? Why did it emerge initially as ulcerative colitis but now Crohn's disease has become the predominate form of IBD in developed nations? Why is IBD emerging in recent years in developing nations and why is it that ulcerative colitis is the predominate form in these countries? In this chapter we will explore what is known about environmental issues that impact on disease presentation and where they provide opportunities for therapy. Managing smoking cessation in Crohn's disease is substantiated by evidence showing that smokers have a worse course of disease than non-smokers or than persons who quit smoking. Introducing nicotine to patients with ulcerative colitis has not brought the positive results anticipated with the widespread observation that smoking cessation was associated with flaring of this disease. Assessing and managing stress in both Crohn's disease and ulcerative colitis has emerged as an important consideration for clinicians caring for patients with IBD, especially for patients with active disease who may develop maladaptive coping mechanisms. Recent data suggest that stress may antedate flares. It is unknown what may induce changes in the gut flora of patients with IBD compared to controls. There are suggestions that antibiotic use in childhood and specific diets particularly those lower in ω-3 fatty acids may impact on disease presentation and the common mechanism may be through alteration of gut flora. For at-risk families (where there are affected family members) perhaps greater vigilance with antibiotic use in childhood and ensuring diets are higher in ω-3 fatty acids can be considered. In the future there may be approaches to modulate gut flora either with antibiotics targeted against identified noxious microbes or with selective probiotics that can rebalance the gut dysbiosis.
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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 | 0.014 | 0.039 |
| Meta-epidemiology (narrow) | 0.002 | 0.001 |
| Meta-epidemiology (broad) | 0.005 | 0.003 |
| Bibliometrics | 0.004 | 0.003 |
| Science and technology studies | 0.002 | 0.006 |
| Scholarly communication | 0.007 | 0.023 |
| Open science | 0.004 | 0.004 |
| Research integrity | 0.008 | 0.017 |
| Insufficient payload (model declined to judge) | 0.015 | 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".