In contrast, during pregnancy, effect estimates were null for sensitization to any allergens (aOR = 1.02; 95% CI: 0.86, 1.22) and for sensitization to food allergens (aOR = 1.00; 95% CI: 0.77, 1.61).
The majority of risk estimates were null, except for the highest exposure group for cumulative exposure (>34 years, OR = 2.60, 95% CI: 1.0-6.4) anumberber of embalmings (>3068 embalmings, OR = 2.3, 95% CI: 1.00-5.70).
Nevertheless, our point estimates are close to null, strongly suggesting true equipoise until a definitive randomized trial with sufficient power (i.e. a much larger sample size) rigorously tests the relative efficacy of these interventions.
Therefore, it is important to assess how far variation estimates are from the null hypothesis, and how precise the statistics are in each particular situation.
PFOA was not associated with overweight in male offspring, and RR estimates were consistently null.
Most of the study estimates are centred around the null, however findings from India, Indonesia and Pakistan (all in relation to suicide) show evidence of an increased risk in individuals who were unemployed (OR range from 3 7).
Analyses by sex showed significant reductions in body weight with LCSs among women (−0.72; 95% CI: −1.19, −0.25; fixed-effect WGMD = −0.62); the summary estimate for men was null but based on only 2 trials (no evidence of small-study bias was observed) (30, 32).
This corresponds to the statistical expectation that, given nondifferential misclassification, corrected relative risk estimates are further away from the null than the uncorrected estimates.
These limitations lead to misclassification of exposure, but as this is unlikely to vary by case status, the effect estimates are probably shifted toward the null.
In contrast, 2-sample IV estimates are known to be biased towards the null, even when the confounded estimate is biased away from the null (4, 5).
