Motivator: A twitter comment “Isn’t the implication that the large effect size is a direct byproduct of the lack of power? i.e. that if the the study had more power, the effect size would have been found to be smaller.”1 2 A thought: our belief in the magnitude of an observed effect should be based on our priors, which, hopefully, are formed from good mechanistic models and not sample size“.3

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“A more efficient design would be to first group the rats into homogeneous subsets based on baseline food consumption. This could be done by ranking the rats from heaviest to lightest eaters and then grouping them into pairs by taking the first two rats (the two that ate the most during baseline), then the next two in the list, and so on. The difference from a completely randomised design is that one rat within each pair is randomised to one of the treatment groups, and the other rat is then assigned to the remaining treatment group.

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1 Why reported effect sizes are inflated 2 Setup 3 Exploration 1 4 Unconditional means, power, and sign error 5 Conditional means 5.1 filter = 0.05 5.2 filter = 0.2 1 Why reported effect sizes are inflated This post is motivated by many discussions in Gelman’s blog but start here When we estimate an effect1, the estimate will be a little inflated or a little diminished relative to the true effect but the expectation of the effect is the true effect.

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The post motivated by a tweetorial from Darren Dahly In an experiment, do we adjust for covariates that differ between treatment levels measured pre-experiment (“imbalance” in random assignment), where a difference is inferred from a t-test with p < 0.05? Or do we adjust for all covariates, regardless of differences pre-test? Or do we adjust only for covariates that have sustantial correlation with the outcome? Or do we not adjust at all?

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“GPP (n=4 per site) increased from the No Wildlife site to the Hippo site but was lowest at the Hippo + WB site (Fig. 6); however, these differences were not significant due to low sample sizes and high variability.” If we know these are not significant due to low sampe size and high variability, why even do the test? “TRE led to a modest, but not significant, increase in sleep duration to 449.

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This post has been updated. A skeleton simulation of different strategies for NHST for count data if all we care about is a p-value, as in bench biology where p-values are used to simply give one confidence that something didn’t go terribly wrong (similar to doing experiments in triplicate – it’s not the effect size that matters only “we have experimental evidence of a replicable effect”). tl;dr - At least for Type I error at small \(n\), log(response) and Wilcoxan have the best performance over the simulation space.

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Researchers frequently report results as relative effects, for example, “Male flies from selected lines had 50% larger upwind flight ability than male flies from control lines (Control mean: 117.5 cm/s; Selected mean 176.5 cm/s).” where a relative effect is \[\begin{equation} 100 \frac{\bar{y}_B - \bar{y}_A}{\bar{y}_A} \end{equation}\] If we are to follow best practices, we should present this effect with a measure of uncertainty, such as a confidence interval. The absolute effect is 59.

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Author's picture

R doodles. Some ecology. Some physiology. Much fake data.

Thoughts on R, statistical best practices, and teaching applied statistics to Biology majors.

Jeff Walker, Professor of Biological Sciences

University of Southern Maine, Portland, Maine, United States