Variance estimation when matching with replacement

“Matching with replacement induces two types of correlations that must be accounted for when estimating the variance of estimated treatment effects. The first is a within-matched set correlation in outcomes. Matched subjects within the same matched set have similar values of the propensity score. Subjects who have the same value of the propensity score have measured baseline covariates that come from the same multivariate distribution. In the presence of confounding, baseline covariates are related to the outcome. Thus, matched subjects are more likely to have similar outcomes compared to two randomly selected subjects. The second source of correlation is induced by repeated use of control subjects. Failure to account for this correlation and acting as though the matched control subjects were independent observations will likely result in estimated standard errors that are artificially small and estimated confidence intervals that are artificially narrow. Added complexity is introduced by having subjects cross-classified with matched sets such that the same control subject can belong to more than one matched set.”

Austin, P. C., & Cafri, G. (2020, p. 1625). [Variance estimation when using propensity‐score matching with replacement with survival or time‐to‐event outcomes. Statistics in Medicine, 39(11), 1623–1640.]

Privacy implications of hashing data, by John Cook

Cryptographic hash functions are sometimes used to create pseudo IDs from identifiable info like NHS numbers. An advantage of this approach is that two sites that have no way to communicate with each other will generate the same pseudo ID, allowing data to be linked. A disadvantage is that, although in general hashes are impossible to inverse, a rainbow table lookup attack can be used to inverse the hash when the space of inputs is relatively small, as is the case for ID numbers. John Cook explores.

Baseline balance in experiments and quasi-experiments

Baseline balance is important for both experiments and quasi-experiments, just not in the way researchers sometimes believe. Here are excerpts from three of my favourite discussions of the topic.

Don’t test for baseline imbalance in RCTs. Senn (1994,  p. 1716):

“… the following are two incontrovertible facts about a randomized clinical trial:

1. over all randomizations the groups are balanced;

2. for a particular randomization they are unbalanced.

Now, no ‘[statistically] significant imbalance’ can cause 1 to be untrue and no lack of a significant balance can make 2 untrue. Therefore the only reason to employ such a test must be to examine the process of randomization itself. Thus a significant result should lead to the decision that the treatment groups have not been randomized…”

Random sequence generators will randomise the groups. What can go wrong is that people can subvert the randomisation -sometimes with the best of intentions – if you’re not careful to prevent them doing so.

Balancing covariates between treatment groups, e.g., using permuted blocks or minimisation, can increase the efficiency of covariate adjustment. Senn (1994, p. 1721):

“… what is the value of balance as regards validity of an inference? Answer: none. This does not mean that balance is not useful. Its use is that, having decided to condition, we minimize the standard errors of our treatment effects if our covariate is orthogonal to treatment. This is the true value of balance which is an issue of efficiency, not validity.”

Do examine baseline imbalance in quasi-experiments; however, not by using statistical tests. Sample descriptives, such as a difference in means, suffice. Imai et al. (2008, p. 497):

“… from a theoretical perspective, balance is a characteristic of the sample, not some hypothetical population, and so, strictly speaking, hypothesis tests are irrelevant…”

Using p-values from t-tests and similar can lead to erroneous decisions of balance. As you prune a dataset to improve balance, power to detect effects decreases. Imai et al. (2008, p. 497 again):

“Since the values of […] hypothesis tests are affected by factors other than balance, they cannot even be counted on to be monotone functions of balance. The t-test can indicate that balance is becoming better whereas the actual balance is growing worse, staying the same or improving. Although we choose the most commonly used t-test for illustration, the same problem applies to many other test statistics…”

If your matching has led to baseline balance, then you’re good, even if the matching model is misspecified. (Though not if you’re missing key covariates, of course.) Rosenbaum (2023, p. 29):

“So far as matching and stratification are concerned, the propensity score and other methods are a means to an end, not an end in themselves. If matching for a misspecified and misestimated propensity score balances x, then that is fine. If by bad luck, the true propensity score failed to balance x, then the match is inadequate and should be improved.”

References

Imai, K., King, G., & Stuart, E. A. (2008). Misunderstandings between experimentalists and observationalists about causal inference. Journal of the Royal Statistical Society: Series A (Statistics in Society), 171(2), 481–502.

Rosenbaum, P. R. (2023). Propensity score. In J. R. Zubizarreta, E. A. Stuart, D. S. Small, & P. R. Rosenbaum, Handbook of Matching and Weighting Adjustments for Causal Inference (pp. 21–38). Chapman and Hall/CRC.

Senn, S. (1994). Testing for baseline balance in clinical trials. Statistics in Medicine, 13, 1715–1726.

A Word on Critical Realism, by Kieran Healy (2013)

I’ve just remembered this:

“[Critical realism] presents itself in a way that some social scientists—with next to no real background in philosophy—feel gives them just what they need to shore up their empirical research and metaphysical intuitions. You want to be realist in your philosophy of social science? Sure! You want your preferred level of analysis to also be an ontologically emergent level of reality? No problem! You want to talk about social structures as irreducible in some serious-but-not-really-analyzed fashion? You got it. You want your theory to be critical? I mean, who doesn’t, right? Just call yourself a Critical Realist and cite some Bhaskar. After all, he has repeatedly asserted that his work is a “Copernican Revolution” in the philosophy of science […]”

And:

“The diffusion of CR was slightly hampered by the transformation of Bhaskar from fringe philosopher of science to full-blown guru. Having recruited followers in sociology on the basis of his realism, he began to pull the rug out from under them in the late 1990s, first with the merely absurd Plato, Etc and then with the frankly embarrassing From East to West: Odyssey of a Soul (which closed with a final chapter titled “The Dance of Shiva in the Age of Aquarius”). This work, in retrospect, seems like the culmination of the unpleasant cult of personality that grew up around Bhaskar in CR circles in the 1980s and which he seems to have done little to discourage.”

One section is constructive, providing alternatives to critical realism:

“Sociologists interested in emergence or macro-level explanations have no need to run together that interest with the specific CR position or view. (This was the point of my old article on Archer, Mouzelis, and CR.) There are large and immediately accessible literatures on all of these topics in philosophy, leading naturally to more technical or specialist work. Consider the SEP article on Emergent Properties, for instance, and the one on Supervenience, or the one on Scientific Explanation, or Scientific Realism. Go from there to, say, Jonathan Schaffer’s Is there a Fundamental Level? (for the metaphysics) or Michael Strevens’ Depth for one take on the philosophy of science, or—for something in parts similar to Bhaskar but far more creative and central—read Nancy Cartwright on laws of nature. I feel confident in asserting that different sociologists could ally themselves with quite incompatible positions in these debates and much of our work would go on as before.”

Regression to the mean

Suppose we were to run an uncontrolled pre-post evaluation of an intervention to alleviate psychological distress. We screen participants for distress and invite those with scores 1.5 SDs or more above the mean to take part. Then, following the intervention, we collect data on distress again to see if it has reduced. The measure we have chosen has a test-retest reliability of 0.8.

Here is a picture of simulated findings (scores have been scaled so that they have a mean of 0 and SD of 1). Red points denote data from people who have been included the study.

I have setup the simulation so that the intervention had no effect, in the sense that outcomes would have been identical in the absence of the intervention. However, looking at the right hand side, it appears that there has been a reduction in distress of 1.1 SDs – a huge effect. This is highly “statistically significant”, p < .001. What happened?!

Tweaking the simulation

Let’s try a different simulation. This time, without any screening, so everyone is included in the intervention regardless of their levels of distress (so all the data points are red):

Looking at the right hand side, the pre-post change is 0 and p is close to 1. There is no change.

Next, select participants whose scores are at the mean or above:

The pre-post change is now statistically significant again, with improvement of 0.27 SDs.

Select participants with more extreme scores, 1.5 SDs or above at baseline, and we see the magnitude of change has increased again:

What happens if we increase the test-retest reliability of the measure to 0.9?

Firstly, the scatterplot on the left is a little less fuzzy. The magnitude of change has reduced to 0.48 SDs.

Finally, let’s make the measure perfectly reliable so that the scatterplot on the left is a fuzz-free straight line:

Now there is no change.

What’s going on?

I have simulated the data so that the intervention had zero impact on outcomes, and yet for many of the analyses above it does appear to have alleviated distress.

The extent to which the effect illustrated above, called regression to the mean, occurs partly depends on how selective we are in inviting participants to join the study. At one extreme, if there is no selection, then the mean change is still zero. At the other extreme, when we are highly selective, then change is over 1 SD.

This is because by selecting people with particularly high scores at baseline, there’s an increased chance that we include people who had, for them, a statistically rare score. Perhaps they had a particularly bad day, which wasn’t indicative of their general levels of distress. Since we selected them when they happened to have a bad day, on measuring again after the intervention, there was a good chance they had a much less extreme score. But this reduction was entirely unrelated to the intervention. We know this because the simulation was setup so that the intervention had zero effect.

Making test-retest reliability perfect also eliminates regression to the mean. However, this is unlikely to be possible for most of the characteristics of people that are of interest for interventions.

You can play around with the app I developed to simulate the data over here.

Regression to the mean is just one reason why interventions can spuriously appear to have an effect. Carefully chosen control groups, where possible with random assignment to intervention or control, can take account of alternative explanations of change.

Evaluating What Works, by Dorothy Bishop and Paul Thompson

“Those who work in allied health professions aim to make people’s lives better. Often, however, it is hard to know how effective we have been: would change have occurred if we hadn’t intervened? Is it possible we are doing more harm than good? To answer these questions and develop a body of knowledge about what works, we need to evaluate interventions.

“As we shall see, demonstrating that an intervention has an impact is much harder than it appears at first sight. There are all kinds of issues that can arise to mislead us into thinking that we have an effective treatment when this is not the case. On the other hand, if a study is poorly designed, we may end up thinking an intervention is ineffective when in fact it is beneficial. Much of the attention of methodologists has focused on how to recognize and control for unwanted factors that can affect outcomes of interest. But psychology is also important: it tells us that own human biases can be just as important in leading us astray. Good, objective intervention research is vital if we are to improve the outcomes of those we work with, but it is really difficult to do it well, and to do so we have to overcome our natural impulses to interpret evidence in biased ways.”

(Over here.)

History repeating in psychedelics research

Interesting paper by Michiel van Elk and Eiko Fried (2023) on flawed evaluations of psychedelics to treat mental health conditions and how to do better. Neat 1966 quotation at the end:

“Given the current state of research, strong caution is warranted regarding the hype around psychedelics as treatments: there is not enough robust evidence to draw any firm conclusions about the safety and efficacy of psychedelic therapy. […] For psychedelic research in particular, we are not the first to raise concerns and can only echo the warning expressed more than half a century ago [Masters & Houston, 1966]:

“‘To be hopeful and optimistic about psychedelic drugs and their potential is one thing; to be messianic is another. Both the present and the future of psychedelic research already have been grievously injured by a messianism that is as unwarranted as it has proved undesirable.'”

References

Van Elk, M., & Fried, E. I. (2023). History repeating: Guidelines to address common problems in psychedelic science. Therapeutic Advances in Psychopharmacology, 13.

“Randomista mania”, by Thomas Aston

Thomas Aston provides a helpful summary of RCT critiques, particularly in international evaluations.

Waddington, Villar, and Valentine (2022), cited therein, provide a handy review of comparisons between RCT and quasi-experimental estimates of programme effect.

Aston also cites examples of unethical RCTs. One vivid example is an RCT in Nairobi with an arm that involved threatening to disconnect water and sanitation services if landlords didn’t settle debts.

Five questions to ask of social research

  1. Why should I care about this sample? Is the sample itself of interest, whether 1 person (e.g., a biography-like case study) or 1,000?
  2. If generalisation to a broader population is intended or implied, how is the case made that the findings do generalise?
  3. To what extent do findings depend on participants being able to explain why they acted the way they did? People sometimes tell more than they can know.
  4. If the researchers state that X caused or contributed to Y, what evidence is provided that if X hadn’t been the case, then Y would have been different?
  5. What political agendas do the researchers and their institutions have, e.g., as influenced by who funds them?

Myers-Briggs

People are rightly critical of the Myers–Briggs Type Indicator (MBTI). But some of the types are moderately correlated with the Big Five dimensions, which are seen as more credible in differential psychology. MBTI extraversion correlates with… wait for it… Big Five extraversion (50% shared variance). MBTI intuition correlates with openness to new experiences (40% shared variance). The opposite poles correlate as you’d expect.

Here are the key correlations (Furnham et al., 2003, p. 580, gender and linear effects of age have been partialed out):

“Neuroticism was most highly correlated with MBTI Extraversion (r = -.30, p = .001) and Introversion (r = .31, p < .001). Costa and McCrae’s Extraversion was most highly correlated with Myers-Briggs Extraversion (r = .71, p < .001) and Introversion (r=-.72, p < .001). Openness was most highly correlated with Sensing (r = -.66, p < .001) and Intuition (r = .64, p < .001). Agreeableness was most highly correlated with Thinking (r=-41, p < .001) and Feeling (r = .28, p < .001). Conscientiousness was most highly correlated with Judgment (r = .46, p<.001) and Perception (r=-.46, p < .001).”

Dichotomising is still silly, particularly for scores close to thresholds, where a light breeze might flip someone’s type from, say, I to E or vice verse. But the same can be said of any discretisation taken too seriously. Consider also clinical bands on mental health questionnaires and attachment styles on the Experience in Close Relationships Scale.

Also silly are tautologous non-explanations of the form: they behave that way because they’re E. Someone is E because they ticked a bunch of boxes saying they consider themselves extraverted! The types are defined transparently in terms of thoughts, feelings, and behaviour. They help structure self-report, but don’t explain why people are the way they are. Explanations require mechanisms.

References

Furnham, A., Moutafi, J., & Crump, J. (2003). The relationship between the revised NEO-Personality Inventory and the Myers-Briggs Type Indicator. Social Behavior and Personality, 31, 577–584.