I am an experimental and behavioral economist, studying the interplay of beliefs and individual decision-making with applications to health, discrimination, and machine learning.
We propose a simple, incentive compatible procedure based on binarized linear scoring rules to elicit beliefs about real-valued outcomes - multiple point predictions. Simultaneously eliciting multiple point predictions with linear incentives reveals the subjective probability distribution without pre-defined intervals or probabilistic statements. We show that the approach is theoretically as robust as existing methods, while adapting flexibly to different beliefs. In a laboratory experiment, we compare our procedure to the standard approach of eliciting discrete probabilities on pre-defined intervals. We find that elicitation with multiple point predictions is faster, perceived as less difficult and more consistent with a subsequent decision. We further find that multiple point predictions are more ac- curate if beliefs vary between participants. Finally, we provide experimental evidence that pre-defined intervals anchor reports.
We test in an experiment if a monetary incentive or a charity incentive can motivate people to fill in the German organ donor card and thereby increase the number of organ donors. We find that a monetary incentive significantly increases the number of organ donors whereas the charity incentive does not.
Identifying the cause of discrimination is crucial to design effective policies and to understand discrimination dynamics. Building on traditional models, this paper introduces a new explanation for discrimination: discrimination based on motivated reasoning. By systematically acquiring and processing information, individuals form motivated beliefs and consequentially discriminate based on these beliefs. Through a series of experiments, I show the existence of discrimination based on motivated reasoning and demonstrate important differences to statistical discrimination and taste-based discrimination. Finally, I demonstrate how this form of discrimination can be alleviated by limiting individuals’ scope to interpret information.
Using a unique dataset from a German health check-up provider including detailed individual questionnaire data as well as medical test data, I apply a random forest to predict several health risk factors. I evaluate the prediction performance using various metrics and find decent prediction qualities across all outcomes. By identifying the most relevant predictor variables, I compile concise and validated questionnaire tools to identify individuals’ blood pressure, blood glucose, and cholesterol levels, their risk of a coronary heart disease, whether or not they suffer from plaque or a metabolic syndrome as well as their relative fitness levels. In a second step, I compare the prediction results to physician predictions of the same patient observations. I find that the random forest outperforms the physicians if predictions are based on the same information set. When additionally providing the physicians with the random forest predictions for a particular patient observation, the physicians align with the random forest predictions. Finally, while the random forest considers various psychological scales, the physicians focus on family health history information instead.
The root causes of dementia are still largely unclear, and the medical community lacks highly effective preventive and therapeutic pharmaceutical agents for dementia despite large investments into their development. There is growing interest in the question if infectious agents play a role in the development of dementia, with herpesviruses attracting particular attention. To provide causal as opposed to merely correlational evidence on this question, we take advantage of the fact that in Wales eligibility for the herpes zoster vaccine (Zostavax) for shingles prevention was determined based on an individual’s exact date of birth. Those born before September 2 1933 were ineligible and remained ineligible for life, while those born on or after September 2 1933 were eligible to receive the vaccine. By using country-wide data on all vaccinations received, primary and secondary care encounters, death certificates, and patients’ date of birth in weeks, we first show that the percentage of adults who received the vaccine increased from 0.01% among patients who were merely one week too old to be eligible, to 47.2% among those who were just one week younger. Apart from this large difference in the probability of ever receiving the herpes zoster vaccine, there is no plausible reason why those born just one week prior to September 2 1933 should differ systematically from those born one week later. We demonstrate this empirically by showing that there were no systematic differences (e.g., in pre-existing conditions or uptake of other preventive interventions) between adults across the date-of-birth eligibility cutoff, and that there were no other interventions that used the exact same date-of-birth eligibility cutoff as was used for the herpes zoster vaccine program. This unique natural randomization, thus, allows for robust causal, rather than correlational, effect estimation. We first replicate the vaccine’s known effect from clinical trials of reducing the occurrence of shingles. We then show that receiving the herpes zoster vaccine reduced the probability of a new dementia diagnosis over a follow-up period of seven years by 3.5 percentage points (95% CI: 0.6 – 7.1, p=0.019), corresponding to a 19.9% relative reduction in the occurrence of dementia. Besides preventing shingles and dementia, the herpes zoster vaccine had no effects on any other common causes of morbidity and mortality. In exploratory analyses, we find that the protective effects from the vaccine for dementia are far stronger among women than men. Randomized trials are needed to determine the optimal population groups and time interval for administration of the herpes zoster vaccine to prevent or delay dementia, as well as to quantify the magnitude of the causal effect when more precise measures of cognition are used. Our findings strongly suggest an important role of the varicella zoster virus in the etiology of dementia.
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