Wednesday, July 21, 2021

Due to the social desirability bias, software pirates deny it when filling surveys; 47pct actual piracy rate vs 19pct self-reported piracy rate

Liar, liar, pants on fire! Social desirability bias in software piracy research. Marton Gergely & V. Srinivasan (Chino) Rao. Behaviour & Information Technology, Jul 19 2021.

Abstract: Measures of ethical behaviours in research may be subject to social desirability bias (SDB). Most behavioural aspects of software piracy research are a subset of ethical research. Few studies of software piracy have explicitly addressed the issue of SDB. In this article, the extent of SDB that may be present in software piracy is empirically assessed. This was done by comparing SDB in software piracy under three conditions using the 40-item Balanced Inventory of Desirable Responding (BIDR) scale. First, software piracy behaviour was examined in an experimental setting with actual money at stake. This allowed subject behaviour to be observed rather than inferred from self-report responses. Second, a survey was conducted to test the extent of software piracy based on subject self-report responses. Third, the extent of software piracy was also assessed based on peer-report responses (i.e.: the subject reported whether their peers would pirate). A comparison of the responses in the three conditions allows us to draw inferences about SDB in software piracy research. Self-report surveys exhibited high levels of SDB. The behaviour in the experimental condition, and responses in the peer-report survey method, did not exhibit SDB.

Keywords: Software piracyinformation system ethicsdigital mediaintellectual property theftsocial desirability bias

Haptic stimulation of endorphin acts to bond relationships in primates and humans; humans have found ways to trigger the endorphin system virtually without touch, allowing us to ‘groom’ at a distance with more individuals

Virtual touch and the human social world. Robin IM Dunbar. Current Opinion in Behavioral Sciences, Volume 43, February 2022, Pages 14-19.


• Haptic stimulation of endorphin acts to bond relationships in primates and humans.

• Humans have found ways to trigger the endorphin system virtually without touch.

• Virtual ‘touch’ allows humans to ‘groom’ at a distance with more individuals.

Abstract: Touch forms a central component of social bonding, both in primates and in humans, via the brain’s endorphin system. In primates, this involves social grooming, acting via the CT neuron system. Although humans still use soft touch for bonding relationships, they have had to find ways of triggering the endorphin system without the need for physical touch in order to be able to increase the size of their social groups beyond the size of those characteristic of monkeys and apes. These behaviors include laughter, singing, dancing, the rituals of religion, feasting and emotional storytelling, and act functionally as a form of ‘virtual touch’. I summarise recent behavioral, neurobiological and genetic evidence demonstrating that these behaviors both enhance bonding and act through the endorphin system.

Reviewing theory and experimental evidence, they suggest that spontaneous BOLD activity may be more closely aligned with off-line plasticity and homeostatic processes than on-line fluctuations in cognitive content

Brain activity is not only for thinking. Timothy OLaumann, Abraham ZSnyder. Current Opinion in Behavioral Sciences, Volume 40, August 2021, Pages 130-136.

Abstract: The human brain is a complex organ with multiple competing imperatives. It must perceive and interpret the world, incorporate new information, and maintain its functional integrity over the lifespan. Neural activity is associated with all of these processes. Spontaneous BOLD signals have been invoked as representing neural activity associated with all of these processes. However, their exact role in these processes remains controversial. Here, we review learning machine theory, molecular mechanisms of synaptic plasticity and homeostasis, and recent experimental evidence to suggest that spontaneous BOLD activity may be more closely aligned with off-line plasticity and homeostatic processes than on-line fluctuations in cognitive content.


The existence of unceasing spontaneous brain activity has been recognized since at least the 1930s [1]. However, the functions of this activity have remained mysterious [2]. Over the last three decades, blood oxygen level dependent (BOLD) fMRI has become the dominant tool for measurement of brain activity in humans. Soon after the adoption of fMRI, it was observed that fMRI signals exhibit constant fluctuations unrelated to the task [3]. In the context of task fMRI, this activity was conventionally regarded as ‘physiological noise’ [4]. However, it is now clear that this ‘physiological noise’ is temporally correlated within functional systems [5,6]. It is this property of spontaneous brain activity that constitutes the basis of resting state functional connectivity (RSFC) [7]. The existence of this well-structured organization implies that spontaneous brain activity is physiologically consequential.

The meaning of spontaneous BOLD signal fluctuations has been variably interpreted along two different perspectives. According to one view, spontaneous BOLD fluctuations are proposed to reflect unconstrained cognitive processes, for example, retrospection, prospection, reflection, environmental monitoring — the ‘stream of consciousness’ — attendant to our subjective experience. Given the centrality of perception and action to mental life, it is appealing to assume that all observed brain activity is directly related to moment-to-moment cognition and behavior. This perspective has been reinforced by a massive accumulation of PET and fMRI experiments in which brain activity has been imaged with the objective of localizing cognitive operations [8]. More recently, the observation of ‘dynamic’ functional connectivity during wakeful rest and changes in functional connectivity between rest and task states have, at times, been interpreted as reflecting cognition [9,10].

We have previously articulated several problems with the notion that all ongoing BOLD activity directly reflects cognition and behavior (Box 1; [11]): (1) The topography of BOLD fMRI correlations remains largely intact during slow-wave sleep [12] and even anesthesia [13], states in which cognition is presumed to be either absent or greatly attenuated; (2) The extent to which task paradigms modify the correlation structure of spontaneous BOLD signal fluctuations is very limited [14,15,16]; (3) While unconstrained cognition might be expected to vary from scan to scan within an individual, RSFC remains remarkably consistent across sessions [17,18]. RSFC is also relatively stable within a given scan, discounting fluctuations attributable to drowsiness [11] or arousal [19], which likely relate to fluctuations in BOLD signals, at least partly due to alterations in respiratory behavior and pCO2 [20]. Moreover, brain metabolic activity is high at all times and minimally affected by task performance [21].

Box 1

Evidence that RSFC structure is largely independent of cognitive content


RSFC structure is similar during wake and sleep. For instance, DMN structure is observed through wake, S1, S2, and SWS [12,100].


RSFC structure is present under anesthesia [13,101], although covariance does diminish with increased sedation [102].


RSFC structure is minimally altered by task state [1415].


RSFC structure within subject is consistent across sessions [16,11,103].


RSFC structure within subject is similar over long time scales [18,17].


RSFC structure is consistent across subjects at the population level [104,105].


Similar RSFC structure is evident across mammalian species [106107108].

For all of these reasons, unconstrained cognition does not fully explain ongoing spontaneous activity. An alternative view proposes that spontaneous BOLD activity may more closely relate to mechanisms associated with learning and memory [22,23]. In the following, we review prior literature supporting the perspective that a substantial fraction of spontaneous brain activity represents homeostatic and consolidative signaling, the function of which is to enable neural plasticity while maintaining the brain's functional integrity through time. We also review recent evidence that BOLD RSFC may be intimately tied to these processes.

Learning machine theory

When considering the role of ongoing neural activity in brain function, it is important to recognize that one of the brain’s primary capacities is its ability to learn new information about its environment. Theoretical considerations, initially formulated by David Marr [24], suggest that any associative learning machine functions optimally if it is allowed to alternate between two states: (1) a learning phase, during which the machine is connected to inputs and connections are enhanced between simultaneously active elements and (2) a restorative phase during which the machine is disconnected from inputs and connections between elements are rebalanced in a manner that increases randomness (entropy) [25,26]. In multi-layer perceptrons, this principle is expressed as iterative alternation between a forward phase, during which prediction error is evaluated, and a backward phase, during which connection weights are adjusted by back-propagation [27]. The starkest expression of the state alternation principle in living organisms is sleep versus wake. This alternation appears to be necessary: all organisms capable of learning alternate between wake versus sleep states [28]. In vertebrates, events experienced during wake are registered in the hippocampus and the cerebral cortex [29,30]. During slow wave sleep (SWS), reactivation of the same circuits leads to the creation of stable (consolidated) episodic memory [31].

Understanding how state alternation is implemented in brains requires consideration of the cellular and molecular events underlying synaptic weight modification. Activity-dependent synaptic plasticity plays a crucial role in brain development well before birth [323334]. For example, retino-tectal connections have been shown to be sculpted by spontaneous retinal waves during prenatal development of the visual system [35]. Following birth, spontaneous activity continues to refine neural connections using sensory feedback [36,37]. During early life critical periods, experience-dependent synaptic plasticity tunes the response properties of cortical sensory neurons (e.g. ocular dominance columns) [38]. As the brain matures, metabolic ‘brakes’ limit neural plasticity to mechanisms centered on inhibitory interneurons [394041]. Although neural plasticity in adults is more restricted, the underlying activity-dependent processes likely follow similar principles.

Molecular mechanisms of activity-dependent synaptic plasticity

Activity-dependent synaptic plasticity is conventionally discussed under the headings of long-term potentiation (LTP) and long-term depression (LTD). But LTP/LTD are deceptively simple terms encompassing a wide range of molecular processes [42,43]. The early phase of LTP (E-LTP) is triggered by Ca2+ influx linked to post-synaptic depolarization, which sets in motion molecular cascades mediated by phosphorylation and dephosphorylation of regulatory molecules (e.g. protein kinase C (PKC) and Ca2+-calmodulin-dependent protein kinase (CamKII)) that govern neurotransmitter receptor trafficking. E-LTP lasts 1−3 hours and is independent of gene expression. The late phase of LTP (L-LTP) begins with the transcription of immediate early genes (IEGs; e.g. Arc, Zif268) that control translational processes, which lead, on a time scale of hours, to structural changes in dendritic spines [444546]. Thus, whereas electrophysiological event-related responses may last up to a few hundred millisec and BOLD hemodynamic responses typically evolve over ∼16−20 s, the metabolic traces of the evoked activity persist over much longer time scales. These traces may underlie the observation that fMRI responses to task A are modulated by having performed unrelated task B during the past half hour [47].

The Hebbian principle (‘fire together → wire together’) is often invoked to account for resting state functional connectivity [48,49]. The mechanism underlying Hebbian learning, that is, spike-timing dependent synaptic plasticity (STDP), has been elucidated in considerable detail [50,51]. In brief, neural back-propagation of depolarization induced by a first excitatory stimulus removes the Mg2+ block at NMDA receptors, thereby allowing a second stimulus (if it occurs within a 20–85 ms window) to induce local Ca2+ entry, which initiates the LTP molecular cascade, ultimately reinforcing the association between the paired stimuli. Hebbian mechanisms undoubtedly play a central role in adult learning. Accordingly, it is reasonable to posit that synchronous spontaneous BOLD fluctuations that give rise to RSFC are due to a history of prior co-activation. However, a system dominated by unopposed Hebbian plasticity inevitably becomes either infinitely active or silent.

In contrast to Hebbian plasticity, which adjusts synaptic weights in the same direction as an applied stimulus, the brain also employs various mechanisms of homeostatic plasticity, which adjusts synaptic strengths in the opposite direction to return excitatory/inhibitory (E/I) balance and mean firing rate to prior set points [52]. Homeostatic plasticity includes cell-autonomous mechanisms that directly adjust neuronal excitability to counteract environmental stimuli, as well as multiplicative synaptic scaling, which preserves relative strengths between neighboring synapses, thereby maintaining currently represented information [53]. These homeostatic mechanisms operate at the level of dendritic branches [45], individual neurons [53], and large-scale circuits [54], and are active over multiple time scales [55,56]. A correlate of these homeostatic processes is ongoing turnover of synaptic proteins and lipids with half-lives on the order of ‘minutes, hours, days, weeks’ [57]. Modeling experiments suggest that homeostatic regulation of E/I balance plays a crucial role in maintaining the characteristic features of spontaneous brain activity [58]. Importantly, synaptic homeostasis is inseparable from consolidation, the process whereby brief changes in neural activity ultimately lead to stable memory [59,60]. Thus, it is reasonable to posit that spontaneous activity includes both Hebbian and homeostatic signaling.

There is encouraging evidence of an association between low total cholesterol and aggression towards others as well as suicidality in schizophrenia; association was strongest for low total cholesterol

How do lipids influence risk of violence, self-harm and suicidality in people with psychosis? A systematic review. Piyal Sen et al. Australian & New Zealand Journal of Psychiatry, July 9, 2021.


Objectives: Low cholesterol has been linked with violent and suicidal behaviour in people with schizophrenia. This association, if consistently present, may be a promising biological marker that could assist clinicians in decision making regarding risk and treatment. We conducted a systematic review to assess whether there is a reliable association between lipid profile (total cholesterol, high- and low-density lipoprotein cholesterol, and triglycerides) and aggression, self-harm or suicide in people with schizophrenia, and whether effects are similar in males and females.

Method: Relevant databases were searched to identify primary research studies (up to November 2020) that (1) involved adults (some samples also included 16- to 18-year olds) with a confirmed diagnosis of schizophrenia, schizoaffective disorder or psychosis; and (2) included a standardised assessment of verbal aggression, physical aggression against objects, physical aggression against self (including suicide) or others. The search yielded 23 studies eligible for inclusion following a quality appraisal.

Results: Suicidality was the most commonly assessed subtype of aggression (20 studies). For suicidality, about half the studies, including the study with the largest sample size, found a link with total cholesterol. An association between low total cholesterol and violence towards others was found in six of nine studies that investigated this. The evidence for a link with violence was the strongest for total cholesterol, followed by low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, and the weakest for triglycerides. Only a few studies investigated sex differences and yielded mixed evidence. Studies focussed on self-harm as well as involving females in forensic settings were lacking.

Conclusion: There is encouraging evidence of an association between low total cholesterol and aggression towards others as well as suicidality in schizophrenia. Future studies should systematically explore this association in people with schizophrenia who have a significant history of violence, suicidality and self-harm, both inpatients and community, and also investigate underlying mechanisms.

Keywords: Cholesterol, aggression, suicide, schizophrenia, sex

There were three main findings in relation to the primary objectives of this systematic review.

First, there were many more studies which reported on a link between low cholesterol and violence to others than those which did not find a link. All researchers investigating forensic samples found such a relationship. However, the relationship was not only with low TC but also with other parameters of the lipid profile, such as low LDL and low HDL. It is thus important not just to collect data on TC, but LDL and HDL as well. The evidence was weaker for the link between TG and violence, with only two studies finding a link, but one with high TG, the other with low TG. It is to be noted that the study with the largest sample size failed to find a link (Hjell et al., 2020). However, one of the issues in this study was the relatively low rate of baseline violence in the study population, thus offering some indication that the link is likely to be more valid in groups where there is a greater prevalence of violence (i.e. forensic populations).

The biological mechanism behind cholesterol–violence association has been hypothesised to involve serotonin. Animal studies have found an increase in violent behaviour in monkeys assigned to a low-cholesterol diet (Kaplan et al., 19911994). Kaplan et al. (1991) suggested that low cholesterol may reduce cell viscosity and reduce serotonergic receptor activity. This may lead to a depressive state (Marcinko et al., 2005), increased impulsivity (Carver and Miller, 2006Paaver et al., 2007) and aggressive behaviour (Chakrabarti et al., 2004). This finding was observed in Kaplan et al. (1994), where monkeys with experimentally lowered cholesterol had higher concentrations of serotonin metabolites than monkeys given high-cholesterol diets. However, the exact biological mechanism underlying cholesterol–violence (towards self/others) association in humans is still unclear.

Second, there was mixed evidence for a link between low cholesterol and suicidality in schizophrenia, with almost equal number of studies in favour and against such a link. The majority of studies used suicide as the method of assessing aggression. Eight studies found a statistically significant association between low cholesterol and suicide attempts, two of which only found this association in females (Misiak et al., 2015Shrivastava et al., 2017). Seven studies failed to find a link. However, the study with the largest sample size (Sankaranarayan et al., 2020) did find a link, thus suggesting that methodological flaws, particularly low power, might have contributed to the variation in findings.

The evidence for a specific relationship between lipid profile and violent suicidal attempts was even more mixed. Ruljancic et al. (2007) found a significant association between low cholesterol and non-violent suicide attempts, in contrast to two other studies (Marcinko et al., 2005Tripodianakis et al., 2002), reporting an association between low cholesterol and violent suicide attempts. While the two studies showing a positive association had smaller sample sizes, such findings are supported by other literature (Garland et al., 2000Vevera et al., 2003). A meta-analysis found 50% more violent deaths in males with relatively low cholesterol than in participants with higher levels of cholesterol (Jacobs et al., 1992). This meta-analysis also found a higher prevalence of depressive symptoms in males with low serum cholesterol.

An association between low cholesterol and depression has frequently been observed (Grussu et al., 2007Ploeckinger et al., 1996Troisi et al., 2002). It is plausible that the causal pathway from low cholesterol to suicidality in schizophrenia patients involves depression. Kunugi et al. (1997) did not find a significant difference in cholesterol level between suicidal and non-suicidal inpatients with schizophrenia spectrum disorders. However, significantly lower cholesterol levels were found in suicide attempters with mood disorders compared with controls. Similarly, Modai et al. (1994) found a significant association between lower cholesterol and suicidality in patients with depression, but not in schizophrenia patients. Around 40% of people with schizophrenia have depression, with depression being the most significant factor in completed suicide (Upthegrove et al., 2016). People with schizophrenia and comorbid depression also have a significantly increased risk of violence and suicidality (Conley et al., 2007) and poorer clinical outcomes (Gardsjord et al., 2016Upthegrove et al., 2009). The studies included in this systematic review did not control for depressive symptoms in schizophrenia patients. Although findings of low cholesterol and depression are inconsistent, with a number of researchers not finding a significant association (Cepeda et al., 2020Van Dam et al., 1999), it is plausible that suicidality seen in schizophrenia patients with low cholesterol may be a consequence of depressive symptoms.

Third, most of the studies had similar findings for males and females. However, low HDL was seen in two studies to be a better predictor of violence than low TC for males (Eriksen et al., 20172018). Another study found female sex and low TC levels could be used, in part, as predictors of violence in patients with schizophrenia (Chen et al., 2015). One study found higher TC and LDL levels to be associated with suicidality in females but not males with first-episode schizophrenia, thus suggesting that the link between lipids and violence is somewhat complex (Misiak et al., 2015). Future studies need to be designed to explore the nature of the link separately for females and males. All studies (Chakrabarti et al., 2004Marcinko et al., 20052007, 2008; Repo-Tiihonen et al., 2002) investigating only male schizophrenia patients found a significant association between low cholesterol and suicidality, except one group (Turkoglu et al., 2009) who did not report a significant association. On the contrary, three study authors observed an association only in female participants: two for suicidality (Misiak et al., 2015Shrivastava et al., 2017) and one for violence towards others in patients with schizophrenia (Chen et al., 2015). However, one study (Eriksen et al., 2017) did not find this specific correlation in female participants.

Thus, it can be concluded that cholesterol levels could be used, in part, as predictors of violence in patients with schizophrenia. The evidence for a clear link with sex remains inconclusive. This is an important area for further work given that rates of violence in psychiatric patients following discharge tend to be higher in men than in women (Robbins et al., 2003). In addition, the neurobiology of violence, factors like body mass index (BMI), incidence of metabolic syndrome following antipsychotic medication and the effects of cholesterol are different between men and women, suggesting that discrete effects may occur in each sex (Golomb, 1998).


There were several limitations regarding the studies reviewed. First, in many of the studies reviewed, the main focus was on suicide and physical aggression to others. As a result, most patients observed were clinically ill enough to warrant inpatient treatment. Few studies evaluated aggression as physical against property and verbal, potentially deemed less severe and more likely to be seen in community or outpatient-based studies. A representative view of schizophrenia patients of all severities, including inpatients and outpatients, was therefore not specifically assessed in this review. Second, confounding factors, including sex, medication and age, may have affected the findings of this review. According to the Gender Paradox in Suicide, men are more likely to die by suicide than women, while women are more likely to engage in suicidal behaviour and deliberate self-harm (Canetto and Sakinofsky, 1998). However, self-harm was not frequently assessed in these studies. There is some indication of a link between low TC, HDL, LDL and impulsivity, which could translate into risk of self-harm, but this link needs to be explored through studies in populations with higher self-harming behaviours, like inpatient female wards. Medication, such as certain antipsychotics like risperidone, stimulate serotonergic output in cortical and subcortical areas more than other antipsychotics (Amato, 2015), and this may contribute to changes in aggressive behaviour independent of cholesterol level. In addition, with age comes a natural variance in cholesterol level, with a tendency of increased serum cholesterol with increasing age (Morgan et al., 2016). Aggressive behaviour may be independent of low cholesterol in younger participants as they, typically, would have a lower cholesterol level when compared to older patients. The effects of age as well as medication were not accounted for in a number of studies. Finally, the lack of statistical analysis using a 95% confidence interval in a number of studies (see Table 4) limited the review by making it difficult to assess precision and risk in data obtained.

In addition, there are limitations to the review itself. First, the review may have been limited by only allowing diagnosis of schizophrenia by a variant of DSM or ICD classifications. This excluded foreign classifications such as T-SCL-90-R. Second, selection bias arose when only considering studies reported in English. The inclusion and exclusion criteria stated that participants must be adults only, unless unavoidable. As a result, three included studies (Chen et al., 2015Repo-Tiihonen et al., 2002Ruljancic et al., 2007) had some participants below the age of 18, leading to wide variations in the age range of the study participants.

Sweden: Parental absences tend to be associated with earlier first births, and more reliably so for women; recent changes in effects may mean that fathers start influencing sons and daughters more similarly

Historical Context Changes Pathways of Parental Influence on Reproduction: An Empirical Test from 20th-Century Sweden. Cristina Moya et al. Soc. Sci. 2021, 10(7), 260, Jul 8 2021.

Abstract: Several studies have found that parental absences in childhood are associated with individuals’ reproductive strategies later in life. However, these associations vary across populations and the reasons for this heterogeneity remain debated. In this paper, we examine the diversity of parental associations in three ways. First, we test whether different kinds of parental availability in childhood and adolescence are associated with women’s and men’s ages at first birth using the intergenerational and longitudinal Uppsala Birth Cohort Study (UBCoS) dataset from Sweden. This cultural context provides a strong test of the hypothesis that parents influence life history strategies given that robust social safety nets may buffer parental absences. Second, we examine whether investments in education help explain why early parental presence is associated with delayed ages at first birth in many post-industrial societies, given that parents often support educational achievement. Third, we compare parental associations with reproductive timing across two adjacent generations in Sweden. This historical contrast allows us to control for many sources of heterogeneity while examining whether changing educational access and norms across the 20th-century change the magnitude and pathways of parental influence. We find that parental absences tend to be associated with earlier first births, and more reliably so for women. Many of these associations are partially mediated by university attendance. However, we also find important differences across cohorts. For example, the associations with paternal death become similar for sons and daughters in the more recent cohort. One possible explanation for this finding is that fathers start influencing sons and daughters more similarly. Our results illustrate that historical changes within a population can quickly shift how family affects life history.

Keywords: fertility; reproductive timing; family structure; life history strategies; educational attainment; cohort effects

Sex differences are consistent in rest state fMRI and should be considered seriously in any study; features that discriminate males and females were found to be distributed across several different brain regions

Machine Learning Evidence for Sex Differences Consistently Influences Resting-State fMRI Fluctuations Across Multiple Independently-Acquired Datasets. Obada Al Zoubi et al. Brain Connectivity, Jul 16 2021.


Background/Introduction: Sex classification using functional connectivity (FC) from resting-state fMRI (rs-fMRI) has shown promising results. This suggested that sex difference might also be embedded in the blood-oxygen-level-dependent (BOLD) properties like the amplitude of low-frequency fluctuation (ALFF) and the fraction of ALFF (fALFF). This study comprehensively investigates sex differences using a reliable and explainable machine learning (ML) pipeline. Five independent cohorts of resting-state fMRI with over than 5500 samples were used to assess sex classification performance and map the spatial distribution of the important brain regions.

Methods: Five rsfMRI samples were used to extract ALFF and fALFF features from predefined brain parcellations and then were fed into an unbiased and explainable ML pipeline with a wide range of methods. The pipeline comprehensively assessed unbiased performance for within-sample and across sample validation. Additionally, the parcellation effect, classifiers selection, scanning length, spatial distribution, reproducibility, and feature importance were analyzed and evaluated thoroughly in the study.

Results: The results demonstrated high sex classification accuracies from healthy adults (area under the curve (AUC) > 0.89) while degrading for non-healthy subjects. Sex classification showed moderate to good intraclass correlation coefficient (ICC) based on parcellation. Linear classifiers outperform non-linear classifiers. Sex differences could be detected even with a short rs-fMRI scan (e.g., 2 minutes). The spatial distribution of important features overlaps with previous results from Studies.

Discussion: Sex differences are consistent in rs-fMRI and should be considered seriously in any study design, analysis, or interpretation. Features that discriminate males and females were found to be distributed across several different brain regions, suggesting a complex mosaic for sex differences in resting-state fMRI.

The evidence is consistent with the possibility that urgent care centers—which are increasingly owned by or contract with hospital systems—induce greater spending on hospital care

Do Urgent Care Centers Reduce Medicare Spending? Janet Currie, Anastasia Karpova & Dan Zeltzer. NBER Working Paper 29047. Jul 2021. DOI 10.3386/w29047

Abstract: We examine the impact of the opening of a new urgent care center (UCC) on health care costs and the utilization of care among nearby Medicare beneficiaries. We focus on 2006–2016, a period of rapid UCC expansion. We find that total Medicare spending rises when residents of a zip code are first served by a UCC, relative to spending in yet-to-be-served zip codes, while mortality remains flat. We explore mechanisms by looking at categories of spending and by examining utilization. Increases in inpatient visits are the largest contributor to the overall increase in spending, rising by 6.65 percent within six years after UCC entry. The number of emergency room visits that result in a hospital admission also increases by 3.7 percent. In contrast, there is no change in the number of ER visits that do not result in admission to hospital, in visits to physicians outside a UCC, or in imaging and tests. Overall, these results provide little evidence that UCCs replace costly ER visits or that they crowd out visits to patients' regular doctors. Instead, the evidence is consistent with the possibility that UCCs—which are increasingly owned by or contract with hospital systems—induce greater spending on hospital care.