Elucidating the role of macro- and neighborhood-level exposures in adolescent psychotic experiences could be particularly informative for early intervention efforts, because the clinical relevance of psychotic phenomena increases later in adolescence.Cities have higher rates of violent crime and tend to be more threatening and less socially cohesive.Additionally, 16–24 year-olds in the United Kingdom are 3 times more likely than other age groups to be victimized by a violent crime.Therefore, many adolescents raised in cities are not only embedded in more socially adverse neighborhoods, but are also more likely be personally victimized by crime compared to other age groups and peers living in rural neighborhoods. Given that cumulative trauma is implicated in risk for psychosis,we hypothesized that one of the reasons that young people in urban settings are at increased risk for psychotic phenomena is that they experience a greater accumulation of neighborhood-level social adversity and personal experiences of violence during upbringing. No study has yet explored the potential cumulative effects of adverse neighborhood social conditions and personal crime victimization on the emergence of psychotic experiences during adolescence. The present study addresses this topic with data from a nationally-representative cohort of over 2000 British adolescents, who have been interviewed repeatedly up to age 18, with comprehensive assessments of victimization and psychotic experiences and high-resolution measures of the built and social environment. We asked: Are psychotic experiences more common among adolescents raised in urban vs rural settings? And does this association hold after controlling for neighborhood-level deprivation,vertical rack as well as individual- and family-level factors, that might otherwise explain the relationship? Can the association between urban upbringing and adolescent psychotic experiences be explained by urban neighborhoods having lower levels of social cohesion and higher levels of neighborhood disorder ?
Are psychotic experiences more common among adolescents who have been personally victimized by a violent crime? And Is there a cumulative effect of neighborhood social adversity and personal crime victimization on adolescent psychotic experiences? In addition, the present study conducted sensitivity analyses using adolescent psychotic symptoms as the outcome .We conducted analyses following 5 steps. First, logistic regression was used to test whether psychotic experiences were more common among adolescents raised in urban neighborhoods. We controlled for family- and individual-level factors and for neighborhood-level deprivation to check that the association was not explained by these characteristics which could potentially differ between urban vs rural residents. We also examined the association between urbanicity and adolescent major depression to check for specificity of the previous findings. Second, because urban neighborhoods are characterized by lower levels of social cohesion and higher levels of neighborhood disorder we tested whether levels of these neighborhood characteristics accounted for the association between urbanicity and adolescent psychotic experiences, and we also estimated the separate associations of social cohesion and neighborhood disorder with adolescent psychotic experiences. Third, using logistic regression we checked whether adolescents who had lived in the most socially adverse neighborhoods were more likely to be personally victimized by violent crime and, in turn, whether psychotic experiences were more common among adolescents who had been victimized. Fourth, using interaction contrast ratio analysis we investigated potential cumulative and interactive effects of adverse neighborhood social conditions and personal victimization by violent crime on adolescent psychotic experiences. Four exposure categories were created for this analysis by combining neighborhood social adversity with personal crime victimization . Finally, sensitivity analyses were conducted using the clinically-verified adolescent psychotic symptoms as the outcome measure. All analyses were conducted in STATA 14.2 , and accounted for the non-independence of twin observations using the “CLUSTER” command.
This procedure is derived from the Huber-White variance estimator, and provides robust standard errors adjusted for within cluster correlated data.Note: ordinal logistic regression was used in analyses where adolescent psychotic experiences was the dependent variable, because this was on an ordinal scale.This study investigated the role of urbanicity, neighborhood social conditions, and personal crime victimization in adolescent psychotic experiences and revealed 3 initial findings. First, the association between growing up in an urban environment and adolescent psychotic experiences remained after considering a range of potential confounders including family SES, family psychiatric history, maternal psychosis, adolescent substance problems, and neighborhood-level deprivation. This association between urbanicity and psychotic experiences was explained, in part, by 2 features of the neighborhood social environment, namely lower levels of social cohesion and higher levels of neighborhood disorder. Second, personal victimization by violent crime was nearly twice as common among adolescents in the most socially adverse neighborhoods, and adolescents who had experienced such victimization had over 3 times greater odds of having psychotic experiences. Third, the cumulative effect of neighborhood social adversity and personal crime victimization on adolescent psychotic experiences was substantially greater than either exposure alone, highlighting a potential interaction between these exposures. That is, adolescents who had lived in the most adverse neighborhood conditions and been personally victimized were at the greatest risk for psychotic experiences during adolescence. The present findings extend previous evidence from this cohort implicating childhood urbanicity and neighborhood characteristics in the occurrence of childhood psychotic symptoms.Here we show that the effects of urban and socially adverse neighborhood conditions on psychotic experiences are not limited to childhood, but continue into adolescence when psychotic phenomena become more clinically relevant.These findings support previous evidence demonstrating higher rates of psychosis-proneness and prodromal status among adolescents and young adults in urban,threatening,and socially fragmented neighborhoods.
Late adolescence heralds the peak age at which psychotic disorders are typically diagnosed.If a degree of aetiological continuity truly exists between adolescent psychotic experiences and adult psychotic disorder, ours and other recent findings tentatively support a mechanism linking adverse neighborhood conditions during upbringing with psychosis in adulthood. In our study,microgreen flood table the combined effect of adverse neighborhood social conditions and personal victimization by violent crime was greater than the independent effects of each. This is consistent with cumulative stress models and previous studies showing that risk for psychosis phenotypes increases as the frequency and severity of stressful exposures increase.Several biological and psychological mechanisms could explain why adolescents who were exposed to neighborhood social adversity and violent crime during upbringing were more prone to psychotic experiences. Prolonged and acute early-life stress is purported to dysregulate the biological stress response and lead to dopaminergic sensitization, which is the leading hypothesized neurochemical pathway for the positive symptoms of psychosis.In addition, adolescents who grow up in threatening neighborhoods with weak or absent community networks could develop psychosislike cognitive schemas such as paranoia, hypervigilance, and negative attributional styles.A cognitive pathway could explain why effects were apparent for psychotic experiences but not major depression. Our findings tentatively suggest a mechanism whereby childhood exposure to neighborhood social adversity sensitizes individuals to subsequent stressful experiences such as crime victimization. This hypothesized mechanism is supported by recent evidence of neurological differences in social stress reactivity between adults with urban vs rural upbringing.Further research into the influence of neighborhood exposures on childhood neurocognitive development could shed light on this hypothesized mechanism.Several limitations should be considered. First, causality of findings from this observational study cannot be assumed. Noncausal mechanisms, such as the selection of genetically high-risk families into urban and adverse neighborhoods, remain possible,though our findings were not explained by proxy indicators of genetic and familial risk. Second, neighborhood conditions were measured approximately 5 years before adolescent psychotic experiences were assessed. However, the vast majority of adolescents reported that they did not move house between ages 12 and 18. Third, though crime victimization was more common in adverse neighborhoods, we do not know the extent to which these victimization experiences occurred outside the home. Perpetrators of physical violence are often family members,suggesting that our measure of violent crime captured victimization inside as well as outside the home. Fourth, psychotic experiences are associated with adult psychosis but also with other serious psychiatric conditions; while a degree of specificity was suggested in that the effect of urbanicity on psychotic experiences was not replicated for adolescent depression and was not explained by adolescent substance problems, it is probable that the mental health implications of growing up in an urban setting extend beyond psychosis.
In addition, associations arising for the clinically-verified psychotic symptoms were often non-significant. It is possible that the low prevalence of psychotic symptoms in this sample restricted our power to detect associations. However, it is also possible that the self-report measure of adolescent psychotic experiences captured genuine experiences as well as psychotic phenomena . This may have inflated the associations arising for adolescent psychotic experiences, though it is reassuring that point estimates were fairly similar to those produced for psychotic symptoms. Finally, our findings come from a sample of twins which potentially differ from singletons. However, E-Risk families closely match the distribution of UK families across the spectrum of urbanicity and neighborhood level deprivation.Furthermore, the prevalence of adolescent psychotic experiences among E-Risk participants is similar to non-twin samples of adolescents and young adults.Acute pancreatitis is an acute, inflammatory, potentially life-threatening condition of the pancreas. With over 100000 hospital admissions per annum, acute pancreatitis is the leading gastrointestinal cause of hospitalization in the United States and the 10th most common non-malignant cause of death among all gastrointestinal, pancreatic, and liver diseases . It is a major cause of morbidity and healthcare expenditure not only in the United States, but worldwide. There are numerous established etiologies of acute pancreatitis, among which gallstones and alcohol are the most common. The remaining cases are primarily attributable to the following etiologic factors: Hypertriglyceridemia, autoimmune, infection, hyper/hypocalcemia, malignancy, genetics, endoscopic retrograde cholangiopancreatography, and trauma. Despite accounting for approximately only 1%-2% of cases overall, drug-induced pancreatitis has become increasingly recognized as an additional and vitally important, albeit often inconspicuous, etiology of acute pancreatitis. The World Health Organization database lists 525 different medications associated with acute pancreatitis.Unfortunately, few population-based studies on the true incidence of DIP exist, limiting knowledge of true incidence and prevalence. In this setting, we review the ever-increasing diversity of DIP, with emphasis on the wide range of drug classes reported and their respective pathophysiologic mechanisms – in an attempt to raise awareness of the true and underestimated prevalence of DIP. We hope this manuscript will aid in increasing secondary prevention of DIP ultimately leading to a decrease in overall acute pancreatitis-related hospitalizations and economic burden on the health care system. As there is no standardized approach to stratifying patients to determine their risk of developing acute pancreatitis, primary prevention for the majority of etiologies cannot be fully implemented. Secondary prevention of acute pancreatitis, on the other hand, can more easily be executed. For example, abstinence from alcohol reduces the risk of alcoholic pancreatitis, cholecystectomy reduces the risk of gallstone pancreatitis, and tight control of triglycerides reduces the risk of recurrent episodes of pancreatitis secondary to hypertriglyceridemia. On this notion, unique to DIP, is the fact that it can be prevented in both the primary and secondary fashion. Unfortunately, however, most of the available data in reference to DIP is derived from case reports, case series, or case control studies. In this vein, the causality between specific medications and acute pancreatitis has been established in only a minority ofcases. In addition, oftentimes, lack of a known etiology for acute pancreatitis directly increases length of hospitalization due to delayed diagnosis and subsequent treatment. Moreover, patients unaware of an adverse drug reaction to a prior medication may continue taking that medication leading to repeat hospitalizations. Finally, with the rapid expansion of pharmacologic agents, widespread legalization of cannabis, increase in recognized medications, supplements, and alternative medications reported to induce pancreatitis, the need to become familiar with this esoteric group remains imperative, and knowledge in the form of awareness regarding certain medications is warranted.First, the lack of mandatory adverse drug reporting systems allow many cases to go unreported. Second, bias exists, in the sense that clinicians tend to forgo linking unusual medication suspects to a rare adverse event. Third, it is often difficult to rule out other, more common, causes of drug-induced pancreatitis, especially in patients who have multiple comorbidities and underlying risk factors. Fourth, many cases lack a re-challenge test or drug latency period to definitively link acute pancreatitis to a particular drug. Finally, evidence is lacking to support the use of any serial monitoring technique – namely, imaging or pancreatic enzymes to help detect cases of drug-induced pancreatitis.