Books on the topic 'Health status - Morbidity and mortality rates'

This handbook signals a paradigm shift in health research. Population-based disciplines have employed large national samples to examine how sociodemographic factors contour rates of morbidity and mortality. Behavioral and psychosocial disciplines have studied the factors that influence these domains using small, nonrepresentative samples in experimental or longitudinal contexts. Biomedical disciplines, drawing on diverse fields, have examined mechanistic processes implicated in disease outcomes. The collection of chapters in this handbook embraces all such prior approaches and, via targeted questions, illustrates how they can be woven together. Diverse contributions showcase how social structural influences work together with psychosocial influences or experiential factors to impact differing health outcomes, including profiles of biological risk across distinct physiological systems. These varied biopsychosocial advances have grown up around the Midlife in the United States (MIDUS) national study of health, begun over 20 years ago and now encompassing over 12,000 Americans followed through time. The overarching principle behind the MIDUS enterprise is that deeper understanding of why some individuals remain healthy and well as they move across the decades of adult life, while others succumb to differing varieties of disease, dysfunction, or disability, requires a commitment to comprehensiveness that attends to the interplay of multiple interacting influences. Put another way, all of the disciplines mentioned have reliably documented influences on health, but in and of themselves, each is inherently limited because it neglects factors known to matter for health outside the discipline’s purview. Integrative health science is the alternative seeking to overcome these limitations.

Increasing numbers of studies of correctional populations have emphasized diagnosis with structured clinical instruments over the past two decades. These studies have primarily focused on serious mental illness (i.e., psychotic and mood disorders), substance use disorders, and personality disorders. The focus has made sense because of the need to identify the severely mentally ill who are incarcerated and to identify the most common disorders. Anxiety disorders include generalized anxiety disorder, social anxiety disorder, panic disorder, and specific phobias. One anxiety disorder that stands apart from others is PTSD, which is prevalent at much higher rates in both incarcerated men and women than in the community. Despite this fact, other anxiety disorders are often co-morbid and add to overall disease burden and impair ability to function. Individuals with a greater disease burden (i.e., number of diagnoses, symptom counts) have worse outcomes than those with uncomplicated disorders. These impaired outcomes include a deteriorating trajectory of illness, increased health service utilization, poor prognosis, and increased likelihood of morbidity and mortality. Thus, while anxiety disorders may not be the primary focus of the correctional system, they must be recognized as important. Unrecognized anxiety disorders can result in behavior that is disruptive and may appear to be volitional. They can also lead to overutilization of health services that are already facing substantial demands. Appropriate, available, and consistent assessment, diagnosis, and treatment that are well integrated can successfully intervene in the range of anxiety disorders that present in correctional settings.

Sleep disorders are associated with several morbidities, most strongly with psychiatric disorders, cognitive impairment, and impaired quality of life, as well as with increased mortality. Sleep problems are common across the lifespan from childhood to adolescence and adulthood. Physiological sleep continuity with respect to circadian rhythms is considered to be important for the maintenance of cardiovascular, metabolic, and immune function, physiological homeostasis, and psychological balance. Nowadays, it is reasonable to include sleep disturbances among the top 10 potentially modifiable cardiovascular disease (CVD) risk factors. The links between sleep disorders and morbidity as CVD show bidirectional associations. Because these disorders are chronic, they may also have a deleterious societal impact on a patient’s employment status, ability to work, risk of accident, and health. The relationship between work performance and sleep quality is reciprocal and potentially complex. This chapter illustrates the principal sleep disorders and their relevance as indicators of health status.

As a public good, antimicrobial medicines require rational use if their effectiveness is to be preserved. However, up to 50% of antibiotic use is inappropriate, adding considerable costs to patient care, and increasing morbidity and mortality. In addition, there is compelling evidence that antimicrobial resistance is driven by the volume of antimicrobial agents used. High rates of antimicrobial resistance to common treatments are currently reported all over the world, both in health care settings and in the community. For over two decades, the Region of the Americas has been a pioneer in confronting antimicrobial resistance from a public health perspective. However, those efforts need to be stepped up if we are to have an impact on antimicrobial resistance and want to quantify said impact.

The relationship between socioeconomic status (SES) and cancer is complex, dynamic, and evolving. Associations depend on SES measures, cancer type, sociodemographic factors including race/ethnicity, and historical trends. However, socioeconomic disadvantage is often associated with a higher risk of cancer, particularly cancers diagnosed at a late stage, as well as worse prognosis once diagnosed. Research on secular trends over the past 70 years has shown reversals of the socioeconomic gradient for lung and colorectal cancer consistent with differential trends by SES in patterns of smoking, diet, and obesity. Rates of these cancers are now currently higher in socioeconomically disadvantaged groups. SES is considered to be a “fundamental” determinant of health outcomes, and this appears true throughout the cancer spectrum—from cancer incidence to detection, treatment, and survival. Investigations over the past decade have increasingly considered the simultaneous impact of individual SES and area-level SES (as a contextual influence) on health outcomes.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.

This chapter points out that some researchers explain the higher mortality rates among blacks in the United States as “nature”, blaming such rates primarily on blacks' genetic makeup. Others explain the phenomenon as “nurture”, blaming social status differences stemming from systemic discrimination. For a genetic difference to be used to explain an observed health disparity, the identified causal variant would have to have a large effect on the disease phenotype risk and would have to have a substantially different prevalence in the two racial populations, and the disease would have to be a significant contributor to mortality in the racial population. Genetic studies were done on cardiovascular disease, type II diabetes, homicide, and more. In evaluating results from these studies and previous knowledge, 3% of the entire racial disparity in mortality can be accounted for, which leaves 97% of disparities to social origin.

Compared with episodic depression, chronic depression and treatment resistant depression have higher rates of comorbidity, more persistent social and vocational disability, an increased risk of suicide, greater medical morbidity and mortality, and greater health care utilization and costs. A large number of antidepressant medications and other psychotropic drugs, depression-focused psychotherapies, and neuromodulation therapies are available for the treatment of depression. Many drugs or psychotherapies are used for the treatment of other psychiatric disorders or medical conditions, and they should be considered relevant when these comorbidities exist with depression. Selecting treatments for depression must take into account the clinical implications of the presence of any comorbidities. Because comorbidity is associated with depressive chronicity and treatment resistance, various approaches to treating chronic depression or TRD have been investigated. Treating depressed patients with comorbid psychiatric, personality, or medical disorders is a clinical challenge that requires effective multidisciplinary collaboration.

Bipolar disorder is a chronic and debilitating mental illness affecting a significant proportion of the world’s population. It is associated with significant impairments in health-related quality of life and psychosocial functioning, and has significant illness-related morbidity and heightened mortality rates due to medical co-morbidities and suicide. The management of this disorder requires a complex combination of pharmacological and psychosocial interventions which can be challenging for clinicians. This book provides readers with a concise and comprehensive guide to the integrative management of bipolar disorder. This resource contains 31 chapters on the various management choices available, from both established and novel treatment areas, such as psychoeducation, psychotherapeutic interventions, neuromodulatory approaches, and novel therapeutic targets. The complexity and diversity of the management choices available makes this a continually evolving field and necessitates forward thinking. By discussing both the current management of bipolar disorder and the future developments available, this book provides all clinicians working with patients with bipolar disorder an up-to-date and reflective guide to its management and what the future holds.

Globally, tuberculosis (TB) is a major cause of morbidity and mortality among people who use drugs (PWUD), particularly those co-infected with HIV. This chapter describes how TB is prevalent in several prison systems by virtue of the concentration of PWUD and people living with HIV. TB is further amplified within this system through overcrowding, poor ventilation, and delayed access to quality prevention and treatment services. In many countries, individuals cycling through prisons are inadequately screened and treated for TB, and affected individuals may have frequent treatment interruptions. For PWUD, relapse to drug use immediately after release from custody can impede continuity of care, which may contribute to the development of drug-resistant TB. Particularly in countries with high incarceration rates, prisons act as amplifiers of TB and drug-resistant TB in the community. The World Health Organization’s recommendations for integration of TB, HIV, and addiction treatment are seldom achieved, especially within prisons. Other factors contributing to poor TB outcomes among PWUD interfacing with prisons include insufficient support to promote medication adherence and co-morbidities, like viral hepatitis that potentiate hepatic toxicity, both of which are prevalent among PWUD.

Since 9/11 2001, international attention has once again focused on the risks to human and animal health from the deliberate release of infectious or toxic chemical agents. In theory any agent could be used by terrorists and disaffected people, but the most serious risk for infectious agents are mainly zoonotic (Franz et al. 1997). Three modes of exposure may be anticipated, inhalation of powder or spray or dust from explosives, direct contact or inoculation from an explosion, and ingestion. Centers for Disease Control (CDC) list 19 bioterrorism agents or groups of agents of which 14 are zoonotic. In Category A are 6 agents which can be easily disseminated or transmitted from person to person, that result in high mortality rates and have the potential for major public health impact, which might cause public panic and social disruption and which require special action from public health preparedness. Of these 6, four are zoonoses — Anthrax, Plague, Tularaemia and Viral Haemorrhagic Fevers. In Category B, are 12 groups of agents, which are moderately easy to disseminate and cause moderate morbidity. Of these 12 groups, 8 contain zoonoses: Brucellosis, Food Safety threats (e.g. Salmonella, E.coli 0157, Campylobacter), Meliodiosis, Psittacoccosis, Q Fever, Typhus, Viral encephalitis, Water safety threats (e.g. Cryptosporidium).

AbstractSchistosomiasis is a parasitic disease that affects millions of people in 78 countries, where it is held responsible for considerable morbidity and mortality. It is caused by a blood fluke, which provokes an immunological response to hundreds of its antigens. This induces multi-organ pathology through the formation of tissue granulomata or circulating immune complexes. In addition, it is amyloidogenic and carcinogenic, through the interaction of immunological perturbation with confounding metabolic and genetic factors. The primary targets of schistosomiasis are urinary and hepatointestinal.The lower urinary tract is mainly affected in S. haematobium infection, and may lead to chronic pyelonephritis and/or obstructive nephropathy. The colon and liver are the targets of S. mansoni and S. japonicum infection, leading to hepatic fibrosis, portal hypertension, and liver failure. S. mansoni may also lead to immune complex glomerulonephritis, which is discussed elsewhere. Both S. haematobium and S. mansoni ova may be carried with the venous circulation to the lungs, where they provoke granulomatous and immune-mediated endothelial injury leading to cor-pulmonale. Ova may be subsequently carried with the arterial circulation to form ‘metastatic’ granulomas in other tissues, notably the brain (S. japonicum), spinal cord (S. haematobium), skin, conjunctiva, and genital organs.Schistosomiasis is preventable. World Health Organization programmes have successfully eradicated or reduced the incidence of infection in many countries, particularly Egypt and China. Prevention strategies include health education, raising hygiene standards, and interruption of the parasite’s life cycle by snail control and mass treatment. The search for a vaccine continues. Effective antiparasitic treatment is now possible with high elimination rates. Available agents include praziquantel and artemether for all species, metrifonate for S. haematobium, and oxamniquine for S. mansoni. Successful outcome correlates with early intervention, before fibrosis has occurred.

The development of haemodialysis for the treatment of chronic kidney disease was a remarkable step in medicine that moved what was once a universally fatal organ failure to a condition that is regarded as treatable. Over the decades since that remarkable advancement, mechanical methods of blood purification to correct the uraemic condition have gained a prominent and often expected role in the care of the patient with end-stage kidney failure. Even so, patients with end-stage kidney disease still experience high rates of morbidity and mortality, at times surpassing other chronic conditions such as cancer. The goal of haemodialysis should be not only to maintain life but also to restore the afflicted individual to a state of health, thus rehabilitating them so that they can lead a meaningful, fulfilling life. Currently utilized methods of haemodialysis, while effective at acutely reversing the uraemic condition, often fall short of the goal of rehabilitation. This observation, among others, has led many scientists and physicians to suspect that contemporary dialytic therapy is inadequate and has led to vigorous pursuit of the question: what is the adequate dose of dialysis? While extensive effort has been devoted to the pursuit of this question, it has yet to be definitively answered to the satisfaction of the scientific community. This chapter will predominantly focus on currently popularized and frequently utilized methods for measurement of dialysis dose with the stipulation that the reader understands that the determination of the adequate dose of dialysis is an evolving field and in clinical practice should require more diligence than simple surveillance of urea clearance. The adequacy of volume management, which is arguably of equal importance to the adequacy of uraemic retention solute clearance is covered in other chapters within this book.