Wednesday, 4 January 2017

What is fever? |


Causes and Symptoms

Although the symptoms that often accompany a fever are familiar to everyone—shivering, sweating, thirst, hot skin, and a flushed face—what causes fever and its function during illness are not fully clear even among medical specialists. Considerable literature exists on the differences between warm-blooded organisms (endotherms) and cold-blooded organisms (ectotherms) in what is called the normal state, when no symptoms of disease are present. Cold-blooded organisms depend on temperature conditions in their external environment to maintain various levels of temperature within their bodies. These fluctuations correspond to the various levels of activity that they need to sustain at given moments. Thus, reptiles, for example, may “recharge” themselves internally by moving into the warmth of the sun. Warm-blooded organisms, on the other hand, including all mammals, utilize energy released from the digestion of food to maintain a constant level of heat within their bodies. This level—a “normal” temperature—is approximately 37 degrees Celsius (98.6 degrees Fahrenheit) in humans. An internal body temperature that rises above this level is called a febrile temperature, or a fever.



If the temperature in the surrounding environment is low, warm-blooded animals must raise their metabolic rate (a measurement, in calories, of converted energy) accordingly to maintain a normal internal body temperature. In humans, this rate of energy expenditure is about 1,800 calories per day. If insufficient food is taken in to supply the necessary potential energy for this metabolic conversion into heat, the body will draw on its storage resource—fat—to fulfill this vital need. The potentially fatal condition called hypothermia, in which the body is too fatigued to maintain metabolic functions or has exhausted all of its stores of calories, occurs when the internal temperature falls below normal. Although cold-blooded animals must also protect themselves against the danger that their body heat may fall too low to sustain life functions, they can support adjustments in their own internal temperature down to about 20 degrees Celsius. At the same time, metabolic expenditures, as measured in calories, are very low in cold-blooded animals; for example, alligators must expend only 60 calories per day to create the same amount of heat as 1,800 calories per day in warm-blooded humans.


The question of internal temperature in warm-blooded animals is closely tied to management efficiency in the body. This function becomes critical when one considers abnormally high internal temperature, or fever. Generally speaking, all essential biochemical functions in the human body can be carried out at optimal levels of efficiency at the set point of 37 degrees Celsius. In the simplest of terms, any increase or decrease in temperature creates either more or less kinetic energy and has the potential to affect the chemistry of all body functions.


Endotherms are able to tolerate a certain range of involuntary change in their internal body temperature (brought about by disease or illness), but there is an upper limit of 45 degrees Celsius, which constitutes a high fever. If the self-regulating higher set point associated with fever goes beyond this point, destructive biochemical phenomena will occur in the body—in particular, a breaking down of protein molecules. If these phenomena are not checked, they can bring about death.


Modern scientific approaches to the internal body processes that lead to fever, like a medical discussion of the effects that occur once fever is operating in the body, are much more complicated. They revolve around the concept of a change in the set point monitored in the brain. When this change in the brain’s normal (37 degree) thermostatic signal is called for, a process called phagocytosis begins, leading to a higher internal body heat level throughout the organism.


Phagocytosis, the ingestion of a solid substance (especially foreign material such as invading bacteria), involves the appearance in the host’s system of large numbers of leukocyte cells. When these cells ingest the bacteria, small quantities of protein called leukocytic pyrogens are produced. According to most modern theories, these protein pyrogens trigger the biochemical reactions in the brain that alter the body’s temperature set point. After this point, changes that occur throughout the system and raise the body’s internal temperature depend on a component of the bacterial cell wall called endotoxin. By the end of the 1960s, researchers had drawn attention to at least twenty effects that activated endotoxins may have on the host organism. Key effects include enhancement of the production of new white blood cells (leukocytosis), enhancement of various forms of immunological resistance, reduction of serum iron levels, and lowering of blood pressure.


Most, if not all, of these effects brought about by endotoxins are accompanied by higher levels of heat throughout the body, the definition of fever. Closer biochemical examination of the source of the added heat yielded the suggestion, made by P. B. Beeson in 1948, that the host’s endotoxin-affected cells begin to produce a distinct form of protein, now called endogenous pyrogens. Pyrogens are thought to induce the first stage of fever by interacting with cells in tissues very close to the brain, specifically in the brain stem itself. Laboratory experiments in the first half of the twentieth century allowed researchers to produce almost immediate fever reactions when they injected pyrogen protein material into rabbits. Studies of the induced febrile state in laboratory animals, and therefore presumably also in humans, linked fever to immunological (virus-resistant and bacteria-resistant) reactions, not necessarily in the initially affected tissues around the brain but in various places throughout the organism. Scientific research into the effect of pyrogens on thermoregulation and into the febrile process in general remains ongoing.




Treatment and Therapy

The febrile response has been noted in five of the seven extant classes of vertebrates on earth (Agnatha, such as lampreys, and Chondrichthyes, such as sharks, are excluded). Scientists have determined that its function as a reaction to bacterial infection can be traced back as far as 400 million years in primitive bony fishes. The question of whether the natural phenomenon of fever actually aids in combating disease in the body, however, has not been fully resolved.


In ancient and medieval times, it was believed that fever served to “cook” and separate out one of the four essential body “humors”—blood, phlegm, yellow bile, and black bile—that had become excessively dominant. Throughout the centuries, such beliefs even caused some physicians to try to induce higher internal body temperatures as a means of treating disease. Use of modern antipyretic drugs to reduce fever remained unthinkable until the nineteenth century.


It was the German physician Carl von Liebermeister who, by the end of the nineteenth century, set some of the guidelines that are still generally observed in deciding whether antipyretic drugs should or should not be used to reduce a naturally occurring fever during illness. Liebermeister insisted that the phenomenon of fever was not one of body temperature gone “out of control” but rather a sign that the organism was regulating its own temperature. He also demonstrated that part of the process leading to increased internal temperature could be seen in reactions that actually reduce heat loss at the body’s surface, notably decreases in skin blood flow and evaporative cooling through perspiration. Liebermeister determined that one of the positive effects of higher temperatures inside the body was to impede the growth of harmful microorganisms. At the same time, however, other side effects of fever during illness were deemed to be negative, such as loss of appetite, and, in some cases, actual degeneration of key internal organs. Liebermeister’s generation of physicians, therefore, tended to rely on antipyretic drugs only when high fevers persisted for long periods of time. Moderate fevers or even high fevers, if they did not continue too long, were deemed to contribute to the overall process of natural body resistance to disease.


In fact, a limited school of physicians followed the teaching of 1927 Nobel laureate Julius Wagner-Jauregg, who claimed that “fever therapy” methods should be adopted for the treatment of certain diseases. Wagner-Jauregg himself had pioneered this theory by inoculating victims of neurosyphilis with fever-producing malaria. Part of his argument in favor of this experimental therapy was that malaria, with its accompanying fever, was a treatable disease (through the use of quinine) and could be controlled at regular intervals during its “service” as a fighter against a disease that still had no known cure. Later use of fever therapy for treatment of other sexually transmitted diseases, specifically gonorrhea, proved to be moderately successful. When typhoid vaccine was used to induce fevers in some patients, however, side effects such as hypotension (low blood pressure) or cardiovascular shock introduced what some considered to be dangerous risk factors. Nevertheless, certain fields of medicine, especially those involved with eye diseases and related eye ailments, have proved that fever-inducing agents (specifically those contained in typhoid and typhoid-paratyphoid vaccines) also induce beneficial secretion of the anti-inflammatory hormone cortisol.


By the second half of the twentieth century, the medical use of antipyretic drugs, containing such components as salicylates and indomethacin, had become widespread. This phenomenon was not caused by any compelling reversal of earlier general assumptions that moderate levels of fever, being a natural body reaction, were not necessarily harmful to patients suffering from a wide variety of diseases. Rather, physicians may have opted to use such drugs as much for their pain-relieving qualities as for their fever-reducing characteristics. Although patients receiving such drug treatment notice a diminishing of severe pains or general aching, the cause of the disease has not been combated merely by the removal of such symptoms as fever and pain.


Modern medical science has tended to support further study of particular circumstances in which induced fevers can actually produce disease-combating reactions. A newly emerging field by the late 1970s, for example, involved studying the benefits of higher temperatures in newborn infants fighting viral infections. Although specific circumstances and the nature of disease prevent a generalized conclusion in terms of the use of induced fevers as a form of treatment, researchers have shown that an elevated body temperature serves to increase the speed at which white blood cells, the body’s natural enemies against disease, move to infected areas.




Perspective and Prospects

Although doctors have been aware of the symptoms of fever since the beginnings of medical history, centuries passed before its importance as an indicator of disease was accepted. A certain degree of sophistication in the study of fevers became possible largely as a result of the development of the common thermometer, in a rudimentary form in the seventeenth century and then with greater technical accuracy in the eighteenth century. Systematic use of the thermometer in the eighteenth century enabled doctors to observe such phenomena as morning remission and evening peaking of fever intensity. Studies involving the recording of temperature in healthy individuals also yielded important discoveries. One such discovery was made in 1774, when use of the thermometer showed that, even in a room heated to the boiling point of water (100 degrees Celsius), healthy subjects maintained an internal body heat that was very close to the normal 37-degree level.


Medical reports as late as the end of the eighteenth century, however, indicate that even internationally recognized pioneers of science were still not close to understanding the causes of fever. The English doctor John Hunter, for example, declared himself opposed to the prevailing view that rising body heat came from the circulation of warmer blood throughout the body. Hunter suspected that the warmth was produced by an entirely different agent that was independent of the circulatory system. He never learned what that agent might be, however, and failed in defense of his theory that the source of added body heat was in the stomach. Even the famous French chemist Antoine-Laurent Lavoisier erred when he tried to explain fever in terms of some form of chemical “combustion” involving hydrogen and carbon. Lavoisier identified the lungs as the possible location for this spontaneous production of internal body heat.


Although these theories were identified as erroneous, the late eighteenth and early nineteenth century left one legacy that would develop into the twentieth century and is still practiced by physicians: systematic thermometry. In essence, thermometry involves the tracing of the upward or downward direction of fever during illness in order to judge the course of the disease and the effects brought about by different stages of treatment. In many diseases, for example, clinical records of the full course of previous cases can be studied by doctors responsible for treating an individual patient. With thermometry, the doctor is able to determine how far the body’s struggle against a certain disease has progressed. If thermometry shows a marked departure from what clinical records have charted as the normal course of disease under certain forms of treatment, then the physician may look for signs of another disease.




Bibliography


Best, Elspeth V., and Mark D. Schwartz. "Fever." Evolution, Medicine, and Public Health 2014, no. 1 (April, 2014): 92.



Brassfield, Krista, and Kenneth P. Steckel. Fevers: Types, Treatments and Health Risks (Human Anatomy and Physiology). Hauppauge: Nova Biomedical, 2013.



Kemper, Kathi J. The Holistic Pediatrician: A Pediatrician’s Comprehensive Guide to Safe and Effective Therapies for the Twenty-five Most Common Ailments of Infants, Children, and Adolescents. Rev. ed. New York: Quill, 2002.



Kluger, Matthew J. Fever: Its Biology, Evolution, and Function. Princeton: Princeton University Press, 1979.



Kluger, Matthew J., Tamas Bartfai, and Charles A. Dinarello, eds. Molecular Mechanisms of Fever. New York: New York Academy of Sciences, 1998.



Litin, Scott C., ed. Mayo Clinic Family Health Book. 4th ed. New York: HarperResource, 2009.



Mackowiak, Philip A., ed. Fever: Basic Mechanisms and Management. 2d ed. Philadelphia: Lippincott-Raven, 1997.



Nathanson, Laura Walther. The Portable Pediatrician: A Practicing Pediatrician’s Guide to Your Child’s Growth, Development, Health, and Behavior from Birth to Age Five. 2d ed. New York: HarperCollins, 2002.



Polsdorfer, Ricker. "Fever of Unknown Origin." Health Library, July 3, 2013.



Vasey, Christopher. The Healing Power of Fever: Your Body's Natural Defense Against Disease. Rochester: Healing Arts, 2011.

Tuesday, 3 January 2017

What is rhubarb as a dietary supplement?


Overview

The stalk of the intensely flavored rhubarb plant has been used in European cooking since the seventeenth century. Before this time, rhubarb species were utilized medicinally in traditional Chinese herbal medicine. Traditional uses include treatment of constipation, diarrhea, fever, menstrual problems, jaundice, sores (when applied topically), ulcers, and burns. Although there are many species of rhubarb, the one most studied is Rheum rhaponticum.






Uses and Applications

Rhubarb root contains lindleyin, a substance with estrogen-like properties. On this basis, extracts of rhubarb have been tried for the control of menopausal symptoms. In a twelve-week, double-blind, placebo-controlled trial of 109 women with menopause-related symptoms, the use of a standardized R. rhaponticum extract significantly improved symptoms compared with placebo. Improvements were particularly seen in rate and severity of hot flashes. While this is meaningful supporting evidence, additional independent trials are necessary to establish that this rhubarb extract is a safe and effective treatment for menopause.


Other potential uses of rhubarb lack reliable supporting evidence. One human trial purportedly found evidence that rhubarb could reduce the impairment of lung function that may occur when people with lung cancer receive radiation therapy. However, this study had a number of significant flaws, and its results cannot be regarded as reliable.


In another human trial, this one using a cream containing sage and rhubarb, researchers failed to find more than modest benefits for the treatment of herpes. Additional proposed uses of rhubarb are supported only by test-tube studies. For example, various rhubarb species have shown hints of potential value for the treatment of diabetes, kidney disease, liver disease, allergies, and pancreatitis. However, the vast majority of effects seen in test-tube studies do not recur in human trials.




Dosage

A typical dosage of rhubarb root is one-half to one teaspoonful of the root boiled for ten minutes in a cup of water, three times daily. In the foregoing menopause study, a standardized extract was used. Such extracts should be used according to label instructions.




Safety Issues

As a widely consumed food, rhubarb is thought to be relatively safe if consumed in moderation. However, the plant contains high levels of oxalic acid, and rhubarb consumption can markedly increase oxalic acid levels in the urine. This could lead to increased risk of kidney stones and other problems. Rhubarb leaf contains the highest oxalic acid content. The roots and stems contain less oxalic acid but higher levels of anthraquinones, laxative substances similar to those found in senna or cascara. It is safest to use rhubarb standardized extracts that have been processed to remove oxalic acid.


Contrary to some reports, consumption of rhubarb probably does not impair calcium absorption. Weak evidence hints that excessive consumption of rhubarb could increase the risk of stomach or colon cancer. Maximum safe doses in pregnant or nursing women, young children, and people with severe liver or kidney disease have not been established.




Bibliography


Choi, S. Z., et al. “Antidiabetic Stilbene and Anthraquinone Derivatives from Rheum undulatum.” Archives of Pharmacy Research 28 (2005): 1027-1030.



Heger, M., et al. “Efficacy and Safety of a Special Extract of Rheum rhaponticum (ERr 731) in Perimenopausal Women with Climacteric Complaints.” Menopause 13 (2006): 744-759.



Vollmer, G., A. Papke, and O. Zierau. “Treatment of Menopausal Symptoms by an Extract from the Roots of Rhapontic Rhubarb: The Role of Estrogen Receptors.” Chinese Medicine 5 (2010): 7.



Yu, H. M., et al. “Effects of Rhubarb Extract on Radiation Induced Lung Toxicity via Decreasing Transforming Growth Factor-Beta-1 and Interleukin-6 in Lung Cancer Patients Treated with Radiotherapy.” Lung Cancer 59 (2008): 219-226.



Zhao, Y. Q., et al. “Protective Effects of Rhubarb on Experimental Severe Acute Pancreatitis.” World Journal of Gastroenterology 10 (2004): 1005-1009.

Monday, 2 January 2017

What are support groups? |


Introduction

Humans are social animals in that they live in groups. These networks among people are powerful in shaping behavior, feelings, and judgments. Groups can lead to destructive behavior, such as mob violence and aggression, but they can also encourage loyalty, nurturing of others, and achievement, as found in cancer-support groups. Scientific investigation of how groups affect human behavior began as early as 1898, but the main body of research on group functioning began only in the 1940s and 1950s. The study of groups is still a major topic of scientific enquiry.


































D. R. Forsyth defined a group as “two or more individuals who influence each other through social interaction.” A group may be permanent or temporary, formal or informal, structured or unstructured. Those groups known as support groups may share any of these characteristics.


Why do human beings seek out groups? Social learning theorists
believe that humans learn to depend on other people because most are raised within families, where they learn to look to other people for support, validation, amusement, and advice. Exchange theorists, on the other hand, reason that groups provide both rewards (such as love and approval) and costs (such as time and effort). Membership in a group will “profit” the individual if the rewards are greater than the costs. Yet another set of theorists, the sociobiologists, argue that humans form groups because this has a survival benefit for the species. They hypothesize a genetic predisposition toward affiliation with others. It is within groups that the fittest have the greatest chance of survival.


Whatever the reason for forming groups, all groups have important characteristics that must be addressed in seeking to understand why support groups work. First of all, group size is important. Larger groups allow more anonymity, while smaller groups facilitate communication, for example. Group structure includes such elements as status differences, norms of conduct, leaders and followers, and subgroups. Individuals in groups develop social roles—those expected behaviors associated with the individual’s position within the group. Roles are powerful in influencing behavior and can even cause individuals to act contrary to their private feelings or their own interests. These roles carry varying degrees of status within the group—who is influential and respected and who is less so. Groups may have subgroups, based on age, residence, roles, interests, or other factors. These subgroups may contribute to the success of the whole or may become cliquish and undermine the main group’s effectiveness.


Groups also have varying degrees of cohesion. Cohesion reflects the strength of attachments within the group. Sometimes cohesion is a factor of how well group members like one another, sometimes a factor of the need to achieve an important goal, and sometimes a factor of the rewards that group membership confers. All groups have communication networks, or patterns of openness and restrictions on communication among members.


Group norms are those attitudes and behaviors that are expected of members. These norms are needed for the group’s success because they make life more predictable and efficient for the members. Leadership may be formal or informal, may be task oriented or people oriented, and may change over time. Finally, all groups go through fairly predictable stages as they form, do their work, and conclude. The comprehensive term for the way a group functions is
group dynamics
.




How Groups Influence Individuals

Researchers have found that for all animals, including human beings, the mere presence of other members of the same species may enhance performance on individual tasks. This phenomenon is known as social facilitation. However, with more complex tasks the presence of others may decrease performance. This is known as social inhibition or impairment. It is not clear whether this occurs because the presence of others arouses the individual, leads individuals to expect rewards or punishments based on past experience, makes people self-conscious, creates challenges to self-image, or affects the individual’s ability to process information. Most theorists agree that the nature of the task is important in the success of a group. For example, the group is more likely to succeed if the individual members’ welfare is closely tied to the task of the group.


Groups provide modeling of behavior deemed appropriate in a given situation. The more similar the individuals doing the modeling are to the individual who wants to learn a behavior, the more powerful the models are. Groups reward members for behavior that conforms to group norms or standards and punish behaviors that do not conform. Groups provide a means of social comparison—how one’s own behavior compares to others’ in a similar situation. Groups are valuable sources of support during times of stress. Some specific factors that enhance the ability of groups to help individuals reduce stress are attachment, guidance, tangible assistance, and embeddedness. Attachment has to do with caring and attention among group members. Guidance may be provision of information or it may be advice and feedback provided by the group to its members. Tangible assistance may take the form of money or of other kinds of service. Embeddedness refers to the sense the individual has of belonging to the group. Some researchers have shown that a strong support system actually increases the body’s immune functioning.




Alcoholics Anonymous

The most well-known support group is Alcoholics Anonymous (AA), formed in Akron, Ohio, in the late 1930s. AA groups now number in the tens of thousands and are found across the globe. What is less well known is that AA is an outgrowth of the Oxford Group, an evangelical Christian student and athlete group formed at Oxford University in England in 1908. The Oxford Group’s ideals of self-examination, acknowledgment of character defects, restitution for harm done, and working with others directly influenced the steps to recovery practiced by members of AA and other so-called twelve-step groups, including Al-Anon, Narcotics Anonymous, and Smokers Anonymous.


For addicts, support groups are important for a number of reasons. They provide peer support for the effort to become “clean and sober.” They provide peer pressure against relapsing into substance use. They assure addicts that they are not alone—that others have suffered the destruction brought about by drinking or drug use. Addicts in twelve-step groups learn to interact with others on an emotional level. Importantly, members of AA and other support groups for addicts are able to confront the individual’s maladaptive behaviors and provide models for more functional behavior. The norm for AA is sobriety, and sobriety is reinforced by clear directions on how to live as a sober person. Another important aspect of AA is the hope that it is able to inspire in persons who, while using, saw no hope for the future. This hope comes not only from seeing individuals who have successfully learned to live as sober persons but also from the group’s emphasis on dependence on a higher power and the importance of a spiritual life.




Other Support Groups

Not all support groups are for addicts. Support groups exist for family and friends of addicts as well as for adoptive parents, children who have been adopted, persons with acquired immunodeficiency syndrome (AIDS), caregivers for patients with Alzheimer’s disease, amputees—and that is just the beginning. Why are these groups so popular? Some writers believe that Americans have turned away from the “rugged individualism” that has characterized the national psyche in the past and are searching for meaning in groups to replace the extended families found in other societies. However, this does not explain why support groups are also popular in other parts of the world. The answer probably lies in the characteristics of groups.


Support groups are generally composed of small numbers of people who are facing similar challenges in their lives. They meet, with or without a trained facilitator, to explore their reactions, problems, solutions, feelings, frustrations, successes, and needs in relation to those challenges. They build bonds of trust. Members show compassion for one another. Groups may provide material support or simply assure the individual member he or she is not alone. They help minimize stress and maximize coping. They model strategies for dealing with the given challenge. They provide information. They nurture their members. They encourage application of new learning. Through this sharing, each member grows, and through individual growth, the group matures.


Support groups have traditionally met in person, but the Internet has altered this expectation. Many support groups now meet online. These may take the form of synchronous or asynchronous chat groups, bulletin boards, Web sites with multiple links to information sources, referrals, and collaboration with professionals. These groups, while not well studied, seem to serve the same purposes as in-person groups. In addition, they provide a possible advantage: The anonymity of the Web makes it possible to observe and to learn from observing without actually participating until one is comfortable doing so.


Support groups may not be sufficient in and of themselves to solve individual problems. They are probably most effective as a part of an integrated plan for addressing the challenge in the individual’s life that involves other resources as appropriate. For example, the caregiver of a person with Alzheimer’s disease may also need social services support, adult daycare or respite care facilities, medical assistance for control of problem behaviors, and home health services to deal successfully with the day-to-day challenges of caring for the patient. The support group can facilitate access to these other resources in addition to serving as an important stress reducer and support system for the caregiver.




Bibliography


Carlson, Hannah. The Courage to Lead: Start Your Own Mutual Help Support Group—Mental Illnesses and Addictions. Madison: Bick, 2001. Print.



Galinsky, Maeda J., and Janice H. Schopler, eds. Support Groups: Current Perspectives on Theory and Practice. New York: Routledge, 2013. Print.



Klein, Linda L. The Support Group Sourcebook: What They Are, How You Can Find One, and How They Can Help You. New York: Wiley, 2000. Print.



Kleinberg, Jeffrey L., ed. The Wiley-Blackwell Handbook of Group Psychotherapy. Malden: Wiley, 2012. Print.



Mowat, Joan. Using Support Groups to Improve Behaviour. Thousand Oaks: PCP/Sage, 2007. Print.



Nichols, Keith, and John Jenkinson. Leading a Support Group: A Practical Guide. New York: Open UP, 2006. Print.



O’Halloran, Sean. Talking Oneself Sober: The Discourse of Alcoholics Anonymous. Amherst: Cambria, 2008. Print.



"Support Groups: Make Connections, Get Help." Mayo Clinic. Mayo Foundation for Medical Education and Research, 1 Aug. 2012. Web. 15 July 2014.

What is comorbidity? |


Introduction

People with primary psychiatric disorders have high rates of substance abuse and addictive disorders and vice versa. These clinical conditions are defined in the
Diagnostic and Statistical Manual of Mental Disorders: DSM 5
(2013) of the American Psychiatric Association, which is the widely used nomenclature for mental disorders. In the fields of clinical psychology and psychiatry, the terms comorbidity or dual diagnosis, generally apply to the presence of one or more serious mental disorders (SMDs) and one or more substance use disorders (SUDs). However, comorbidity can also refer to the co-occurrence of two or more serious mental disorders such as personality disorders .











Prevalence


Substance use disorders and addictive disorders are the most common and clinically severe disorders that affect people with serious mental disorders, which include major depression, bipolar disorder, anxiety disorders, and schizophrenia. The Substance Abuse and Mental Health Services Administration reported in 2009 that almost 9 million adults in the United States have co-occurring mental and substance use disorders. Estimates of the percentages of people with both lifetime serious mental and substance use disorders vary among different studies. The Epidemiological Catchment Area Study, which involved structured psychiatric interviews with more than twenty thousand randomly selected participants, found that nearly half of those diagnosed with schizophrenia (48 percent) and more than half (56 percent) of those diagnosed with bipolar disorder had one or more substance use disorders.




Causes and Consequences

Significant research has been conducted to attempt to determine why serious mental and substance use disorders co-occur. Studies of close family members and twins have suggested an inherited susceptibility to serious mental and substance use disorders, and investigations are pointing to the potential for overlapping genetic vulnerabilities. A 2010 report from the National Institute on Drug Abuse (NIDA), a division of the US Department of Health and Human Services, indicated an individual's vulnerability to addiction is 40–60 percent genetic, and a more recent (2013) study in the journal Nature Genetics linked five major mental disorders—schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders, and attention-deficit hyperactivity disorder (ADHD)—to the same genetic variations. Furthermore, specific areas of the brain, such as those that use the neurotransmitter dopamine are affected by addictive substances and are known to be involved in several mental illnesses such as schizophrenia and depression. NIDA also reported that individuals diagnosed with mood or anxiety disorders and antisocial syndromes, such as antisocial personality disorder and its childhood precursor conduct disorder, are almost twice as likely to suffer from substance use disorder. Conversely, those suffering from substance use disorder are about twice as likely to also suffer from mood and anxiety disorders. It is unknown whether substance use causes mental illness or if the presence of a serious mental illness contributes to substance use disorder.


Anecdotal evidence suggests that individuals with mental disorders such as anxiety or depression or with negative side effects from a psychopharmacological course of treatment use certain substances to self-medicate to alleviate their symptoms. For example, people with depressive disorders often choose drugs that have stimulating effects, such as cocaine or amphetamines. Conversely, people with anxiety-inducing disorders often choose drugs that have sedative effects, such as opiates or alcohol.


Research suggests that people who have a mental illness are hypersensitive to the effects of drugs and alcohol. Small amounts of drugs and alcohol in people with a mental illness, compared with individuals with no mental illness, are more likely to impair the person’s performance in cognitive and motor tasks. Furthermore, small amounts of drugs and alcohol can result in more abuse and dependence problems, as well as other negative consequences, for mentally ill individuals than for those who are not mentally ill.




Treatment Options

Comorbid disorders differ from single disorders in their clinical courses and treatment protocols. Individuals with comorbidity are generally more difficult to diagnose and treat, primarily because of the similarities between the symptoms of substance use disorder and major mental illnesses. Individuals with comorbidity often experience a greater number of psychotic symptoms, require more specialized and intensive treatment, and have poorer treatment outcomes than those with only a serious mental or substance use disorder. People with dual diagnoses also have more difficulty accessing treatment. According to 2009 report from the Substance Abuse and Mental Health Services Administration, only 7.4 percent of individuals with co-occurring disorders receive treatment for both conditions with 55.8 percent receiving no treatment at all.


Treatment programs for people with serious mental or substance use disorders have historically been administered through separate systems with different criteria for client services and different training, education, and certification requirements for service providers. Individuals with comorbidity usually have participated in sequential treatment in which they are expected to be free of either their serious mental or substance use disorder before receiving treatment for the other disorder. Another option is for such individuals to receive parallel treatment, thus participating in both treatments simultaneously but with different practitioners who work at different agencies or clinics.


Sequential and parallel treatments have led to fragmented and ineffective care for people with dual diagnoses. Such treatments force them to navigate the mental health and substance abuse systems separately and to struggle with the disparate messages that they receive from each about treatment goals and pathways to recovery. For example, many drug treatment programs prohibit patients from taking psychiatric medications, the mainstay of care for people with serious mental illness.


Integrated treatments for co-occurring disorders are delivered by professionals who view both serious mental and substance use disorders as “primary” conditions, provide coordinated care for co-occurring disorders, and adhere to consistent and shared philosophies and treatment plans. The essential ingredients of integrated treatments for people with comorbidity include assertive outreach procedures; case management models; comprehensive services; shared decision making with staff, clients, and clients’ families; progressive stages that engage clients in treatment and help them avoid relapses; team approaches to service delivery; long-term commitment to services; cross-training for program staff; and the use of self-help groups and psychopharmacological interventions.


Integrated treatment for co-occurring disorders is more effective than either sequential or parallel treatments. Studies have found that people with co-occurring disorders who are in integrated treatment programs have sustained remission rates from substance use that are two to four times higher than those in nonintegrated treatment programs. Other benefits of integrated treatment for comorbidity include longer retention in treatment, lower rates of victimization, and less time in the hospital. The treatment dropout rates of people with dual diagnoses are very high, owing to their low motivation, cognitive impairment, and disorganized lives. Therefore, clinicians in integrated programs concentrate their services in the community, aggressively bringing comprehensive services to clients rather than expecting clients to seek such services. Comprehensive services encompass all areas of clients’ lives and are aimed at improving their potential for obtaining employment, having stable housing, and living independently.


Treatment plans are more readily accepted and adhered to when people with comorbidity—and their families—have a role in developing and modifying such plans. Moreover, systematic or stage-wise models to treatment recognize that clients must be engaged in services, be motivated to change, be helped to achieve abstinence, and be taught to prevent relapses from serious mental and substance use disorders. Medications for serious mental and substance use disorders are instrumental in reducing and managing symptoms. If left untreated or treated with nonintegrated approaches, co-occurring serious mental and substance use disorders usually become more severe and chronic. People with dual diagnoses need considerable time to recover. Hence, integrated programs take a long-term view of success with such patients.


People with comorbidity are common in both the mental health and substance abuse treatment systems and in the criminal justice system. They present significant challenges to treatment providers and place tremendous strain on resources. Patients with dual disorders suffer from a wide range of public health problems and are unlikely to recover without long-term care. Offenders with comorbid serious mental and substance use disorders are more likely to recidivate, engage in violent behaviors, and have infectious diseases. Integrated programs have the best chance of helping them achieve more satisfying and productive lives.


The War on Drugs in the United States has swelled the country’s probation, jail, and prison populations with unprecedented numbers of drug-abusing and drug-dependent offenders, and has lead to the implementation and evaluation of numerous drug treatment programs in correctional settings. Lost in the emphasis on providing drug treatment to offenders, however, is the very high rates of comorbid psychiatric disorders. The lack of specific programs for offenders with co-occurring disorders has resulted in high rates of rearrests and reincarcerations and has increased the likelihood of violent behaviors within this population.


Although the nation’s correctional populations continue to grow, adequate and well-designed treatment programs are needed more urgently than ever to address psychiatric comorbidities among offender populations. Despite high rates of psychiatric comorbidity among offender populations, drug treatment programs in criminal justice settings and the general community have concentrated on drug treatment and have failed to address psychiatric comorbidity adequately. Unfortunately for those with comorbidity, not enough effective programs are available to meet the demand for such care.




Bibliography


Boden, Matthew Tyler, and Rudolf Moos. "Predictors of Substance Use Disorder treatment Outcomes Among Patients with Psychotic Disorders." Schizophrenia Research 146.1–3 (2013): 28–33. Print.



Drake, R. E., et al. “A Review of Integrated Mental Health and Substance Abuse Treatment for Patients with Dual Disorders.” Schizophrenia Bulletin 24 (1998): 589–608. Print.



Epstein J., P. Barker, M. Vorburger, and C. Murtha. Serious Mental Illness and Its Co-occurrence with Substance Use Disorders, 2002. DHHS Publication No. SMA 04–3905, Analytic Series A-24. Rockville: Substance Abuse and Mental Health Services Administration, Office of Applied Studies, 2004. Print.



Hills, H. A. Creating Effective Treatment Programs for Persons with Co-occurring Disorders in the Justice System. Delmar: GAINS Center, 2000. Print.



Kessler, R. C., et al. “Lifetime Co-occurrence of DSM-III-R Alcohol Abuse and Dependence with Other Psychiatric Disorders in the National Comorbidity Survey.” Archives of General Psychiatry 54 (1997): 313–21. Print.



Lee, S. Hong. "Genetic Relationship Between Five Psychiatric Disorders Estimated from Genome-Wide SNPs." Nature Genetics 45 (2013): 984–94. Print.



Mueser, K. T., R. E. Drake, and M. A. Wallach. “Dual Diagnosis: A Review of Etiological Theories.” Addictive Behaviors 23 (1998): 717–34. Print.



National Institute on Drug Abuse. "Comorbidity: Addiction and Other Mental Illnesses." Research Report Series (2010). Print.

What is hepatitis? |


Causes and Symptoms

Hepatitis, an inflammation of the liver, may result from any of a variety
of causes but commonly follows bacterial or viral infection. Hepatitis may be
associated with an autoimmune phenomenon in which the body produces antibodies
against liver tissue. Liver inflammation may also be an aftereffect of the use of
alcohol or various hepatotoxic chemicals, either through the taking of illegal
drugs or as a side effect of prescription pharmacological agents. Among the
pharmaceuticals that can cause liver damage are antibiotics
such as isoniazid and sulfa drugs, the painkiller acetaminophen, tetracyclines,
and anabolic steroids.



Symptoms associated with hepatitis are a reflection of the function of the liver.
The liver is arguably the most complex organ in the body. More than five hundred
different functions have been associated with the organ, including the production
of bile for emulsification of fats and the secretion of
glucose, proteins, or vitamins for use elsewhere in the body. The liver plays a
major role in the detoxification of the blood, removing alcohol, nicotine, and
other potentially poisonous substances. The Kupffer cells in the liver function in
the removal of infectious agents or foreign material from the blood. More than 10
percent of the blood supply in the body is found within the liver at any time.


Among the functions of the liver is the removal of hemoglobin in the blood, which
is released as a result of the lysis (disintegration) of red blood cells. A
breakdown product of hemoglobin is the yellowish compound bilirubin. It
is the buildup of bilirubin in blood that results in the appearance of
jaundice in cases of inadequate liver function, such as
during hepatitis.


Although hepatitis may develop from a variety of causes, it most commonly results
from infection of the liver. Nearly any infectious agent may potentially damage
the liver, but generally these involve one of several types of viruses, bacteria,
parasites, fungi, or amoebas. Liver disease may also be significantly exacerbated
by alcohol abuse, as is seen in patients with cirrhosis.
Regardless of the specific cause, symptoms of liver disease remain similar in most
cases. The liver is often enlarged and tender to physical examination. The person
may feel tired and run a low-grade fever. It is not unusual for the person to feel
nauseous and lose weight. Jaundice is common in most patients; the concentrations
of the enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
may rise. Levels of these enzymes, however, are not necessarily indications of the
severity of liver disease; in any event, their levels often fall over the course
of the disease.


Three particular viruses have been associated with most forms of viral hepatitis
(hepatitis viruses A, B, and C), while a fourth (type D) appears as a passenger
during some cases of hepatitis B. Several additional viruses, designated hepatitis
E (HEV) through hepatitis G (HGV), have also been linked to forms of the disease.
Hepatitis
A results from infection with the hepatitis A virus (HAV), a
virus classified in the same group as the poliovirus and rhinoviruses
(cold viruses). The disease is transmitted through a fecal-to-oral method and is
self-limited (running a definite and limited course). Often the disease is
subclinical (undetectable), particularly as seen in children. Replication of the
virus occurs in hepatocytes (liver cells); the virus then passes into the
intestine and is eliminated with the feces. A long incubation period following
ingestion may occur, sometimes as long as one month, and during the incubation
period, the person is capable of transmitting the disease. In otherwise healthy
individuals, recovery is complete and occurs over several weeks. Anti-HAV
antibodies are present in the blood of about 30 to 40 percent of the general
population, reflecting the widespread nature of the disease.



Hepatitis
B (HBV), formerly called serum hepatitis, is a potentially
much more severe form of the disease. The disease in young children is frequently
asymptomatic, with the appearance of symptoms in older individuals being more
common. In general, however, the most frequent result of primary infection with
HBV is a mild or subclinical course of infection. The disease is most commonly
seen in patients aged fifteen to thirty-five years, in part reflecting its method
of transmission (through blood or body fluids).


Persistent infection with HBV, occurring in approximately 1 to 3 percent of
patients, can be associated with either an asymptomatic carrier state or chronic
hepatitis. The chronic state may be severe, with progression to cirrhosis and
cellular degeneration or inflammation. In fact, it is the immune response to the
presence of HBV that may contribute to liver degeneration. HBV infection results
in the expression of viral antigens, which stimulate an immune response on the
surface of liver cells. Among the inflammatory cells present at the sites of
infection are a large proportion of lymphocytes. These include cytotoxic T cells,
which are lymphocytes associated with the killing of virally infected cells.
Because immunologically impaired individuals infected with HBV often suffer a mild
form of the disease, the possibility exists that it is the immune response itself
that contributes to the ensuing liver damage.


Hepatitis B transmission occurs through blood or bodily fluids, including semen
and vaginal secretions. Because HBV is also found in saliva, the disease may be
transmitted among family members through nonsexual contact. Maternal-neonatal
transmission may occasionally occur while the fetus is in the uterus but more
likely during the labor or birth process. There is, however, no evidence for
transmission through food or water or by an airborne means.


Clinical features of HBV infections are similar to those associated with other
forms of hepatitis. In the asymptomatic form of type B disease, AST or ALT levels
may be elevated, but jaundice is absent. Adults with symptomatic hepatitis B may
suffer jaundice (referred to as icteric hepatitis), or they may
not (nonicteric hepatitis). There is generally a mild fever, fatigue, and
weakness.


Accompanying an indeterminant number of HBV infections is a second virus,
designated the hepatitis D virus (HDV). HDV is a defective virus and is
capable of replication only in the presence of HBV. Not surprisingly, its
geographic distribution and mode of transmission are similar to those of HBV. The
prevalence of HDV has been found to be as high as 70 percent in some outbreaks of
HBV and nonexistent in others. In most cases, HDV infection results in subclinical
or mild hepatitis. In about 15 percent of cases, the disease may progress to a
more severe form. HDV may itself be cytopathic (causing pathological changes) for
hepatocytes.


Based on the exclusion of other types of etiologic agents, including HAV, HBV,
Epstein-Barr
virus, and cytomegalovirus, non-A, non-B (NANB)
hepatitis was considered a clinical entity. During the late 1980s, NANB hepatitis
was determined to be caused by a newly isolated infectious agent, designated
hepatitis
C virus (HCV). The study of HCV was hampered by the inability
to grow the virus in cell culture. Ironically, the virus was cloned and
characterized before it was even physically observed, allowing for the development
of a screening assay used for the detection of contaminated serum. Before
screening procedures were put into place in 1992, HCV infection was the major
complication of blood transfusions or transfusions of blood products. Infection
now occurs primarily through sexual intercourse, the sharing of intravenous
needles, and accidental needle punctures among health care workers. HCV has been
increasingly recognized as a major health threat, and HCV and HBV together are the
leading cause of liver cancer in the world, accounting for more than 75
percent of cases. HAC creates serious liver damage and is the leading cause of
liver
transplants. It is all the more dangerous because patients
are often asymptomatic and learn of the infection when their blood is screened for
other reasons. As a result, many people are unknowing carriers of the virus.


Outbreaks of an enterically transmitted NANB hepatitis (NANB hepatitis transmitted
through the intestines), designated hepatitis E, have also been found in
some parts of the world. Although hepatitis E was first documented in 1955, it was
not until the late 1980s that it was determined to be a unique form of the
disease. Transmission occurs through eating or drinking contaminated food or
water, though there is evidence that household contact with infected persons may
also transmit the disease. Hepatitis E is most common in low-income countries of
Asia, with sporadic outbreaks elsewhere. The few cases found in the United States
have involved travelers to these areas.


Acute hepatitis is less commonly associated with infection by other viruses. These
include the herpes family of viruses, such as herpes simplex,
cytomegalovirus, and Epstein-Barr virus. Because the prevalence of these viruses
is quite high, immunosuppressed or immunodeficient patients may be at particular
risk.


Certain forms of hepatitis are associated with an autoimmune response. In these
cases, the cause is not an infectious agent but rather a form of rejection by the
body of its own liver tissue. Autoimmune hepatitis is suspected in individuals in
which the disease persists for at least six months with no evidence of exposure to
an infectious agent or hepatotoxin. In nearly one-third of these individuals,
other immunological diseases such as lupus or arthritis may be present. The
clinical manifestations of autoimmune hepatitis are similar to those of other
forms of the disease. Most patients exhibit jaundice, a mild fever, weakness, and
weight loss. The liver is often enlarged and tender. Unlike other forms of
hepatitis, found equally in men and women, autoimmune hepatitis is most commonly
found in women. Prognosis of the disease is unclear, as an unknown percentage of
cases are subclinical. Severe forms have a high fatality rate.




Treatment and Therapy

Treatment for the various forms of viral hepatitis is, for the most part,
symptomatic and supportive. Hospitalization may be required in severe cases, but,
in general, any restriction of activity is left up to the patient. Recovery often
involves a long convalescence. As long as a healthy diet and adequate hydration is
maintained, no special dietary requirements exist, but a high-calorie diet is
often preferable. Drugs or chemicals that are potentially damaging to the liver,
including alcohol and certain antibiotics or painkillers, should be avoided.


Hepatitis induced by other forms of infectious agents such as bacteria or fungi
may be treated using an appropriate course of antibiotic therapy. In cases of
drug-induced disease, avoidance of the chemical is a key to recovery.
Bacterial
infections of the liver are often associated with patients
who are malnourished, such as the elderly or alcoholics, or who may be
immunosuppressed. These problems must also be addressed during the course of
treatment.


Prevention of the disease is preferable, however, and because the means of viral spread has been well established in most cases, appropriate measures can often be taken. For the most part, the viruses associated with hepatitis have little in common with one another aside from their predilection for hepatocytes. Thus, preventing their spread involves different strategies.


HAV is almost always spread through a fecal-oral means of transmission. Often the
source is an infected person involved in the preparation of uncooked foods. Common
sense dictates that the person should wash after every use of a toilet, but this
is often not the case. Not surprisingly, children attending day-care centers
frequently become infected. Contaminated groundwater is also a potential source of
outbreak in areas in which proper sewage treatment does not take place. Less
commonly, HAV is spread directly from person to person through sexual contact. A
method called immunoprophylaxis can prevent the development of symptoms in
individuals exposed to hepatitis A by utilizing a form of passive immunity.
Developed during World War II, the procedure involves the pooling of serum from
immune individuals. In most cases, inoculation is effective in prevention of the
disease. Management of HAV includes avoidance of alcohol and acetaminophen, rest,
and adequate nutrition and hydration. Oral corticosteroids may also be used.


In 1994, SmithKline Beecham Pharmaceuticals developed and received approval from
the US Food and Drug Administration (FDA) for the first vaccine shown to be safe
and effective in preventing HAV infection. Manufactured under the trade name
Havrix, the vaccine consists of a formalin-inactivated strain of HAV to be
administered in three doses to children. In 1996, a similar vaccine was developed
by Merck to be sold under the trade name Vagta. In 2001, a combined hepatitis A
and hepatitis B vaccine was developed and approved in the United States for use in
individuals eighteen and older. It is given in three doses over a period of six
months. In 2002, the US Centers for Disease Control recommended that any
individuals at risk for hepatitis A infection or those at risk for becoming
seriously ill if infected should receive immunization against the virus.


The transmission of HBV generally involves passage via contaminated blood or body
secretions. Before blood screening was standard procedure, blood transfusions were
the most common means of spreading the disease—hence the designation “serum
hepatitis.” Since the 1980s, however, the most common means of documented spread
has been through either sexual contact or through the sharing of contaminated
hypodermic needles. Semen, vaginal secretions, and saliva from infected
individuals all contain the active virus, and limiting exchange of these fluids is
key to prevention of transmission. Even so, the means of infection in nearly
one-third of symptomatic cases remains unknown.


In 2002, the Centers for Disease Control recommended that certain groups of
individuals who are at high risk for exposure to HBV be vaccinated against the
virus: children (newborn to eighteen years old), intravenous drug users, sexually
active heterosexuals and homosexual men, healthcare workers, and those in contact
with hepatitis B-infected individuals. It was also recommended that those who
would become seriously ill if they contracted the virus be vaccinated: newborns,
individuals with hemophilia, those with any chronic liver disease, and those
waiting for a liver transplant.


HBV medications do not eradicate the virus and have limited long-term efficacy;
however, medications for the treatment of HBV include interferons such as
peginterferon alfa-2a and interferon alfa-2a and nucleoside or nucleotide analogs
such as entecavir and tenofovir.


Because the hepatitis D virus is defective in replication and requires the presence of HBV, no specific measures of prevention are necessary. Immunization against HBV is sufficient to prevent the spread of HDV.


HCV is treated with antiviral agents, such as sofosbuvir, ribavirin, and
peginterferon-alfa. Abstinence from smoking and alcohol is recommended, as well as
vaccination against hepatitis A and B. Patients with active HCV infection should
receive education to help reduce progression of liver disease and to prevent
transmission of HCV.


Hepatitis E is also transmitted through a fecal-oral route. Drinking water
contaminated by sewage has been the most common source of transmission. Because no
active means of prevention has been developed, prevention of exposure requires
that the individual avoid any food or water potentially contaminated with sewage.
This is particularly true in areas of the world in which hepatitis E is found.
Though the precaution may seem obvious, the safety of the water, as well as any
object washed in the water, is not always readily apparent.


Autoimmune hepatitis results from an aberrant immune system rather than from an
infectious agent. Pretreatment with vaccination against hepatitis A and B is
recommended. Treatment generally involves the use of immunosuppressive drugs to
limit the immune response. Corticosteroids such as prednisone,
often taken in combination with azathioprine, have proven effective in the therapy
of many patients. Treatment generally is carried out over a long period of time,
at least a year, and relapses are common. Often, the patient requires lifetime
therapy. The immunosuppressive activity of the therapy may also leave the patient
more susceptible to infection. Adjunctive therapies for bone disease due to
immunosuppression include vitamin D, calcium, and bisphosphonates. In some cases,
liver transplantation has proven effective, at least in the short term. Because
the liver rejection was caused by an autoimmune response in the first place, the
transplant may also be subject to the same phenomenon.




Perspective and Prospects

Inflammation of the liver resulting in hepatitis can develop from a variety of mechanisms. Most often, these mechanisms are associated with either a chemical injury or infection by a microbiological agent.


Infections of the liver generally involve one of several viral agents. The
association of liver disease, or at least jaundice, with an infectious agent was
suspected as early as the fifth century BCE when Hippocrates described a syndrome
that was undoubtedly viral hepatitis. The disease was also described in the
Babylonian Talmud about eight hundred years later. Epidemics of the disease, which
most likely involved outbreaks of hepatitis A, have been reported since the Middle
Ages. The spread of this disease through personal contact was confirmed in the
1930s.


Hepatitis B was described as a clinical entity by A. Lurman in 1855. Lurman
observed that 15 percent of shipyard workers in Bremen, Germany, who received a
smallpox vaccine containing human lymph developed jaundice within the following
six months. In the early years of the twentieth century, jaundice frequently
developed among patients who received vaccines prepared from convalescent serums
or who underwent procedures such as venipuncture using instruments that had not
been properly sterilized. By 1926, the blood-borne nature of the disease had been
confirmed. In 1942, more than twenty-eight thousand American soldiers developed
jaundice after being vaccinated against yellow fever with a vaccine prepared
from pooled human serums. By then it had become obvious that at least two forms of
infectious agents were associated with viral hepatitis.


The isolation of HBV occurred as a result of studies initiated by Baruch Blumberg
in 1963. Blumberg was actually attempting to correlate the development of diseases
such as cancer with particular patterns of proteins found in the
serum of individuals. His approach was to collect blood from persons in various
parts of the world and then analyze their serum proteins. Blumberg found an
antigen, a protein, in the blood of Australian Aborigines that reacted with
antibodies in the blood of an American with hemophilia. Blumberg called the
protein the Australia (Au) antigen. It later became apparent that the Au antigen
could be isolated from the blood of patients with serum hepatitis. By 1970, it was
established that what Blumberg had referred to as the Au antigen was in fact the
HBV particle.


HBV is associated with more than simply viral hepatitis. Chronic hepatitis
associated with HBV can often develop into hepatocellular carcinoma, or cancer of
the liver. The precise reason is unclear; the cancer may result from the chronic
damage to liver tissue associated with long-term infection by HBV.


Cases of HCV continue to climb because of the high numbers of asymptomatic
carriers. According to the World Health Organization (WHO), 130 to 150 million
people worldwide have chronic HCV infection, and 350,000 to 500,000 people die
each year from hepatitis C–related liver diseases. The WHO also reports that more
than 780,000 people die annually due to hepatitis B and estimates that there are
1.4 million cases of hepatitis A each year. According to the WHO, an estimated 57
percent of cases of liver cirrhosis and 78 percent of cases of primary liver
cancer result from hepatitis B or C viral infection.




Bibliography


Boyer, Thomas D.,
Michael P. Manns, and Arun J. Sanyal, eds. Zakim and Boyer’s
Hepatology: A Textbook of Liver Disease
. 6th ed. Philadelphia:
Saunders/Elsevier, 2011. Print.



Cox, Jeffrey T., and Dedrick I. Owen, eds.
Hepatitis B: New research. New York: Nova, 2012.
Print.



Everson, Gregory T.,
and Hedy Weinberg. Living with Hepatitis C: A Survivor’s
Guide
. 5th ed. New York: Hatherleigh, 2009. Print.



Frank, Steven A.
Immunology and Evolution of Infectious Disease.
Princeton: Princeton UP, 2002. Print.



Gorbach, Sherwood L.,
John G. Bartlett, and Neil R. Blacklow, eds. Infectious
Diseases
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Print.



"Hepatitis." World Health
Organization
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Hepatitis Foundation International. http://www.hepatitisfoundation.org.



Humes, H. David, et
al., eds. Kelley’s Textbook of Internal Medicine. 4th ed.
Philadelphia: Lippincott, 2000. Print.



Levine, Arnold.
Viruses. New York: Freeman, 1992. Print.



Palmer, Melissa.
Dr. Melissa Palmer’s Guide to Hepatitis and Liver
Disease
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Print.



Perez Gonzales, Alvaro, and Angel Alonso
Verracruz, eds. Hepatitis C Virus: Epidemiology, Pathogenesis and
Treatment
. New York: Nova, 2012. Print.



Porter, Lucinda K.
Hepatitis C Treatment One Step at a Time. New York:
Demos Health, 2013. Print.



Shaw, Michael, ed.
Everything You Need to Know About Diseases. Springhouse:
Springhouse, 1996. Print.



Spector, Steven.
Viral Hepatitis: Diagnosis, Therapy, and Prevention.
Totowa: Humana, 1999. Print.



Thomas, Howard C., et al., eds.
Viral Hepatitis. 4th ed. Hoboken: Wiley, 2014.
Print.

Sunday, 1 January 2017

What is memory? |


Introduction

Human memory is among the most complex phenomena in the universe. A Russian newspaper reporter once flawlessly recalled a list of fifty unrelated words he had studied for only three minutes fifteen years before. On the other hand, as everyone knows from personal experience, the memory system is also capable of losing information presented only seconds in the past. Errors in memory create so many problems that it seems imperative to know all that is possible about human memory. For that, a theory is needed.






A scientific theory is a systematic way to understand complex phenomena that occur in nature. A theory is judged to be useful insofar as its claims can be supported by the findings of empirical tests, especially experimentation, and insofar as it leads to further research studies. A theory is not right or wrong; it is simply a tool to describe what is known and to suggest what needs further study.


Three major forms of memory are generally described: short-term, long-term, and sensory memory. Short-term memory represents the temporary retention of newly acquired information. Generally, short-term memory lasts no longer than about twenty seconds. This is useful for short-term tasks, such as the recall of speech during discussions or discourse with another person. Short-term memory is rapidly lost, sometimes referred to as a process of decaying. Alan Baddeley, a major researcher in the field of memory, has suggested that a concept of working memory may be substituted for short-term. Repeat stimulation, or rehearsal, may transfer short-term memory into that of long-term.



Long-term memory involves storage of information over longer periods of time, potentially as long as the life of the individual. Some researchers into the subject consider long-term memory to include two major areas: episodic and semantic. Episodic memory addresses events that have a temporal relationship with a person’s life. This may include recall of when events or information appeared. Semantic memory represents the concepts or skills, represented in part by learning, that people acquire through the course of their lives.


Sensory memories are those that can be retrieved as a result of sensory stimuli. For example, a particular odor may result in the recall of events from the past. The unusual smell of a cleaning solution may cause the recall of a college dormitory from years past. This form of recall has been called olfactory memory. The image of a flower may result in the memory of a teenage boyfriend. Such a visual stimulus is sometimes referred to as iconic memory.


Theories of memory have been important to psychology for a long time, often occupying the time and interest of researchers throughout their careers. Memory, which is always connected to learning, is defined as the mental process of preserving information acquired through the senses for later use. The cognitive approach to memory places emphasis on mental processes, which result in the ability to comprehend or recall what is learned. The basis is found in changes that occur in the regions of the brain, such as the hippocampus, associated with memory. In a sense, memory is the record of the experiences of a lifetime. Without it, a person could not re-experience the past; everything at every moment would be brand-new. A person could not even recognize the face of a loved one or learn from any experience. A person would thus have a greatly reduced chance for survival and would have no sense of personal identity. Memory is, in short, critical to functioning as a human being.




Associationism, Cognitive Theory, and Neuropsychology

The goal of a theory of memory is to explain the structures (hardware) and the processes (software) that make the system work. Explaining how such a complex system works is a massive undertaking. The attempts have taken the form of large-scale theories, which seek to deal with all major operations of the memory systems. The major theories of memory are associationism and theories from cognitive psychology and neuropsychology. The theories differ primarily in views of the retention and retrieval functions of memory. They also differ in terms of their conception of memory as active or passive.


Associationism, the oldest of the three, is the theory that memory relies on forming links or bonds between two unrelated things. This theory stems from the work of Hermann Ebbinghaus, who started the use of laboratory methods in the study of memory in the late nineteenth century. According to this theory, the ability to remember depends on establishing associations between stimuli and responses (S-R). Establishing associations depends on the frequency, recency, and saliency of their pairing. If these bonds become very strong, the subject is said to have developed a habit. Associationism also assumes the existence of internal stimuli that produce behavioral responses. These responses then become stimuli for other unobservable internal responses, thus forming chains. In this way, complex physical behaviors and mental associations can be achieved. Associationists tend to view the memory system as essentially passive, responding to environmental stimuli.


Cognitive theory emphasizes studying complex memory in the real world; it is concerned with the ecological validity of memory studies. Most of this work stems from the research of Sir Frederic C. Bartlett, who was not satisfied with laboratory emphasis on “artificial memory,” but rather chose to study what he called meaningful memory. Meaningful memory, he said in his book Remembering: A Study in Experimental and Social Psychology (1932), is a person’s effort to make sense of the world and to function effectively in it. Cognitive psychology recognizes subjective experiences as inescapably linked to human behavior. It centers on internal representation of past experiences and assumes that intentions, goals, and plans make a difference in what is remembered and how well it is remembered. The focus in memory research is on semantic memory—the knowledge of words, categories, concepts, and meanings located in long-term memory. People have highly complex networks of concepts, which helps account for their behavior in the real world. These networks are called schemas. New experiences and new information are viewed in light of old schemas so that they are easier to remember. Cognitive theory emphasizes how the individual processes information, and it uses the computer as its working model of memory.


Neuropsychology has contributed the third major theory of memory. Although psychology has always recognized the connection between its concerns and those of biology and medicine, the technology now available has made neuropsychological analysis of brain structure and functioning possible. Karl Lashley was an early researcher who sought to find the location of memory in the brain. He ran rats through mazes until they had learned the correct pathway. His subsequent surgical operations on experimental rats’ brains failed to show localization of memory.


The search for the memory trace, the physiological change that presumably occurs as a result of learning, continued with Donald O. Hebb, who had assisted Lashley. The brain consists of billions of nerve cells, which are connected to thousands of other neurons. Hebb measured the electrical activity of the brain during learning, and he discovered that nerve cells fire repeatedly. He was able to show that an incoming stimulus causes patterns of neurons to become active. These cell assemblies discovered by Hebb constitute a structure for the reverberating circuits, a set of neurons firing repeatedly when information enters short-term memory. This firing seems to echo the information until it is consolidated in long-term memory. Other researchers have found chemical and physical changes associated with the synapses and in the neurons themselves during learning and when the learning is consolidated into long-term memory. The discovery of the memory trace, a dream of researchers for a long time, may become a reality. Neuropsychology sees memory as a neural function controlled by electrical and chemical activity.




Clinical Approaches to Memory Disorders

Human memory is so important to daily life that any theory that could explain its structures and processes and thus potentially improve its functioning would be invaluable. Memory is inextricably tied to learning, planning, reasoning, and problem solving; it lies at the core of human intelligence.


None of the three theories is by itself sufficient to explain all the phenomena associated with memory. Over the years, a number of ideas have been developed in the attempt to improve memory functioning through passive means. Efforts to induce learning during sleep and to assess memory of patients for events taking place while under anesthesia have had mixed results but on the whole have not succeeded. Memory enhancement through hypnosis has been attempted but has not been shown to be very effective or reliable. Pills to improve memory and thereby intelligence have been marketed but so far have not been shown to be the answer to memory problems. Research has begun on the possibility that certain drugs (such as tacrine) may interactively inhibit memory loss in people afflicted with certain kinds of dementia (for example, Alzheimer’s disease). Work in neuropsychology has shown the influence of emotion-triggered hormonal changes in promoting the memory of exciting or shocking events (such as one’s first kiss or an earthquake). This has led to an understanding of state-dependent memory: Things learned in a particular physical or emotional state are more easily remembered when the person is in that state again. This helps explain the difficulties in remembering events that took place when a person was intoxicated or depressed. In fact, heavy use of alcohol may result in significant memory loss. A person may not even remember having injured someone in a car accident. Although not fully researched, it may be that certain kinds of memory are mood-congruent. Perhaps memories of events that occurred when a person was in a certain mood may become available to the person only when that mood is again induced.


More active means for memory improvement have met with greater success. Associationist theory has demonstrated the value of the use of mnemonics, devices or procedures intentionally designed to facilitate encoding and subsequent recall. The use of rhymes, acronyms, pegwords, and the like enables people to recall factual information such as the number of days in each month (“Thirty days hath September . . . ”), the names of the Great Lakes (the acronym HOMES), and the colors of the visible spectrum (ROY G. BIV). Visual cues, such as tying a string around one’s finger or knotting one’s handkerchief, are traditional and effective ways to improve prospective memory. Cognitive psychology has demonstrated the importance of emotional factors—how and why something is learned—to the effectiveness of memory. It has provided the research base to demonstrate the effectiveness of study strategies such as the SQ3R (survey, question, read, recite, review) technique. Cognitive theory has also shown that metamemory, a person’s knowledge about how his or her memory works, may be important for the improvement of memory.


In clinical settings, much research has been concerned with memory impairment as a means to test the applicability of theories of memory. Head injuries are a common cause of amnesia in which events immediately prior to an accident cannot be recalled. Damage to the hippocampus, a part of the brain that is vital to memory, breaks down the transfer of information from short-term to long-term memory. One dramatic case concerns “H. M.,” a patient who had brain surgery to control epileptic seizures. After surgery, H. M.’s short-term memory was intact, but if he was momentarily distracted from a task, he could not remember anything about what he had just been doing. The information was never transferred to long-term memory. Such patients still remember information that was stored in long-term memory before their operation, but to them everyday experiences are always strangely new. They can read the same paragraph over and over, but each time the material will be brand-new. In H. M.’s case, it was discovered that his intelligence as measured by standardized tests actually improved, yet he was continually disoriented and unable to learn even the simplest new associations. Intelligence tests are made to measure general information, vocabulary, and grammatical associations; these things were stored in H. M.’s long-term memory and were apparently not affected by brain surgery. In cases less dramatic than H. M.’s, damage to particular areas of the brain can still have devastating effects on the memory. Damage can be caused by accidents, violent sports activity, strokes, tumors, and alcoholism. Alzheimer’s disease is another area to which research findings on memory may be applied. In this fatal disease, a patient’s forgetfulness increases from normal forgetting to the point that the patient cannot remember how to communicate, cannot recognize loved ones, and cannot care for his or her own safety needs.


Associationism, cognitive psychology, and neuropsychology can each explain some of the structures and processes involved in these and other real-world problems, but it seems as though none of the theories is sufficient by itself. Memory is such a complex phenomenon that it takes all the large-scale theories and a number of smaller-scale ones to comprehend it. The truth probably is that the theories are not mutually exclusive but rather are complementary to one another.




Physiological Basis of Memory

Theories of learning and memory have been of great concern to philosophers and psychologists for a long time. They have formed a major part of the history of psychology. Each of the theories has been ascendant for a time, but the nature of theory building requires new conceptions to compensate for perceived weaknesses in currently accepted theories and models. Associationism was the principal theory of memory of stimulus-response psychology, which was dominant in the United States until the mid-1950s. Cognitive psychology evolved from Gestalt psychology, from Jean Piaget’s work on developmental psychology, and from information-processing theory associated with the computer, and was extremely important during the 1970s and 1980s. Neuropsychology developed concurrently with advanced technology that permits microanalysis of brain functioning. It has resulted in an explosion of knowledge about how the brain and its systems operate.


Formation of memory seems to involve two individual events. Short-term memory develops first. Repeated rehearsal transfers this form of memory into long-term storage. At one time, it was believed both these forms of memory involved similar events in the brain. However, experimental models have shown such a theory to be incorrect. Two experimental approaches have addressed this issue: the separation of memory formation involving “accidental” or intentional interference with brain function, and development of an animal model for the study of memory.


Electroshock treatment of depression in humans has been shown to interfere with short-term memory formation. However, these persons are still perfectly able to recall the memory of earlier events stored within long-term memory. Accidental damage to temporal lobes of the brain does not appear to interfere with short-term memory but may inhibit the ability to recall events from the past.


The experimental use of an animal model in the study of memory formation was developed by Eric R. Kandel at Columbia University. Kandel has used the sea slug Aplysia in his study of memory. The advantage of such a model is its simplicity—instead of the approximately one trillion neurons that make up the nervous system of humans, Aplysia contains a “mere” twenty thousand.


Using a variety of stimuli on the animal and observing its response, Kandel has shown that the physiological basis for short-term memory differs from that of long-term. Specifically, short-term memory involves stimulus to only a small number of individual neurons. Long-term memory involves de novo (new) protein synthesis in the affected cells and formation of extensive neural circuits. Kandel was awarded the Nobel Prize in Physiology or Medicine in 2000 for this work.




Memory Retrieval

The basis for memory recall remains an active area of study. Memory retrieval can be of two types: recognition and recall. In recognition, the individual is presented with information that had been previously learned. The subject remembers he or she has already observed or learned that information. In effect, it is analogous to seeing a movie or book for the second time. In recall, information is reproduced from memory, as in response to a question. The physiological basis for retrieval probably involves the activation of regions of the brain that were involved in the initial encoding.




Bibliography


Baddeley, Alan D. Human Memory: Theory and Practice. Rev. ed. Hove, East Sussex, England: Psychology Press, 2005. Print.



Collins, Alan, ed. Theories of Memory. Mahwah: Erlbaum, 1994. Print.



Holcomb, Orval, and Dannie M. Hendrix. Psychology of Memory. New York: Nova Science, 2012. Digital file.



Kandel, Eric. “The Molecular Biology of Memory Storage: A Dialogue Between Genes and Synapses.” Science 294 (2001): 1030–1038. Print.



Kellogg, Ronald Thomas. Fundamentals of Cognitive Psychology. 2d ed. Los Angeles: Sage, 2012. Print.



Klingberg, Torkel. The Learning Brain: Memory and Brain Development in Children. New York: Oxford UP, 2013.



Neisser, Ulric. Cognition and Reality: Principles and Implications of Cognitive Psychology. San Francisco: Freeman, 1981. Print.



Norman, Donald A. The Psychology of Everyday Things. New York: Basic, 2008. Print.



Nyberg, Lars, et al. “Reactivation of Encoding-Related Brain Activity During Memory Retrieval.” Proceedings of the National Academy of Sciences of the United States of America 97 ( 2000): 11,120–121,124. Print.



Weisberg, Robert W., and Lauretta Reeves. Cognition: From Memory to Creativity. Hoboken: Wiley, 2013. Digital file.

What is brief therapy? |


Introduction

Brief therapy is a form of psychotherapy that uses short-term treatment methods to help people handle current life problems and crises. The distinctive features of brief therapy include a time limit and a focus on specific problems and topics. During brief therapy, the therapist takes an active role in directing the participant to specific issues and limiting the exploration of other aspects of the person’s life. This approach contrasts with traditional open-ended therapy, which seeks to explore numerous topics as they are uncovered during psychotherapy.








Although brief therapy is time limited, there is no consensus concerning the ideal number of therapy sessions for this form of treatment. It may last anywhere from a single session to twenty or more. Brief therapy is also known as time-limited psychotherapy or short-term psychotherapy. Consensus is also lacking regarding the type of person who benefits most from this form of therapy. Sometimes focusing on a particular problem may bring forth additional problems that cannot be addressed in the time-limited format.


Because of the time-limited nature of brief therapy, the costs associated with psychotherapy are less than with traditional forms. Brief therapy has become popular with managed-care organizations, as it helps to contain treatment costs.




Historical Trends

The foundations for brief therapy were laid by Franz Alexander
and Thomas French in 1946, when they identified the critical elements for a time-limited form of psychotherapy. They suggested that new ways of thinking, acting, and feeling could be promoted in individuals through the establishment of a corrective emotional experience during treatment. If the individuals being treated were highly motivated and worked effectively with a therapist, they could achieve change in a short time.


In the 1950s, while working in London, David Malan developed brief focal psychotherapy as a time-limited treatment. In this type of therapy, the patient and therapist formulate a focus for the treatment and set a termination date before the therapy begins. The average number of sessions for this treatment is twenty meetings. To be selected for this therapy, a person must be able to think in feeling terms, have a high motivation level, and respond to the trial interpretations from the therapist. Trial interpretations are explanations provided by the therapist about why a person is behaving in a certain manner.


Also developed during the 1950s was short-term anxiety-provoking psychotherapy. Peter Sifneos identified individuals who could select a specific problem in their lives and had the motivation to solve the problem in therapy. For those persons, Sifneos confronted their problems using forced-choice questions, which do not permit a person to avoid problems or ideas that may be upsetting. The focus of this form of brief therapy is on anything related to the identified problem that provokes worry and anxiety.


James Mann developed time-limited psychotherapy in the 1970s while working at Boston University. Mann selected individuals who had an easily identifiable central conflict in their lives and limited treatment to only twelve sessions. The conflicts usually related to problems with maturation and psychological development. For example, a young man may be having difficulty moving away from his parents and be afraid of living alone. This conflict of independence versus dependence would become the central focus of the time-limited psychotherapy. The treatment would then focus on possible solutions to this conflict.




Current Issues

One of the major similarities among all brief therapies is the importance of the therapist’s behavior during the sessions. In brief therapy, the therapist is very active in the process of focusing on specific problems and confronting the patient to solve his or her problem. Because the therapist is very direct with the patient, there is a dynamic interaction between them that is designed to obtain solutions in the least amount of time. Modern brief therapy uses many cognitive and behavioral techniques to facilitate the changes sought from the person seeking treatment. Cognitive techniques focus on modifying how a person thinks about the surrounding environment. Behavioral techniques attempt to reinforce desired behaviors and remove actions that are causing problems in a person’s life. Specific exercises are performed to solve problems and improve interpersonal skills. Research investigations of brief therapy have shown that it is effective for a specific range of mental-health problems, but controversy has emerged over its extensive use.


Brief therapy is frequently the treatment of choice for managed-care organizations, which often discourage long-term treatments. Outpatient psychotherapy is usually approved for six to eight sessions of brief therapy. Critics charge that the mental-health profession is being driven by economic considerations rather than the needs of its patients. The support that brief therapy receives from managed-care organizations has created a conflict with those providing psychotherapy that may take years to resolve.




Bibliography


Engler, Jack, and Daniel Goleman. The Consumer’s Guide to Psychotherapy. New York: Simon, 1992. Print.



Franklin, Cynthia, et al., eds. Solution-Focused Brief Therapy: A Handbook of Evidence-Based Practice. New York: Oxford UP, 2012. Print.



Horowitz, Mardi Jon. Personality Styles and Brief Psychotherapy. Northvale: Aronson, 2001. Print.



Lazarus, Arnold. Brief but Comprehensive Psychotherapy. New York: Springer, 2006. Print.



MacKenzie, K. Roy. “Principles of Brief Intensive Psychotherapy.” Psychiatric Annals 21.7 (1991): 398–404. Print.



Piper, William E., and Anthony S. Joyce. “A Consideration of Factors Influencing the Utilization of Time-Limited, Short Term Group Therapy.” International Journal of Group Psychotherapy 46.3 (1996): 311–28. Print.



Ratner, Harvey, Evan George, and Chris Iveson. Solution Focused Brief Therapy: 100 Key Points and Techniques. New York: Routledge, 2012. Print.



Strosahl, Kirk, Patricia Robinson, and Thomas Gustavsson. Brief Interventions for Radical Change: Principles and Practice of Focused Acceptance and Commitment Therapy. Oakland: New Harbinger, 2012. Print.

In Parts 1 and 2, we have seen bravery on the part of Odysseus as he faces countless monsters. What is similar about the ways he faces danger for...

Odysseus is really brave in the face of danger, and he is willing to encounter danger himself for good reason.  When he forms his plan to kill the Cyclops, Polyphemus, he knows the risk of being one of the men to plunge the stake into the Cyclops' eye (as they have to stand on the monster in order to accomplish this), yet he insists that he be one of the men to take this risk....

Odysseus is really brave in the face of danger, and he is willing to encounter danger himself for good reason.  When he forms his plan to kill the Cyclops, Polyphemus, he knows the risk of being one of the men to plunge the stake into the Cyclops' eye (as they have to stand on the monster in order to accomplish this), yet he insists that he be one of the men to take this risk.  Further, when he and his crew land in Aeaea, he confronts Circe -- a dangerous proposition -- even though he knows that she has incredible powers, because he needs to save his men.  Then, after Calypso releases him, he sets out -- alone, on a raft, in the sea -- despite the fact that he has deeply angered Poseidon by blinding his son, Polyphemus.  He is quite willing to put himself in danger when the benefit seems to outweigh the risk.


Odysseus is actually more willing to endanger himself than he is willing to endanger his crew.  When their ship approaches Scylla, he arms himself so that he can try to kill her before she has a chance to attack his men.  Further, when their ship passes the Sirens, he stops his crew's ears with wax so that they will not be tempted by their song.  He has them lash him to the mast so that he, alone, will hear and be tortured by the song; his crew will not have to bear it.  Even in the land of the lotus-eaters, when the three scouts do not come back to the ship because they've eaten the lotus fruit and now no longer want to return home, Odysseus goes himself to physically force them back, risking his own safety instead of leaving them behind or endangering another crew member.


Ultimately, Odysseus is very willing to face danger to preserve himself or his crew, and he treats them -- for the most part -- generously and kindly.  He sincerely mourns the loss of each man.

How can a 0.5 molal solution be less concentrated than a 0.5 molar solution?

The answer lies in the units being used. "Molar" refers to molarity, a unit of measurement that describes how many moles of a solu...