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Scientists have long suspected that abnormalities in brain enzymes or receptors are major contributors to the causes of mental illness and have been searching for an enzyme or receptor deficiency that could be identified as the cause of specific psychiatric disorders blood sugar foods generic metformin 850mg without a prescription. Such tools available for use in humans include studies of enzymes diabetes videos metformin 500 mg fast delivery, receptors diabetic diet sample meal plan metformin 500 mg discount, and genes in postmortem brain tissues and in peripheral tissues that can be ethically 102 Essential Psychopharmacology Table 4-2 diabetes alert dogs in virginia purchase genuine metformin online. Metabolites of neurotransmitters can be studied in cerebrospinal fluid, plasma, and urine. Receptors for neurotransmitters can also be studied indirectly by using selective drug probes, which cause hormones to be released into the blood that can be measured and therefore serve as a reflection of brain receptor stimulation. Unfortunately, little progress has been made yet in defining the biological causes of mental illnesses by using these approaches. No single reproducible abnormality in any neurotransmitter or in any of its enzymes or receptors has been shown to cause any common psychiatric disorder. Indeed, it is no longer considered likely that one will be found, given the complexity of psychiatric diagnosis and the profound interaction of environmental factors with genetics in psychiatric disorders. More Chemical Neurotransmission as the Mediator of Disease Actions 103 recently, biological psychiatry has shifted from a strategy of pursuing a single unique biochemical lesion as the cause of each psychiatric disorder to the discovery and enumeration of risk factors that do not cause illness by themselves but contribute to the risk of a psychiatric disorder. This approach is sometimes called complex genetics because it is indeed complicated, as we shall see below. The potential usefulness of this approach is underscored by findings from genetic studies of mental illnesses. Despite strong evidence from twin studies that genetic susceptibility exists for both bipolar disorder and schizophrenia, no specific gene has been unambiguously identified for the usual forms of any common mental disorder. Rather, the genetics of major psychiatric disorders are likely to be at best contributors in multiple complex ways to these illnesses, just as is currently suspected for coronary artery disease, diabetes, and hypertension. Methods to approach the complex genetics of mental illnesses are just evolving and include such techniques as linkage, linkage disequilibrium, and association studies to name a few. Rather, a whole list of abnormally acting genes and their corresponding gene products, triggered by both inherited and acquired risk factors, are hypothesized to act together or in just the right sequence to cause clusters of symptoms that appear in different psychiatric disorders. Once the complete list of genes and environmental factors that comprise all the vulnerabilities to a psychiatric illness is determined, it will be necessary to understanding how all the corresponding gene products participate in the neuronal functioning and especially the chemical neurotransmission that mediate the mental illness. The long-term hope, of course, is that by knowing this, a logical biochemical rationale can be found for reversing these abnormalities with drug therapies. The question of how this could lead to a rational drug therapy to halt, reverse, or compensate for these multiple simultaneous biochemical events leaves us in a complete quandary at present. It might be possible to pursue treatments based on this knowledge if the abnormal gene products proved to be enzymes or receptors that could be stimulated or blocked by drugs. However, it is not likely to be this simple, as multiple simultaneous drugs acting to compensate for each genetic abnormality that contributes to the disease vulnerability might prove to be necessary. At any rate, the biological psychiatry hunt is on, but treatments based on this approach certainly do not appear to be right around the corner. Psychopharmacology Limited definition the use of drugs to treat symptoms of mental illness the science of drug discovery, targeting enzymes and receptors Approach Studies in patients with psychiatric disorders Serendipitous clinical observations In clinical investigations, the use of drugs with known mechanisms of action to provoke biological or behavioral responses that would provide clues where abnormalities in brain functioning may exist in specific psychiatric disorders In drug discovery, theory-driven targeting of enzymes and receptors hypothesized to regulate symptoms in a psychiatric disorder Psychopbarmacological results In clinical investigations, the first observation is often a serendipitous discovery of clinical efficacy, after which the biochemical mechanism of action is discovered In drug discovery, specific enzymes or receptors are first targeted for drug action. That is, if a drug with a well understood mechanism of action on a receptor or enzyme causes reproducible effects on the symptoms of a patient with a brain disorder, it is likely that those symptoms are also linked to the same receptor that the drug is targeting. Using drugs as tools in this manner can help map which receptors and enzymes are linked to which psychiatric or neurological disorder. Since drug actions are much better known than disease actions at the present time, the use of drug tools in this manner has so far proved to be the more productive approach to understanding diseases as compared with the biological psychiatry approach of looking for abnormal receptors, enzymes, or genes. Indeed, much of what is known, hypothesized, or theorized about the neurochemical abnormalities of brain disorders is derived from the approach of using drugs as tools. Thus, pathophysiology is inferred rather than proved, since we do not yet know the primary enzyme, receptor, or genetic deficiency in any given psychiatric or neurological disorder. These theories, in fact, direct the biological psychiatry researcher where to look for proof of disease abnormalities. Thus, psychopharmacology is bidirectional in the sense that certain drugs, namely, those that have a known neurochemical mechanism of action and that are also effective in treating brain disorders, help to generate hypotheses about the causes of those brain disorders. The other direction of psychopharmacology is that in the case of a brain disorder with a known or suspected pathophysiology, drugs can be rationally designed to act on a specific receptor or enzyme to correct the known or suspected pathophysiology and thereby treat the disorder. It would be advantageous for new drug development to proceed from knowledge of pathophysiology to the invention of new therapeutics, but this must await the elucidation of such pathophysiologies, which, as emphasized here, are yet largely unknown.

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By contrast diabetes type 2 and insulin generic 500 mg metformin mastercard, in women the incidence of depression mirrors their changes in estrogen across the life cycle diabetic cookies generic metformin 500mg line. As estrogen levels rise during puberty diabetes type 1 uptodate order metformin line, the incidence of depression skyrockets diabetes symptoms teenagers discount 850 mg metformin amex, falling again after menopause. Thus, women have the same frequency of depression as men before puberty and after menopause. However, during their childbearing years when estrogen is high and cycling, the incidence of depression in women is two to three times as high as in men. Several other issues are of particular importance to women in terms of assessing their vulnerability to the onset and recurrence of mood disorders across their lifetimes. These are linked to shifts in reproductive hormone status, as outlined in Figure 14-28. First episodes of depression often begin in puberty or early adulthood, when estrogen is first rising; unfortunately these episodes are frequently unrecognized and untreated. During the early phase of the cycle, estradiol levels rise, and this trophic influence induces dendritic spine formation and synaptogenesis. Progesterone administration rapidly potentiates this, so spine formation is at its greatest when both estrogen and progesterone peak just after the first half of the cycle. However, once estrogen levels fall significantly and progesterone continues to rise, the presence of progesterone without estrogen triggers down regulation of these spines and removal of the synapses by the end of the estrus cycle. One hypothesis to explain the mechanism of cyclical formation and removal of synapses every menstrual (estrus) cycle in females is that estrogen may exert its trophic influence through low levels of glutamate activation, leading to spine formation and synaptogenesis. This, however, is followed by too much glutamate activation in the absence of estrogen, when progesterone alone leads to excitotoxicity and destruction of these same spines and synapses. In other patients, this end-of-the-cycle worsening is unmasking a mood disorder that is actually present during the whole cycle but is sufficiently worse at the end of the cycle that it becomes obvious in a phenomenon called menstrual magnification. This may be a harbinger of further worsening or may also represent a state of incomplete recovery from a previous episode of depression. Estrogen levels shift dramatically across the female life cycle, all in relation to various types of reproductive events. Estrogen levels plummet precipitously immediately postpartum, and regular menstrual cycles begin again once nursing stops. Although the median age of menopause, when all menstruation stops, is 51, women do not stop menstruation overnight. The transition period from regular menstrual periods to complete cessation of menstruation is called perimenopause and can begin 5 to 7 years prior to menopause. In men, the incidence of depression rises in puberty and then is essentially constant throughout life, despite a slowly declining testosterone level from age 25 on. In women, the incidence of depression mirrors their changes in estrogen across the life cycle. As estrogen levels rise during puberty, the incidence of depression also rises, and it falls again during menopause, when estrogen levels fall. However, during their childbearing years when estrogen is high and cycling, the incidence of depression in women is two to three times as high as in men. The first is the postpartum period, when skyrocketing levels of estrogen plummet immediately after delivery of the child. The second occurs during perimenopause, when chaotic hormonal status characterizes the transition from regular menstrual cycles to menopause with no menstrual cycles. There is an increasing risk that a woman will have a recurrence of a major depressive episode after any shift in her estrogen status across her lifetime, a phenomenon some experts have called "kindling. A woman who has a depressive episode triggered by any endocrine shift is quite vulnerable to a recurrence of depression after another reproductive "event" later in her life cycle, such as those shown in Figure 14 - 28, which include puberty, miscarriage, postpartum, perimenopause, taking oral contraceptives, and taking hormone replacement therapy, especially progestins. The increasing chances of a recurrent episode of depression in women whose episodes are linked to reproductive events and shifts in estrogen status may be related to the phenomenon of recurrence in other psychiatric disorders, such as bipolar disorder and schizophrenia. Thus, it is possible that certain mental illnesses, including recurrent depression, are potentially damaging to the brain owing to excitotoxic brain damage (see Chapters 4 and 10). Perhaps life cycle shifts in estrogen status trigger excitotoxicity, just as they seem to do every menstrual cycle.

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Blogging as a social medium in undergraduate courses: Sense of community best predictor of perceived learning diabetes vascular disease discount metformin 500mg free shipping. The site allows registered users to post short (280-character maximum) messages ("tweets") diabetes test without blood buy 500mg metformin visa, which are then available for other users (depending on privacy settings) to read diabetes symptoms hunger buy metformin 500mg, reply to diabetes diet soft drinks metformin 500mg otc, or retweet. As of the writing of this chapter, there were 328 million monthly active users of Twitter worldwide, 82 percent of whom used it via mobile phones (Twitter, 2017). Its cultural impact is widespread, as social commentators credit Twitter for energizing social movements ranging from the Arab Spring and Black Lives Matter to the 2016 election of Donald Trump, who has continued as U. The paucity of experimental studies on the effects of Twitter on student engagement in higher education at that time is what led to the study described in this chapter. Fortunately, since that chance encounter with students Tweeting during class, experimental research on the use of Twitter in the classroom has grown, although it still lags behind studies about Facebook in educational settings (Fleck, Richmond, & Hussey, 2013; Tang & Hew, 2017). In this chapter, we will review such research, and introduce our own experiment performed in an introductory psychology course. Welch and Bonnan-White (2012), however, found no effect on student engagement when P a g e 295 comparing sociology and anthropology courses requiring and not requiring Twitter, although they did find a positive relationship between self-reported Twitter enjoyment and perceived engagement. Blessing, Blessing, and Fleck (2012) compared psychology class sections where instructors tweeted either daily course-related material or daily jokes, and found that students receiving the course-related tweets remembered more concepts than those receiving the joke tweets. Kassens-Noor (2012) in a small, exploratory, mostly qualitative study, allowed students in an urban planning course to choose to either tweet or keep diaries relating to environmentally unsustainable practices they witnessed, and found that students in the Twitter group identified more unsustainable practices, but recalled fewer practices and generated fewer remedies for those practices, compared to the diary group. It is notable, however, that in these three studies, tweets were either generated by the instructors (Blessing et al. Munoz, Pelligrini-Lafont, and Cramer (2014) allowed for independent student-generated tweets in their study comparing an online teacher education course section using Twitter, an online section using a Blackboard-based (Learning Management System) microblog, and a face-to-face section using Twitter. Kuznekoff, Munz, and Titsworth (2015) were able to simulate a classroom setting via a true experiment in which participants were randomly assigned to one of several conditions including whether they were texting while taking notes, tweeting while taking notes, or simply note-taking during a lecture they would be later quizzed about. Participants performed better in the note-taking-only condition than in the tweeting condition, even when they were asked to tweet about lecture content, suggesting that tweeting while in class can be more of a distraction than a help. The lack of consistent findings from the aforementioned studies points to the need for more research on the use of Twitter in education, at least as long as Twitter remains ubiquitous in popular culture. Large-scale reviews have been relatively scarce, as well, but are presented here to conclude this introduction. Gao, Luo, and Zhang (2012) performed an early critical analysis of studies about microblogging in education published from 2008 to 2011, reviewing 21 studies. They highlighted the need for more systematically designed research on using Twitter in education, noting that many studies relied on case studies or descriptive data. The authors provided guidance about incorporating social media in the classroom in general, with a focus on both Facebook and Twitter. Of these 51 studies, only six involved experimental comparisons of Twitter to nonTwitter methods and utilized quantitative outcomes. True experiments, with each participant randomly assigned to a condition, are difficult to achieve in a real educational setting given that students in higher education choose their course sections based on a variety of both practical (e. It would also be logistically difficult for one instructor to structure a single course section with students in both Twitter and control groups. Thus, in the current study we employed a quasi-experimental design, with entire sections assigned to either use Twitter or not. Eight lecture-based sections of introductory psychology participated in the study over four 15-week academic semesters. This questionnaire included demographic items and instruments measuring student engagement and social media use (discussed in more detail below). For the sections comprising the treatment group, we integrated Twitter into curriculum as described below. In the Twitter sections, we provided students with brief tutorials on how to use Twitter, and made clear our expectations for how it would be used during the semester. Each week, students had to compose at least one original tweet regarding something they learned about psychology during that week. These tweets could be informative, humorous, reflective, observational, or inquisitive, and follow standards of relevance and respect that we set for typical classroom discussion.

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