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Clinical Issues and Case Histories
Published in Albert A. Kurland, S. Joseph Mulé, Psychiatric Aspects of Opiate Dependence, 2019
Albert A. Kurland, S. Joseph Mulé
The next 2 years were spent convalescing and Goering finally returned to Sweden. Now 32, he was described by his doctor as a sick man, with a body like an elderly woman, fat, pale and white. He was unemployed, dependent on his wife’s family, and had become a morphine addict injecting himself daily to keep despair at bay. In the months that followed he displayed the worst symptoms of morphine addiction.
Challenges Facing the American Healthcare System
Published in Kant Patel, Mark Rushefsky, Healthcare Politics and Policy in America, 2019
Unfortunately, many veterans got hooked on morphine and morphine addiction came to be called “the army’s disease” (“Opioid Crisis Fast Facts” 2017; Stobbe 2017). In the 1800s, opium had become an addictive and dangerous drug given to patients for pain who had trouble sleeping. The drug was also used by people to get “high.” Ironically, cocaine and heroin were developed in part to help morphine addiction. In the early 1900s cocaine use became epidemic and its recreational use came to be associated with prostitution and violent crimes. In 1914 Congress passed the Harrison Act, which required that cocaine and heroin could be sold only as prescription medicines. The widespread use of cocaine had for the time being been prevented by economics and politics. During the Great Depression, very few individuals had the disposable income to engage in illicit drug habits, and World War II pretty much stopped the supply of drugs from overseas. However, during the 1960s and 1970s, heroin used surged, especially among Vietnam War soldiers who were exposed to it while fighting overseas. President Nixon’s “War on Drugs” focused on the “supply” side by attacking the drug problem through beefed-up law enforcement and tougher sentences for users and dealers. By the late 1970s, heroin use faded but cocaine was on its way back in the form of the crack epidemic in the 1980s. The crack epidemic died out in the 1990s (“Opioid Crisis Fast Facts” 2017; Stobbe 2017). During the 1980s, under the Reagan administration, First Lady Nancy Reagan’s simplistic “Just Say No” campaign focused on the “demand” side of the drug problem.
The methadone game: control strategies and responses
Published in Jane Fountain, Dirk J Korf, Drugs in Society, 2019
The history of drug addiction includes the history of the search for a medical cure for it. Examples of so-called miracle or therapeutic cures are plentiful. In the late eighteenth century, morphine was believed to cure cocaine addiction, injected morphine was used to cure opium addiction, and heroin was explicitly marketed as a non-addictive cure for morphine addiction.1,18 In the 1930s, a series of new synthetic analgesics were marketed and accepted as safe and curative, including what is now known as methadone, an opiate-like drug synthesised in Germany during the Second World War, and commercially produced under many different trade names from 1947.19 Although mainly prescribed for its pain-killing properties, methadone was also used for detoxification purposes.20,21 However, it was not until the mid-1960s that it was discovered to be an effective medical substitute for illicit opioids. Vincent Dole and Marie Nyswander had found that when it was administered orally and in an adequate dose, the pharmacological effects of methadone would prevent withdrawal symptoms for 24–36 hours, relieve drug craving and block the euphoric effects of heroin.22 Significantly, the results of Dole and Nyswander’s pioneering study indicated that when stabilised on methadone, their patients were able to reorganise their lives socially and productively. Since then, treatment with methadone has expanded substantially to become the predominant form of drug treatment in most western countries.23,24
Linalool attenuates acquisition and reinstatement and accelerates the extinction of nicotine-induced conditioned place preference in male mice
Published in The American Journal of Drug and Alcohol Abuse, 2021
Linalool may demonstrate an attenuating effect on nicotine-induced CPP linked to multiple pharmacological mechanisms. Many studies confirmed that administration of nicotine causes dopamine release in the brain reward system. Furthermore, some studies demonstrate that NMDA antagonists reduce extracellular dopamine in the brain’s reward area and have a reducing effect on nicotine and other substance dependence (6,11,39,58–60). Linalool significantly decreased potassium-stimulated glutamate release as well as glutamate uptake, but did not interfere with basal glutamate release (61,62). In addition, linalool demonstrated a reducing effect on the behavioral nociceptive responses caused by proinflammatory cytokines Il-1β and TNF-α through inhibition of NMDA receptors (16,22). It was suggested in several studies that NMDA antagonists decrease the acquisition and expression of nicotine-induced CPP (30,31). It was also indicated in studies that linalool reduces morphine dependence and morphine-induced conditioned place preference (38,39). The effect of linalool on morphine addiction was interpreted through NMDA receptors. Therefore, linalool may decrease the nicotine-linked CPP via the NMDA receptor. These results are in line with previous studies as mentioned before (30,31,63).
Trauma and Addiction
Published in Psychiatry, 2019
The first case described a man with morphine addiction who had 15 failed treatments of psychotherapy. From the onset, two major problems were identified that likely led to the patient’s failed therapies: His difficulty presenting a problem; and his lack of will to work on the problem. This patient had intense anxiety about having a wish for help. His anxiety was simply too high to form a therapeutic alliance. In ISTDP parlance, this means that his anxiety was either experienced in the body as somatic symptoms or as cognitive and/or perceptual confusion. Frederickson cautions that it is easy for therapists, with our own anxieties and defenses, to assume a patient is “on board” when they are not. When the man began to face his history and the possibility of something different, he began sobbing. No doubt the audience was moved.
Long non-coding RNA MEG3 attends to morphine-mediated autophagy of HT22 cells through modulating ERK pathway
Published in Pharmaceutical Biology, 2019
Shuibo Gao, Enyao Li, Haixia Gao
Morphine is a very effective opiate analgesic drug widely used to ease both acute and chronic pain (Du 2018). However, morphine has become a commonly abused recreational drug due to its widespread availability and a high potential for addiction (Kim et al. 2016). Researching the pathogenesis of morphine addiction can provide new ideas and theoretical basis for elucidating the molecular mechanism of opioid addiction and clinical treatment. Earlier experimental studies have indicated that neuronal cell mitochondrial dysfunction happens in morphine addiction process, which in turn induces cell autophagy (Lixia et al. 2010; Cai et al. 2016; Su et al. 2017). Su et al. (2017) reported that compared to wild-type mice, mice specific knockout of autophagy-related 5 (Atg5) and Atg7 in dopaminergic neurons had lower sensitivities to constructing morphine-induced addictive behaviours. Orexin1 receptor (OX1R) is a G-protein-coupled receptor in central nervous system, which contributed to the establishment of morphine addiction (Baimel et al. 2015). c-fos is a proto-oncogene that expressed in central neurons after adverse stimulation (Dziopa et al. 2011). Studies in rats revealed that c-fos protein took part in the neurobiological responses to morphine in dopamine neurons (Dziopa et al. 2011). Besides, both ERK and PKC pathways have been found to participate in the morphine-mediated drug addiction (Liu et al. 2016; Pena et al. 2018).