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Pharmacotherapy of Anxiety Disorders in the 21St Century: a Call for Novel Approaches

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Pharmacotherapy of Anxiety Disorders in the 21St Century: a Call for Novel Approaches Open access Review Gen Psych: first published as 10.1136/gpsych-2019-100136 on 11 December 2019. Downloaded from Pharmacotherapy of anxiety disorders in the 21st century: A call for novel approaches Eric Bui,1,2 Franklin King,1,2 Andrew Melaragno1,2 To cite: Bui E, King F, ABSTRACT (FDA)- approved antianxiety medications, Melaragno A. Pharmacotherapy While limited advances have occurred in the past 30 years also date back to the 1950s, and target the of anxiety disorders in the in the pharmacological management of anxiety and stress- gamma- aminobutyric acid (GABA) receptor 21st century: A call for novel related disorders, novel molecular pathways both within approaches. General Psychiatry in a similar fashion to their more toxic prede- and without the monoamine systems are currently under 2019;32:e100136. doi:10.1136/ cessors, meprobamate and the barbiturates, gpsych-2019-100136 investigation and offer promising new avenues for more effective future treatments. Enhancing psychotherapy whose use dates back to the beginning of the Received 17 October 2019 approaches with pharmacological compounds offers 20th century. Moreover, the use of benzodiaz- Revised 09 November 2019 the potential to not only transform the standard of care epines is now more limited due to concerns Accepted 13 November 2019 of these conditions, but more broadly would introduce of abuse, dependence and mortality in poly- a paradigm shift in the way medications and their role pharmacy with concomitantly prescribed (or in psychiatric care are conceptualised. Although further abused) opioids.2 Clearly, since the advent of human trials and more translational research are sorely fluoxetine, no major breakthrough has been needed, continuing to pursue innovative mechanisms achieved in the pharmacological treatment of and treatments is hoped to yield substantial results in the anxiety disorders in the past three decades, coming decades and a departure from the reliance on chemical agents of the 20th century. with advances being mostly incremental. The factors contributing to this lack of major advances are many, but at least three interconnected ones should be highlighted. PHARMACOLOGIcaL TREatMENT OF ANXIETY First, research efforts and the majority of DISORDERS IN THE paST 30 YEARS FDA- approved medications for anxiety have Over 30 years after the introduction of fluox- long revolved around the monoamine and etine in 1986, the first-line pharmacotherapy http://gpsych.bmj.com/ the GABA systems, restricting the range of of anxiety disorders still relies on selective possible innovation to incremental steps serotonin reuptake inhibitor (SSRI) and within a narrow framework. Second, the devel- serotonin- norepinephrine reuptake inhibitor (SNRI) antidepressants, two closely related opment of drugs has developed somewhat classes of drugs derived from fluoxetine.1 serendipitously in parallel with the rigorous Admittedly, these SSRI and SNRI drugs, accumulation of basic science supporting a along with serotonin 5- hydroxytryptamine more comprehensive understanding of the on October 1, 2021 by guest. Protected copyright. 1A (5- HT1A) receptor agonists such as molecular and cellular pathophysiology and buspirone, also introduced in 1986, have brain circuit dysfunction involved in anxiety significantly improved the pharmacological disorders. A gap in translational research has treatment of anxiety by offering options that created a situation where the leaps gained © Author(s) (or their from the former are not effectively used to employer(s)) 2019. Re- use were significantly more tolerable to patients permitted under CC BY-NC. No and vastly safer in overdose than prior treat- inform the latter. For example, most FDA- commercial re- use. See rights ments. Nevertheless, if we consider SSRIs/ approved treatments for anxiety were initially and permissions. Published by SNRIs as belonging to a broader class of medi- developed or tested for another condition, BMJ. usually depression. Furthermore, develop- 1 cations that modulate levels of central nervous Department of Psychiatry, ment efforts usually focus on identifying Massachusetts General Hospital, system monoamine neurotransmitters (prin- Boston, Massachusetts, USA cipally serotonin and norepinephrine, but drugs based on their affinity to brain recep- 2Department of Psychiatry, also dopamine), then no major innovation tors but do not account for the complex Harvard Medical School, Boston, in terms of therapeutic targets has occurred interaction between different circuits, nor for Massachusetts, United States since the introduction of monoamine oxidase the upregulation and downregulation that Correspondence to inhibitors and tricyclic antidepressants in the can occur when a new drug is introduced. Dr Eric Bui; 1950s. Benzodiazepines, the other major Third, the conceptualisation of how drugs tebui@ mgh. harvard. edu class of Food and Drug Administration work for anxiety disorders largely follows a Bui E, et al. General Psychiatry 2019;32:e100136. doi:10.1136/gpsych-2019-100136 1 General Psychiatry Gen Psych: first published as 10.1136/gpsych-2019-100136 on 11 December 2019. Downloaded from medical model3—that is to say, chronic administration of of PTSD.23 Second, the renin–angiotensin system has a drug to compensate for a chronic deficit, much like the become the focus of attention of recent translational lifelong administration of insulin to a patient with type 1 research.24 Preclinical data suggest that blocking the diabetes. This frame is partially at odds with the efficacy of angiotensin 1 receptor may enhance the extinction of psychotherapeutic approaches, which in many cases have fear memory in rodents.25 In another recent animal study, actually been demonstrated to be curative in nature,4 the administration of the angiotensin II receptor antag- reversing underlying biological abnormalities evidenced onist losartan mitigated artificially induced deficits in by neuroimaging findings.5 In fact, there is no satisfac- extinction in female rodents.26 A clinical trial in humans tory explanatory model for how both antidepressants and of daily administration of losartan for PTSD is currently psychotherapy could be efficacious in anxiety disorders. under way (NCT02709018). We therefore propose that future research in anxiety More importantly, while the large majority of phar- disorders should focus on novel neurotransmitter path- macological treatments for anxiety disorders available ways, building on a better understanding of the molec- to date have relied on the traditional model of chronic ular and cellular pathophysiology of (pathological) drug administration to treat putatively chronic, lifelong anxiety, with an aim to fully and definitively restore func- disorders, these recent advances in our understanding tions altered. of fear learning have been the stepping-stone for new approaches aiming to pharmacologically manipulate fear consolidation and extinction learning. Data have NOVEL PROMISING PHARMACOLOGIcaL patHWAYS suggested that stored memories are rendered labile The oxytocin system that is implicated in reproductive during retrieval, and that these memories undergo a and prosocial behaviours6 has also been found to play a reconsolidation process after being retrieved. This has role in stress- related7 8 and anxiety disorders.9 Empirical led to efforts to block memory reconsolidation using evidence suggests that targeting the oxytocin system may the beta- blocker propranolol for PTSD.27 Recently, in a reduce avoidance,10 anxiety and stress.11 Oxytocin admin- randomised controlled trial of six sessions of propranolol istration has thus been proposed as a potential treat- (vs placebo) administration 90 min before a brief memory ment target for stress-related and anxiety disorders;12 13 retrieval were found efficacious for PTSD.28 This may be however, to date no efficacy data from prospective clinical relevant to other anxiety disorders, although findings trials are available. have not been extended to other conditions to date. Both Ketamine, an N- methyl- D- aspartate receptor (NMDA) recent animal and human studies report that propranolol receptor antagonist, has been recently shown to rapidly may enhance extinction,29 30 suggesting that propranolol reduce the severity of depression symptoms.14 Preliminary administration might act as a fear extinction learning data also suggest a potential efficacy in post-traumatic enhancer rather than a postretrieval amnesia inducer, stress disorder (PTSD),15 obsessive-compulsive disorder,16 and future studies should test whether propranolol could 17 and social and generalised anxiety disorders. enhance fear extinction learning during exposure-based http://gpsych.bmj.com/ Research has demonstrated the involvement of the therapies. endocannabinoid system in the regulation of various In fact, several other strategies focused on enhancing physiological operations including pain, inflammation, fear extinction learning through the administration of gastrointestinal, metabolic and cardiovascular function, pharmacological compounds during sessions of exposure and has been recently proposed as a potential therapeutic have also been examined for fear- based disorders.31 32 The target in psychiatry and for anxiety disorders.18 In partic- NMDA partial agonist D-cycloserine has been the most ular, preclinical studies reported that inhibition of the studied potential pharmacological enhancer of exposure- on October 1, 2021 by guest. 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