多幸感

多幸感（たこうかん、英: euphoria）、ユーフォリアとは、非常に強い幸福感、ウェルビーイングのことである。 特定の自然報酬、有酸素運動、笑い、音楽の聴取、作曲、ダンスなどの社会的活動は、多幸感を引き起こしうる 愛情による至福感や、競技で勝利したときの陶酔感、オーガズムは、多幸感の例である。 また、多幸感は宗教的儀式や瞑想によっても生じうる。 特定の薬物の副作用として生じる場合もあり、また、精神や神経の疾患によって生じる場合もある。 高齢者が自然と感じるようになる幸福感も多幸感の一種とされる（老年的超越）。 脳内で、快楽などを司るA10神経のシナプス間に、幸福感を司る神経伝達物質であるドーパミンが、大量に放出されている状態とされる[要出典]。 娯楽的な薬物使用（英語版）とは、活力や、多幸感や喜びを生じさせるという目的での薬物の使用を描写する、医学的でない用語である。すべての薬物が薬物依存症を引き起こすわけではなく、薬物が引き起こす喜びは、急性の作用（ラッシュ）と、続く多幸感から成り立ち、依存へとつながる精神的な動因がもたらされる。多くは乱用薬物として規制されている。 精神賦活薬、自然報酬、社会的活動など、さまざまな種類の刺激が多幸感を引き起こしうる。単極性躁病または双極性障害などの感情障害は、多幸感の症状を伴うことがある。 継続的な身体運動、特に有酸素運動は多幸感を引き起こしうる。たとえばマラソンはしばしば「ランナーズハイ」に関連付けられ、これは運動によって多幸感が顕著となった状態である。 運動は側坐核のドーパミン信号伝達に影響を及ぼし、その結果、3つの神経化学物質生合成が増加することで、幸福感を生み出すことが知られている。それはアナンダミド（エンドカンナビノイド）β-エンドルフィン（内因性オピオイド）、フェネチルアミン（微量アミンとアンフェタミンアナログ）と特定されている。 多幸感は、音楽に合わせて踊ったり、音楽を作曲したり、感情を刺激する音楽を聴いたりすることで発生する神経イメージング研究によって、音楽による多幸感の発生は、報酬系が中心的な役割を果たしていることが実証されている。 一部の人々により、性交のさまざまなステージにおいて多幸感が誘発されると説明されることもある。さまざまなアナリストは、交尾の全行為、オルガスムに至る瞬間、またはオルガスム自体を、人間の快楽または多幸感の頂点と表現している。 断食をすることは、気分、ウェルビーイング、そして時には多幸感の改善に関連する。様々なメカニズムが提案されており、うつ病の治療における適用可能性が検討されている。 オピオイドは、モルヒネ、ヘロイン、コデインなどを含む鎮痛麻薬を指す厳密な用語で、これらは鎮痛作用を超える作用として、鎮静、強い多幸感、呼吸抑制、便秘などの作用がある。 テトラヒドロカンナビノール (THC) 大麻に含まれる成分で、多幸感、不安の緩和、鎮静、眠気を生じさせる。ドロナビノール（マリノール）やナビキシモルス（サティベックス）のような、大麻をもとにした医薬品は、副作用として（薬として目的とする作用ではないので）多幸感を生じさせる。合成カンナビノイドは、大麻の多幸感を模倣する作用を持つ。 メチレンジオキシメタンフェタミン (MDMA)の急性作用は、健康な感覚、多幸感、他者への開放性（共感）が増加することである。 ケタミンの多幸感は急速に生じ、それは量に伴って高くなる。最初のラッシュでの忘我的な多幸感は数分で生じる。 γ-ヒドロキシ酪酸 (GHB) の娯楽的使用者は、副作用としてリビドーと多幸感を生じさせる。パーティでの使用は多く多幸感や社交性を求めて使用され、少数では多幸感に加え睡眠の強化や性的な目的で使用し、頻繁な使用者は依存症と関連して睡眠を誘導したり離脱症状を緩和するために使用する。 ほか（未詳細） コカイン シンナー ステロイドホルモン（医薬品） ^ a b "Addicted to Euphoria": The History, Clinical Presentation, and Management of Party Drug Misuse. International Review of Neurobiology. 120. (2015). 205–33. doi:10.1016/bs.irn.2015.02.005. ISBN 9780128029787. PMID 26070759. "Eating, drinking, sexual activity, and parenting invoke pleasure, an emotion that promotes repetition of these behaviors, are essential for survival. Euphoria, a feeling or state of intense excitement and happiness, is an amplification of pleasure, aspired to one's essential biological needs that are satisfied. People use party drugs as a shortcut to euphoria. Ecstasy (3,4-methylenedioxymethamphetamine), γ-hydroxybutyric acid, and ketamine fall under the umbrella of the term "party drugs," each with differing neuropharmacological and physiological actions."  ^ “The SEEKING mind: primal neuro-affective substrates for appetitive incentive states and their pathological dynamics in addictions and depression”. Neuroscience and Biobehavioral Reviews 35 (9): 1805–1820. (2011). doi:10.1016/j.neubiorev.2011.03.002. PMID 21396397. "Recent human data have demonstrated that the SEEKING brain circuitry, as predicted, is involved in the emergence of a characteristic appetitive affective state, which may be described as “enthusiastic positive excitement” or “euphoria” (Drevets et al., 2001; Volkow and Swanson, 2003) and that do not resemble any kind of sensory pleasure (Heath, 1996; Panksepp et al., 1985) ... However, in our view, cognitive processes, are only one “slice of the pie”, and gamma oscillations may be more globally viewed as the overall emotional–motivational neurodynamics through which the SEEKING disposition is expressed, accompanied by a feeling of excitement/eurphoria (not ‘pleasure’) that is evolutionarily designed to achieve a diversity of useful outcomes"  ^ a b “Key DSM-IV Mental Status Exam Phrases”. Gateway Psychiatric Services. 2013年11月13日時点のオリジナルよりアーカイブ。2014年2月17日閲覧。 ^ a b c “Rowers' high: behavioural synchrony is correlated with elevated pain thresholds”. Biol. Lett. 6 (1): 106–8. (2010). doi:10.1098/rsbl.2009.0670. PMC 2817271. PMID 19755532. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817271/. "This heightened effect from synchronized activity may explain the sense of euphoria experienced during other social activities (such as laughter, music-making and dancing) that are involved in social bonding in humans and possibly other vertebrates."  ^ "Psychophysical Correlates of the Practice of Tantric Yoga Meditation". Corby, Roth, Zarcone, & Kopell. Archives of General Hackett, 1978. ^ “Euphoria”. Wrong Diagnosis. Health Grades Inc.. 2011年6月23日閲覧。 ^ Rhodri Hayward "euphoria" The Oxford Companion to the Body. Ed. Colin Blakemore and Sheila Jennett. Oxford University Press, 2001. Oxford Reference Online. Oxford University Press. 28 July 2011 ^ “NHKクローズアップ現代「“百寿者”　知られざる世界～幸せな長生きのすすめ～」（2014年10月15日放送）”. 2014年10月15日閲覧。 ^ a b c d e f g Bearn, Jenny; O'Brien, Matthew (2015). ““Addicted to Euphoria””. Int. Rev. Neurobiol. 120: 205–233. doi:10.1016/bs.irn.2015.02.005. PMID 26070759.  ^ “Neuronal reward and decision signals: from theories to data”. Physiological Reviews 95 (3): 853–951. (2015). doi:10.1152/physrev.00023.2014. PMC 4491543. PMID 26109341. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491543/. "The feeling of high that is experienced by sports people during running or swimming, the lust evoked by encountering a ready mating partner, a sexual orgasm, the euphoria reported by drug users, and the parental affection to babies constitute different forms (qualities) rather than degrees of pleasure (quantities)."  ^ a b Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. (2009). pp. 191, 350–351, 367–368, 371–375. ISBN 9780071481274. "Changes in appetite and energy may reflect abnormalities in various hypothalamic nuclei. Depressed mood and anhedonia (lack of interest in pleasurable activities) in depressed individuals, and euphoria and increased involvement in goal-directed activities in patients, who experience mania, may reflect opposing abnormalities in the nucleus accumbens, medial prefrontal cortex, amygdala, or other structures. ... Although short-term administration of glucocorticoids often produces euphoria and increased energy, the impact of long-lasting increases in endogenous glucocorticoids produced during depression can involve complex adaptations such as those that occur in Cushing syndrome (Chapter 10). ... Exposure to addictive chemicals not only produces extreme euphoric states that may initially motivate drug use, but also causes equally extreme adaptations in reinforcement mechanisms and motivated behavior that eventually lead to compulsive use. Accordingly, the evolutionary design of human and animal brains that has helped to promote our survival also has made us vulnerable to addiction."  ^ a b “Phenylethylamine, a possible link to the antidepressant effects of exercise?”. Br J Sports Med 35 (5): 342–343. (2001). doi:10.1136/bjsm.35.5.342. PMC 1724404. PMID 11579070. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1724404/. "The 24 hour mean urinary concentration of phenylacetic acid was increased by 77% after exercise. ... These results show substantial increases in urinary phenylacetic acid levels 24 hours after moderate to high intensity aerobic exercise. As phenylacetic acid reflects phenylethylamine levels3, and the latter has antidepressant effects, the antidepressant effects of exercise appear to be linked to increased phenylethylamine concentrations. Furthermore, considering the structural and pharmacological analogy between amphetamines and phenylethylamine, it is conceivable that phenylethylamine plays a role in the commonly reported "runners high" thought to be linked to cerebral β-endorphin activity. The substantial increase in phenylacetic acid excretion in this study implies that phenylethylamine levels are affected by exercise. ... A 30 minute bout of moderate to high intensity aerobic exercise increases phenylacetic acid levels in healthy regularly exercising men. The findings may be linked to the antidepressant effects of exercise."  ^ “Physical activity and the endocannabinoid system: an overview”. Cell. Mol. Life Sci. 71 (14): 2681–2698. (2014). doi:10.1007/s00018-014-1575-6. PMID 24526057. "The traditional view that PA engages the monoaminergic and endorphinergic systems has been challenged by the discovery of the endocannabinoid system (ECS), composed of endogenous lipids, their target receptors, and metabolic enzymes. Indeed, direct and indirect evidence suggests that the ECS might mediate some of the PA-triggered effects throughout the body. ... the evidence that PA induces some of the psychotropic effects elicited by the Cannabis sativa active ingredient Δ9-tetrahydrocannabinol (Δ9-THC, Fig. 1), like bliss, euphoria, and peacefulness, strengthened the hypothesis that endocannabinoids (eCBs) might mediate, at least in part, the central and peripheral effects of exercise [14]. ... To our knowledge, the first experimental study aimed at investigating the influence of PA on ECS in humans was carried out in 2003 by Sparling and coworkers [63], who showed increased plasma AEA content after 45 min of moderate intensity exercise on a treadmill or cycle ergometer. Since then, other human studies have shown increased blood concentrations of AEA ... A dependence of the increase of AEA concentration on exercise intensity has also been documented. Plasma levels of AEA significantly increased upon 30 min of moderate exercise (heart rate of 72 and 83 %), but not at lower and significantly higher exercise intensities, where the age-adjusted maximal heart rate was 44 and 92 %, respectively ... Several experimental data support the hypothesis that ECS might, at least in part, explain PA effects on brain functions, because: (1) CB1 is the most abundant GPCR in the brain participating in neuronal plasticity [18]; (2) eCBs are involved in several brain responses that greatly overlap with the positive effects of exercise; (3) eCBs are able to cross the blood–brain barrier [95]; and (4) exercise increases eCB plasma levels [64–67]."  ^ “Effects of exercise and physical activity on depression”. Ir J Med Sci 180 (2): 319–325. (2011). doi:10.1007/s11845-010-0633-9. PMID 21076975. "According to the 'endorphins hypothesis', exercise augments the secretion of endogenous opioid peptides in the brain, reducing pain and causing general euphoria. ... Based upon a large effect size, the results confirmed the endorphins hypothesis demonstrating that exercise leads to an increased secretion of endorphins which, in turn, improved mood states. β-Endorphin, an endogenous μ-opioid receptor selective ligand, has received much attention in the literature linking endorphins and depression or mood states. ... exercise of sufficient intensity and duration can increase circulating β-endorphin levels. ... Moreover, a recent study demonstrated that exercise and physical activity increased β-endorphin levels in plasma with positive effects on mood. The researchers reported that, independently of sex and age, dynamic anaerobic exercises increased β-endorphin, while resistance and aerobic exercises seem to only have small effects on β-endorphins. ... The results showed that mood tends to be higher in a day an individual exercises as well as that daily activity and exercise overall are strongly linked with mood states. In line with these findings, a recent study showed that exercise significantly improved mood states in non-exercises, recreational exercisers, as well as marathon runners. More importantly, the effects of exercise on mood were twofold in recreational exercisers and marathon runners."  ^ “A renaissance in trace amines inspired by a novel GPCR family”. Trends Pharmacol. Sci. 26 (5): 274–281. (2005). doi:10.1016/j.tips.2005.03.007. PMID 15860375. "The pharmacology of TAs might also contribute to a molecular understanding of the well-recognized antidepressant effect of physical exercise [51]. In addition to the various beneficial effects for brain function mainly attributed to an upregulation of peptide growth factors [52,53], exercise induces a rapidly enhanced excretion of the main β-PEA metabolite β-phenylacetic acid (b-PAA) by on average 77%, compared with resting control subjects [54], which mirrors increased β-PEA synthesis in view of its limited endogenous pool half-life of ~30 s [18,55]."  ^ “The potential of trace amines and their receptors for treating neurological and psychiatric diseases”. Rev Recent Clin Trials 2 (1): 3–19. (2007). doi:10.2174/157488707779318107. PMID 18473983. "It has also been suggested that the antidepressant effects of exercise are due to an exercise-induced elevation of [phenethylamine] [151]."  ^ “Anatomically distinct dopamine release during anticipation and experience of peak emotion to music”. Nat. Neurosci. 14 (2): 257–262. (2011). doi:10.1038/nn.2726. PMID 21217764. "Music, an abstract stimulus, can arouse feelings of euphoria and craving, similar to tangible rewards that involve the striatal dopaminergic system. ... the caudate was more involved during the anticipation and the nucleus accumbens was more involved during the experience of peak emotional responses to music. ... Notably, the anticipation of an abstract reward can result in dopamine release in an anatomical pathway distinct from that associated with the peak pleasure itself."  ^ a b “Music and the nucleus accumbens”. Surg Radiol Anat 37 (2): 121–125. (March 2015). doi:10.1007/s00276-014-1360-0. PMID 25102783. "The functional connectivity between brain regions mediating reward, autonomic and cognitive processing provides insight into understanding why listening to music is one of the most rewarding and pleasurable human experiences. Musical stimuli can significantly increase extracellular DA levels in the NA. NA DA and serotonin were found significantly higher in animals exposed to music. Finally, passive listening to unfamiliar although liked music showed activations in the NA. ... Music can arouse feelings of euphoria and craving, similar to tangible rewards that involve the striatal DAergic system [16]. Reward value for music can be coded by activity levels in the NA, whose functional connectivity with auditory and frontal areas increases as a function of increasing musical reward [19]. ... Listening to pleasant music induces a strong response and significant activation of the VTA-mediated interaction of the NA with the hypothalamus, insula and orbitofrontal cortex [1]. Conclusions Listening to music strongly modulates activity in a network of mesolimbic structures involved in reward processing including the NA. Music, acting as a positive pleasant emotion, increases NA DAergic activity. Specifically the NA is more involved during the experience of peak emotional responses to music. Reward value of music can be predicted by increased functional connectivity of auditory cortices, amygdala and ventromedial prefrontal regions with the NA. Further research is needed to improve our understanding of the NA role in the influence of music in our lives."  ^ “Musical pleasure and reward: mechanisms and dysfunction”. Ann. N. Y. Acad. Sci. 1337 (1): 202–211. (March 2015). Bibcode: 2015NYASA1337..202Z. doi:10.1111/nyas.12677. PMID 25773636. https://zenodo.org/record/3456475. "Most people derive pleasure from music. Neuroimaging studies show that the reward system of the human brain is central to this experience. Specifically, the dorsal and ventral striatum release dopamine when listening to pleasurable music, and activity in these structures also codes the reward value of musical excerpts. Moreover, the striatum interacts with cortical mechanisms involved in perception and valuation of musical stimuli. ... Development of a questionnaire for music reward experiences has allowed the identification of separable factors associated with musical pleasure, described as music-seeking, emotion-evocation, mood regulation, sensorimotor, and social factors. Applying this questionnaire to a large sample uncovered approximately 5% of the population with low sensitivity to musical reward in the absence of generalized anhedonia or depression. Further study of this group revealed that there are individuals who respond normally both behaviorally and psychophysiologically to rewards other than music (e.g., monetary value) but do not experience pleasure from music despite normal music perception ability and preserved ability to identify intended emotions in musical passages."  ^ “Evidence against involvement of endorphins in sexual arousal and orgasm in man”. Archives of General Psychiatry 34 (10): 1179–1180. (1977). doi:10.1001/archpsyc.1977.01770220061006. PMID 199128.  ^ “Fasting in mood disorders: neurobiology and effectiveness. A review of the literature”. Psychiatry Research 209 (3): 253–258. (2013). doi:10.1016/j.psychres.2012.12.018. PMID 23332541. オリジナルの19 July 2018時点におけるアーカイブ。. https://web.archive.org/web/20180719195929/http://www.hal.inserm.fr/inserm-00789122/file/PRISMA_FLOW_DIAGRAMM_FASTING_07_12_12.pdf 14 November 2018閲覧。.  ^ 世界保健機関 (1994) (pdf). Lexicon of alchol and drug term. World Health Organization. pp. 47, 49. ISBN 92-4-154468-6. http://whqlibdoc.who.int/publications/9241544686.pdf  （HTML版 introductionが省略されている） ^ Ghelardini, C (2015). “The pharmacological basis of opioids”. Clinical Cases in Mineral and Bone Metabolism (3): 219–21. doi:10.11138/ccmbm/2015.12.3.219. PMC 4708964. PMID 26811699. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4708964/.  ^ “Cannabis drug profile”. 欧州薬物・薬物依存監視センター (EMCDDA) (Update: 08 January 2015). 2016年12月28日閲覧。 ^ H. Valerie Curran; Philip Wiffen; David J. Nutt; Willem Scholten=. Cannabis and Cannabis Resin Pre-Review Report (pdf) (Report). DrugScience. p. 28. ISBN 978-1-5272-0260-3. 2016年12月28日閲覧。 ^ Debruyne, Daniele; Le Boisselier, Reynald (2015). “Emerging drugs of abuse: current perspectives on synthetic cannabinoids”. Substance Abuse and Rehabilitation: 113. doi:10.2147/SAR.S73586. PMC 4622447. PMID 26543389. https://www.dovepress.com/emerging-drugs-of-abuse-current-perspectives-on-synthetic-cannabinoids-peer-reviewed-fulltext-article-SAR.  ユーフォリア 表示 編集 表示 編集