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a prolonged disorder of eating due to loss of appetite

PrepTutorEJDIC

(神経性の)食欲減退(不振)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/09/17 16:13:41」(JST)

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「Anorexia nervosa」はこの項目へ転送されています。フランスのシンフォニックブラックメタルバンドについては「アノレクシア・ネルヴォサ」をご覧ください。

神経性無食欲症（しんけいせいむしょくよくしょう、英: Anorexia nervosa ; AN）は、病的な痩せを呈する摂食障害であり、精神疾患の一種である^[1]。一般には拒食症（きょしょくしょう）、アノレキシアとも言われる。若年層に好発し、ボディ・イメージの障害（「自分は太っている」と考えること）、食物摂取の不良または拒否、体重減少を特徴とする。神経性食欲不振症、神経性食思不振症、思春期やせ症とも言う。

当疾患および神経性過食症（過食症）をあわせた「中枢性摂食異常症（摂食障害）」は厚生労働省の特定疾患に該当し、重点的に研究が進められている。

日本精神神経学会のDSM‒5病名・用語翻訳ガイドラインでは神経性やせ症に名称変更した^[2]。

概要

神経性無食欲症は心理的要因・社会的要因・生物学的要因によって生じる、摂食行動の障害となって現れる精神疾患である。特に心理的要因（ストレス）によるところが多く、慢性経過をとることが多い。近年日本において増加傾向にあり、また抑うつを伴ったり身体的疾患を合併することもあり、心身に与える影響は大きい。

摂食障害は大きく拒食症、過食症に分類される。拒食と過食は相反するもののように捉えがちだが、拒食症から過食症に移行するケースが約60 - 70%みられたり、「極端なやせ願望」あるいは「肥満恐怖」などが共通し、病気のステージが異なるだけの同一疾患と考えられている^[3]^[4]。よって拒食症、過食症を区別する指標は、基本的には正常最低限体重を維持しているかどうかのみである。アメリカでは平均体重の85%以下が拒食症に分類されているが、日本では80%以下とされている^[5]。

精神分析医のヒルデ・ブルックは摂食障害を「これは食欲の病気ではありません。人からどう見られるのかということに関連する自尊心の病理です」と指摘している。摂食障害患者は根源的否定感を抱えており、食行動の異常の背景には茫漠たる自己不信が横たわっていると理解される。その不安を振り払うために強迫的に完全を志向するのである。摂食障害は境界性パーソナリティ障害、自己愛性パーソナリティ障害との合併、あるいはそれらパーソナリティ障害の部分症状として顕在化しているケースも多い^[6]。

典型的なANの患者では、体重を落とすために始めたダイエットで達成感が得られ、体重を落とすことを止められなくなってしまう。低体重であっても自分の体重を多すぎると感じ、さらに体重を減らすことを望む。鏡を見ても「まだまだ痩せられる」と感じるのみであり、体重が低すぎるとは考えない。宗教上の理由から断食をする場合、政治的目的から断食によるストライキを行う場合、あるいはカロリーを制限することで長寿が達成できるという健康上の信念を持っている場合に、食事を摂らないか極端に食事の摂取量を減らす例があるが、これらはANではない。

時にANは拒食の反動から過食を伴ったり、その他非定型性の摂食障害へと病像が変化する場合がある。

歴史

古くは宗教的な意味合いから拒食になるケースが多く、増え始めたのは13世紀頃である。一般的に、19世紀までは病気として扱われたことはなかった。ルドルフ・ベルの『聖なる拒食』(Holy Anorexia)には中世イタリアのカトリック261人の拒食聖女の記録がある。これらの聖女はほとんどが思春期の女性であった。聖カタリナは16歳頃からパンと生野菜と水しか摂取せず、25歳までにはほとんどの食事を採らなくなったが、非常に活動的で各地を渡り歩いた。聖クララは月水金は何も食べず、他の曜日もわずかしか食べず病気になり、聖フランシスコとアッシジ司教が毎日1.5オンスのパンを食べるように命じ、回復したという。^[7]これらの聖人の拒食は、禁欲業としての断食のレベルをはるかに超えるものであった。彼女達は貴族や富裕層の出身であり、親の結婚強要など、世俗の慣習から免がれる為に、宗教的救いを求めた結果の拒食とも言えるであろう。^[要出典]

その一方で、医学的な捉え方は17世紀末から出始めている。1689年にジェイムズ二世の侍医であるリチャード・モートンが、拒食症の症例を初めて病気として記述した。^[8]その後の1874年には、ヴィクトリア女王の御典医であったウィリアム・ガルが初めて「Anorexia Nervosa（神経性無食欲症）」と呼称した。19世紀後半以降から、英米仏の中産階級の子女たちの間で拒食症は大流行する。この病気の流行はこの時代の家父長制度によって抑圧され、出口を失った女性の生のエネルギーが自己破壊に向かったものとする見方がある^[9]。また、現代に至り痩身イコール女性美と考える社会風潮が拒食症を増やす要因にであることは周知の事実であろう。^[要出典]

症状

自分の思う通りにならない自分を、摂食行動において完璧にコントロールし、痩せを維持できることは、万能感・高揚感を与えてくれる体験である。食事をコントロールし、自らの体を過度にコントロールしようとする心性の背後には慢性的な不安が控えており、摂食障害者は一様に強迫的な性格傾向を有する^[10]。

ANは精神神経疾患の中では致死率が高い疾患のひとつであり、最終的な致死率は5%-20%程度である。主な死因は極度の低栄養による感染症や不整脈である。患者は自己の体重が減少することに恍惚を感じるため、自殺が死因となることは神経性大食症(過食症)と比較して少ないが、抑うつを伴い自殺を企図する例もある。ANは自らが太ることに対する恐怖感や、体重を落とすことに対する快感を覚える精神的要因から無食欲状態に陥り、食事を摂らないか、極端に少量しか摂らなくなり、無理して食べると嘔吐してしまう。あるいは飢餓状態から突如過食をし、その後自己誘発嘔吐などの代償行為を行う。

主な合併症は以下のとおりである。

極度の体重減少
無月経（女性）
若年性更年期障害
活動性の上昇、易興奮性、睡眠障害
抑うつ症状
食物への興味の上昇…しばしば料理関係の情報を収集する
強迫的な思考
強い拘り（強迫的傾向）
感情の統制水準が低下する
物事に興味・関心がなくなる・笑わなくなる
自傷行為
手掌・足底の黄染（高カロテン血症）
低血圧
低体温
徐脈
便秘、腹痛
貧血
電解質代謝異常、特に低カリウム血症
骨粗鬆症
続発性甲状腺機能低下症
色素性痒疹…胸や肩などに痒みの強い発疹が出現する皮膚疾患

電解質代謝異常は利尿剤の乱用が見られる症例では起こりやすく、時に低カリウム血症から致死性の不整脈をきたし急死することがある。またこれらの個人に属する症状に加えて、極度の体重減少や易刺激性が、周囲との関係不良をもたらすことも大きな問題となる。

診断基準

DSM-IV-TR

DSM-IV-TRでは次の4項目を満たすと神経性無食欲症と診断される。排出行動が見られるかによって、制限型とむちゃ食い/排出型に分かれる^[11]。

A. 年齢と身長に対する正常体重の最低限、またはそれ以上を維持することの拒否 (例: 期待される体重の85%以下の体重が続くような体重減少；または成長期間中に期待される体重増加がなく、期待される体重の85%以下になる)

B. 体重が不足している場合でも、体重が増えること、または肥満することに対する強い恐怖

C. 自分の体重または体型の感じ方の障害、自己評価に対する体重や体型の過剰な影響、または現在の低体重の重大さの否認

D. 初潮後の女性の場合は、無月経、すなわち月経周期が連続して少なくとも3回欠如する (エストロゲンなどのホルモン投与後にのみ月経が起きている場合, その女性は無月経とみなされる)

病型: 制限型：現在の神経性無食欲症のエピソード期間中、その人は規則的にむちゃ食いや排出行動（つまり、自己誘発性嘔吐、または下剤、利尿剤、または浣腸の誤った使用）を行ったことがない; むちゃ食い/排出型：現在の神経性無食欲症のエピソード期間中、その人は規則的にむちゃ食いや排出行動（すなわち、自己誘発性嘔吐、または下剤、利尿剤、または浣腸の誤った使用）を行ったことがある

ICD-10

確定診断のためには，以下の障害のすべてが必要である^[12]。

（a）体重が（減少したにせよ、はじめから到達しなかったにせよ）期待される値より少なくとも15％以上下まわること、あるいはQuetelet's body-mass index（BMI）が17.5以下、前思春期の患者では、成長期に本来あるべき体重増加がみられない場合もある。

（b）体重減少は「太る食物」を避けること。また、自ら誘発する嘔吐、緩下薬の自発的使用、過度の運動、食欲抑制薬および/または利尿薬の使用などが1項以上ある。

（c）肥満への恐怖が存在する。その際、特有な精神病理学的な形をとったボディイメージのゆがみが、ぬぐい去りがたい過度の観念として存在する。そして患者は自分の体重の許容限度を低く決めている。

（d）視床下部下垂体性腺系を含む広汎な内分泌系の障害が、女性では無月経、男性では性欲、性的能力の減退を起こす（明らかな例外としては、避妊用ピルとして最もよく用いられているホルモンの補充療法を受けている無食欲症の女性で、性器出血が持続することがある）。また成長ホルモンの上昇、甲状腺ホルモンによる末梢の代謝の変化、インスリン分泌の異常も認められることがある。

（e）もし発症が前思春期であれば、思春期に起こる一連の現象は遅れ、あるいは停止することさえある（成長の停止。少女では乳房が発達せず、一次性の無月経が起こる。少年では性器は子どもの状態のままである）。回復すれば思春期はしばしば正常に完了するが、初潮は遅れる。

疫学

摂食障害全体が日本で増加し始めたのは1970年代からであり、現代における有病率はアメリカやヨーロッパの先進各国と同水準である^[13]。ダイエットが若年層の一大関心事である日本におけるANは、若年層、特に青年期の女性に非常に多いことが特徴である。若年男性でのANの発症も見られるが、男女比はおよそ1対20である。発症年齢が年々低年齢化しており、小学生での発症も増加している。近年では思春期以降で発症する人も増加傾向にある。治療は一般に困難であり、長い時間がかかる。合併症や自殺のために経過の途中で死亡する例もある（5%～15%程度）。一方で、近代的なダイエットとは無縁のアフリカにおいてAN様の病像を呈する症例の報告があり、宗教的信念との関連が考えられている。

病理学

摂食障害は拒食と過食が主な症状であるが、相互に排他的な疾患ではないため、背景にある精神病理を把握することが求められる。

拒食

神経性無食欲症が爆発的に増加したのは、1960年代から1970年代にかけてと言われる。1966年にはイギリス出身のモデルであるレズリー・ホーンビーがデビューし、ツイッギー（小枝）という愛称で親しまれた。「妖精」と謳われた華奢な体型の彼女は、ロンドンで行われた人気アンケートで年々順位を上げ、1976年には首位に立っている。社会の価値観はそれまでのグラマラスな女性像に代わり、スリムな女性を理想像として迎えた^[14]。痩せていることは克己心、禁欲、美しさ、高い精神性などの隠喩が込められており、今や「痩せることは女性にとって価値があること」になった。摂食障害の人にとって、この「価値があること」がキーワードなのである。

自分には何の取り柄も無いという自己不信を根底に抱える人は、その抑うつを防衛するために、人とは際立って違う、優れた、特別な自分であり続けなければならない。彼らは幼い頃から常に「自分が自分以上でなければならない」という強迫観念に支配されている。痩せを実現するには、食欲を抑え、自分に打ち勝つ必要がある。やせる事に成功した時には、自分をコントロールすることが出来たという万能感が得られる。幼い頃から課題に挑戦し、自分に打ち勝って結果を得てきた彼らは、結果を出す事で得られる賞賛と万能感により、中核にある自己不信を救済する^[15]。

彼らは負けず嫌いであり、そしていつも負けていると思っている。現実の中で特別な価値の獲得に失敗した人は、「せめて痩せていないと取り柄がない」という感覚から、誰もが望み、簡単には出来ないダイエットへと挑戦する。やせることは最も身近な外的価値の収得であり、ダイエットの成功は直接的に自己価値を高める。それはやせることには価値があり、その為には努力しなければならないからである。価値意識は「どれだけやせているか」へと変換され、体重増加は恐ろしいほどの価値の低下に繋がる。他と変わらない体重は「並」「平凡」「普通」であるため、輝くことで自己不信を払拭してきた彼らには決して許容することが出来ない。痩せを希求する女性にとって、男性はほとんど意識されておらず、その競争相手は同じ女性である。人より痩せていることは、現代社会の価値観においては「勝った」ことに繋がる。人より痩せる事は、常に人より上に立ちたい、勝ちたい、輝きたいと願う彼らの存在証明でもある。拒食は自己愛の病理と深く関連しており、自己愛性心性を扱うことが求められる^[16]^[17]^[18]。

詳細は「摂食障害#病理学」を参照

原因

摂食障害の病因についてこれまで様々な仮説が唱えられてきた。肥満蔑視・やせに価値があるという社会文化的要因、成熟拒否や自己同一性獲得の失敗等の心理的要因、脳機能の異常に原因を求める生物学的要因等である。しかし現代においてはそれらが相互に複雑に関連し合って発症に至ると考えられている^[19]。これはANについても同様である。

社会文化的要因

社会文化的要因はANの発症に深く関与している。メディアにおいてやせた女性、元気で快活な女性が賞賛され、内面よりも外見を重視するような風潮はANの発症の大きな要因であろう。実際に12~21歳の2862人の思春期少女を18か月間追跡調査したところ、90人が摂食障害を新たに発症したが、発症に関与した因子として一人で食事をすること、少女雑誌をよく読むことやラジオをよく聴くことが挙げられた^[20]という研究もあり、スリムな体型に高い価値を置くという現代の社会背景の影響がうかがわれる。

芸能界やモデル業界などの美を競う業界や、痩せていることが重要だと考えられているスポーツ選手においてANにかかる患者がいることが注目を集めている。2006年にはファッションモデルのアナ・カロリナ・レストンが21歳の若さで死亡したことで話題となった。2007年にはイタリアでの拒食症啓発キャンペーンポスターにモデルのイザベル・カロが出演。極端に痩せたヌード姿をさらし、細身の体形が常識とされていたファッションモデル界に一石を投じた。カロは13歳の頃から拒食症に苦しみ、撮影時の身長は165cm、体重は30kgだった。2010年に死去。

心理的要因

心理的要因が発病に影響しているのは明らかである。海外の研究においては摂食障害の患者は健康な人間よりも高い確率で幼少期に性的虐待を含む虐待を受けた経験をもつという報告もあるが、他の精神疾患においても高い確率で性的虐待の既往が報告されており、摂食障害と性的虐待を直接的な因果関係は不明である^[21]。また、かつて1970年代などの初期の研究において、高学歴や家庭の経済状態がよいことなどがANの罹患率と相関するという報告がなされ広く信じられていたが、その後の研究ではこの説を支持しないか、むしろ逆の結果が示されることもある^[22]。その他にも力動精神医学的な観点から様々な考察がなされている。

性的な成熟に対する恐怖・女性であることの否定：女性は第二次性徴を迎えると、皮下脂肪をたくわえ身体が丸みを帯び、乳房がふくらむなど身体が変化する。これらの変化に伴い、男性の性的関心の対象となるのを嫌悪・拒絶する心理がAN発症の因子となる。
肥満恐怖：肥満への恐怖・嫌悪が存在することが多い。「太っている」などとからかわれることが発症のきっかけとなる場合も多い。これは自尊心の易傷性が特徴である。
母親となることの拒絶：摂食拒否によって母親になることを拒絶しているという説。
対人関係の障害：原因なのか結果なのかは不明であるが、対人関係に障害を有する症例が多い。
失感情症（アレキシサイミア）：自らの感情に気づくことができない・できにくいことを「失感情症（アレキシサイミア）」という。ANも失感情症の要素があることが指摘されており、自らのストレスやつらい気持ちに気づかず（否認して）、その代わり身体症状で表現しているという可能性がある。
完璧主義・強迫性はAN患者においてよくみられる性格標識である。
嗜癖（依存症）としての要素：ANの初期に摂食量を制限して体重が減るという結果を得て満足し、更に摂食量制限にふけり、独特の気分高揚を示すことがある。この心性は薬物依存やギャンブル依存などの嗜癖行動との共通点があると言われている。

生物学的要因

様々な研究が報告されている。器質的な脳の病変の存在は明らかにされていないが、二卵性双生児よりも一卵性双生児の方が一致率が高いこと、AN患者の家族にはうつ病、アルコール依存、強迫性障害や摂食障害が多いことから遺伝的要因の関与も考えられている。ANの発病に関連する遺伝子もいくつか見いだされてはいるが、結論は出ていない。視床下部におけるドパミン、ノルアドレナリン活性の異常を指摘する研究もある。出産時の合併症（頭蓋内出血、低体重など）がANの罹患率を増加させるという疫学的研究もある^[23]。

治療

拒食と過食は周期的に繰り返される場合が多く、心療内科医・精神科医など医師や心理カウンセラーの心理的なカウンセリングを受けることが有効である。しかし専門性の高い医師は多くはないのが現状である。拒食や過食の食行動異常が注目されやすいが、たとえ体重が適性値に戻っても、その背景にある心の問題が解決されないと再び摂食障害に陥ってしまうことがある。背景の問題解決には周囲の協力が必要である。特に家族ガイダンスは有効である^[24]^[25]。

治療は精神療法が中心となる。対症療法として抑うつ症状には薬物療法が用いられる。家族カウンセリングが行われる場合もある。患者が病気であることを否認する場合や、ANの存在を容認したとしても治療拒否の姿勢を示す場合はよくみられる。さらには治療を認める姿勢を見せて、実際には出された食事を隠れて捨てるなどの行為がとられる場合もある。

治療にあたっては体重増加のみを治療目的とすべきではない。「とにかく食べろ」といった強硬な姿勢を家族や治療者が見せることは逆効果となる。長い間ANと戦っている患者にとって、食物を食べること自体が大変な苦痛・恐怖につながるためである。また体重増加以外にも患者の主体性を重視し、人間としての成熟、対人関係の充実、実生活での適応などを援助することが重要である。摂食障害全般を扱う自助グループが全国に存在する。治療により軽快した場合、再発や、神経性大食症の発症に注意する必要がある。厚生労働省の特定疾患に該当し、治療法についても重点的に研究が進められている。

精神療法

精神療法としては、力動的精神療法、行動療法、認知療法、対人関係療法、家族療法などがある。栄養リハビリテーションも必要である。

薬物療法

摂食障害は心の病理を有する障害であり、薬物療法の効果は限局的であることから、他の治療法を容易にする、あるいは効果を高める補助療法として用いられる^[26]。

人物

日本では、ANは一般的には「拒食症」の名前で知られており、その患者の実態はたびたびドキュメンタリーとしてメディアに取り上げられることがある。

カーペンターズのカレン・カーペンターが拒食症から心臓発作を起こして死亡した際、本症は日本やアメリカで大きな話題を呼び、注目される疾患となった。なお、鈴木その子の息子も同様の病気で没している。
オーストリアのエリーザベト皇后も、嫁姑問題を契機にANを発症したといわれている。
90年代には、ともさかりえ、宮沢りえが拒食症による極端なやせ方をした為、「りえ痩せ」という言葉があり、比較的若い女性や生殖可能年齢に達した少女にも見られるケースがある。
鈴木明子（フィギュアスケート）、女優の釈由美子なども拒食・過食嘔吐体験をマスコミにカミングアウトしている。

脚注

^ 水島広子 (2009) pp. 14 - 15.
^ “DSM‒5 病名・用語翻訳ガイドライン（初版）”. 日本精神神経学会 (2014年5月28日). 2014年5月28日閲覧。
^ 切池信夫 (2004) p. 32.
^ 高木洲一郎、浜中禎子 (2011) p. 10.
^ 水島広子 (2001) p. 37.
^ 市橋秀夫 (2012) p. 32, 134.
^ 魔女と聖女池上俊一
^ 「神経性消耗病（nervous consumption）」リチャード・モートン著 1689年
^ 健康文化 16号「拒食症と文化」渡辺美樹[1]
^ 下坂幸三 (2007) pp. 309 - 310.
^ アメリカ精神医学会 DSM-IV-TR (2004) pp. 559 - 565.
^ 世界保健機関 ICD-10 (2005) p. 187.
^ 西園マーハ文 (2010) p. 2.
^ スティーヴン・ワイリー・エメット (1986)
^ 市橋秀夫「肥満恐怖の社会文化的影響」、『精神科治療学』第12巻第12号、1997年、 1405-1412頁。
^ 市橋秀夫 (2006) pp. 134 - 142.
^ 松木邦裕 (1997) pp. 21 - 33.
^ 松木邦裕 (2008) pp. 17 - 20.
^ 切池信夫 (2009) pp. 41 - 59.
^ Martinez-Gonzalez MA, Gual P, Lahortiga F, Alonso Y, de Irala-Estevez J, Cervera S. (2003). “Parental factors, mass media influences, and the onset of eating disorders in a prospective population-based cohort.”. Pediatrics. 111 (2): 315-320. PMID 12563057.
^ Deep AL, Lilenfeld LR, Plotnicov KH, Pollice C, Kaye WH. (1999). “Sexual abuse in eating disorder subtypes and control women: the role of comorbid substance dependence in bulimia nervosa.”. Int J Eat Disord. 25 (1): 1-10. PMID 9924647.
^ Gard MC, Freeman CP. (1996). “The dismantling of a myth: a review of eating disorders and socioeconomic status.”. Int J Eat Disord. 20 (1): 1-12. PMID 8807347.
^ Cnattingius S, Hultman CM, Dahl M, Sparen P. (1999). “Very preterm birth, birth trauma, and the risk of anorexia nervosa among girls.”. Arch Gen Psychiatry. 56 (7): 634-638. PMID 10401509.
^ 西園文 (2004) pp. 16 - 18.
^ 野間俊一 (2003) pp. 149 - 154.
^ 日本摂食障害学会 (2012) p. 127.

参考文献

診療ガイドライン

高橋三郎、大野裕、染矢俊幸（訳）『DSM‐IV‐TR 精神疾患の診断・統計マニュアル新訂版』医学書院、2004年（原著2002年）。ISBN 9784260118897。

融道男、中根允文、小見山実他（監訳）『ICD‐10 精神および行動の障害—臨床記述と診断ガイドライン新訂版』医学書院、2005年（原著1992年）。ISBN 9784260001335。

日本摂食障害学会（監）「摂食障害治療ガイドライン」作成委員会（編）『摂食障害治療ガイドライン』医学書院、2012年。ISBN 9784260014434。

ほかの医学書・一般書

市橋秀夫『心の地図〈上〉—こころの障害を理解する』星和書店、1997年。ISBN 9784791103553。

市橋秀夫『ダイエット依存症を乗りこえる！正しい治し方と知識』日東書院本社、2012年。ISBN 9784528016996。

スティーヴン・ワイリー・エメット（編）篠木満、根岸鋼（訳）『神経性食思不振症と過食症』星和書店、1986年（原著1985年）。ISBN 9784791101481。

上島国利（監）市橋秀夫（編）『精神科臨床ニューアプローチ 5 パーソナリティ障害・摂食障害』メジカルビュー社、2006年。ISBN 9784758302302。

切池信夫（監）『拒食症と過食症』講談社、2004年。ISBN 9784062593328。

切池信夫『摂食障害―食べない、食べられない、食べたら止まらない第2版』医学書院、2009年。ISBN 9784260008181。

下坂幸三『拒食と過食の心理—治療者のまなざし』岩波書店、1999年。ISBN 9784000225021。

下坂幸三『アノレクシア・ネルヴォーザ論考新装版』金剛出版、2007年。ISBN 9784772409681。

高木洲一郎、浜中禎子『最新版拒食症・過食症の治し方がわかる本』主婦と生活社、2011年。ISBN 978-4391140460。

西園文『生活しながら治す摂食障害』女子栄養大学出版部、2004年。ISBN 9784789554299。

西園マーハ文『摂食障害のセルフヘルプ援助—患者の力を生かすアプローチ』医学書院、2010年。ISBN 9784260010443。

野間俊一『ふつうに食べたい―拒食・過食のこころとからだ』昭和堂、2003年。ISBN 9784812203064。

ヒルデ・ブルック（著）岡部祥平、溝口純二（訳）『思春期やせ症の謎—ゴールデンケージ』星和書店、1979年（原著1978年）。ISBN 9784791100354。

ヒルデ・ブルック（著）ダニタ・クウゼウスキー、メラニー・シュー（編）岡部祥平、溝口純二（訳）『やせ症との対話—ブルック博士、思春期やせ症患者と語る』星和書店、1993年（原著1988年）。ISBN 9784791102501。

松木邦裕『摂食障害の治療技法—対象関係論からのアプローチ』金剛出版、1997年。ISBN 9784772405607。

松木邦裕『摂食障害というこころ—創られた悲劇／築かれた閉塞』新曜社、2008年。ISBN 9784788511064。

水島広子『「やせ願望」の精神病理―摂食障害からのメッセージ』 PHP研究所、2001年。ISBN 9784569615899。

水島広子『焦らなくてもいい!拒食症・過食症の正しい治し方と知識』日東書院本社、2009年。ISBN 9784528016880。

外部リンク

ウィキメディア・コモンズには、神経性無食欲症に関連するカテゴリがあります。

脳科学辞典 - 摂食障害
厚生労働省 - 摂食障害
難病情報センター - 中枢性摂食異常症

wiki en

[Wiki en表示]

Anorexia nervosa is an eating disorder characterized by immoderate food restriction, inappropriate eating habits or rituals, obsession with having a thin figure, and an irrational fear of weight gain, as well as a distorted body self-perception. It typically involves excessive weight loss and is diagnosed approximately nine times more often in females than in males.^[1] Due to their fear of gaining weight, individuals with this disorder restrict the amount of food they consume. Outside of medical literature, the terms anorexia nervosa and anorexia are often used interchangeably; however, anorexia is simply a medical term for lack of appetite, and the majority of individuals afflicted with anorexia nervosa do not, in fact, lose their appetites.^[2] Patients with anorexia nervosa often experience dizziness, headaches, drowsiness, fever, and a lack of energy. To counteract these side effects, particularly the latter, individuals with anorexia may engage in other harmful behaviors, such as smoking, excessive caffeine consumption, and excessive use of diet pills, along with an increased exercise regimen.

Anorexia nervosa is often coupled with a distorted self image^[3]^[4] which may be maintained by various cognitive biases^[5] that alter how the affected individual evaluates and thinks about their body, food, and eating.^[6] People with anorexia nervosa often view themselves as overweight or "big" even when they are already underweight.^[7]

Anorexia nervosa most often has its onset in adolescence and is more prevalent among adolescent females than adolescent males. In general, men appear to be more comfortable with their weight and perceive less pressure to be thin than women.^[8] ^[9]

While the majority of people with anorexia nervosa continue to feel hunger, they deny themselves all but very small quantities of food.^[6] The caloric intake of people with anorexia nervosa can vary significantly between individuals and over time, depending on whether they engage in binging and/or purging behavior.^[10] Extreme cases of complete self-starvation are known. It is a serious health condition with a high incidence of comorbidity and similarly high mortality rate to serious psychiatric disorders.^[7] People with anorexia have extremely high levels of ghrelin (the hunger hormone that signals a physiological need for food) in their blood. The high levels of ghrelin suggests that their bodies are desperately trying to make them hungry; however, that hunger call is being suppressed, ignored, or overridden. Sufferers may commonly engage in self-harm behaviors in order to override their feelings of hunger.

1 Diagnosis
- 1.1 Psychological
  - 1.1.1 DSM-5 Criteria
  - 1.1.2 ICD-10 Criteria
- 1.2 Medical
  - 1.2.1 Medical Tests
2 Signs and symptoms
- 2.1 Complications
3 Causes
- 3.1 Biological
- 3.2 Sociological
  - 3.2.1 Media effects
- 3.3 Relationship to autism
- 3.4 Differential diagnoses
4 Treatment
- 4.1 Dietary
- 4.2 Medication
- 4.3 Therapy
5 Prognosis
- 5.1 Relapse
6 Epidemiology
7 History
8 See also
9 References
10 External links

Diagnosis

Psychological

Not only does starvation result in physical complications, but mental complications as well.^[11] P. Sodersten and colleagues suggest that effective treatment of this disorder depends on re-establishing reinforcement for normal eating behaviours instead of unhealthy weight loss.^[2]

Anorexia nervosa is classified as an Axis I^[12] disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-V), published by the American Psychiatric Association. The DSM-V should not be used by laypersons to diagnose themselves.

The DSM-V has replaced the previously used volume DSM-IV-TR, and in the new DSM-V there have been several changes made to the criteria for anorexia nervosa, most notably that of the amenorrhea criterion being removed. However, significant changes in wording have also been made to each remaining criterion.

DSM-5 Criteria

Persistent restriction of energy intake leading to significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory, and physical health).
Either an intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain (even though significantly low in weight).
Disturbance in the way one's body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.^[13]

Subtypes:

Restricting type: Individual does not utilize binge eating nor displays purging behavior as their main strategy for weight loss. Instead, the individual uses restricting food intake, fasting, diet pills, and/or exercise as a means for losing weight.^[14]
Binge-eating/purging type: Individual utilizes binge eating or displays purging behavior as a means for losing weight.^[14]

Levels of Severity:

Body mass index (BMI) is used by the DSM-V as an indicator of the level of severity of anorexia nervosa. The DSM-V states these as follows:

Mild: BMI of 17-17.99
Moderate: BMI of 16-16.99
Severe: BMI of 15-15.99
Extreme: BMI of less than 15

ICD-10 Criteria

F 50.0: A disorder characterized by deliberate weight loss, induced and sustained by the patient. It occurs most commonly in adolescent girls and young women, but adolescent boys and young men may also be affected, as may children approaching puberty and older women up to the menopause. The disorder is associated with a specific psychopathology whereby a dread of fatness and flabbiness of body contour persists as an intrusive overvalued idea, and the patients impose a low weight threshold on themselves. There is usually undernutrition of varying severity with secondary endocrine and metabolic changes and disturbances of bodily function. The symptoms include restricted dietary choice, excessive exercise, induced vomiting and purgation, and use of appetite suppressants and diuretics.^[15]

Medical

The initial diagnosis should be made by a competent medical professional. There are multiple medical conditions, such as viral or bacterial infections, hormonal imbalances, neurodegenerative diseases and brain tumors which may mimic psychiatric disorders including anorexia nervosa.

Medical Tests

Medical tests to check for signs of physical deterioration in anorexia nervosa may be performed by a general physician or psychiatrist. These are done as each doctor deems necessary. Some of the medical testing possibilities include the following:

Complete Blood Count (CBC): a test of the white blood cells, red blood cells and platelets used to assess the presence of various disorders such as leukocytosis, leukopenia, thrombocytosis and anemia which may result from malnutrition.^[16]
Urinalysis: a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health^[17]
ELISA: Various subtypes of ELISA used to test for antibodies to various viruses and bacteria such as Borrelia burgdoferi (Lyme Disease)^[18]
Western Blot Analysis: Used to confirm the preliminary results of the ELISA^[19]
Chem-20: Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes such as potassium, chlorine and sodium and tests specific to liver and kidney function.^[20]
Glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycystic ovary syndrome^[21]^[22]
Secritin-CCK Test: Used to assess function of the pancreas and gall bladder^[23]^[24]
Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition^[25]
Liver Function Test: A series of tests used to assess liver function some of the tests are also used in the assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, and Crohn's Disease.^[26]
Lh response to GnRH: Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH): Tests the pituitary glands' response to GnRh a hormone produced in the hypothalamus. Central hypogonadism is often seen in anorexia nervosa cases.^[27]
Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatine kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).^[28]^[29]
Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabolism first formed in the liver then removed from the body by the kidneys. The BUN test is primarily used to test kidney function. A low BUN level may indicate the effects of malnutrition.^[30]
BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various conditions. A high BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, and intestinal bleeding. A low BUN/creatinine ratio can indicate a low protein diet, celiac disease, rhabdomyolysis, or cirrhosis of the liver.^[31]^[32]^[33]
Electrocardiogram (EKG or ECG): measures electrical activity of the heart. It can be used to detect various disorders such as hyperkalemia^[34]
Electroencephalogram (EEG): measures the electrical activity of the brain. It can be used to detect abnormalities such as those associated with pituitary tumors^[35]^[36]
Upper GI Series: test used to assess gastrointestinal problems of the middle and upper intestinal tract^[37]
Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3)^[38]
Parathyroid hormone (PTH) test: tests the functioning of the parathyroid by measuring the amount of (PTH) in the blood. It is used to diagnose parahypothyroidism. PTH also controls the levels of calcium and phosphorus in the blood (homeostasis).^[39]
Barium enema: an x-ray examination of the lower gastrointestinal tract^[40]

Signs and symptoms

Please note that not all individuals with anorexia nervosa exhibit the same symptoms, nor are all of these symptoms are required to be diagnosed with anorexia. Please consult the Diagnosis section for more detail.

Anorexia nervosa is an eating disorder that is characterized by attempts to lose weight, to the point of self-starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary in each case and may be present but not readily apparent. Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.^[41]^[42]^[43]

Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis.

Between 50% and 75% of individuals with an eating disorder experience depression. In addition, one in every four individuals who are diagnosed with anorexia nervosa also exhibit obsessive-compulsive disorder.^[44]

Symptoms of a person with anorexia nervosa may include:

Refusal to maintain a normal body mass index for their age^[45]
Amenorrhea, a symptom that occurs after prolonged weight loss; causes menses to stop, hair becomes brittle, and skin becomes yellow and unhealthy^[45]
Fearful of even the slightest weight gain and takes all precautionary measures to avoid weight gain and becoming overweight^[45]
Obvious, rapid, dramatic weight loss at least 15% under normal body weight^[46]
Lanugo: soft, fine hair growing on the face and body^[47] – one theory is that this is related to hypothyroidism, as there are several reports of a similar hypertrichosis occurring in hypothyroidism^[48]^[49]
Obsession with calories and fat content of food
Preoccupation with food, recipes, or cooking; may cook elaborate dinners for others, but not eat the food themselves^[50]
Food restriction despite being underweight
Food rituals, such as cutting food into tiny pieces, refusing to eat around others, or hiding or discarding food
Purging: May use laxatives, diet pills, ipecac syrup, or water pills; may engage in self-induced vomiting; may run to the bathroom after eating in order to vomit and quickly get rid of ingested calories^[51]^[52] (see also bulimia nervosa)
May engage in frequent, strenuous, or compulsive exercise^[53]
Perception of self as overweight despite being told by others they are too thin
Intolerance to cold and frequent complaints of being cold; body temperature may lower (hypothermia) in an effort to conserve energy^[54]
Hypotension and/or orthostatic hypotension
Bradycardia or tachycardia
Depression: may frequently be in a sad, lethargic state^[55]
Solitude: may avoid friends and family; becomes withdrawn and secretive
Cheeks may become swollen because of enlargement of the salivary glands caused by excessive vomiting^[56]
Swollen joints^[57]
Abdominal distension
Halitosis (from vomiting or starvation-induced ketosis)
Dry hair and skin, as well as hair thinning^[58]^[59]
Fatigue^[60]
Rapid mood swings
Absence of menses

Dermatological signs of anorexia nervosa^[61]
xerosis cutis	telogen effluvium	carotenoderma	acne vulgaris	hyperpigmentation
seborrhoeic dermatitis	acrocyanosis	chilblains	petechiae	livedo reticularis
interdigital intertrigo	paronychia	generalized pruritus	acquired striae distensae	angular stomatitis
prurigo pigmentosa	edema	linear erythema craquele	acrodermatitis enteropathica	pellagra

Possible medical complications of anorexia nervosa
constipation^[62]	diarrhea^[63]	electrolyte imbalance^[64]	cavities^[65]	tooth loss^[66]
cardiac arrest^[67]	amenorrhoea^[68]	edema^[69]	osteoporosis^[70]	osteopenia^[71]
hyponatremia^[72]	hypokalemia^[73]	optic neuropathy^[74]	brain atrophy^[75]^[76]	leukopenia^[77]^[78]

The prevalent symptoms for anorexia nervosa (as discussed above) such as decreased body temperature, obsessive-compulsivity, and changes in psychological state, can actually be attributed to symptoms of starvation. This theory can be supported by a study by Routtenberg in 1968 involving rats who were deprived of food; these rats showed dramatic increases in their activity on the wheel in their cage at times when not being fed.^[79] These findings could explain why those with anorexia nervosa are often seen excessively exercising; their overactivity is the result of fasting, and by increasing their activity they could raise their body temperature, increase their chances of stumbling upon food, or become distracted from their desire for nourishment (because they do not, in fact, lose their appetite). While it is commonly believed that those with AN do not have a normal appetite, this is not the case. Those with AN are typically obsessive about food, cooking often for others, but not eating the food themselves. Despite the fact that the physiological cause behind each case of anorexia nervosa is different, the most common theme seen across the board is the element of self-control. The underlying cause behind the disorder is rarely about the food itself; it is about the individual attempting to gain complete control over an aspect of their lives, in order to prove themselves, and distract them from another aspect of their lives they wish they could control. For example, a child with a destructive family life who restricts food intake in order to compensate for the chaos occurring at home.^[79]

Complications

Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation, or the attainment of peak bone mass.^[80] Complications specific to adolescents and children with anorexia nervosa can include the following:

Growth retardation – height gain may slow and can stop completely with severe weight loss or chronic malnutrition. In such cases, provided that growth potential is preserved, height increase can resume and reach full potential after normal intake is resumed.^[80] Height potential is normally preserved if the duration and severity of illness are not significant and/or if the illness is accompanied with delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may negate the deleterious effects of undernutrition on stature by allowing for a longer duration of growth compared to controls.^[81] In such cases, appropriate early treatment can preserve height potential and may even help to increase it in some post-anorexic subjects due to the aforementioned reasons in addition to factors such as long-term reduced estrogen-producing adipose tissue levels compared to premorbid levels.^[82]^[83]^[84]^[85]
Pubertal delay or arrest – both height gain and pubertal development are dependent on the release of growth hormone and gonadotrophins (LH and FSH) from the pituitary gland. Suppression of gonadotrophins in patients with anorexia nervosa has frequently been documented.^[80] However, a study demonstrated that growth hormone levels were not a predictor of height measures in anorexic patients, which is suggestive of a resistance to growth hormone effects at the growth plate, similar to the resistance to growth hormone of bone-formation markers.^[81] Instead, insulin-like growth factor had a larger effect, with lower IGF-I levels and longer durations of illness tending to result in lower height measures than vice versa, although IGF-I levels in anorexic subjects may not necessarily be low enough to affect height measures.^[81] In some cases, especially where onset is pre-pubertal, physical consequences such as stunted growth and pubertal delay are usually fully reversible.^[86]
Reduction of Peak Bone Mass – bone accretion is the highest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, bone mass may remain low.^[80]
Hepatic steatosis – fatty infiltration of the liver is an indicator of malnutrition in children.^[80]
Heart disease and arrythmias
Neurological disorders- seizures, tremors
Acute gastric dilation, infarction and perforation,^[87]
Death (Anorexia nervosa has the highest rate of mortality of any psychological disorder):^[88] [5-9 percent]^[89]

Causes

Studies have hypothesized the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed normal controls exhibit many of the behavioral patterns of anorexia nervosa (AN) when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self-perpetuating cycle.^[90]^[91]^[92]^[93] Studies have suggested the initial weight loss such as dieting may be the triggering factor in developing AN in some cases, possibly because of an already inherent predisposition toward AN. One study reported cases of AN resulting from unintended weight loss that resulted from varied causes, such as a parasitic infection, medication side effects, and surgery. The weight loss itself was the triggering factor.^[94]^[95] Even though anorexia does not affect males as often in comparison to females, studies have shown that males with a female twin have a higher chance of getting anorexia. Therefore anorexia may be linked to intrauterine exposure to female hormones.^[96]

Biological

Obstetric complications: various prenatal and perinatal complications may factor into the development of anorexia nervosa, such as maternal anemia, diabetes mellitus, preeclampsia, placental infarction, and neonatal cardiac abnormalities. Neonatal complications may also have an influence on harm avoidance, one of the personality traits associated with the development of AN.^[97]^[98]
Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%.^[99]^[100]^[101] Twin studies have shown a heritability rate of 56%.^[102]^[103] Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1.^[104] In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia.^[105]
- epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequence. They are heritable, as was shown in the Överkalix study, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.^[106] "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."^[106]^[107]
  
  Dysregulation of the dopamine and serotonin pathways has been implicated in the etiology, pathogenesis and pathophysiology of anorexia nervosa.^[108]^[109]^[110]^[111]
Addiction to the chemicals released in the brain during starving and physical activity;^[112] people affected with anorexia often report getting some sort of high from not eating. The effect of food restriction and intense activity causes symptoms similar to anorexia in female rats,^[112] though it is not explained why this addiction affects only females.
Serotonin dysregulation; brain imaging studies implicate alterations of 5-HT1A and 5-HT2A receptors and the 5-HT transporter. Alterations of these circuits may affect mood and impulse control as well as the motivating and hedonic aspects of feeding behavior.^[113] Starvation has been hypothesized to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety.^[113] Other studies of the 5HT_2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics associated with AN and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.^[114] Another study found AN to be significantly associated with the S allele and S carrier (SS + LS) genotype.^[115]
Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it also plays a role in learning, memory and in the hypothalamic pathway that controls eating behavior and energy homeostasis. BDNF amplifies neurotransmitter responses and promotes synaptic communication in the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression.^[116]^[117] Exercise increases levels of BDNF^[118]
Leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of satiety. Ghrelin is an appetite inducing (orexigenic) hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity both have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.^[119] A 2013 study revealed that anorectic subjects may have reduced ghrelin bioactivity due to altered carrier-antibody affinity, leading to less efficient transport of ghrelin to the brain and thus reduced hunger sensation.^[120]
Orexin; orexin is a neurotransmitter that regulates appetite and is responsible for increasing the craving for food.^[121]
Cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic patients, which may be a predisposing factor in the onset of AN.^[122]
Autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.^[123]
Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. PANS is an acronym for Pediatric acute-onset neuropsychiatric syndrome, a hypothesis describing children who have abrupt, dramatic onset of obsessive-compulsive disorder (OCD) or anorexia nervosa coincident with the presence of two or more neuropsychiatric symptoms.^[124]
Nutritional deficiencies
- Zinc deficiency may play a role in anorexia. It is not thought responsible for causation of the initial illness but there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.^[125]

Sociological

Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations. There is a possible connection between anorexia nervosa and culture; culture may be a cause, a trigger, or merely a kind of social address or envelope which determines in which segments of society or in which cultures anorexia nervosa will appear. The thesis of this connection is that culture acts as a cause by providing a blueprint for anorexia nervosa. A moderate thesis is that specific cultural factors trigger the illness which is determined by many factors including family interactions, individual psychology, or biological predisposition. Culture change can trigger the emergence of anorexia in adolescent girls from immigrant families living in highly industrialized Western Societies.^[126] According to a study published in 1980, people in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career,^[127] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.^[128]

Anorexia nervosa is more likely to occur in a person's pubertal years, especially for girls.^[129] Female students are 10 times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female high school students, "85% who were a normal weight wanted to be thinner and 45% who were 10–20% underweight wanted to be thinner."^[130] Teenage girls concerned about their weight and who believe that slimness is more attractive among peers trend to weight-control behaviors. Teen girls learn from each other to consume low-caloric, low-fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.^[131]

It has also been noted that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent. It has been suggested that anorexia nervosa results from a sexually selected evolutionary drive to appear youthful in populations in which size becomes the primary indicator of age.^[132]

There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia^[133] and also a deficit in certain emotional functions. A research study showed that this was the case in both adult and adolescent anorexia nervosa patients.^[134]

Early theories of the cause of anorexia linked it to sexual abuse or dysfunctional families. Some studies reported a high rate of reported child sexual abuse experiences in clinical groups of people who have been diagnosed with anorexia. One found that women with a history of eating disorders were twice as likely to have reported childhood sexual abuse compared to women with no history of eating disorders.^[135] The joint effect of both physical and sexual abuse resulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria.^[135] The conclusion was that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting function, associated with eating behaviour.^[135]

In contrast to the above, a metastudy of published research examining causes of anorexia found no conclusive link between abuse, parenting and eating disorders.^[136] The American Psychiatric Association writes: "No evidence exists to prove that families cause eating disorders."^[137]

Efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as the misconception that families, in particular mothers, are responsible for their daughter developing an eating disorder.^[138]

Media effects

There is no evidence^{[disputed – discuss]} that the media is a cause of eating disorders, and advances in neuroscience point to a more complex combination of genetic and environmental influences.^[139]

Mass media interventions may offer a distorted vision of the world, and it may be difficult for children and adolescents to distinguish whether what they see is real or not, so that they are more vulnerable to the messages transmitted. Field, Cheung, et al.'s survey of 548 preadolescent and adolescent girls found that 69% acknowledged that images in magazines had influenced their conception of the ideal body, while 47% reported that they wanted to lose weight after seeing such images.^[140] There was also the survey by Utter et al. who studied 4,746 adolescent boys and girls demonstrating the tendency of magazine articles and advertisements to activate weight concerns and weight management behaviour. He discovered that girls who frequently read fashion and glamour magazines and girls who frequently read articles about diets and issues related to weight loss were seven times more likely to practice a range of unhealthy weight control behaviours and six times more likely to engage in extremely unhealthy weight control behaviours (e.g., taking diet pills, vomiting, using laxatives, and using diuretics). There was not stated though wether this behavior was a possible cause of anorexia nervosa or a result of the disease.^[140] Websites that stress the message of thinness as the ideal have surfaced on the Internet and have managed to embed themselves as an increasing source of influence. The possibility that pro-anorexia websites may reinforce restrictive eating and exercise behaviours is an area of concern. Pro-anorexia websites contain images and writing that support the pursuit of an ideal thin body image. Research has shown that these websites stress thinness as the ideal choice for women and in some websites ideal images of muscularity and thinness for men^[141] It has also been shown that women who had viewed these websites at least once had a decrease in self-esteem and reports also show an increased likelihood of future engagement in many negative behaviours related to food, exercise, and weight.^[141] Evidence of the value of thinness in majority U.S culture is found in Hollywood's elite and the media promotion of waif models in fashion and celebrity circles (e.g. Nicole Richie, Mary Kate Olsen, Kate Moss, and Lady Gaga^[142]).

Relationship to autism

A summary of the strategy Zucker et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.^[143]

Since Gillberg's (1983 & 1985)^[144]^[145] and others' initial suggestion of relationship between anorexia nervosa and autism,^[146]^[147] a large-scale longitudinal study into teenage-onset anorexia nervosa conducted in Sweden confirmed that 23% of people with a long-standing eating disorder are on the autism spectrum.^[148]^[149]^[150]^[151]^[152]^[153]^[154] Those on the autism spectrum tend to have a worse outcome,^[155] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.^[156]^[157] Other studies, most notably research conducted at the Maudsley Hospital, furthermore suggest that autistic traits are common in people with anorexia nervosa; shared traits include, e.g., poor executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation and understanding facial expressions.^[158]^[159]^[160]^[161]^[162]^[133]

Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to right).^[143] A pilot study into the effectiveness of cognitive behaviour therapy, which based its treatment protocol on the hypothesised relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism and rigidity in 17 out of 19 participants.^[163]

Some autistic traits are more prominent during the acute phase of AN.^[164]

Differential diagnoses

A variety of medical and psychological conditions have been misdiagnosed as anorexia nervosa; in some cases the correct diagnosis was not made for more than ten years. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital.^[165]

Other psychological issues may factor into anorexia nervosa; some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 "clusters", A, B and C. The causality between personality disorders and eating disorders has yet to be fully established.^[166] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.^[167]^[168]^[169] Some develop them afterwards.^[170] The presence of Axis I and/or Axis II psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults.^[171]^[172] In particular, substance abuse and borderline personality appear more frequent among anorexics who binge or purge.^[173]^[174] And obsessive-compulsive personality disorder—according to some studies, the most common personality disorder among anorexics—and particular traits of this diagnosis such as perfectionism are linked with more severe symptomatology and worse prognosis.^[175]^[176]

Comorbid Disorders
Axis I	Axis II
depression^[177]	obsessive compulsive personality disorder^[178]
substance abuse, alcoholism^[179]	borderline personality disorder^[180]
anxiety disorders^[181]
obsessive compulsive disorder^[182]^[183]
Attention-Deficit-Hyperactivity-Disorder^[184]^[185]^[186]^[187]

Body dysmorphic disorder (BDD) is listed as a somatoform disorder that affects up to 2% of the population. BDD is characterized by excessive rumination over an actual or perceived physical flaw. BDD has been diagnosed equally among men and women. While BDD has been misdiagnosed as anorexia nervosa, it also occurs comorbidly in 25% to 39% of AN cases.^[188]

BDD is a chronic and debilitating condition which may lead to social isolation, major depression, suicidal ideation and attempts. Neuroimaging studies to measure response to facial recognition have shown activity predominately in the left hemisphere in the left lateral prefrontal cortex, lateral temporal lobe and left parietal lobe showing hemispheric imbalance in information processing. There is a reported case of the development of BDD in a 21-year-old male following an inflammatory brain process. Neuroimaging showed the presence of new atrophy in the frontotemporal region.^[189]^[190]^[191]^[191]^[192]

The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make as there is considerable overlap between patients diagnosed with these conditions. Seemingly minor changes in a patient's overall behavior or attitude can change a diagnosis from "anorexia: binge-eating type" to bulimia nervosa. A main factor differentiating binge-purge anorexia from bulimia is the gap in physical weight. Someone with bulimia nervosa is ordinarily at a healthy weight, or slightly overweight. Someone with binge-purge anorexia is commonly underweight.^[193] It is not unusual for a person with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time.^[143]

Treatment

There is no conclusive evidence that any particular treatment for anorexia nervosa works better than others; however, there is enough evidence to suggest that early intervention and treatment are more effective.^[194] Treatment for anorexia nervosa tries to address three main areas.

Restoring the person to a healthy weight;
Treating the psychological disorders related to the illness;
Reducing or eliminating behaviours or thoughts that originally led to the disordered eating.^[195]

Although restoring the person's weight is the primary task at hand, optimal treatment also includes and monitors behavioral change in the individual as well.^[45] Not all anorexia nervosa patients recover completely; About 20% develop anorexia nervosa as a chronic disorder.^[196] If anorexia nervosa is not treated, serious complications such as heart conditions and kidney failure can arise and eventually lead to death. "As many as 6 percent of people with the disorder die from causes related to it."^[197]

Dietary

Diet is the most essential factor to work on in patients with anorexia nervosa, and must be tailored to each patient's needs. Initial meal plans may be low in calories, about 1200, in order to build comfort in eating, and then food amount can gradually be increased. Food variety is important when establishing meal plans as well as foods that are higher in energy density. Other more specific dietary treatments are listed below.^[198]

Zinc: Zinc supplementation has been shown in various studies to be beneficial in the treatment of AN even in patients not suffering from zinc deficiency, by helping to increase weight gain. Patients with anorexia nervosa have a high likelihood of being zinc deficient, and this probability increases if they are vegetarians. Vegetarianism is adopted by many patients with eating disorders because it is widely acclaimed as healthy and easy to manage calorie intake.^[199] Sufficient Zinc must be available during recovery, and normal zinc levels were seen in the Notre Dame study to increase weight gain at a faster rate. Zinc supplementation can also help reduce reproductive issues for patients with anorexia nervosa. Leptin levels, which regulate hunger and metabolism, decrease from zinc deficiency and even more with AN sufferers due to the reduction in size of adipose tissue. Reproductive tissues have been discovered to contain leptin receptors, thus a decrease in leptin concentration would lead to a lower rate of fertility. Despite the connection to weight gain and reproduction, zinc supplementation seems to be largely under-appreciated and many do not consider zinc deficiency as an important factor in regard to anorexia nervosa.^[200]
Calories: Patients must be fed adequate calories at a measured pace for improvement of their condition to occur. The best level for calorie intake is to start by providing 1200 to 1500 calories daily and increasing this amount by 500 each day. This process should continue until the level of 4000 calories (for male patients) or 3500 calories (for female patients) is achieved. This system should also decrease effects such as apathy, lethargy, and food-related obsessions.^[201]
Essential fatty acids: The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have been shown to benefit various neuropsychiatric disorders. There was reported rapid improvement in a case of severe AN treated with ethyl-eicosapentaenoic acid (E-EPA) and micronutrients.^[202] DHA and EPA supplementation has been shown to be a benefit in many of the comorbid disorders of AN including attention deficit/hyperactivity disorder (ADHD), autism, major depressive disorder (MDD),^[203] bipolar disorder, and borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.^[204]^[205]
Nutritional counseling.^[206]^[207]
Medical Nutrition Therapy (MNT), also referred to as Nutrition Therapy, is the development and provision of a nutritional treatment or therapy based on a detailed assessment of a person's medical history, psychosocial history, physical examination, and dietary history.^[208]^[209]^[210]

Medication

Olanzapine: There have been some claims that olanzapine is effective in treating certain aspects of AN including helping raise the body mass index and reducing obsessionality, including obsessional thoughts about food.^[211]^[212] Olanzapine does not increase the rate of body mass index growth in patients with anorexia.^[213]

Therapy

Family-based treatment

Family-based treatment (FBT) has been shown in randomized controlled trials to be more successful than individual therapy in most treatment trials.^[45] Several components of family therapy for patients with AN are:

the family is seen as a resource for the adolescent^[214]
anorexia nervosa is reframed in benign, non blaming terms^[214]
directives are provided to parents so that they may take charge of their child or adolescent's eating routine^[214]
a structured behavioral weight gain program is implemented^[214]
after weight gain, control over eating is gradually returned to the child or adolescent^[214]
as the child or adolescent begins to eat and gain weight, the therapeutic focus broadens to include family interaction problems, growth and autonomy issues and parent–child conflicts^[214]

Various forms of family-based treatment have been proven to work in the treatment of adolescent AN including "conjoint family therapy" (CFT), in which the parents and child are seen together by the same therapist, "separated family therapy" (SFT) in which the parents and child attend therapy separately with different therapists. "Eisler's cohort show that, irrespective of the type of FBT, 75% of patients have a good outcome, 15% an intermediate outcome ...".^[215]^[216] Proponents of Family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment.^[217]
A four- to five-year follow up study of the Maudsley family therapy, an evidence-based manualized model, showed full recovery at rates up to 90%.^[218] Although this model is recommended by the NIMH,^[219] critics claim that it has the potential to create power struggles in an intimate relationship and may disrupt equal partnerships.^[220]

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) is an evidence based approach which in studies to date has shown to be useful in adolescents and adults with anorexia nervosa.^[221]^[222]^[223] Components of using CBT with adults and adolescents with anorexia nervosa have been outlined by several professionals as:

the therapist focuses on using cognitive restructuring to modify distorted beliefs and attitudes about the meaning of weight, shape and appearance^[214]
specific behavioral techniques addressing the normalization of eating patterns and weight restorations, examples of this include the use of a food diary, meal plans, and incremental weight gain^[214]
cognitive techniques such as restructuring, problem solving, and identification and expression of affect^[214]
When using CBT with adolescents and children with AN, several professionals have expressed concerns about the minimum age and level of cognition necessary for implementing cognitive behavioral techniques.^[214] Modified versions and elements of CBT can be implemented with children and adolescents with AN. Such modifications may include the use of behavioral experiments to disconfirm distorted beliefs and absolutistic thinking in children and adolescents.^[214]

Acceptance and commitment therapy

Acceptance and commitment therapy is a type of CBT, which has shown promise in the treatment of AN" participants experienced clinically significant improvement on at least some measures; no participants worsened or lost weight even at 1-year follow-up."^[224]

Cognitive remediation therapy

Cognitive remediation therapy (CRT) is a cognitive rehabilitation therapy developed at King's College in London designed to improve neurocognitive abilities such as attention, working memory, cognitive flexibility and planning, and executive functioning which leads to improved social functioning. Neuropsychological studies have shown that patients with AN have difficulties in cognitive flexibility. In studies conducted at Kings College^[225] and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa,^[225] in the United States clinical trials are still being conducted by the National Institute of Mental Health^[226] on adolescents age 10–17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.^[227]

Prognosis

The long-term prognosis of anorexia nervosa is more on the favorable side. The National Comorbidity Replication Survey was conducted among more than 9,282 participants throughout the United States; ` found that the average duration of anorexia nervosa is 1.7 years. "Contrary to what people may believe, anorexia is not necessarily a chronic illness; in many cases, it runs its course and people get better ..."^[228] However, 5–20% of people diagnosed with anorexia nervosa die from it, and the cause of death is mostly because of the direct health effects of the eating disorder on the body.^[229]

In cases of adolescent anorexia nervosa where family-based treatment is used, 75% of patients have a good outcome and an additional 15% show an intermediate yet more positive outcome.^[215] In a five-year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%.^[230]

Some remedies, however, are proven to not have any value in resolving anorexia. "Incarceration in hospital" prohibits patients from many basic rights, such as using the bathroom independently. Therefore, it has been seen as catalytic in increasing weight and pushing patients away from the path to recovery.^[231]

According to a 1997 study, even in severe cases of AN, despite a noted 30% relapse rate after hospitalization, and a lengthy time to recovery ranging from 57 to 79 months, the full recovery rate was still 76%. There were minimal cases of relapse even at the long term follow-up conducted between 10–15 years.^[232] The long-term prognosis of anorexia nervosa is changeable: a fifth of patients stay severely ill, another fifth of patients recover fully and three fifths of patients have a fluctuating and chronic course.^[233]

Although overall the prognosis may seem favorable, this is not the case for all patients of anorexia nervosa. Among psychiatric disorders, anorexia nervosa has one of the highest mortality rates because of side effects of the disorder, such as cardiac complications or suicide. In intermediate to long-term studies with juveniles, death rates, on average, have ranged anywhere from 1.8 to 14.1%.^[234] Recovery can be lifelong for some; energy intake and eating habits may never return to normal.^[198] Many studies have attempted to study relapse and recovery through longitudinal studies but this is difficult, time consuming, and costly. Recovery is also viewed on a spectrum rather than black and white. According to the Morgan-Russell criteria patients can have a good, intermediate, or poor outcome. Even when a patient is classified as having a "good" outcome, weight only has to be within 15% of average and normal menstruation must be present in females. The good outcome also excludes psychological health. Recovery for patients with anorexia nervosa is undeniably positive, but recovery does not mean normal.^[234]

Relapse

According to the Eckert study, relapse is greatest in the first year after normal body weight is obtained. This includes right after release from inpatient institutions. Relapse includes a return to food restriction as well as a shift to binge eating habits.

As stated above, higher energy density in dietary plans is important. Patients with lower dietary energy density in their meals, prior to being discharged, had worse outcomes within the year, therefore a higher likelihood of relapse. This is speculated to be due to fat and fluid consumption. Patients whose dietary plans included fats and foods containing fats were forced to eat a more realistic and "normal" plan than those with lower energy density. Therefore, when released from inpatient treatment, the patients with higher dietary energy density plans had adopted healthier and more balanced eating habits. A greater food variety in inpatient dietary plans may help lower rates of relapse as well.^[235] Relapse, binging or starving after initial weight gain, occurs in 40–70% of anorexia patients.^[236] Prevention of relapse can be helped by cognitive-behavioral therapy and pharmacological therapies.^[236] Link of OCD with anorexia shows treatments for OCD such as serotonin re-uptake inhibitors (SSRI) helps in preventing relapse.^[236]

Several clinically significant variables that could predict relapse among AN patients were identified in a study conducted by a team at the University of Toronto. First, patients with binge-purge type AN were twice as likely to have a relapse as those with restricting subtype AN. The second predictor of relapse was the level of motivation to recover. When patients' motivation to recover fell during the first 4 weeks of inpatient treatment, the risk of relapse rose. The third predictor identified in the study was higher pre-treatment severity of checking behaviors, as reported on the Padua Inventory (PI) Checking Behavior scale, a measure of obsessive-compulsive disorder symptoms.^[237]

Epidemiology

Anorexia has an average prevalence of 0.3–1% in women and 0.1% in men for the diagnosis in developed countries.^[238] The condition largely affects young adolescent women, with those between 15 and 19 years old making up 40% of all cases. Approximately 75% of people with anorexia are female.^[239] Anorexia nervosa is more prevalent in the upper social classes and it is thought to be rare in less-developed countries.^[233] Anorexia is more prevalent in females and males born after 1945.^[240] The lifetime incidence of atypical anorexia nervosa, a form of ED-NOS in which not all of the diagnostic criteria for AN are met, is much higher, at 5–12%.^[241]

The question of whether the incidence of AN is on the rise has been under debate. Most studies show that since at least 1970 the incidence of AN in adult women is fairly constant, while there is some indication that the incidence may have been increasing for girls aged between 14 and 20.^[242] It is difficult to compare incidence rates at different times and possibly different locations due to changes in methods of diagnosing, reporting and changes in the population numbers, as evidenced on data from after 1970.^[243]^[244]^[245]

History

Two images of an anorexic female patient published in 1900 in "Nouvelle Iconographie de la Salpêtrière". The case was entitiled "Un cas de anorexia hysterique" (A case of hysteria anorexia).

The term anorexia nervosa was coined in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.^[246] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), thus meaning a lack of desire to eat.^[247]

The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era^[248] and continuing into the medieval period. A number of well known historical figures, including Catherine of Siena and Mary, Queen of Scots are believed to have suffered from the condition.^[249]^[250]

The medieval practice of self-starvation by women, including some young women, in the name of religious piety and purity also concerns anorexia nervosa; it is sometimes referred to as anorexia mirabilis. By the thirteenth century, it was increasingly common for women to participate in religious life and to even be named as saints by the Catholic Church. Many women who ultimately became saints engaged in self-starvation, including Saint Hedwig of Andechs in the thirteenth century and Catherine of Siena in the fourteenth century. By the time of Catherine of Siena, however, the Church became concerned about extreme fasting as an indicator of spirituality and as a criterion for sainthood. Catherine of Siena was told by Church authorities to pray that she would be able to eat again, but was unable to give up fasting.^[249]

The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton in 1689.^[248] Case descriptions fitting anorexic illnesses continued throughout the 17th, 18th and 19th centuries. They include the cases of an 18-year-old girl treated by Richard Morton in 1689 who refused to eat and died 3 months later.^[251] Noah Webster writes of an instructor at Yale College in the 1770s who refused to eat because he believed food was "dulling his mind."^[252]

However, it was not until the late 19th century that anorexia nervosa was widely accepted by the medical profession as a recognised condition. In 1873, Sir William Gull, one of Queen Victoria's personal physicians, published a seminal paper which coined the term anorexia nervosa and provided a number of detailed case descriptions and treatments. However, Gull was unable to provide an explanation for the condition.^[251] In the same year, French physician Ernest-Charles Lasègue similarly published details of a number of cases in a paper entitled De l'Anorexie Histerique.

Awareness of the condition was largely limited to the medical profession until the latter part of the 20th century, when German-American psychoanalyst Hilde Bruch published The Golden Cage: the Enigma of Anorexia Nervosa in 1978. This book created a wider interest in anorexia nervosa among lay readers. Bruch postulated that anorexia nervosa is a "desperate struggle for a self-respecting identity". Despite major advances in neuroscience,^[139] Bruch's theories tend to dominate popular thinking. A further important event was the death of the popular singer and drummer Karen Carpenter in 1983, which prompted widespread ongoing media coverage of eating disorders. Anorexia has the highest mortality rate of any mental illness^[253] and continues to be in the public eye. "Pro-ana" websites range from those claiming to be a safe-space for anorexics to discuss their problems, to those supporting anorexia as a lifestyle choice and offering "thinspiration," or photos and videos of thin or emaciated women. A survey by Internet security firm Optenet found a 470% increase in pro-ana and pro-mia (as in bulimia) sites from 2006 to 2007.^[254] Many celebrities have come forward discussing their struggles with anorexia, increasing awareness of the disease. Celebrities who have come forward publicly to discuss their experiences with anorexia include singer Fiona Apple, who purposely lost weight to discourage unwanted sexual advances after being raped at age 12,^[255] Portia de Rossi,^[256] Calista Flockhart,^[257] Tracey Gold,^[258] whose difficult recovery was well publicized by the media after her weight dropped to 80 pounds (36 kg) on her 5 ft 3 in (1.60 m) frame and she was hospitalized,^[259] Mary-Kate Olsen,^[260] Alanis Morissette,^[261] and French model Isabelle Caro, who died due to complications related to anorexia.

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^ le Grange D, Eisler I (2009). "Family interventions in adolescent anorexia nervosa". Child and Adolescent Psychiatric Clinics of North America 18 (1): 159–73. doi:10.1016/j.chc.2008.07.004. PMID 19014864.
^ "Eating Disorders". National Institute of Mental Health (NIMH). 2011. Retrieved 29 September 2013.
^ "Couples Therapy Helps Combat Anorexia Nervosa". Eating Disorders Review 23 (6). 2012.
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^ Ball J, Mitchell P (2004). "A randomized controlled study of cognitive behavior therapy and behavioral family therapy for anorexia nervosa patients". Eating Disorders 12 (4): 303–14. doi:10.1080/10640260490521389. PMID 16864523.
^ Berman MI, Boutelle KN, Crow SJ (2009). "A case series investigating acceptance and commitment therapy as a treatment for previously treated, unremitted patients with anorexia nervosa". European Eating Disorders Review 17 (6): 426–34. doi:10.1002/erv.962. PMID 19760625.
^ ^a ^b Tchanturia K, Davies H, Campbell IC (2007). "Cognitive remediation therapy for patients with anorexia nervosa: preliminary findings". Annals of General Psychiatry 6 (1): 14. doi:10.1186/1744-859X-6-14. PMC 1892017. PMID 17550611.
^ NIMH · Eating Disorders. Nimh.nih.gov (2011-08-23). Retrieved on 2012-02-04.
^ Studies – Eating Disorders Program – Stanford University School of Medicine. Edresearch.stanford.edu (2008-06-20). Retrieved on 2012-02-04.
^ Hudson JI, Hiripi E, Pope HG, Kessler RC (2007). "The Prevalence and Correlates of Eating Disorders in the National Comorbidity Survey Replication". Biological Psychiatry 61 (3): 348–58. doi:10.1016/j.biopsych.2006.03.040. PMC 1892232. PMID 16815322.
^ Shaw, Gina. Anorexia: The Body Neglected. Webmd.com. Retrieved on 2013-04-29.
^ Eisler I, Le Grange D, Asen KE (2003). "Family interventions". In Treasure J, Schmidt U, van Furth E. Handbook of eating disorders (2nd ed.). Chichester: Wiley. pp. 291–310.
^ Morris J, Twaddle S (2007). "Anorexia nervosa". BMJ 334 (7599): 894–898. doi:10.1136/bmj.39171.616840.BE. PMC 1857759. PMID 17463461.
^ Strober M, Freeman R, Morrell W (1997). "The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study". The International Journal of Eating Disorders 22 (4): 339–60. doi:10.1002/(SICI)1098-108X(199712)22:4<339::AID-EAT1>3.0.CO;2-N. PMID 9356884.
^ ^a ^b Gelder, Michael; Mayou, Richard and Geddes, John (2005) Psychiatry, Oxford; New York: Oxford University Press, ISBN 0-19-852863-9.
^ ^a ^b Strober M, Freeman R, Morrell W (1997). "The long-term course of severe anorexia nervosa in adolescents: Survival analysis of recovery, relapse, and outcome predictors over 10-15 years in a prospective study". International Journal of Eating Disorders 22 (4): 339–360. doi:10.1002/(SICI)1098-108X(199712)22:4<339::AID-EAT1>3.0.CO;2-N. PMID 9356884.
^ Schebendach J, Mayer LE, Devlin MJ, Attia E, Walsh BT (2012). "Dietary energy density and diet variety as risk factors for relapse in anorexia nervosa: A replication". International Journal of Eating Disorders 45 (1): 79–84. doi:10.1002/eat.20922. PMID 21448937.
^ ^a ^b ^c Halmi, K. A.; Mitchell, J.; Agras, S. (1996). "Anorexia nervosa: Prevention of relapse". Biological Psychiatry 39 (7): 666. doi:10.1016/0006-3223(96)84502-1.
^ "Tackling Relapse Among Anorexia Nervosa Patients". Eating Disorders Review 24 (1). 2013.
^ Treasure J, Claudino AM, Zucker N (2010). "Eating disorders". Lancet 375 (9714): 583–93. doi:10.1016/S0140-6736(09)61748-7. PMID 19931176.
^ Gowers S, Bryant-Waugh R (2004). "Management of child and adolescent eating disorders: the current evidence base and future directions". Journal of Child Psychology and Psychiatry, and Allied Disciplines 45 (1): 63–83. doi:10.1046/j.0021-9630.2003.00309.x. PMID 14959803.
^ Bulik CM, Sullivan PF, Tozzi F, Furberg H, Lichtenstein P, Pedersen NL (2006). "Prevalence, Heritability, and Prospective Risk Factors for Anorexia Nervosa". Archives of General Psychiatry 63 (3): 305–312. doi:10.1001/archpsyc.63.3.305. PMID 16520436.
^ Zanetti, Tatiana (2013). "Epidemiology of Eating Disorders". Eating Disorders and the Skin. pp. 9–15. doi:10.1007/978-3-642-29136-4_2. ISBN 978-3-642-29135-7.
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^ Gull WW (1997). "Anorexia nervosa (apepsia hysterica, anorexia hysterica). 1868". Obesity Research 5 (5): 498–502. doi:10.1002/j.1550-8528.1997.tb00677.x. PMID 9385628.
^ Costin, Carolyn (1999). The Eating Disorder Sourcebook. Linconwood: Lowell House. p. 6. ISBN 0-585-18922-6.
^ ^a ^b Pearce JM (2004). "Richard Morton: Origins of Anorexia nervosa". European Neurology 52 (4): 191–192. doi:10.1159/000082033. PMID 15539770.
^ ^a ^b Hepworth, Julie (1999) The Social Construction of Anorexia Nervosa. Thousand Oaks, CA: Sage Publications, ISBN 0-7619-5309-4.
^ McSherry JA (1985). "Was Mary, Queen of Scots, anorexic?". Scottish medical journal 30 (4): 243–5. PMID 3912990.
^ ^a ^b Sir William Withey Gull (1894). T D Acland, ed. Medical Papers. p. 309.
^ Kendall, Joshua C. (2011). The Forgotten Founding Father: Noah Webster's Obsession and the Creation of an American Culture. Penguin. p. 368. ISBN 978-0-399-15699-1.
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^ A survey by Internet security firm Optenet found a 470% increase in pro-ana and pro-mia sites from 2006 to 2007
^ Heath, Chris (22 Jan 1998). "The Caged Birds Sings". Rolling Stone 778.
^ Katrandjian, Olivia (3 Nov 2010). "Portia de Rossi: "I would strave myself daily"". ABC news. Retrieved 23 October 2012.
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^ Soriano, César G. (2004-06-22). "Mary-Kate Olsen seeks treatment for eating disorder". USA Today. Retrieved 23 October 2012.
^ Felts, Susannah. "How Alanis Morissette Beat Her Eating Disorder How Alanis Morissette Beat Her Eating Disorder". Health Magazine. Retrieved 23 October 2012.

External links

National Association of Anorexia Nervosa and Associated Disorders
International Eating Disorder Referral and Information Center
Anorexia nervosa
Society of Clinical Child and Adolescent Psychology – What is Anorexia Nervosa?
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001510/#adam_000479.disease.symptoms

UpToDate Contents

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1. 成人における神経性無食欲症：認知行動療法（CBT） anorexia nervosa in adults cognitive behavioral therapy cbt
2. 成人および思春期における神経性食思不振症：内科的合併症およびそのマネージメント anorexia nervosa in adults and adolescents medical complications and their management
3. 成人における神経性食思不振症：診断、随伴する臨床的特徴、および評価 anorexia nervosa in adults diagnosis associated clinical features and assessment
4. 成人における神経性食思不振症：薬物療法 anorexia nervosa in adults pharmacotherapy
5. 成人および思春期における神経性食思不振症：再栄養症候群 anorexia nervosa in adults and adolescents the refeeding syndrome

English Journal

Low baseline startle in anorexia nervosa patients.

Bellodi L, Martoni RM, Galimberti E, Cavallini MC.SourceDepartment of Clinical Neuroscience, San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, School of Psychology, Milan, Italy.
Progress in neuro-psychopharmacology & biological psychiatry.Prog Neuropsychopharmacol Biol Psychiatry.2013 Jan 10;40:26-9. doi: 10.1016/j.pnpbp.2012.08.007. Epub 2012 Aug 27.
This study examined baseline startle magnitude, using eye blink response and skin conductance response in anorexia nervosa patients. Twenty female in-patients with anorexia nervosa and an equal number of female healthy controls were tested. Baseline startle response was assessed during blank screens
PMID 22954471

Meal support using mobile technology in Anorexia Nervosa. Contextual differences between inpatient and outpatient settings.

Cardi V, Lounes N, Kan C, Treasure J.SourceKing's College London, Institute of Psychiatry, Psychological Medicine, Section of Eating Disorders, 103 Denmark Hill, London SE58AF, UK. Electronic address: valentina.cardi@kcl.ac.uk.
Appetite.Appetite.2013 Jan;60(1):33-9. doi: 10.1016/j.appet.2012.10.004. Epub 2012 Oct 17.
The aim of this study was to examine the impact of a "supported eating" intervention using mobile technology in patients with Anorexia Nervosa (AN). Twenty Inpatients and 18 Outpatients with AN underwent a test meal on two occasions, whilst listening to either a short video-clip ('vodcast'), or musi
PMID 23085476

Japanese Journal

The physiological significance and potential clinical applications of ghrelin.

Akamizu Takashi,Kangawa Kenji
European journal of internal medicine 23(3), 197-202, 2012-04
… Clinical trials have already been performed to assess the utility of ghrelin for the treatment of several disorders including anorexia, cachexia, and GH-related disorders. …
NAID 120003988362

摂食障害の病理とマインドフルネス-「時間」と「身体」からの考察

花澤寿,ハナザワヒサシ,HANAZAWA Hisashi
千葉大学教育学部研究紀要 60, 395-400, 2012-03
… Anorexia nervosaは,拒食とやせにこだわり続け「今この瞬間」から目を背けることで発達の危機状況を防衛していると考えられ,あえてそこに目を向けさせようとするマインドフルネス・アプローチの適用は困難であると考えられた。 …
NAID 120003987547

Related Pictures

★リンクテーブル★

リンク元	「神経性食思不振症」「100Cases 30」「摂食障害」「視床下部性無月経」「拒食症」
関連記事	「nervosa」

「神経性食思不振症」

Anorexia nervosa
	Classification and external resources
	"Miss A—" pictured in 1866 and in 1870 after treatment. She was one of the earliest anorexia nervosa case studies. From the published medical papers of Sir William Gull
ICD-10	F50.0-F50.1
ICD-9	307.1
OMIM	606788
DiseasesDB	749
MedlinePlus	000362
eMedicine	emerg/34 med/144
Patient UK	Anorexia nervosa
MeSH	D000856

神経性無食欲症
	分類及び外部参照情報
	治療前の17歳（1866年）及び治療後の21歳（1870年）時に描かれた女性の肖像。彼女は神経性無食欲症の記録に残る最も早期の患者であり、ウィリアム・ガルによって報告された
ICD-10	F50.0-F50.1
ICD-9	307.1
OMIM	606788
DiseasesDB	749
MedlinePlus	000362
eMedicine	emerg/34 med/144
MeSH	D000856
	プロジェクト:病気／Portal:医学と医療
	テンプレートを表示

　　[★]

ラ: anorexia nervosa, AN
同: 神経性食欲不振症、神経性無食欲症; also see KPS. 798

概念

器質的・特定の精神的疾患がないのに、拒食や過食などの食行動の異常、極端なやせ、無月経など種々の身体・精神症状をきたす病態。

身体像(ボディイメージ)の障害、やせ願望や肥満恐怖などによる。

病型

制限型：少食でやせを維持
むちゃ食い/排出型：過食しながら自己嘔吐や下剤・利尿薬の乱用でやせを維持

病因

1. 遺伝的要因
2. 環境要因(人格的脆弱性、生活環境、社会文化的要因)など　→　ストレスを適切に処理できないために発症

性格：内向的、自己中心的、小心、完全癖、潔癖症など
生活環境：家庭内の葛藤、学業や人間関係の悩み

病態的には、心理的ストレスが大脳皮質を介して視床下部摂食中枢のコルチコトロピン放出ホルモン系を活性化することなどにより、食欲抑制や性機能障害をきたす。

疫学

1980年代より増加傾向。日本の有病率は0.4-1.0%(摂食異常調査表による調査)(IMD.922)
12-25歳に好発(YN.D-166)。10代後半-20代前半、15歳以下の発症例も増加傾向(IMD.922)。
99%が女性(YN.D-166)。男性例は5%以下(IMD.922)

症状

やせ、無月経
病識なし、活動性亢進、むちゃ食い/排出型の場合は自己嘔吐や下剤・利尿薬乱用の習慣化
飢餓症候群

生活すべてが食とやせの維持に振り回され、ついには飢餓に伴う精神症状が出現
集中力・判断力の低下、抑うつ、不安、過敏性、不眠、自傷行為など

身体所見(IMD.922, YN.D-166)

低栄養だが、性ホルモンは比較的維持。

低血圧、低体温、便秘、徐脈　←　自律神経失調
(背中)うぶ毛密生、貧血、浮腫、肝機能障害、
カロチン症
循環障害による皮膚色の変化や凍瘡、末梢神経麻痺
やせに比して乳房は比較的保たれ、腋毛・恥毛は脱落しないことが多い。

検査

白血球数減少、貧血、血小板減少
肝機能障害、低血糖、低蛋白血症
(むちゃ食い/排出型)低Na・低K血症、代謝性アルカローシスや高アミラーゼ血症　←　低K血症(循環血漿量減少　→　RAA系の亢進　→　アルドステロンによるKの排出)
血清コレステロール値：(軽症)上昇、(重症)低下
骨密度の低下
甲状腺：T4：→/↑、T3：↓、reverse T3：↑(低T3症候群)。
成長ホルモン：↑、インスリン様成長因子-I(IGF-I)：↓　　←　末梢でIGF-Iの産生が低下、負のフィードバックにより成長ホルモンが増加
ACTH、コルチゾール：↑

卵胞刺激ホルモン(FSH)：→/↑
黄体ホルモン(LH)：↓

血算	ヘモグロビン	減少(貧血)
	白血球	減少
	リンパ球	比較的増加
生化学	Na	低Na血症(自己嘔吐・下剤使用例)
	K	低Ka血症(自己嘔吐・下剤使用例)
	AST	上昇
	ALT	上昇
	LDH	上昇
	T-Cho	上昇
	血糖	低下
血清学	IgG	低下(易感染性はない)
内分泌	T3	低下
	reverse T3	上昇
	GH	↑
	LH	↓
	FSH	→ or ↑
	コルチゾール	→ or ↑

診断

診断基準(厚生省特定疾患・神経性食欲不振症調査研究班, 1990年)

(2) 標準体重の－20%以上のやせ
(3) 食行動の異常(不食、大食、隠れ食いなど)
(4) 体重や体型についての歪んだ認識(体重増加に対する極端な恐怖など)
(1) 発症年齢：30歳以下
(5) (女性ならば)無月経
(6) やせの原因と考えられる器質性疾患がない

やせや無月経をきたす器質性疾患：視床下部腫瘍、下垂体機能低下症、糖尿病、慢性膵炎、甲状腺機能亢進症、炎症性腸疾患、結核などの感染症、悪性腫瘍

鑑別診断

食思不振症とか錐体機能低下症の比較 IMD.923改変

		神経性食思不振症	下垂体機能低下症	ANについて
好発年齢		思春期	全年齢
性差		女>>男	なし
体重		著明に減少	不定
食欲不振		高度	希
食行動の異常		高頻度	なし
精神運動異常		活発	無欲状
月経異常		あり(体重減少に先行)	あり
産毛の増加		あり	なし？
恥毛・腋毛脱落		なし	あり	LH, FSHが少しは存在するため。
乳腺萎縮		軽度やせに比して乳房は保たれる	著明	LH, FSHが少しは存在するため。
下垂体機能	GH	正常～高値	低値	IGF-I低値
	ACTH	正常～高値	低値
	LH, FSH	低値	低値
	TSH	正常	低値
甲状腺機能		低T3症候群	機能低下	T4正常、reverse T3上昇
副腎皮質機能		正常 (コルチゾール高値例あり)	機能低下 (コルチゾール低値)
頭部CT・MRI		異常なし	異常例有り (下垂体腫瘍, empty sellaなど)
症状		背部のうぶ毛の増加、便秘、低血圧、徐脈、下腿浮腫、循環障害による皮膚色の変化や凍瘡、末梢神経麻痺、カロチン症など

神経性食思不振症では成長ホルモンと糖質コルチコイドの上昇、末梢の甲状腺ホルモンの異常(reverse T3↑のこと？)、インスリン分泌の異常が認められることがある。(参考6)　　←　甲状腺、副腎機能は正常と言い切っている書物もあるが、、、

治療

医師と患者の信頼関係が重要。体重増加を受け入れてもらう
栄養療法：少量・低エネルギー食より開始。栄養不良が著しい場合には静脈栄養/経腸栄養
心理社会的療法(認知行動療法)

予後

改善50%、不変25%、悪化25%、死亡率5-8%(YN.D-167)　←　過食性食思不振症に比して予後が悪い

参考

1. 思春期やせ症

http://www.aiiku.or.jp/aiiku/jigyo/contents/kaisetsu/ks0712/ks0712_4.pdf

5. [charged] Patient information: Anorexia nervosa (TheBasics) - uptodate [1]
6. [charged] 成人における神経性食思不振症：診断、随伴する臨床的特徴、および評価 - uptodate [2]
7. [charged] 成人における神経性食思不振症：合併症の評価およびこれらの合併症管理のための入院基準 - uptodate [3]
8. [charged] 成人における神経性食思不振症：薬物療法 - uptodate [4]
9. [charged] 成人および思春期における神経性食思不振症：再栄養症候群 - uptodate [5]
10. [charged] 成人および思春期における神経性食思不振症：内科的合併症およびその管理 - uptodate [6]
11. [charged] 摂食障害：疫学、病因、および臨床的特徴の概要 - uptodate [7]
12. [charged] 摂食障害：治療および転帰 - uptodate [8]

「100Cases 30」

　　[★]

☆case30　無月経

■症例

23歳　女性　女優

主訴：無月経

現病歴：5ヶ月前からの無月経である。初経は13歳で、これまで月経周期は整であった。食欲はあると言っているが昨年から(over the pas year)体重が8kg減少した。

嗜好品：アルコール10 unit/week(缶ビール(350ml)6本弱本/週)。

既往歴：なし

社会歴：現在は無職。

服用薬：なし

生活歴：一年前、彼氏と別れた。

身体所見 examination

　四肢と殿部の筋肉が喪失。身長1.7m、体重41kg、BMI 13.7(標準的:20＜　＜24)。頬、首、前腕で毛が過剰に生えている。脈拍52/分。血圧96 /60 mmHg

検査所見 investigations

　ECG

血液生化学

　K↓, Cl↓, HCO3-↑, Cre↓, Alb(保たれているのか・・・)

問診(S)

　5ヶ月前からの無月経

　昨年から8kg体重が減少。

　無職

　1年前に彼氏と別れた

身体所見(O)

　四肢と殿部の筋肉が喪失。

　身長1.7m

　体重41kg

　BMI 13.666666666666666

　頬、首、前腕で毛が過剰に生えている。

　脈拍52/分

　血圧96/60 mmHg

検査(O)

　K↓, Cl↓, HCO3-↑, Cre↓

・なにをすべきか？

　・無月経の鑑別診断？

　・体重減少の原因

■診断

　神経性食思不振症, anorexia nervosa, AN

■要点

・嘔吐　→　H+,Cl-喪失。

・減少した血漿量　→　アルドステロン分泌亢進　→　尿細管ではナトリウム保持、カリウム分泌、(本来分泌されるべき)H+の枯渇

・アルカローシス(血中：Cl-低値、HCO3-高値。尿：Cl-低値、K+高値)

・尿中のCl-：<10mmol/day：嘔吐していることを暗示(imply vomitting)。高値：利尿剤の乱用

・anorexia nervosaで見られる検査値もチェックしておこう

　・LH, FSH, エストロゲンは低値

■key points

・神経性食思不振症は若年女性の中で無月経の主要な原因である。

・低カリウム性代謝性アルカローシスは特徴的な代謝異常

・神経性食思不振症は利尿剤や下剤の濫用と結びついていることがある。

■参考文献

　DIF　Differential Diagnosis in Primary Care Fourth Edition版 Lippincott Williams & Wilkins

■major cases of secondary amenorrhea

　・視床下部、下垂体の疾患：ex. 下垂体機能低下症、高プロラクチン血症

　・性腺不全：ex. 自己免疫性卵巣不全、多能性卵巣

　・副腎不全：ex. クッシング病

　・甲状腺疾患：ex. [甲状腺機能低下症]]、甲状腺機能亢進症

　・重症慢性疾患：ex. 癌、慢性腎不全

□アルコールのunit

　1 unit = 10 ml of ethanol

　350ml アルコール5%　→　350x0.05/10=1.75 unit

■glossary

buttock　

　n. 殿部、尻。船尾

interrelate　

　vi. 相互関係を持つ(有する)

　vt. 相互に関係(関連)づける

contract　

　v. 収縮する

lanugo

　n. 毳毛、うぶ毛

無月経の原因 NGY.153

	原発性無月経	続発性無月経
視床下部性無月経	カルマン症候群	視床下部の機能障害
	フレーリヒ症候群	神経性食欲不振症
	Laurence-Moon-Biedl症候群	体重減少性無月経
	プラダ・ウィリ症候群	高プロラクチン血症
		Chiari-Frommel症候群
		Argonz-del Castillo症候群
下垂体性無月経	先天性ゴナドトロピン欠損症	シーハン症候群
	empty sella症候群	下垂体腺腫
		Forbes-Albright症候群
卵巣性無月経	性腺形成不全	早発卵巣機能不全
	ターナー症候群	多嚢胞性卵巣症候群
		卵巣摘出
		卵巣の放射線障害
子宮性無月経	ロキタンスキー・キュスター・ハウザー症候群	アッシャーマン症候群
	子宮奇形	子宮内膜炎
	処女膜閉鎖	子宮摘出術後
膣性無月経	処女膜閉鎖症
膣性無月経	膣閉鎖症
その他	半陰陽(先天性副腎過形成、アンドロゲン不応症)	Cushing症候群
		Addison病
		Basedow病
		甲状腺機能低下症
		糖尿病
生理的		妊娠、産褥、授乳、閉経

「摂食障害」

　　[★]

英: eating disorder ED, eating disturbance, eating pathology, anorexia, feeding disorder, problem with eating
同: 食行動異常
関: 神経性過食症、食欲不振、食欲不振症、無食欲、食欲低下、食思不振、栄養補給障害、幼児摂食障害
ICD-10: F50

分類

ICD-10

F50	Eating disorders
	F50.0	anorexia nervosa
	F50.1	atypical anorexia nervosa
	F50.2	bulimia nervosa
	F50.3	atypical bulimia nervosa
	F50.4	overeating associated with other psychological disturbances
	F50.5	vomiting associated with other psychological disturbances
	F50.8	other eating disorders
	F50.9	eating disorder, unspecified

参考

分類

http://priory.com/psych/ICD.htm http://www.swedauk.org/disorders/definitions.htm

「視床下部性無月経」

　　[★]

英: hypothalamic amenorrhea
同: 間脳性無月経 diencephalic amenorrhea

分類

原発性

続発性

「拒食症」

　　[★]

ラ: anorexia nervosa、cibophobia
関: 神経性食欲不振症、神経性無食欲症、拒絶症

「nervosa」

　　[★]

adj.

神経性の

関: neural、neurally、neurogenic、neurologic、neurological、neuronally; anorexia nervosa、bulimia nervosa

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Anorexia nervosa
Classification and external resources
"Miss A—" pictured in 1866 and in 1870 after treatment. She was one of the earliest anorexia nervosa case studies. From the published medical papers of Sir William Gull
ICD-10	F50.0-F50.1
ICD-9	307.1
OMIM	606788
DiseasesDB	749
MedlinePlus	000362
eMedicine	emerg/34 med/144
Patient UK	Anorexia nervosa
MeSH	D000856

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anorexia nervosa

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★リンクテーブル★

「神経性食思不振症」

概念

病型

病因

疫学

症状

身体所見(IMD.922, YN.D-166)

検査

診断

診断基準(厚生省特定疾患・神経性食欲不振症調査研究班, 1990年)

鑑別診断

食思不振症とか錐体機能低下症の比較 IMD.923改変

治療

予後

参考

「100Cases 30」

無月経の原因 NGY.153