Jadłowstręt psychiczny – Patofizjologia i mechanizm

Jadłowstręt psychiczny
Patofizjologia i mechanizm

Jadłowstręt psychiczny (anorexia nervosa, AN) to złożone zaburzenie o wysokim wskaźniku śmiertelności, którego patogeneza obejmuje interakcje czynników genetycznych, neurobiologicznych, endokrynologicznych i psychospołecznych. Dziedziczność szacowana jest na 28-58%, z ryzykiem 12-krotnie wyższym u krewnych pierwszego stopnia. Geny ESRRA i HDAC4 zwiększają ryzyko odpowiednio o 90% i 85%. Neurobiologicznie obserwuje się deficyty dopaminy, serotoniny i acetylocholiny, szczególnie w prążkowiu, co sprzyja kompulsywnemu samogłodzeniu. Zaburzenia endokrynologiczne obejmują dysfunkcje osi gonadowej, tarczycowej i nadnerczowej, z obniżonym poziomem leptyny i zmienionymi peptydami jelitowymi (grelina, peptyd YY, amylina). Dysbioza mikrobioty jelitowej oraz zmniejszona produkcja krótkołańcuchowych kwasów tłuszczowych przyczyniają się do stanu prozapalnego i zaburzeń regulacji apetytu i emocji. Psychologicznie AN cechuje się zniekształceniem obrazu ciała, obsesyjnym lękiem przed przytyciem, perfekcjonizmem i niską elastycznością poznawczą.

Mechanizmy patogenezy jadłowstrętu psychicznego

Czynniki genetyczne i dziedziczenie
Neurobiologiczne podstawy jadłowstrętu psychicznego
Zaburzenia endokrynologiczne i metaboliczne
Wpływ mikrobioty jelitowej na rozwój jadłowstrętu psychicznego
Mechanizmy psychologiczne i neurobehawioralne

Mechanizmy neuroendokrynologiczne i fizjologiczne w jadłowstręcie psychicznym

Wpływ na układ sercowo-naczyniowy
Zaburzenia metabolizmu kostnego
Zmiany w strukturze mózgu
Zaburzenia hormonalne
Mechanizmy neuroadaptacyjne i kompulsywne nawyki

Czynniki psychospołeczne i środowiskowe w patogenezie AN

Wpływ rodziny
Wpływ diety i głodzenia
Wpływ czynników socjokulturowych
Wpływ mediów i wizerunku ciała

Holistyczny model patogenezy jadłowstrętu psychicznego

Implikacje dla diagnostyki i leczenia
Kolejne rozdziały

Mechanizmy patogenezy jadłowstrętu psychicznego

Jadłowstręt psychiczny (anorexia nervosa, AN) jest poważnym zaburzeniem psychicznym charakteryzującym się dążeniem do nadmiernej utraty masy ciała, irracjonalnym lękiem przed przybraniem na wadze oraz zaburzonym obrazem własnego ciała. Schorzenie to wiąże się z najwyższym wskaźnikiem śmiertelności spośród wszystkich zaburzeń psychicznych, a jego patogeneza jest złożona i wieloczynnikowa.¹² Obecne badania wskazują, że u podłoża jadłowstrętu psychicznego leżą zarówno czynniki biologiczne, w tym genetyczne, jak i środowiskowe, które wchodzą ze sobą w złożone interakcje.³

Czynniki genetyczne i dziedziczenie

Badania wykazują, że jadłowstręt psychiczny charakteryzuje się wysokim stopniem dziedziczności, szacowanym na 28-58%, przy czym wiele badań wskazuje na wartości powyżej 50%.⁴⁵ Krewni pierwszego stopnia osób z jadłowstrętem psychicznym mają około 12 razy większe ryzyko rozwoju tego zaburzenia.⁶ Badania bliźniąt konsekwentnie wykazują wyższy współczynnik zgodności występowania AN u bliźniąt jednojajowych (15-55%) w porównaniu do bliźniąt dwujajowych (7-10%).⁷⁸

Badania genomu wskazują na związek z AN około 43 różnych genów, które są powiązane z regulacją zachowań żywieniowych, motywacją, mechanizmami nagrody, osobowością i emocjami.⁹ Szczególnie istotne mogą być geny ESRRA i HDAC4, które zwiększają ryzyko rozwoju zaburzeń odżywiania odpowiednio o 90% i 85%.¹⁰ Badania asocjacyjne całego genomu (GWAS) zidentyfikowały osiem lokalizacji genów, które mogą odgrywać rolę w rozwoju jadłowstrętu psychicznego.¹¹ Niedawne badania wykazały również, że mutacja genetyczna VGLUT3-p.T81 w genie VGLUT3 prowadzi do zmniejszenia poziomu acetylocholiny, co może przyczyniać się do nadmiernego tworzenia nawyków powodujących zagłodzenie u pacjentów z AN.¹²

Neurobiologiczne podstawy jadłowstrętu psychicznego

Badania neurologiczne wykazały, że osoby z jadłowstrętem psychicznym mają zmienioną strukturę i funkcję mózgu.¹³ Zaburzenia te dotyczą przede wszystkim następujących obszarów:

Deficyty neuroprzekaźników: dopaminy (związanej z zachowaniami żywieniowymi i układem nagrody) oraz serotoniny (związanej z kontrolą impulsów i neurotyzmem)¹⁴¹⁵
Zróżnicowana aktywacja układu limbicznego (odpowiedzialnego za apetyt i strach)¹⁶
Zmniejszona aktywność obwodów czołowo-prążkowiowych (odpowiedzialnych za zachowania nawykowe)¹⁷¹⁸

Jednym z najnowszych odkryć jest identyfikacja deficytu acetylocholiny w prążkowiu, obszarze mózgu związanym z układem nagrody, co może prowadzić do nadmiernego formowania nawyków i przyspieszać kompulsywne samogłodzenie obserwowane u osób z jadłowstrętem psychicznym.¹⁹²⁰

Zaburzenia układu serotoninergicznego są szczególnie istotne w patogenezie AN. Badania wykazały, że zaburzenia w tym układzie poprzedzają wystąpienie jadłowstrętu psychicznego i mogą przyczyniać się do występowania objawów lęku, zahamowania oraz podatności na ograniczanie jedzenia.²¹ Receptory 5-HT1A i 5-HT2A wydają się najbardziej wpływowe w patogenezie AN.²² Wysoki poziom serotoniny w obszarach mózgu z receptorem 5HT1A jest szczególnie związany z lękiem, nastrojem i kontrolą impulsów.²³

System dopaminergiczny również odgrywa kluczową rolę. U osób z jadłowstrętem psychicznym obserwuje się nierównowagę aktywności dopaminowej w grzbietowym prążkowiu, co może być wspólnym czynnikiem dla zaburzeń używania substancji i zaburzeń odżywiania.²⁴ Badania sugerują, że AN jest związana ze zwiększoną reaktywnością w mózgowych obwodach nagrody, co może wynikać z nadwrażliwego układu dopaminergicznego.²⁵

Zaburzenia endokrynologiczne i metaboliczne

Jadłowstręt psychiczny wpływa na wiele osi endokrynologicznych, powodując liczne zaburzenia hormonalne:²⁶

Zaburzenia osi gonadowej, tarczycowej i nadnerczowej
Nieprawidłowości w wydzielaniu hormonu wzrostu i insulinopodobnego czynnika wzrostu-1 (IGF-1)
Zmiany w poziomach adipokin, takich jak leptyna
Zaburzenia peptydów jelitowych, jak grelina, peptyd YY i amylina²⁷

Niedawne badania genetyczne wykazały, że jadłowstręt psychiczny ma również komponent metaboliczny. Zidentyfikowano mutacje w instrukcjach kontrolujących metabolizm organizmu, szczególnie tych związanych z poziomem cukru we krwi i tkanką tłuszczową.²⁸ To doprowadziło niektórych badaczy do określenia jadłowstrętu psychicznego jako zaburzenia „metabo-psychiatrycznego”, które ma zarówno przyczyny metaboliczne, jak i psychiatryczne.²⁹³⁰

Szczególnie istotna jest rola leptyny, której poziom jest konsekwentnie obniżony u osób z AN. Poziomy leptyny normalizują się po wyzdrowieniu, co kwalifikuje ją jako potencjalny biomarker stanu AN.³¹ Zaburzenia w poziomach leptyny, greliny i obestatyny mogą odzwierciedlać stres, jakiemu poddawany jest organizm podczas ostrego lub przedłużonego głodzenia.³²

Wpływ mikrobioty jelitowej na rozwój jadłowstrętu psychicznego

Coraz więcej dowodów wskazuje na istotną rolę mikrobioty jelitowej w patogenezie jadłowstrętu psychicznego.³³ Badania wykazały, że u pacjentów z AN występuje dysbioza jelitowa, czyli zaburzenie składu mikrobioty.³⁴ Przedłużony stres fizjologiczny i psychologiczny, w tym poważna utrata masy ciała i ekstremalne nawyki żywieniowe, mogą wpływać na skład mikrobioty jelitowej i w konsekwencji indukować dysbiozę jelitową.³⁵

Niedawne badania omiczne i mechanistyczne sugerują, że zakłócona mikrobiota jelitowa może przyczyniać się do patogenezy AN.³⁶ Badania wykazały głębokie i złożone zaburzenia mikrobioty jelitowej u osób z AN, z konsekwencjami funkcjonalnymi i zmianami metabolitów w surowicy.³⁷ Związki te mogą działać poprzez krążenie krwi lub poprzez szlaki sygnalizacyjne mikrobiota-jelito-mózg, wpływając na regulację apetytu, emocji i zachowania w mózgu.³⁸

Model zaproponowany przez badaczy sugeruje, że nierównowaga w składzie mikrobioty jelitowej prowadzi do zmniejszenia produkcji krótkołańcuchowych kwasów tłuszczowych, przyczyniając się do stanu prozapalnego w AN, który jest również powszechny w innych współwystępujących zaburzeniach psychicznych.³⁹

Mechanizmy psychologiczne i neurobehawioralne

Jadłowstręt psychiczny charakteryzuje się pewnymi cechami psychologicznymi i behawioralnymi, które przyczyniają się do jego rozwoju i utrzymywania:⁴⁰

Zniekształcenie obrazu ciała
Obsesyjny lęk przed przytyciem
Perfekcjonizm i lęk
Niska samoocena
Impulsywne lub obsesyjne zachowania⁴¹

Badania neuropsychologiczne wykazały, że osoby z jadłowstrętem psychicznym mają słabą elastyczność poznawczą, co jest stosunkowo niezawodnym ustaleniem.⁴² Zaburzenia uczenia się i funkcji pamięci, takie jak sztywność poznawcza (słabe przełączanie), słaba spójność centralna i trudności w przetwarzaniu społeczno-emocjonalnym, mogą być częściowo spowodowane niskim spożyciem energii powodującym brak dostępnej energii.⁴³

Niedawno zaproponowano teorię „wyuczonej pracowitości” jako nowy mechanistyczny model wyjaśniający, dlaczego niektóre zachowania utrzymują się pomimo braku przyjemności i pozornej awersyjności. Według tej teorii, zachowania wymagające wysokiego wysiłku mogą być warunkowane, aby nabyć wtórne właściwości wzmacniające poprzez powtarzające się kojarzenie z nagrodą. W rezultacie doznania wysiłku stają się mniej awersyjne, a bardziej apetytywne, zwiększając chęć angażowania się w zachowania wymagające wysiłku.⁴⁴

Mechanizmy neuroendokrynologiczne i fizjologiczne w jadłowstręcie psychicznym

Jadłowstręt psychiczny prowadzi do licznych powikłań medycznych, które są bezpośrednio związane z utratą masy ciała i niedożywieniem. Powikłania te dotyczą większości głównych układów narządów i często obejmują zaburzenia fizjologiczne, takie jak hipotensja, bradykardia, hipotermia i brak miesiączki.⁴⁵

Wpływ na układ sercowo-naczyniowy

Zmiany w układzie sercowo-naczyniowym są jednymi z najpoważniejszych powikłań jadłowstrętu psychicznego:⁴⁶

Zmniejszenie masy mięśnia sercowego
Zmniejszenie wielkości komór serca
Obniżenie pojemności minutowej serca
Częste występowanie wypadania zastawki mitralnej⁴⁷⁴⁸

Atrofia mięśnia sercowego, stanowiąca strukturalny wyznacznik tej choroby, charakteryzuje się zmniejszeniem wskaźnika masy lewej komory i towarzyszącym zmniejszeniem objętości lewej komory. Wypadanie zastawki mitralnej jest powszechne w AN. Chociaż jego mechanizm nie został w pełni wyjaśniony, uważa się, że jest konsekwencją atrofii mięśnia sercowego i zmniejszonego rozmiaru komory lewej komory, prowadzącego do względnej wiotkości zastawki, nawet przy braku zwyrodnienia śluzakowatego zastawki.⁴⁹⁵⁰

Zaburzenia metabolizmu kostnego

Jadłowstręt psychiczny negatywnie wpływa na kości i przysadkę mózgową z powodu głodzenia i niedożywienia.⁵¹ Prowadzi to do następujących zaburzeń:

Niska gęstość mineralna kości (BMD)
Zaburzenia mikroarchitektury kości
Zwiększone ryzyko złamań⁵²

Osteopenia jest powszechnym i zwykle długotrwałym powikłaniem AN, prowadzącym do klinicznych złamań i zwiększonego ryzyka złamań przez całe życie. Badanie kobiet z AN w wieku około 25 lat wykazało, że 55% z nich miało osteopenię, a 35% osteoporozę, przy czym tylko 15% miało normalną BMD we wszystkich badanych lokalizacjach szkieletowych.⁵³

Etiologia tej intensywnej utraty gęstości mineralnej kości jest prawdopodobnie wieloczynnikowa i obejmuje podwyższony poziom kortyzolu, niski poziom leptyny i hormonów płciowych, niską masę ciała oraz oporność na hormon wzrostu.⁵⁴

Wpływ jadłowstrętu psychicznego na kości jest szczególnie niepokojący w okresie dojrzewania. Hipogonadyzm i późniejszy wiek menarche są znaczącymi czynnikami przyczyniającymi się do niskiej BMD związanej z AN.⁵⁵

Zmiany w strukturze mózgu

Jadłowstręt psychiczny charakteryzuje się wyraźnym zanikiem mózgu widocznym w badaniach obrazowych mózgu. Szczególne obszary mózgu wydają się być preferencyjnie uszkodzone, w tym zarówno istota szara, jak i biała, oraz obszary wyspy i wzgórza.⁵⁶

Badania z wykorzystaniem tomografii komputerowej wykazały powiększone bruzdy i komory, co jest ustaleniem, które ulega odwróceniu wraz z przyrostem masy ciała.⁵⁷ W jednym z badań z wykorzystaniem pozytonowej tomografii emisyjnej stwierdzono, że metabolizm był wyższy w jądrze ogoniastym podczas stanu anorektycznego niż po hiperalimentacji.⁵⁸

Zaburzenia hormonalne

Nieprawidłowości endokrynologiczne są powszechne w jadłowstręcie psychicznym i obejmują:⁵⁹

Niskie poziomy hormonów gonadowych
Łagodnie obniżone poziomy tyroksyny (T4) i trijodotyroniny (T3)
Zwiększone wydzielanie kortyzolu⁶⁰

Głodzenie prowadzi do wielu zmian biochemicznych, takich jak hiperkortyzolemii, braku supresji deksametazonu, zahamowania funkcji tarczycy i braku miesiączki.⁶¹

Zaburzenia neuroendokrynologiczne, czyli zmieniona sygnalizacja peptydów ułatwiających komunikację między jelitami, mózgiem i tkanką tłuszczową, takich jak grelina, leptyna, neuropeptyd Y i oreksyna, mogą przyczyniać się do patogenezy jadłowstrętu psychicznego poprzez zakłócenie regulacji głodu i sytości.⁶²

Mechanizmy neuroadaptacyjne i kompulsywne nawyki

Utrzymujące się stany głodzenia mogą prowadzić do biochemicznie uwarunkowanej oporności na leczenie ze względu na zmiany neuroadaptacyjne, w tym wzrost białka 6 podobnego do angiopoetyny (ANGPTL6), które zwiększają prawdopodobieństwo, że jadłowstręt psychiczny stanie się przewlekły i trwały.⁶³⁶⁴

Charakterystyczną cechą jadłowstrętu psychicznego jest zwiększona aktywność fizyczna. Według literatury, do 40-80% pacjentów z AN wykazuje nadmierny poziom aktywności fizycznej.⁶⁵ Nadaktywność, definiowana jako intensywna aktywność fizyczna połączona z kompulsywną potrzebą ćwiczeń, odgrywa fundamentalną rolę w rozwoju i utrzymywaniu się AN, może poprzedzać ograniczenie jedzenia i przyspieszać utratę masy ciała po rozpoczęciu ograniczenia jedzenia, a także wyraźnie zakłóca proces powrotu do zdrowia i została zgłoszona jako jeden z czynników predykcyjnych wyższego ryzyka nawrotu po wyzdrowieniu.⁶⁶

Natura tej cechy pozostaje niepewna, chociaż została już rozpoznana i opisana przez Gulla i Lasègue’a w XIX wieku. Aktywacja nagradzająca przy zmniejszonym spożyciu energii poprzez dopaminergiczne szlaki wzmacniające, hipoleptynemia i kompensacja termoregulacyjna z powodu hipotermii zostały wysunięte jako główne przyczyny nadaktywności, ale czynniki genetyczne regulujące poziomy aktywności również powinny przyczyniać się do rozwoju choroby.⁶⁷

Te efekty nagradzające, wywołujące euforię i zależność, są pośredniczone przez zwiększone mesolimbiczne uwalnianie dopaminy poprzez aktywację osi podwzgórze-przysadka-nadnercza z wysokim poziomem kortyzolu we krwi z powodu głodzenia i/lub nadaktywności.⁶⁸

Czynniki psychospołeczne i środowiskowe w patogenezie AN

Oprócz czynników biologicznych i neurobiologicznych, w patogenezie jadłowstrętu psychicznego istotną rolę odgrywają również czynniki psychospołeczne i środowiskowe.⁶⁹

Wpływ rodziny

Idea, że specyficzna dysfunkcja rodzinna może prowadzić do jadłowstrętu psychicznego, była wysuwana przez wielu autorów.⁷⁰⁷¹ Już przed pierwszymi badaniami na temat rodzin w schizofrenii niektórzy autorzy zwrócili uwagę na pewne osobliwości, które powtarzały się wyraźnie w rodzinach osób z jadłowstrętem psychicznym.⁷²

Większość autorów przypisywała osobowości matki szczególną rolę w patogenezie. Jednakże Jeammet, Massing i inni podkreślali również duże znaczenie funkcji ojca w rozwoju jadłowstrętu psychicznego. Szkoła z Getyngi zawsze podkreślała specyficzną obecność potężnej babci w tych rodzinach.⁷³

Należy jednak zaznaczyć, że wyniki badań dotyczących funkcjonowania rodziny i jadłowstrętu psychicznego są sprzeczne.⁷⁴ Mimo że terapia rodzinna okazała się skutecznym leczeniem niedawno rozpoznanego jadłowstrętu psychicznego u młodych pacjentów, nie można na tej podstawie wnioskować, że czynniki rodzinne mogą być patogenetyczne.⁷⁵

Wpływ diety i głodzenia

Badanie Minnesota przekonująco wykazało, że przedłużające się półgłodzenie może prowadzić do rozwoju nieprawidłowych zachowań żywieniowych.⁷⁶⁷⁷ Najczęstszym poprzednikiem jadłowstrętu psychicznego jest dieta. Początkowemu pragnieniu utraty kilku kilogramów szybko towarzyszy obsesyjne pragnienie utraty masy ciała. Bycie zdolnym do utraty wagi i bycie szczupłym jest postrzegane i odczuwane jako dobre, tak że stopniowo dieta i utrata masy ciała zaczynają być postrzegane lub doświadczane jako bycie pod kontrolą lub jako jedyne rozwiązanie problemów życiowych.⁷⁸

Przeprowadzono co najmniej 6 badań podłużnych w celu zbadania roli diety w patogenezie jadłowstrętu psychicznego. Pięć z sześciu badań podłużnych zdecydowanie sugeruje, że zachowania dietetyczne narażają jednostkę na wyższe ryzyko rozwoju zaburzeń odżywiania, chociaż oczywiście nie wszyscy stosujący dietę rozwijają zaburzenia odżywiania.⁷⁹⁸⁰

Badania sugerują również, że rezultaty badania Minnesota mogą być wyjaśnieniem dla kontynuacji zaburzonych wzorców odżywiania jako epifenomenów głodzenia. Wyniki badania głodzenia w Minnesota wykazały, że normalne osoby kontrolne wykazują wiele wzorców behawioralnych jadłowstrętu psychicznego, gdy są poddawane głodzeniu. Może to być spowodowane licznymi zmianami w systemie neuroendokrynnym, co prowadzi do samopodtrzymującego się cyklu.⁸¹

Wpływ czynników socjokulturowych

Presja społeczna na szczupłość może przyczyniać się do wystąpienia zaburzeń odżywiania.⁸² Badania socjokulturowe podkreśliły rolę czynników kulturowych, takich jak promowanie szczupłości jako idealnej formy kobiecej w zachodnich krajach uprzemysłowionych, szczególnie poprzez media.⁸³

Niedawne badania epidemiologiczne przeprowadzone na 989 871 mieszkańcach Szwecji wykazały, że płeć, pochodzenie etniczne i status społeczno-ekonomiczny mają duży wpływ na szanse rozwoju jadłowstrętu psychicznego.⁸⁴

Kulturowy nacisk na szczupłość lub mniejsze ciała jako moralny i zdrowotny imperatyw, wraz z normalizacją zamierzonego odchudzania, przyczynia się do wartościowania jednostek na podstawie wyglądu zewnętrznego.⁸⁵

Każda teoria wyjaśniająca patogenezę jadłowstrętu psychicznego musi uwzględniać, dlaczego zaburzenie to jest znacznie częstsze wśród kobiet niż mężczyzn. Większość opublikowanych badań wykazała przewagę kobiet nad mężczyznami w stosunku około 10:1. Wielu klinicystów i badaczy sugerowało, że proces rozwoju psychologicznego naraża niektóre osoby na ryzyko rozwoju zaburzeń odżywiania.⁸⁶

Wpływ mediów i wizerunku ciała

Presja społeczna na szczupłość może również przyczyniać się do rozwoju jadłowstrętu psychicznego. Nierealistyczne obrazy ciała z mediów, takich jak magazyny i telewizja, mogą znacznie wpływać na młodych ludzi i wywoływać pragnienie bycia szczupłym.⁸⁷

Typowy przypadek jadłowstrętu psychicznego dotyczy młodej osoby (nastolatka lub młodego dorosłego), która jest lekko nadwagi lub ma normalną wagę i rozpoczyna plan diety i ćwiczeń, aby schudnąć. Gdy traci na wadze i otrzymuje początkowe pozytywne wzmocnienie dla tego zachowania (np. komplementy od rówieśników na temat swojego wyglądu), nagroda jest wysoka i powoduje niezdolność do zaprzestania tego zachowania po osiągnięciu idealnej wagi.⁸⁸

Na obecnym etapie naszego zrozumienia jadłowstrętu psychicznego spójna teoria jego patogenezy jest trudna do uchwycenia. Jednakże dostępne dane sugerują, że młoda kobieta z rodzinnym wywiadem zaburzeń odżywiania, depresji lub zaburzenia obsesyjno-kompulsywnego, żyjąca w kulturze, która podkreśla szczupłość, może być bardziej narażona na rozwój jadłowstrętu psychicznego, jeśli podejmie rygorystyczną dietę w celu utraty masy ciała, szczególnie jeśli rygorystyczna dieta wynika z niskiej samooceny.⁸⁹⁹⁰

Holistyczny model patogenezy jadłowstrętu psychicznego

Współczesne podejście do patogenezy jadłowstrętu psychicznego wskazuje na złożoną interakcję wielu czynników. Jak podkreślono w przedstawionych badaniach, etiologia AN jest wieloczynnikowa i obejmuje wpływy genetyczne, biologiczne, psychologiczne, rodzinne i socjokulturowe.⁹¹

Warto zauważyć, że wiele zjawisk neurobiologicznych występuje przedchorobowo, jest nasilonych przez niedożywienie i wraca do poziomów przedchorobowych po wyzdrowieniu.⁹² Potwierdza to złożony charakter zaburzenia i wskazuje na konieczność wieloaspektowego podejścia do jego rozumienia i leczenia.

Chociaż większość endokrynopatii związanych z jadłowstrętem psychicznym poprawia się z czasem, długoterminowe konsekwencje, takie jak niski wzrost, osteoporoza i niepłodność, mogą się utrzymywać.⁹³ Obecnie nie ma leków zatwierdzonych przez FDA do leczenia niskiej gęstości mineralnej kości w jadłowstręcie psychicznym; dlatego przyrost masy ciała i powrót miesiączkowania pozostają najskuteczniejszą strategią zwiększania BMD.⁹⁴

Badacze i klinicyści zgodnie podkreślają, że rozumienie jadłowstrętu psychicznego jako zaburzenia o podłożu zarówno biologicznym, jak i psychologicznym, jest kluczowe dla opracowania skutecznych strategii leczenia i profilaktyki.⁹⁵

Implikacje dla diagnostyki i leczenia

Lepsze zrozumienie mechanizmów patogenetycznych jadłowstrętu psychicznego może prowadzić do rozwoju nowych metod diagnostycznych i terapeutycznych.⁹⁶ Identyfikacja deficytu acetylocholiny jako potencjalnego mechanizmu leżącego u podłoża jadłowstrętu psychicznego otwiera nowe możliwości leczenia.⁹⁷

Nedawno naukowcy z Uniwersytetu McGill odkryli, że deficyt acetylocholiny w prążkowiu może prowadzić do nadmiernego formowania nawyków i przyspieszać kompulsywne samogłodzenie obserwowane u osób z jadłowstrętem psychicznym. Badacze są przekonani, że odkrycie to może potencjalnie zaoferować pierwsze leczenie jadłowstrętu psychicznego oparte na mechanizmie.⁹⁸

Innym obiecującym obszarem badań jest rola mikrobioty jelitowej. Dalszy rozwój w tej dziedzinie może wyjaśnić rolę mikrobów jelitowych w patogenezie zaburzeń odżywiania i dostarczyć silnego uzasadnienia dla interwencji probiotycznej jako leczenia dla pacjentów z jadłowstrętem psychicznym.⁹⁹

W kontekście farmakoterapii, badania sugerują, że aripiprazol, jako częściowy agonista D2 i 5-HT1A, może działać inaczej na receptory dopaminowe i serotoninowe niż inne leki przeciwpsychotyczne. Teoretyczne argumenty wskazują, jak stosowanie aripiprazolu w niższych dawkach (zwykle 1-5 mg/dzień, z okazjonalnym miareczkowaniem do 10 mg/dzień) może ułatwić uczenie się i zmianę zachowań u osób z jadłowstrętem psychicznym. Aripiprazol może obniżać aktywność receptora D2, co może poprawiać funkcję mózgu, zmniejszać lęk i wspierać proces psychoterapeutyczny.¹⁰⁰

Warto podkreślić, że rehabilitacja żywieniowa i wsparcie behawioralne dla utrzymania masy ciała są niezbędne i powinny być podstawą leczenia jadłowstrętu psychicznego.¹⁰¹ Leczenie jadłowstrętu psychicznego jest rzadko podejściem uniwersalnym. Może obejmować pracę z różnymi specjalistami w dziedzinie zdrowia i wypróbowanie kilku różnych podejść.¹⁰²

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Materiały źródłowe

#1 Backstage of Eating DisorderâAbout the Biological Mechanisms behind the Symptoms of Anorexia Nervosa
https://www.mdpi.com/2072-6643/12/9/2604
Anorexia nervosa (AN) represents a disorder with the highest mortality rate among all psychiatric diseases, yet our understanding of its pathophysiological components continues to be fragmentary. […] This article reviews the current concepts regarding AN pathomechanisms that focus on the main biological aspects involving central and peripheral neurohormonal pathways, endocrine function, as well as the microbiomeâgutâbrain axis. […] The emphasis is placed on the mechanisms underlying the main symptoms and potential new directions that require further investigation in clinical settings. […] The high prevalence of fitness and thinness, the low prevalence of AN, together with a clear evidence of anorexia occurring in the past centuries, its stereotypic presentation, heritability, and developmentally specific age-of-onset, suggest rather biological accountabilities.
#2 The Neurobiology of Anorexia Nervosa | IntechOpen
https://www.intechopen.com/chapters/64858
Anorexia nervosa is considered the most deadly psychological illness. […] A better understanding of the biological and neurobiological etiology of anorexia nervosa is direly needed to inform new therapies and to identify individuals at risk for the disorder. This paper summarizes the research related to neurotransmitter abnormalities, aberrant brain activity, and genetic and epigenetic mechanisms that may contribute to the etiology of this deadly disorder. […] Many of the neurobiological phenomena to be discussed in this paper are present premorbidly, exaggerated by malnutrition, and return to premorbid levels after recovery. […] There are currently promising lines of research on dopaminergic, serotonergic, and noradrenergic pathways, as well as dysregulations in appetitive functioning, genetic and epigenetic contributions, contributions from gonadal hormones, and aberrations in brain activity.
#3 Anorexia nervosa pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Anorexia_nervosa_pathophysiology
It is clear that there is no single cause for anorexia and that it stems from a mixture of social, psychological and biological factors. Current research is commonly focused on explaining existing factors and uncovering new causes. However, there is considerable debate over how much each of the known causes contributes to the development of anorexia. In particular, the contribution of perceived media pressure on women to be thin has been especially contentious. […] Family and twin studies have suggested that genetic factors contribute to about 50% of the variance for the development of an eating disorder and that anorexia shares a genetic risk with clinical depression. This evidence suggests that genes influencing both eating regulation, and personality and emotion, may be important contributing factors.
#4 Anorexia Nervosa | Abnormal Psychology
https://courses.lumenlearning.com/wm-abnormalpsych/chapter/eating-disorders/
Anorexia nervosa is highly heritable. Twin studies have shown a heritability rate of between 28%58%, with many studies estimating the heritability of the disorder in the higher range, above 50%. First-degree relatives of those with anorexia have roughly 12 times the risk of developing anorexia. Some studies have shown some associations between anorexia and 43 different genes that are connected to regulating eating behavior, motivation, reward mechanics, personality, and emotion. Epigenetic modifications, such as DNA methylation, may contribute to the development or maintenance of anorexia nervosa, though clinical research in this area is in its infancy. […] Neuroendocrine dysregulation, or altered signaling of peptides that facilitate communication between the gut, brain, and adipose tissue, such as ghrelin, leptin, neuropeptide Y, and orexin, may contribute to the pathogenesis of anorexia nervosa by disrupting the regulation of hunger and satiety.
#5 Is Anorexia Genetic?
https://www.healthline.com/health/eating-disorders/is-anorexia-genetic
Anorexia nervosa is an eating disorder that can cause: […] Today, its clear anorexia nervosa is the result of a combination of genetic and environmental factors. […] More than 50 percent of the risk of developing an eating disorder is due to genetic factors. […] While doctors once considered it a psychological condition, newer research has revealed that anorexia nervosa might have a significant genetic component. […] Numerous studies have identified specific chromosomes and genes that may be part of the equation. […] This suggests that problems in signaling pathways in your brain may trigger anorexia. […] Research has also found that these gene mutations run in families. […] A first-degree relative is a parent, sibling, or child. Whats more, your risk of developing any eating disorder is higher if you have a relative with anorexia.
#6 Anorexia Nervosa | Abnormal Psychology
https://courses.lumenlearning.com/wm-abnormalpsych/chapter/eating-disorders/
Anorexia nervosa is highly heritable. Twin studies have shown a heritability rate of between 28%58%, with many studies estimating the heritability of the disorder in the higher range, above 50%. First-degree relatives of those with anorexia have roughly 12 times the risk of developing anorexia. Some studies have shown some associations between anorexia and 43 different genes that are connected to regulating eating behavior, motivation, reward mechanics, personality, and emotion. Epigenetic modifications, such as DNA methylation, may contribute to the development or maintenance of anorexia nervosa, though clinical research in this area is in its infancy. […] Neuroendocrine dysregulation, or altered signaling of peptides that facilitate communication between the gut, brain, and adipose tissue, such as ghrelin, leptin, neuropeptide Y, and orexin, may contribute to the pathogenesis of anorexia nervosa by disrupting the regulation of hunger and satiety.
#7 Pathogenesis of anorexia nervosa. – Document – Gale Academic OneFile
https://go.gale.com/ps/i.do?id=GALE%7CA169678973&sid=googleScholar&v=2.1&it=r&linkaccess=abs&issn=10262121&p=AONE&sw=w
This paper provides a recent review of studies investigating the eating disorder anorexia nervosa, with a view to summarising current knowledge on the pathogenesis of this condition. […] A comprehensive theory of pathogenesis would need to encompass biological, developmental, psychodynamic, familial, and cultural perspectives. […] There is strong evidence supporting a genetic basis to AN. […] Data from 2 of 3 large scale population-based twin studies also support a genetic basis for AN. […] They found a higher pairwise concordance rate for broadly defined AN among MZ twins (15%) than among DZ twins (7%).
#8 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
Anorexia nervosa (AN) is an intriguing disorder. Its incidence is increasing in the West, and it is among the most lethal of all psychiatric disorders. It seems to selectively affect young, intelligent, attractive women of higher social standing. A comprehensive theory of pathogenesis would need to encompass biological, developmental, psychodynamic, familial, and cultural perspectives. This article summarises current knowledge concerning the pathogenesis of AN. […] There is strong evidence supporting a genetic basis to AN. Three studies have specifically addressed this aspect by studying twin pairs in a clinical setting. In the first study of 34 twin pairs and 1 set of triplets, pairwise concordance rates of AN were much higher among monozgyotic (MZ) than dizygotic (DZ) twins (55% vs 7%). In the second study of a further 15 female twin pairs, a significant difference between MZ and DZ twins was again found (71% vs 10%). A later German study of 25 twin pairs also reported a similar difference in concordance rates between MZ and DZ twins (57% vs 9%) with respect to AN.
#9 Anorexia Nervosa | Abnormal Psychology
https://courses.lumenlearning.com/wm-abnormalpsych/chapter/eating-disorders/
Anorexia nervosa is highly heritable. Twin studies have shown a heritability rate of between 28%58%, with many studies estimating the heritability of the disorder in the higher range, above 50%. First-degree relatives of those with anorexia have roughly 12 times the risk of developing anorexia. Some studies have shown some associations between anorexia and 43 different genes that are connected to regulating eating behavior, motivation, reward mechanics, personality, and emotion. Epigenetic modifications, such as DNA methylation, may contribute to the development or maintenance of anorexia nervosa, though clinical research in this area is in its infancy. […] Neuroendocrine dysregulation, or altered signaling of peptides that facilitate communication between the gut, brain, and adipose tissue, such as ghrelin, leptin, neuropeptide Y, and orexin, may contribute to the pathogenesis of anorexia nervosa by disrupting the regulation of hunger and satiety.
#10 Is Anorexia Genetic?
https://www.healthline.com/health/eating-disorders/is-anorexia-genetic
If serotonin is not in balance, it may result in eating disorders, anxiety, or depression. […] If dopamine levels are irregular, it could cause food aversion, weight loss, and even menstrual dysfunction. […] People with low vitamin D3 levels are more likely to have fatigue, depression, and metabolic disorders. […] An imbalance in these hormones can affect reward mechanisms in your brain and make food less desirable. […] If these receptors are blocked or interrupted, you may not feel energized or fulfilled by food intake. […] Recent research has identified eight gene locations that might play a role in developing an eating disorder. […] These two genes, ESRRA and HDAC4, increase a persons chance of developing an eating disorder by 90 and 85 percent, respectively. […] Blockages or interruptions in the appetite pathways may impact how a person interprets hunger.
#11 Is Anorexia Genetic?
https://www.healthline.com/health/eating-disorders/is-anorexia-genetic
If serotonin is not in balance, it may result in eating disorders, anxiety, or depression. […] If dopamine levels are irregular, it could cause food aversion, weight loss, and even menstrual dysfunction. […] People with low vitamin D3 levels are more likely to have fatigue, depression, and metabolic disorders. […] An imbalance in these hormones can affect reward mechanisms in your brain and make food less desirable. […] If these receptors are blocked or interrupted, you may not feel energized or fulfilled by food intake. […] Recent research has identified eight gene locations that might play a role in developing an eating disorder. […] These two genes, ESRRA and HDAC4, increase a persons chance of developing an eating disorder by 90 and 85 percent, respectively. […] Blockages or interruptions in the appetite pathways may impact how a person interprets hunger.
#12 Researchers Identify the Neurological Mechanism Behind Anorexia Nervosa
https://www.pharmacytimes.com/view/researchers-identify-the-neurological-mechanism-behind-anorexia-nervosa
The researchers identified a decrease in ACh caused by a genetic mutation called VGLUT3-p.T81 in the VGLUT3 gene, leading to the excessive habit formation causing self-starvation in patients with AN. […] The identification of VGLUT3-p.T81 provides valuable insights into the neurological mechanisms underlying AN and its connection with other disorders, such as SUD and EDs.
#13 Anorexia Nervosa | Treatment & Management | Point of Care
https://www.statpearls.com/point-of-care/17626
Studies demonstrate biological factors play a role in the development of anorexia nervosa in addition to environmental factors. […] Patients with anorexia nervosa have altered brain function and structure there are deficits in neurotransmitters dopamine (eating behavior and reward) and serotonin (impulse control and neuroticism), differential activation of the corticolimbic system (appetite and fear), and diminished activity among the frontostriatal circuits (habitual behaviors). […] Patients have co-morbid psychiatric disorders such as major depressive disorder and generalized anxiety disorder.
#14 Anorexia Nervosa | Treatment & Management | Point of Care
https://www.statpearls.com/point-of-care/17626
Studies demonstrate biological factors play a role in the development of anorexia nervosa in addition to environmental factors. […] Patients with anorexia nervosa have altered brain function and structure there are deficits in neurotransmitters dopamine (eating behavior and reward) and serotonin (impulse control and neuroticism), differential activation of the corticolimbic system (appetite and fear), and diminished activity among the frontostriatal circuits (habitual behaviors). […] Patients have co-morbid psychiatric disorders such as major depressive disorder and generalized anxiety disorder.
#15 The Neurobiology of Anorexia Nervosa | IntechOpen
https://www.intechopen.com/chapters/64858
The serotonin system includes at least 14 different receptors. The 5-HT1A and 5-HT2A receptors appear most influential in the pathogenesis of AN. […] Given etiological research on the separate roles of dopamine and serotonin, it is not surprising that the most recent research suggests that interactions between serotonin and dopamine activity truly elicit and maintain the eating pathology of AN. […] The etiology of AN is multifaceted, with contributions from genetic factors, biological factors, family dynamics, personality characteristics, and sociocultural influences. […] The development of this disorder and its maintenance remain poorly understood despite a significant increase in rigorous scientific study into risk factors and shared vulnerabilities with other eating disorders and psychological disorders.
#16 Anorexia Nervosa | Treatment & Management | Point of Care
https://www.statpearls.com/point-of-care/17626
Studies demonstrate biological factors play a role in the development of anorexia nervosa in addition to environmental factors. […] Patients with anorexia nervosa have altered brain function and structure there are deficits in neurotransmitters dopamine (eating behavior and reward) and serotonin (impulse control and neuroticism), differential activation of the corticolimbic system (appetite and fear), and diminished activity among the frontostriatal circuits (habitual behaviors). […] Patients have co-morbid psychiatric disorders such as major depressive disorder and generalized anxiety disorder.
#17 Anorexia Nervosa | Treatment & Management | Point of Care
https://www.statpearls.com/point-of-care/17626
Studies demonstrate biological factors play a role in the development of anorexia nervosa in addition to environmental factors. […] Patients with anorexia nervosa have altered brain function and structure there are deficits in neurotransmitters dopamine (eating behavior and reward) and serotonin (impulse control and neuroticism), differential activation of the corticolimbic system (appetite and fear), and diminished activity among the frontostriatal circuits (habitual behaviors). […] Patients have co-morbid psychiatric disorders such as major depressive disorder and generalized anxiety disorder.
#18 Neurobiological model of the persistence of anorexia nervosa | Journal of Eating Disorders | Full Text
https://jeatdisord.biomedcentral.com/articles/10.1186/s40337-016-0106-2
Studies of reward systems in adolescence have also shown increased salience of rewards. […] Indeed, several reward-centered models of the pathophysiology of AN have emerged. […] A range of disturbances in dorsal frontostriatal systems has been described in AN. […] These data have yielded several models proposing frontostriatal dysfunction in AN. […] As these behaviors are learned through reinforcement, the mesolimbic reward system is highly relevant for understanding the development and persistence of AN. […] A key prediction of the habit model of AN is that restrictive intake in AN is associated with activity in the dorsal striatum. […] This study also yielded intriguing behavioral findings that demonstrate the complex relationship between self-control and habit in maladaptive eating behavior.
#19 A treatment for anorexia nervosa? | Channels – McGill University
https://www.mcgill.ca/channels/channels/news/treatment-anorexia-nervosa-357901
A McGill University-led research team working in collaboration with a French team (CNRS, INSERM and Sorbonne university) believes it has identified both the neurological mechanism underlying anorexia nervosa as well as a possible cure. […] Working with mice, the researchers discovered that a deficit in the acetylcholine, a neurotransmitter in an area of the brain called the striatum, which is associated with the reward system, can lead to excessive habit formation and precipitate the compulsive self-starvation seen in people who suffer from anorexia nervosa. […] We found that it fully reversed the anorexia-like behaviour in mice, and we believe that it could potentially offer the first mechanism-based treatment of anorexia nervosa.
#20 Reddit – The heart of the internet
https://www.reddit.com/r/science/comments/1f3i4p3/researchers_have_discovered_the_neurological/
Researchers have discovered the neurological mechanism behind anorexia nervosa in mice: it’s a deficit in acetylcholine, a neurotransmitter in a brain region known as the striatum.
#21 Backstage of Eating DisorderâAbout the Biological Mechanisms behind the Symptoms of Anorexia Nervosa
https://www.mdpi.com/2072-6643/12/9/2604
Brain neuropeptides together with monoamine systems, especially serotoninergic and dopaminergic, are of most interest in AN, yet our understanding of the pathophysiologic role of those systems in patients is still rather limited. […] A disturbance of brain serotoninergic networks predates the onset of AN, and should contribute to premorbid symptoms of anxiety, inhibition, and a vulnerability for restricted eating. […] However, there is only minimal to moderate evidence that available psychiatric medications are effective. […] According to literature, up to 40â80% of AN patients also show excessive levels of physical activity. […] Thus, hyperactivity, defined as rigorous physical activity combined with a compulsive need to exercise, plays a fundamental role in the development and maintenance of AN, may precede food restriction and accelerate body weight loss once food restriction has been initiated, and obviously interferes with the recovery process, and has been reported as one of the predictive factors of a higher risk of relapse after recovery.
#22 The Neurobiology of Anorexia Nervosa | IntechOpen
https://www.intechopen.com/chapters/64858
The serotonin system includes at least 14 different receptors. The 5-HT1A and 5-HT2A receptors appear most influential in the pathogenesis of AN. […] Given etiological research on the separate roles of dopamine and serotonin, it is not surprising that the most recent research suggests that interactions between serotonin and dopamine activity truly elicit and maintain the eating pathology of AN. […] The etiology of AN is multifaceted, with contributions from genetic factors, biological factors, family dynamics, personality characteristics, and sociocultural influences. […] The development of this disorder and its maintenance remain poorly understood despite a significant increase in rigorous scientific study into risk factors and shared vulnerabilities with other eating disorders and psychological disorders.
#23 Anorexia nervosa pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Anorexia_nervosa_pathophysiology
There are strong correlations (but not proven causation) between the neurotransmitter serotonin and various psychological symptoms such as mood, sleep, emesis (vomiting), sexuality and appetite. A recent review of the scientific literature has suggested that anorexia is linked to a disturbed serotonin system, particularly to high levels at areas in the brain with the 5HT1A receptor – a system particularly linked to anxiety, mood and impulse control. […] Recent studies also suggest anorexia may be linked to an autoimmune response to melanocortin peptides which influence appetite and stress responses. […] Zinc deficiency causes a decrease in appetite that can degenerate in anorexia nervosa (AN), appetite disorders and, notably, inadequate zinc nutriture. […] Anorexic eating behavior is thought to originate from feelings of fatness and unattractiveness and is maintained by various cognitive biases that alter how the affected individual evaluates and thinks about their body, food and eating.
#24 Researchers Identify the Neurological Mechanism Behind Anorexia Nervosa
https://www.pharmacytimes.com/view/researchers-identify-the-neurological-mechanism-behind-anorexia-nervosa
Acetylcholine deficit observed in patients with anorexia nervosa suggest potential targeted treatment options. […] Researchers may have identified the underlying neurological mechanism causing anorexia nervosa (AN), according to a study conducted in mice. Their findings suggest that an imbalance in dopamine activity in the dorsal striatum may be a shared factor for substance use disorders (SUDs) and eating disorders (EDs), such as AN, deepening the clinical understanding of the condition and paving pathways to a potential cure. […] The study focused on the dorsal striatum, a region of the brain that is a part of the basal ganglia. The dorsal striatum is involved in the transition from reward-guided, goal-directed behaviors to habitual behaviors, which can eventually lead to compulsion.
#25 Pharmacological Management of Treatment-Resistant Anorexia Nervosa
https://www.psychiatrictimes.com/view/pharmacological-management-of-treatment-resistant-anorexia-nervosa
What may account for this possible difference between olanzapine and aripiprazole in AN? Olanzapine as well as most other current atypical antipsychotics, including quetiapine and risperidone is a 5-HT2A/D2 antagonist. Aripiprazole, in contrast, is a D2 and 5-HT1A partial agonist, meaning it acts differently at dopamine and serotonin receptors. Theoretical arguments have addressed how use of aripiprazole at lower doses (typically, 1-5 mg/d, with occasional titration up to 10 mg/d) may facilitate learning and behavior change in individuals with AN. […] Moreover, neurobiological research suggests that AN is associated with heightened responsiveness in brain reward circuits, which may be due to a hypersensitive dopamine system. Aripiprazole may downregulate D2 receptor activity, which may improve brain function, reduce anxiety, and aid in the psychotherapeutic process.
#26 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Anorexia nervosa (AN) is a persistent psychiatric disorder that is marked by abnormal reduced weight and amenorrhea, which may be primary or secondary. AN affects multiple endocrine axes such as gonadal, thyroid, and adrenal axis, growth hormone, and insulin-like growth factor-1, adipokines such as leptin, gut peptides like ghrelin, peptide YY, and amylin. […] As a result of these changes bone mineral density is reduced, which increases the risk of bone fracture in patients. […] Although the majority of AN-related endocrinopathies improve over time, long-term consequences such as short stature, osteoporosis, and infertility may occur. […] AN affects bones and the pituitary glands negatively due to starvation and malnutrition. […] These contribute to abnormalities in bone metabolism resulting in low bone mass, impaired bone microarchitecture, and increased risk for fracture.
#27 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Anorexia nervosa (AN) is a persistent psychiatric disorder that is marked by abnormal reduced weight and amenorrhea, which may be primary or secondary. AN affects multiple endocrine axes such as gonadal, thyroid, and adrenal axis, growth hormone, and insulin-like growth factor-1, adipokines such as leptin, gut peptides like ghrelin, peptide YY, and amylin. […] As a result of these changes bone mineral density is reduced, which increases the risk of bone fracture in patients. […] Although the majority of AN-related endocrinopathies improve over time, long-term consequences such as short stature, osteoporosis, and infertility may occur. […] AN affects bones and the pituitary glands negatively due to starvation and malnutrition. […] These contribute to abnormalities in bone metabolism resulting in low bone mass, impaired bone microarchitecture, and increased risk for fracture.
#28 Anorexia stems from body as well as mind â study
https://www.bbc.com/news/health-48989359
The origins of the eating disorder anorexia nervosa are in both the mind and the body, according to an international study. […] But doctors at King’s College London showed changes hardwired into some people’s DNA altered the way they processed fats and sugars and may make it easier to starve their bodies. […] The study, published in Nature Genetics, found some mutations also presented in other psychiatric disorders such obsessive-compulsive disorder, anxiety, and schizophrenia. […] But they also found mutations in the instructions that control the body’s metabolism, particularly those involving blood sugar levels and body fat. […] The researchers – at King’s and the University of North Carolina at Chapel Hill – say anorexia should now be considered a „metabo-psychiatric disorder” as it is a disease of mind and body.
#29 Is Anorexia Genetic?
https://www.healthline.com/health/eating-disorders/is-anorexia-genetic
One twin study found that monozygotic twins are more likely to share an anorexia diagnosis than twins born of separate eggs. […] To help understand which genes may be responsible, genome-wide association studies (GWAS) have compared the genes of thousands of people with anorexia nervosa to the genes of those without. […] These genes, as well as some of the others identified by researchers, are involved in signaling your brains appetite. […] These same areas are also related to other health issues, such as anxiety and depression. […] Still, researchers believe hundreds of genes in your chromosomes significantly affect eating disorder development. […] Some researchers call anorexia a metabo-psychiatric illness. That means it has both metabolic and psychiatric causes. […] The metabolic causes may be due to interruptions in the pathways that control several functions in the body.
#30 Anorexia stems from body as well as mind â study
https://www.bbc.com/news/health-48989359
However, they suspect the mutations allow people to starve their bodies for longer. […] „It’s possible that when people lose weight with anorexia nervosa, they haven’t got such strong drivers getting the set-point back to normal.” […] „Now, we know it’s a complex mixture of aspects from the body and the mind that interact and cause this complex disorder.”
#31 A Brief Review of the Biology of Anorexia Nervosa – MedCrave online
https://medcraveonline.com/JPCPY/a-brief-review-of-the-biology-of-anorexia-nervosa.html
Linkage analysis have implicated 1p33-36 for AN, 1q31.3 for quantitative behavioral traits related to AN and 10p14 for BN, as well as other behavioral phenotypes across both disorders. […] More recently, GWAS analysis with microsatellite markers has implicated novel candidate loci for AN at 1q41 and 11q22. […] Studies on epigenetic changes in AN have described hypomethylation or a normal degree of methylation of the genes in AN. […] With regard to the appetite regulating hormones, the most consistent finding is a decrease in leptin levels. […] Leptin levels normalize with recovery from AN and thereby, leptin would qualify as a state biomarker in AN. […] The changes in leptin, ghrelin and obestatin may reflect the stress that the body is under suffering during acute or prolonged starvation. […] The findings concerning biomarkers such as NPY and alpha-MSH are conflicting and the number of studies small so any conclusions cannot be drawn.
#32 A Brief Review of the Biology of Anorexia Nervosa – MedCrave online
https://medcraveonline.com/JPCPY/a-brief-review-of-the-biology-of-anorexia-nervosa.html
Linkage analysis have implicated 1p33-36 for AN, 1q31.3 for quantitative behavioral traits related to AN and 10p14 for BN, as well as other behavioral phenotypes across both disorders. […] More recently, GWAS analysis with microsatellite markers has implicated novel candidate loci for AN at 1q41 and 11q22. […] Studies on epigenetic changes in AN have described hypomethylation or a normal degree of methylation of the genes in AN. […] With regard to the appetite regulating hormones, the most consistent finding is a decrease in leptin levels. […] Leptin levels normalize with recovery from AN and thereby, leptin would qualify as a state biomarker in AN. […] The changes in leptin, ghrelin and obestatin may reflect the stress that the body is under suffering during acute or prolonged starvation. […] The findings concerning biomarkers such as NPY and alpha-MSH are conflicting and the number of studies small so any conclusions cannot be drawn.
#33 Possible role of the gut microbiota in the pathogenesis of anorexia nervosa | BioPsychoSocial Medicine | Full Text
https://bpsmedicine.biomedcentral.com/articles/10.1186/s13030-021-00228-9
Anorexia nervosa (AN), an eating disorder, is characterized by extreme weight loss and fear of weight gain. […] Recent evidence has shown that the gut microbiota plays an important role in pathogenesis of neuropsychiatric disorders including AN. […] Recently, the gut microbiota has emerged as an important factor affecting AN pathogenesis. […] Considering the emerging effects of gut microbes on body weight control or behavioral phenotypes, we speculated that commensal bacteria may play an important role in the onset and exacerbation of AN. […] Prolonged physiological and psychological stress, including severe weight loss and extreme dietary habits, may influence the composition of the gut microbiota and subsequently induce gut dysbiosis. […] Several researchers have investigated whether gut dysbiosis exists in the gut of patients with AN and have shown that patients with AN show dysbiosis, abnormal features of gut microbiota.
#34 Possible role of the gut microbiota in the pathogenesis of anorexia nervosa | BioPsychoSocial Medicine | Full Text
https://bpsmedicine.biomedcentral.com/articles/10.1186/s13030-021-00228-9
Anorexia nervosa (AN), an eating disorder, is characterized by extreme weight loss and fear of weight gain. […] Recent evidence has shown that the gut microbiota plays an important role in pathogenesis of neuropsychiatric disorders including AN. […] Recently, the gut microbiota has emerged as an important factor affecting AN pathogenesis. […] Considering the emerging effects of gut microbes on body weight control or behavioral phenotypes, we speculated that commensal bacteria may play an important role in the onset and exacerbation of AN. […] Prolonged physiological and psychological stress, including severe weight loss and extreme dietary habits, may influence the composition of the gut microbiota and subsequently induce gut dysbiosis. […] Several researchers have investigated whether gut dysbiosis exists in the gut of patients with AN and have shown that patients with AN show dysbiosis, abnormal features of gut microbiota.
#35 Possible role of the gut microbiota in the pathogenesis of anorexia nervosa | BioPsychoSocial Medicine | Full Text
https://bpsmedicine.biomedcentral.com/articles/10.1186/s13030-021-00228-9
Anorexia nervosa (AN), an eating disorder, is characterized by extreme weight loss and fear of weight gain. […] Recent evidence has shown that the gut microbiota plays an important role in pathogenesis of neuropsychiatric disorders including AN. […] Recently, the gut microbiota has emerged as an important factor affecting AN pathogenesis. […] Considering the emerging effects of gut microbes on body weight control or behavioral phenotypes, we speculated that commensal bacteria may play an important role in the onset and exacerbation of AN. […] Prolonged physiological and psychological stress, including severe weight loss and extreme dietary habits, may influence the composition of the gut microbiota and subsequently induce gut dysbiosis. […] Several researchers have investigated whether gut dysbiosis exists in the gut of patients with AN and have shown that patients with AN show dysbiosis, abnormal features of gut microbiota.
#36 The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice | Nature Microbiology
https://www.nature.com/articles/s41564-023-01355-5
Anorexia nervosa (AN) is an eating disorder with a high mortality. […] The pathogenesis of AN probably involves genetics and various environmental factors, and an altered gut microbiota has been observed in individuals with AN using amplicon sequencing and relatively small cohorts. […] Here we investigated whether a disrupted gut microbiota contributes to AN pathogenesis. […] Our omics and mechanistic studies imply that a disruptive gut microbiome may contribute to AN pathogenesis. […] It has been hypothesized that an aberrant gut microbiota may be involved in the pathogenesis of AN. […] Here we explored the hypothesis that a perturbed intestinal gut microbiota and serum metabolome contribute to the complex pathogenesis of AN. […] Our findings lend support to the hypothesis that a disrupted AN gut microbiota and associated bacterial metabolites contribute to AN pathogenesis.
#37 The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice | Nature Microbiology
https://www.nature.com/articles/s41564-023-01355-5
This suggests that the gut microbiota in AN-RS has weakened gut viral-bacterial interactions. […] Our studies of the viral gut microbiota in AN showed a partial uncoupling of the ecological interactions between viral species and short-chain producing bacterial species with impact on brain biology. […] In conclusion, the present multi-omics study uncovers profound and complex disruptions of the gut microbiota in individuals with AN, with functional implications and altered serum metabolites. […] These compounds may act via the blood circulation or via gut-microbiota-brain neuronal signalling pathways affecting brain regulation of appetite, emotions and behaviour. […] Our findings lend support to the hypothesis that a severely disrupted intestinal microbiota contributes to some of the stages in the pathogenesis of AN.
#38 The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice | Nature Microbiology
https://www.nature.com/articles/s41564-023-01355-5
This suggests that the gut microbiota in AN-RS has weakened gut viral-bacterial interactions. […] Our studies of the viral gut microbiota in AN showed a partial uncoupling of the ecological interactions between viral species and short-chain producing bacterial species with impact on brain biology. […] In conclusion, the present multi-omics study uncovers profound and complex disruptions of the gut microbiota in individuals with AN, with functional implications and altered serum metabolites. […] These compounds may act via the blood circulation or via gut-microbiota-brain neuronal signalling pathways affecting brain regulation of appetite, emotions and behaviour. […] Our findings lend support to the hypothesis that a severely disrupted intestinal microbiota contributes to some of the stages in the pathogenesis of AN.
#39 Gut Microbiome Changes in Anorexia Nervosa: A Comprehensive Review
https://www.mdpi.com/1873-149X/31/1/6
Our model suggests that an imbalance in gut microbiota composition leads to reduced short-chain fatty acids, contributing to a proinflammatory state in AN, which is also common in other psychiatric comorbidities. Microbial changes may also contribute to the semistarvation state through endocrine changes and altered energy utilization. […] However, we acknowledge that reduced butyrate is not a finding specific to AN alone, as it is also observed in AN patients with depression or anxiety. There is a growing body of evidence to show that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, similar to our speculation on the proinflammatory state in AN pathogenesis. […] The contribution of Methanobrevibacter smithii to the semistarvation of AN is supported by Million et al., who observed a negative correlation between BMI and Methanobrevibacter smithii.
#40 What Is Anorexia Nervosa? | Eating Disorders Victoria
https://eatingdisorders.org.au/eating-disorders-a-z/anorexia-nervosa/
Anorexia nervosa is a mental illness that has serious physical, emotional and social impacts. Anorexia nervosa is characterised by body image distortion with an obsessive fear of gaining weight, which manifests itself through depriving the body of food. It often coincides with increased levels of exercise. […] There is no single cause of anorexia nervosa, but there are risk factors that increase the likelihood of it developing. These can be biological, psychological and social. […] Evidence tells us that anorexia nervosa has a moderate-high genetic heritability. Ongoing research into this field is analysing hundreds of genes that may influence the chance of developing an eating disorder with the hope of improving treatment and even preventing illness. […] Some psychological risks for anorexia nervosa encompass feelings of inadequacy, personality traits of perfectionism and anxiety, a fear or avoidance of conflict, low self-esteem, competitiveness, and impulsive or obsessive behaviours.
#41 What Is Anorexia Nervosa? | Eating Disorders Victoria
https://eatingdisorders.org.au/eating-disorders-a-z/anorexia-nervosa/
Anorexia nervosa is a mental illness that has serious physical, emotional and social impacts. Anorexia nervosa is characterised by body image distortion with an obsessive fear of gaining weight, which manifests itself through depriving the body of food. It often coincides with increased levels of exercise. […] There is no single cause of anorexia nervosa, but there are risk factors that increase the likelihood of it developing. These can be biological, psychological and social. […] Evidence tells us that anorexia nervosa has a moderate-high genetic heritability. Ongoing research into this field is analysing hundreds of genes that may influence the chance of developing an eating disorder with the hope of improving treatment and even preventing illness. […] Some psychological risks for anorexia nervosa encompass feelings of inadequacy, personality traits of perfectionism and anxiety, a fear or avoidance of conflict, low self-esteem, competitiveness, and impulsive or obsessive behaviours.
#42 Anorexia nervosa pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Anorexia_nervosa_pathophysiology
Research into the neuropsychology of anorexia has indicated that many of the findings are inconsistent across studies and that it is hard to differentiate the effects of starvation on the brain from any long-standing characteristics. Nevertheless, one reasonably reliable finding is that those with anorexia have poor cognitive flexibility. […] Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialised nations, particularly through the media. A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia.
#43 Anorexia Nervosa: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/912187-overview
The impact of anorexia nervosa on neuropsychological functioning has been found to include what are likely estrogen-mediated impairments in learning and memory tasks, such as cognitive inflexibility (poor set shifting), weak central coherence, and social-emotional processing difficulties that may in part be due to low energy intake causing lack of available energy. […] Persistent states of starvation may result in biochemically based treatment resistance due to neuroadaptive changes including increases in angiopoetin-like protein 6 (ANGPTL6) that occur that increase the likelihood that anorexia nervosa will become chronic and persistent.
#44 Learned industriousness as a translational mechanism in anorexia nervosa | Nature Reviews Psychology
https://www.nature.com/articles/s44159-022-00134-z
It remains unexplained why some behaviours persist despite being non-hedonic and ostensibly aversive. […] Anorexia nervosa is one psychiatric disorder in which effortful behaviours that most people find unpleasant (such as restrictive eating) are persistently performed. […] We propose that the social psychology theory of learned industriousness provides a novel mechanistic account for such phenomena. […] This theory posits that high-effort behaviour can be conditioned to acquire secondary reinforcing properties through repeated pairing with reward. […] Accordingly, effort sensations become less aversive and more appetitive, increasing willingness to engage in effortful behaviour. […] In this Perspective, we review pre-clinical behavioural and biological data that support learned industriousness, contrast learned industriousness with other models of non-hedonic persistence (such as habit learning), highlight evidence that supports learned industriousness in individuals with anorexia nervosa and consider implications of the model, including translation to other psychiatric presentations.
#45 Anorexia nervosa in adults and adolescents: Medical complications and their management – UpToDate
https://www.uptodate.com/contents/anorexia-nervosa-in-adults-and-adolescents-medical-complications-and-their-management
Anorexia nervosa is associated with numerous general medical complications that are directly attributable to weight loss and malnutrition. The complications involve most major organ systems and often include physiologic disturbances such as hypotension, bradycardia, hypothermia, and amenorrhea. Medical complications account for approximately half of all deaths in anorexia nervosa, which has one of the highest mortality rates of any psychiatric disorder. […] The medical complications of low weight in anorexia nervosa and the management of these complications are reviewed here. The evaluation for medical complications and criteria for hospitalizing patients with anorexia nervosa; epidemiology and pathogenesis; clinical features, assessment, and diagnosis; treatment of anorexia nervosa; and the refeeding syndrome are discussed separately.
#46 Anorexia Nervosa – Psychiatric Disorders – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/psychiatric-disorders/eating-disorders/anorexia-nervosa
Anorexia nervosa is characterized by a relentless pursuit of thinness, a morbid fear of obesity, a distorted body image, and restriction of intake relative to requirements, leading to a significantly low body weight. […] The etiology of anorexia nervosa is unknown. […] Family and social factors probably play a role. […] Endocrine abnormalities are common in anorexia nervosa; they include low levels of gonadal hormones, mildly reduced levels of thyroxine (T4) and triiodothyronine (T3), and increased cortisol secretion. […] Cardiac muscle mass, chamber size, and output decrease; mitral valve prolapse is commonly detected. […] Endocrine or electrolyte abnormalities or cardiac arrhythmias may develop, and death can occur.
#47 Anorexia Nervosa – Psychiatric Disorders – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/psychiatric-disorders/eating-disorders/anorexia-nervosa
Anorexia nervosa is characterized by a relentless pursuit of thinness, a morbid fear of obesity, a distorted body image, and restriction of intake relative to requirements, leading to a significantly low body weight. […] The etiology of anorexia nervosa is unknown. […] Family and social factors probably play a role. […] Endocrine abnormalities are common in anorexia nervosa; they include low levels of gonadal hormones, mildly reduced levels of thyroxine (T4) and triiodothyronine (T3), and increased cortisol secretion. […] Cardiac muscle mass, chamber size, and output decrease; mitral valve prolapse is commonly detected. […] Endocrine or electrolyte abnormalities or cardiac arrhythmias may develop, and death can occur.
#48 Medical complications of anorexia nervosa | Cleveland Clinic Journal of Medicine
https://www.ccjm.org/content/87/6/361
Anorexia nervosa is a mental illness characterized by self-starvation, marked weight loss, and malnutrition. As the illness worsens, numerous medical complications develop throughout the body. Some of these resolve with effective nutritional rehabilitation and weight gain, whereas others can lead to permanent damage. […] The etiology of AN is complex, with many genetic, psychological, environmental, and social variables at play. Patients who have a first-degree relative with AN, for example, have a 10-fold greater risk of having the illness themselves. […] Myocardial atrophy, the structural hallmark of this disease, is characterized by a reduction in left ventricular mass index and an attendant decrease in left ventricular volume. […] Mitral valve prolapse is common in AN. Although its mechanism has not been fully elucidated, it is thought to be a consequence of myocardial atrophy and reduced left ventricular chamber size leading to relative valvular laxity even in the absence of myxomatous valve degeneration.
#49 Medical complications of anorexia nervosa | Cleveland Clinic Journal of Medicine
https://www.ccjm.org/content/87/6/361
Anorexia nervosa is a mental illness characterized by self-starvation, marked weight loss, and malnutrition. As the illness worsens, numerous medical complications develop throughout the body. Some of these resolve with effective nutritional rehabilitation and weight gain, whereas others can lead to permanent damage. […] The etiology of AN is complex, with many genetic, psychological, environmental, and social variables at play. Patients who have a first-degree relative with AN, for example, have a 10-fold greater risk of having the illness themselves. […] Myocardial atrophy, the structural hallmark of this disease, is characterized by a reduction in left ventricular mass index and an attendant decrease in left ventricular volume. […] Mitral valve prolapse is common in AN. Although its mechanism has not been fully elucidated, it is thought to be a consequence of myocardial atrophy and reduced left ventricular chamber size leading to relative valvular laxity even in the absence of myxomatous valve degeneration.
#50 Medical complications of anorexia nervosa | Cleveland Clinic Journal of Medicine
https://www.ccjm.org/content/87/6/361
The etiology of this exuberant loss of bone mineral density is likely multifactorial and includes elevated cortisol levels, low leptin and sex hormone levels, low body weight, and growth hormone resistance. […] Anorexia nervosa is characterized by marked brain atrophy on brain imaging studies. Particular areas of the brain seem to be preferentially damaged, including both gray and white matter and areas of the insula and thalamus.
#51 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Anorexia nervosa (AN) is a persistent psychiatric disorder that is marked by abnormal reduced weight and amenorrhea, which may be primary or secondary. AN affects multiple endocrine axes such as gonadal, thyroid, and adrenal axis, growth hormone, and insulin-like growth factor-1, adipokines such as leptin, gut peptides like ghrelin, peptide YY, and amylin. […] As a result of these changes bone mineral density is reduced, which increases the risk of bone fracture in patients. […] Although the majority of AN-related endocrinopathies improve over time, long-term consequences such as short stature, osteoporosis, and infertility may occur. […] AN affects bones and the pituitary glands negatively due to starvation and malnutrition. […] These contribute to abnormalities in bone metabolism resulting in low bone mass, impaired bone microarchitecture, and increased risk for fracture.
#52 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Anorexia nervosa (AN) is a persistent psychiatric disorder that is marked by abnormal reduced weight and amenorrhea, which may be primary or secondary. AN affects multiple endocrine axes such as gonadal, thyroid, and adrenal axis, growth hormone, and insulin-like growth factor-1, adipokines such as leptin, gut peptides like ghrelin, peptide YY, and amylin. […] As a result of these changes bone mineral density is reduced, which increases the risk of bone fracture in patients. […] Although the majority of AN-related endocrinopathies improve over time, long-term consequences such as short stature, osteoporosis, and infertility may occur. […] AN affects bones and the pituitary glands negatively due to starvation and malnutrition. […] These contribute to abnormalities in bone metabolism resulting in low bone mass, impaired bone microarchitecture, and increased risk for fracture.
#53 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Physiological estrogen replacement should be used to improve bone resorption rates and measures of trait anxiety in adolescents with AN. […] The only medication that has been demonstrated to improve BMD in women with AN is recombinant human IGF-I; however, it is not yet permitted for this use. […] Osteopenia is a common and typically long-term complication of AN resulting in clinical fractures and an increased risk of fracture throughout life. […] A study of women with AN in their mid-twenties found that 55% of them had osteopenia and 35% had osteoporosis, with only 15% having a normal BMD at all skeletal locations studied. […] During adolescence, the impact of AN on bone is especially concerning. […] Hypogonadism and later menarchal age are significant contributions to low BMD associated with AN.
#54 Medical complications of anorexia nervosa | Cleveland Clinic Journal of Medicine
https://www.ccjm.org/content/87/6/361
The etiology of this exuberant loss of bone mineral density is likely multifactorial and includes elevated cortisol levels, low leptin and sex hormone levels, low body weight, and growth hormone resistance. […] Anorexia nervosa is characterized by marked brain atrophy on brain imaging studies. Particular areas of the brain seem to be preferentially damaged, including both gray and white matter and areas of the insula and thalamus.
#55 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Physiological estrogen replacement should be used to improve bone resorption rates and measures of trait anxiety in adolescents with AN. […] The only medication that has been demonstrated to improve BMD in women with AN is recombinant human IGF-I; however, it is not yet permitted for this use. […] Osteopenia is a common and typically long-term complication of AN resulting in clinical fractures and an increased risk of fracture throughout life. […] A study of women with AN in their mid-twenties found that 55% of them had osteopenia and 35% had osteoporosis, with only 15% having a normal BMD at all skeletal locations studied. […] During adolescence, the impact of AN on bone is especially concerning. […] Hypogonadism and later menarchal age are significant contributions to low BMD associated with AN.
#56 Medical complications of anorexia nervosa | Cleveland Clinic Journal of Medicine
https://www.ccjm.org/content/87/6/361
The etiology of this exuberant loss of bone mineral density is likely multifactorial and includes elevated cortisol levels, low leptin and sex hormone levels, low body weight, and growth hormone resistance. […] Anorexia nervosa is characterized by marked brain atrophy on brain imaging studies. Particular areas of the brain seem to be preferentially damaged, including both gray and white matter and areas of the insula and thalamus.
#57 Eating Disorders
https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/psychiatry-psychology/eating-disorders/
Biologic and psychosocial factors are implicated in the pathophysiology of eating disorders, but the underlying causes and mechanisms remain unknown. […] Endogenous opioids might contribute to denial of hunger in patients with anorexia nervosa. Some hypothesize that dieting can increase the risk for developing an eating disorder. Increased endorphin levels have been described in patients with bulimia nervosa after purging and may induce feelings of wellbeing. Diminished norepinephrine turnover and activity are suggested by reduced levels of 3-methoxy-4-hydroxyphenylglycol in the urine and cerebrospinal fluid of some patients with anorexia nervosa. Antidepressants often benefit patients with bulimia nervosa and support a pathophysiologic role for serotonin and norepinephrine. […] Starvation results in many biochemical changes such as hypercortisolemia, nonsuppression of dexamethasone, suppression of thyroid function, and amenorrhea. Several computed tomography studies of the brain have revealed enlarged sulci and ventricles, a finding that is reversed with weight gain. In one study using positron emission tomography, metabolism was higher in the caudate nucleus during the anorectic state than after hyperalimentation.
#58 Eating Disorders
https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/psychiatry-psychology/eating-disorders/
Biologic and psychosocial factors are implicated in the pathophysiology of eating disorders, but the underlying causes and mechanisms remain unknown. […] Endogenous opioids might contribute to denial of hunger in patients with anorexia nervosa. Some hypothesize that dieting can increase the risk for developing an eating disorder. Increased endorphin levels have been described in patients with bulimia nervosa after purging and may induce feelings of wellbeing. Diminished norepinephrine turnover and activity are suggested by reduced levels of 3-methoxy-4-hydroxyphenylglycol in the urine and cerebrospinal fluid of some patients with anorexia nervosa. Antidepressants often benefit patients with bulimia nervosa and support a pathophysiologic role for serotonin and norepinephrine. […] Starvation results in many biochemical changes such as hypercortisolemia, nonsuppression of dexamethasone, suppression of thyroid function, and amenorrhea. Several computed tomography studies of the brain have revealed enlarged sulci and ventricles, a finding that is reversed with weight gain. In one study using positron emission tomography, metabolism was higher in the caudate nucleus during the anorectic state than after hyperalimentation.
#59 Anorexia Nervosa – Psychiatric Disorders – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/psychiatric-disorders/eating-disorders/anorexia-nervosa
Anorexia nervosa is characterized by a relentless pursuit of thinness, a morbid fear of obesity, a distorted body image, and restriction of intake relative to requirements, leading to a significantly low body weight. […] The etiology of anorexia nervosa is unknown. […] Family and social factors probably play a role. […] Endocrine abnormalities are common in anorexia nervosa; they include low levels of gonadal hormones, mildly reduced levels of thyroxine (T4) and triiodothyronine (T3), and increased cortisol secretion. […] Cardiac muscle mass, chamber size, and output decrease; mitral valve prolapse is commonly detected. […] Endocrine or electrolyte abnormalities or cardiac arrhythmias may develop, and death can occur.
#60 Anorexia Nervosa – Psychiatric Disorders – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/psychiatric-disorders/eating-disorders/anorexia-nervosa
Anorexia nervosa is characterized by a relentless pursuit of thinness, a morbid fear of obesity, a distorted body image, and restriction of intake relative to requirements, leading to a significantly low body weight. […] The etiology of anorexia nervosa is unknown. […] Family and social factors probably play a role. […] Endocrine abnormalities are common in anorexia nervosa; they include low levels of gonadal hormones, mildly reduced levels of thyroxine (T4) and triiodothyronine (T3), and increased cortisol secretion. […] Cardiac muscle mass, chamber size, and output decrease; mitral valve prolapse is commonly detected. […] Endocrine or electrolyte abnormalities or cardiac arrhythmias may develop, and death can occur.
#61 Eating Disorders
https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/psychiatry-psychology/eating-disorders/
Biologic and psychosocial factors are implicated in the pathophysiology of eating disorders, but the underlying causes and mechanisms remain unknown. […] Endogenous opioids might contribute to denial of hunger in patients with anorexia nervosa. Some hypothesize that dieting can increase the risk for developing an eating disorder. Increased endorphin levels have been described in patients with bulimia nervosa after purging and may induce feelings of wellbeing. Diminished norepinephrine turnover and activity are suggested by reduced levels of 3-methoxy-4-hydroxyphenylglycol in the urine and cerebrospinal fluid of some patients with anorexia nervosa. Antidepressants often benefit patients with bulimia nervosa and support a pathophysiologic role for serotonin and norepinephrine. […] Starvation results in many biochemical changes such as hypercortisolemia, nonsuppression of dexamethasone, suppression of thyroid function, and amenorrhea. Several computed tomography studies of the brain have revealed enlarged sulci and ventricles, a finding that is reversed with weight gain. In one study using positron emission tomography, metabolism was higher in the caudate nucleus during the anorectic state than after hyperalimentation.
#62 Anorexia Nervosa | Abnormal Psychology
https://courses.lumenlearning.com/wm-abnormalpsych/chapter/eating-disorders/
Anorexia nervosa is highly heritable. Twin studies have shown a heritability rate of between 28%58%, with many studies estimating the heritability of the disorder in the higher range, above 50%. First-degree relatives of those with anorexia have roughly 12 times the risk of developing anorexia. Some studies have shown some associations between anorexia and 43 different genes that are connected to regulating eating behavior, motivation, reward mechanics, personality, and emotion. Epigenetic modifications, such as DNA methylation, may contribute to the development or maintenance of anorexia nervosa, though clinical research in this area is in its infancy. […] Neuroendocrine dysregulation, or altered signaling of peptides that facilitate communication between the gut, brain, and adipose tissue, such as ghrelin, leptin, neuropeptide Y, and orexin, may contribute to the pathogenesis of anorexia nervosa by disrupting the regulation of hunger and satiety.
#63 Anorexia Nervosa: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/912187-overview
A typical case of anorexia nervosa involves a young person (teenager or young adult) who is mildly overweight or of normal weight and who begins a diet and exercise plan to lose weight. As he or she loses weight and receives initial positive reinforcement for this behavior (eg, compliments by peers on his or her appearance), the reward is high and causes an inability to stop this behavior once an ideal weight is achieved. […] Anorexia nervosa may be difficult to resolve due to persistent starvation from abnormal eating behavior resulting in treatment resistance due to the neuroadaptive changes causing increases in angiopoetin-like protein 6 (ANGPTL6) that cause anorexia nervosa to more likely become chronic and persistent. […] Malnutrition subsequent to self-starvation leads to protein deficiency and disruption of multiple organ systems, including the cardiovascular, renal, gastrointestinal, neurologic, endocrine, integumentary, hematologic, and reproductive systems.
#64 Anorexia Nervosa: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/912187-overview
The impact of anorexia nervosa on neuropsychological functioning has been found to include what are likely estrogen-mediated impairments in learning and memory tasks, such as cognitive inflexibility (poor set shifting), weak central coherence, and social-emotional processing difficulties that may in part be due to low energy intake causing lack of available energy. […] Persistent states of starvation may result in biochemically based treatment resistance due to neuroadaptive changes including increases in angiopoetin-like protein 6 (ANGPTL6) that occur that increase the likelihood that anorexia nervosa will become chronic and persistent.
#65 Backstage of Eating DisorderâAbout the Biological Mechanisms behind the Symptoms of Anorexia Nervosa
https://www.mdpi.com/2072-6643/12/9/2604
Brain neuropeptides together with monoamine systems, especially serotoninergic and dopaminergic, are of most interest in AN, yet our understanding of the pathophysiologic role of those systems in patients is still rather limited. […] A disturbance of brain serotoninergic networks predates the onset of AN, and should contribute to premorbid symptoms of anxiety, inhibition, and a vulnerability for restricted eating. […] However, there is only minimal to moderate evidence that available psychiatric medications are effective. […] According to literature, up to 40â80% of AN patients also show excessive levels of physical activity. […] Thus, hyperactivity, defined as rigorous physical activity combined with a compulsive need to exercise, plays a fundamental role in the development and maintenance of AN, may precede food restriction and accelerate body weight loss once food restriction has been initiated, and obviously interferes with the recovery process, and has been reported as one of the predictive factors of a higher risk of relapse after recovery.
#66 Backstage of Eating DisorderâAbout the Biological Mechanisms behind the Symptoms of Anorexia Nervosa
https://www.mdpi.com/2072-6643/12/9/2604
Brain neuropeptides together with monoamine systems, especially serotoninergic and dopaminergic, are of most interest in AN, yet our understanding of the pathophysiologic role of those systems in patients is still rather limited. […] A disturbance of brain serotoninergic networks predates the onset of AN, and should contribute to premorbid symptoms of anxiety, inhibition, and a vulnerability for restricted eating. […] However, there is only minimal to moderate evidence that available psychiatric medications are effective. […] According to literature, up to 40â80% of AN patients also show excessive levels of physical activity. […] Thus, hyperactivity, defined as rigorous physical activity combined with a compulsive need to exercise, plays a fundamental role in the development and maintenance of AN, may precede food restriction and accelerate body weight loss once food restriction has been initiated, and obviously interferes with the recovery process, and has been reported as one of the predictive factors of a higher risk of relapse after recovery.
#67 Backstage of Eating DisorderâAbout the Biological Mechanisms behind the Symptoms of Anorexia Nervosa
https://www.mdpi.com/2072-6643/12/9/2604
The nature of this feature remains uncertain although it was already recognized and described by Gull and LasÃ¨gue in the 19th century. […] Rewarding activation upon reduced energy intake through dopaminergic reinforcing pathways, hypoleptinemia and thermoregulatory compensation due to hypothermia have been hypothesized as the leading causes of hyperactivity but genetic factors regulating activity levels should also contribute to the development of the disease. […] Those rewarding effects, triggering euphoria and dependence, are mediated by an enhanced mesolimbic dopamine release through an activation of the hypothalamoâpituitaryâadrenal axis with high blood cortisol levels due to starvation and/or hyperactivity. […] Thus, the aim of our review was to summarize current concepts regarding pathogenesis and pathomechanisms of AN, such as alterations of brain neurotransmission, including abnormally functioning corticolimbic circuits involved in appetite, fronto-striatal networks together with autonomic nervous system dysfunction as well as the microbiomeâgutâbrain axis and endocrine alterations.
#68 Backstage of Eating DisorderâAbout the Biological Mechanisms behind the Symptoms of Anorexia Nervosa
https://www.mdpi.com/2072-6643/12/9/2604
The nature of this feature remains uncertain although it was already recognized and described by Gull and LasÃ¨gue in the 19th century. […] Rewarding activation upon reduced energy intake through dopaminergic reinforcing pathways, hypoleptinemia and thermoregulatory compensation due to hypothermia have been hypothesized as the leading causes of hyperactivity but genetic factors regulating activity levels should also contribute to the development of the disease. […] Those rewarding effects, triggering euphoria and dependence, are mediated by an enhanced mesolimbic dopamine release through an activation of the hypothalamoâpituitaryâadrenal axis with high blood cortisol levels due to starvation and/or hyperactivity. […] Thus, the aim of our review was to summarize current concepts regarding pathogenesis and pathomechanisms of AN, such as alterations of brain neurotransmission, including abnormally functioning corticolimbic circuits involved in appetite, fronto-striatal networks together with autonomic nervous system dysfunction as well as the microbiomeâgutâbrain axis and endocrine alterations.
#69 Pathogenesis of Anorexia Nervosa
https://www.easap.asia/index.php/find-issues/past-issue/item/647-0103-v11n3-an-7-12
This paper provides a recent review of studies investigating the eating disorder anorexia nervosa, with a view to summarising current knowledge on the pathogenesis of this condition. […] A comprehensive theory of pathogenesis would need to encompass biological, developmental, psychodynamic, familial, and cultural perspectives. […] There is strong evidence supporting a genetic basis to AN. […] Studies of twins suggest that there is a genetic basis to AN. […] The Minnesota Study convincingly demonstrated that prolonged semi-starvation can lead to the development of abnormal eating behaviors. […] The most common antecedent to AN is dieting. […] At least 6 longitudinal studies have been conducted to explore the role of dieting in the pathogenesis of AN. […] Clearly not all dieters become individuals with an eating disorder.
#70 Pathogenesis of Anorexia Nervosa
https://www.easap.asia/index.php/find-issues/past-issue/item/647-0103-v11n3-an-7-12
Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. […] In summary, the findings with regard to family functioning and AN are conflicting. […] Any theory explaining the pathogenesis of AN must address why the disorder is so much more prevalent among women than men. […] At this point in our understanding of AN, a coherent theory of its pathogenesis is elusive. […] However, available data suggest that a young woman with a family history of eating disorder, depression, or obsessive compulsive disorder, living within a culture that emphasises thinness, may be more likely to develop AN if she embarks on a rigorous diet to lose weight.
#71 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
At least 6 longitudinal studies have been conducted to explore the role of dieting in the pathogenesis of AN. Five of these have been the subject of a previous review, and are summarised only briefly here. Clearly not all dieters become individuals with an eating disorder. In fact, the majority of dieters will never develop an eating disorder. Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. Family therapy has been found to be effective treatment for recent onset AN in young patients but this cannot be used to infer that family factors may be pathogenetic. Recent research, however, has produced no major new findings, and more often than not findings are conflicting or unconvincing.
#72 The Role of the Family in the Pathogenesis of Anorexia Nervosa | SpringerLink
https://link.springer.com/chapter/10.1007/978-1-4684-4697-5_77
Already before the first studies about the family in schizophrenics appeared (Alanen 1958; Lidz 1958; Fleck 1960) some authors had called our attention on certain pecularities that repeated themselves notoriously in the families of the anorexics (A.Dhrssen 1950; Bleuler 1954). […] Most of the authors have ascribed to the personality of the mother a very special role for the pathogenesis. […] Otherwise, Jeammet (1973), Massing (1974) and we (1976) have pointed out the great importance of the fathers function for developing an Anorexia Nervosa. […] Finally, the School of Goettingen, West-Germany (Meyer, Sperling, Massing, Beckers) always has insisted in the peculiar existence of a powerful grandmother within these families.
#73 The Role of the Family in the Pathogenesis of Anorexia Nervosa | SpringerLink
https://link.springer.com/chapter/10.1007/978-1-4684-4697-5_77
Already before the first studies about the family in schizophrenics appeared (Alanen 1958; Lidz 1958; Fleck 1960) some authors had called our attention on certain pecularities that repeated themselves notoriously in the families of the anorexics (A.Dhrssen 1950; Bleuler 1954). […] Most of the authors have ascribed to the personality of the mother a very special role for the pathogenesis. […] Otherwise, Jeammet (1973), Massing (1974) and we (1976) have pointed out the great importance of the fathers function for developing an Anorexia Nervosa. […] Finally, the School of Goettingen, West-Germany (Meyer, Sperling, Massing, Beckers) always has insisted in the peculiar existence of a powerful grandmother within these families.
#74 Pathogenesis of Anorexia Nervosa
https://www.easap.asia/index.php/find-issues/past-issue/item/647-0103-v11n3-an-7-12
Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. […] In summary, the findings with regard to family functioning and AN are conflicting. […] Any theory explaining the pathogenesis of AN must address why the disorder is so much more prevalent among women than men. […] At this point in our understanding of AN, a coherent theory of its pathogenesis is elusive. […] However, available data suggest that a young woman with a family history of eating disorder, depression, or obsessive compulsive disorder, living within a culture that emphasises thinness, may be more likely to develop AN if she embarks on a rigorous diet to lose weight.
#75 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
At least 6 longitudinal studies have been conducted to explore the role of dieting in the pathogenesis of AN. Five of these have been the subject of a previous review, and are summarised only briefly here. Clearly not all dieters become individuals with an eating disorder. In fact, the majority of dieters will never develop an eating disorder. Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. Family therapy has been found to be effective treatment for recent onset AN in young patients but this cannot be used to infer that family factors may be pathogenetic. Recent research, however, has produced no major new findings, and more often than not findings are conflicting or unconvincing.
#76 Pathogenesis of Anorexia Nervosa
https://www.easap.asia/index.php/find-issues/past-issue/item/647-0103-v11n3-an-7-12
This paper provides a recent review of studies investigating the eating disorder anorexia nervosa, with a view to summarising current knowledge on the pathogenesis of this condition. […] A comprehensive theory of pathogenesis would need to encompass biological, developmental, psychodynamic, familial, and cultural perspectives. […] There is strong evidence supporting a genetic basis to AN. […] Studies of twins suggest that there is a genetic basis to AN. […] The Minnesota Study convincingly demonstrated that prolonged semi-starvation can lead to the development of abnormal eating behaviors. […] The most common antecedent to AN is dieting. […] At least 6 longitudinal studies have been conducted to explore the role of dieting in the pathogenesis of AN. […] Clearly not all dieters become individuals with an eating disorder.
#77 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
Although these population twin studies have major methodological flaws, the findings do lend support for the role of genetic factors in the pathogenesis of AN. What could be genetically transmitted to make an individual vulnerable to the development of AN? There are a range of possibilities to consider in this regard. The disorder itself could be transmitted similar to other conditions such as neurofibromatosis. However, it is unlikely that AN is the result of a single, dominant gene inheritance pattern, and such direct inheritance would still leave unexplained the biological mechanisms producing extreme dieting behaviour, and the characteristic mental attitude of weight phobia. […] The Minnesota Study convincingly demonstrated that prolonged semi-starvation can lead to the development of abnormal eating behaviors. The most common antecedent to AN is dieting. An initial desire to lose a few pounds is soon overtaken by an obsessive desire to lose weight. Being able to lose weight and be thin is seen and felt to be good, such that gradually the dieting and weight loss come to be perceived or experienced as being in control, or being the only solution to life’s problems.
#78 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
Although these population twin studies have major methodological flaws, the findings do lend support for the role of genetic factors in the pathogenesis of AN. What could be genetically transmitted to make an individual vulnerable to the development of AN? There are a range of possibilities to consider in this regard. The disorder itself could be transmitted similar to other conditions such as neurofibromatosis. However, it is unlikely that AN is the result of a single, dominant gene inheritance pattern, and such direct inheritance would still leave unexplained the biological mechanisms producing extreme dieting behaviour, and the characteristic mental attitude of weight phobia. […] The Minnesota Study convincingly demonstrated that prolonged semi-starvation can lead to the development of abnormal eating behaviors. The most common antecedent to AN is dieting. An initial desire to lose a few pounds is soon overtaken by an obsessive desire to lose weight. Being able to lose weight and be thin is seen and felt to be good, such that gradually the dieting and weight loss come to be perceived or experienced as being in control, or being the only solution to life’s problems.
#79 Pathogenesis of Anorexia Nervosa
https://www.easap.asia/index.php/find-issues/past-issue/item/647-0103-v11n3-an-7-12
Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. […] In summary, the findings with regard to family functioning and AN are conflicting. […] Any theory explaining the pathogenesis of AN must address why the disorder is so much more prevalent among women than men. […] At this point in our understanding of AN, a coherent theory of its pathogenesis is elusive. […] However, available data suggest that a young woman with a family history of eating disorder, depression, or obsessive compulsive disorder, living within a culture that emphasises thinness, may be more likely to develop AN if she embarks on a rigorous diet to lose weight.
#80 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
At least 6 longitudinal studies have been conducted to explore the role of dieting in the pathogenesis of AN. Five of these have been the subject of a previous review, and are summarised only briefly here. Clearly not all dieters become individuals with an eating disorder. In fact, the majority of dieters will never develop an eating disorder. Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. Family therapy has been found to be effective treatment for recent onset AN in young patients but this cannot be used to infer that family factors may be pathogenetic. Recent research, however, has produced no major new findings, and more often than not findings are conflicting or unconvincing.
#81 Anorexia Nervosa | Abnormal Psychology
https://courses.lumenlearning.com/wm-abnormalpsych/chapter/eating-disorders/
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 when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self-perpetuating cycle. […] Anorexia nervosa is more likely to occur during puberty. Some explanatory hypotheses for the rising prevalence of eating disorders in adolescence are increase of adipose tissue in girls, hormonal changes of puberty, societal expectations of increased independence and autonomy that are particularly difficult for anorexic adolescents to meet; [and] increased influence of the peer group and its values.
#82 Eating disorders: Overview of epidemiology, clinical features, and diagnosis – UpToDate
https://www.uptodate.com/contents/eating-disorders-overview-of-epidemiology-clinical-features-and-diagnosis
Sociocultural pressure for thinness may contribute to onset of eating disorders. Jednak te zaburzenia sÄ coraz czÄÅciej rozumiane jako majÄce biologiczne podstawy wynikajÄce z interakcji indywidualnej podatnoÅci genetycznej i czynnikÃ³w Årodowiskowych. […] W dodatku, fizjologiczne konsekwencje gÅodzenia i zaburzonego zachowania Å¼ywieniowego, zakÅÃ³cenia w nagradzajÄcych i apetytowych obwodach nerwowych oraz nawykowe i warunkowe reakcje uczenia siÄ sÄ uznawane za istotne czynniki przyczyniajÄce siÄ do kompulsywnej natury tych zaburzeÅ.
#83 Anorexia nervosa pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Anorexia_nervosa_pathophysiology
Research into the neuropsychology of anorexia has indicated that many of the findings are inconsistent across studies and that it is hard to differentiate the effects of starvation on the brain from any long-standing characteristics. Nevertheless, one reasonably reliable finding is that those with anorexia have poor cognitive flexibility. […] Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialised nations, particularly through the media. A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia.
#84 Anorexia nervosa pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Anorexia_nervosa_pathophysiology
Research into the neuropsychology of anorexia has indicated that many of the findings are inconsistent across studies and that it is hard to differentiate the effects of starvation on the brain from any long-standing characteristics. Nevertheless, one reasonably reliable finding is that those with anorexia have poor cognitive flexibility. […] Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialised nations, particularly through the media. A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia.
#85 What Is Anorexia Nervosa? | Eating Disorders Victoria
https://eatingdisorders.org.au/eating-disorders-a-z/anorexia-nervosa/
The cultural emphasis on thinness or smaller bodies as a moral and health imperative, along with the normalisation of intentional dieting, contributes to the valuation of individuals based on outward appearance. […] Anorexia nervosa can affect the functioning of the entire body. […] One of the defining features of anorexia nervosa is often a belief that behaviors, such as restricting food intake or engaging in excessive exercise, are rational and necessary. […] Treatment for anorexia nervosa is rarely a one-size-fits-all approach. It can involve working with a range of health professionals and trying several different approaches. […] Accessing treatment requires navigating different parts of the health care system. Treatment options are available in both the public and private health system.
#86 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
Any theory explaining the pathogenesis of AN must address why the disorder is so much more prevalent among women than men. The majority of published studies have found a female to male preponderance of about 10:1. Many clinicians and researchers have suggested that the process of psychological development places some individuals at risk for the development of an eating disorder. […] At this point in our understanding of AN, a coherent theory of its pathogenesis is elusive. However, available data suggest that a young woman with a family history of eating disorder, depression, or obsessive compulsive disorder, living within a culture that emphasises thinness, may be more likely to develop AN if she embarks on a rigorous diet to lose weight, particularly if rigorous dieting arises from low self esteem.
#87 Anorexia Nervosa: Symptoms, Causes, and Treatments
https://www.healthline.com/health/anorexia-nervosa
The exact cause of anorexia nervosa isnt known. People who develop anorexia may have a negative body image. They may be focused on being perfect. They may be looking for ways to control their lives. Other factors like biology, environment, and psychology are believed to play a role. […] Genetics and hormones might have an effect on the development of anorexia nervosa. Some evidence suggests a link between anorexia and serotonin, a chemical produced in the brain. […] Pressure from society to look thin may also contribute to the development of anorexia nervosa. Unrealistic body images from media outlets like magazines and television can greatly influence young people and spark the desire to be thin. […] Someone with obsessive-compulsive disorder (OCD) might be more predisposed to maintaining the strict diet and exercise regimen that those with anorexia nervosa often maintain. Thats because people with OCD are prone to obsessions and compulsions.
#88 Anorexia Nervosa: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/912187-overview
A typical case of anorexia nervosa involves a young person (teenager or young adult) who is mildly overweight or of normal weight and who begins a diet and exercise plan to lose weight. As he or she loses weight and receives initial positive reinforcement for this behavior (eg, compliments by peers on his or her appearance), the reward is high and causes an inability to stop this behavior once an ideal weight is achieved. […] Anorexia nervosa may be difficult to resolve due to persistent starvation from abnormal eating behavior resulting in treatment resistance due to the neuroadaptive changes causing increases in angiopoetin-like protein 6 (ANGPTL6) that cause anorexia nervosa to more likely become chronic and persistent. […] Malnutrition subsequent to self-starvation leads to protein deficiency and disruption of multiple organ systems, including the cardiovascular, renal, gastrointestinal, neurologic, endocrine, integumentary, hematologic, and reproductive systems.
#89 Pathogenesis of Anorexia Nervosa – ProQuest
https://www.proquest.com/scholarly-journals/pathogenesis-anorexia-nervosa/docview/2791682695/se-2
Any theory explaining the pathogenesis of AN must address why the disorder is so much more prevalent among women than men. The majority of published studies have found a female to male preponderance of about 10:1. Many clinicians and researchers have suggested that the process of psychological development places some individuals at risk for the development of an eating disorder. […] At this point in our understanding of AN, a coherent theory of its pathogenesis is elusive. However, available data suggest that a young woman with a family history of eating disorder, depression, or obsessive compulsive disorder, living within a culture that emphasises thinness, may be more likely to develop AN if she embarks on a rigorous diet to lose weight, particularly if rigorous dieting arises from low self esteem.
#90 Pathogenesis of Anorexia Nervosa
https://www.easap.asia/index.php/find-issues/past-issue/item/647-0103-v11n3-an-7-12
Nevertheless, 5 of the 6 longitudinal studies strongly suggest that dieting behaviour places an individual at higher risk for the development of an eating disorder. […] The idea that specific family dysfunction may lead to AN has been advanced by many authors. […] In summary, the findings with regard to family functioning and AN are conflicting. […] Any theory explaining the pathogenesis of AN must address why the disorder is so much more prevalent among women than men. […] At this point in our understanding of AN, a coherent theory of its pathogenesis is elusive. […] However, available data suggest that a young woman with a family history of eating disorder, depression, or obsessive compulsive disorder, living within a culture that emphasises thinness, may be more likely to develop AN if she embarks on a rigorous diet to lose weight.
#91 The Neurobiology of Anorexia Nervosa | IntechOpen
https://www.intechopen.com/chapters/64858
The serotonin system includes at least 14 different receptors. The 5-HT1A and 5-HT2A receptors appear most influential in the pathogenesis of AN. […] Given etiological research on the separate roles of dopamine and serotonin, it is not surprising that the most recent research suggests that interactions between serotonin and dopamine activity truly elicit and maintain the eating pathology of AN. […] The etiology of AN is multifaceted, with contributions from genetic factors, biological factors, family dynamics, personality characteristics, and sociocultural influences. […] The development of this disorder and its maintenance remain poorly understood despite a significant increase in rigorous scientific study into risk factors and shared vulnerabilities with other eating disorders and psychological disorders.
#92 The Neurobiology of Anorexia Nervosa | IntechOpen
https://www.intechopen.com/chapters/64858
Anorexia nervosa is considered the most deadly psychological illness. […] A better understanding of the biological and neurobiological etiology of anorexia nervosa is direly needed to inform new therapies and to identify individuals at risk for the disorder. This paper summarizes the research related to neurotransmitter abnormalities, aberrant brain activity, and genetic and epigenetic mechanisms that may contribute to the etiology of this deadly disorder. […] Many of the neurobiological phenomena to be discussed in this paper are present premorbidly, exaggerated by malnutrition, and return to premorbid levels after recovery. […] There are currently promising lines of research on dopaminergic, serotonergic, and noradrenergic pathways, as well as dysregulations in appetitive functioning, genetic and epigenetic contributions, contributions from gonadal hormones, and aberrations in brain activity.
#93 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Anorexia nervosa (AN) is a persistent psychiatric disorder that is marked by abnormal reduced weight and amenorrhea, which may be primary or secondary. AN affects multiple endocrine axes such as gonadal, thyroid, and adrenal axis, growth hormone, and insulin-like growth factor-1, adipokines such as leptin, gut peptides like ghrelin, peptide YY, and amylin. […] As a result of these changes bone mineral density is reduced, which increases the risk of bone fracture in patients. […] Although the majority of AN-related endocrinopathies improve over time, long-term consequences such as short stature, osteoporosis, and infertility may occur. […] AN affects bones and the pituitary glands negatively due to starvation and malnutrition. […] These contribute to abnormalities in bone metabolism resulting in low bone mass, impaired bone microarchitecture, and increased risk for fracture.
#94 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Estrogen reduces the activity of the receptor activator of nuclear factor k-B ligand (RANKL) and limits the release of proinflammatory cytokines through increasing osteoprotegerin (OPG). […] Higher sclerostin levels are related to increased bone turnover indicators in controls but this association is interrupted in AN. […] Nutritional rehabilitation and behavioral support for bodyweight maintenance are essential and should be the cornerstones of AN treatment. […] AN is a primary psychiatric disorder characterized by severe endocrine disorders and severe bone loss. […] Currently, there are no FDA-approved medications for low BMD treatment in anorexia nervosa; therefore, weight gain and menstruation recovery remain the most effective strategy to increase BMD.
#95 Anorexia stems from body as well as mind â study
https://www.bbc.com/news/health-48989359
However, they suspect the mutations allow people to starve their bodies for longer. […] „It’s possible that when people lose weight with anorexia nervosa, they haven’t got such strong drivers getting the set-point back to normal.” […] „Now, we know it’s a complex mixture of aspects from the body and the mind that interact and cause this complex disorder.”
#96 Neurobiological model of the persistence of anorexia nervosa | Journal of Eating Disorders | Full Text
https://jeatdisord.biomedcentral.com/articles/10.1186/s40337-016-0106-2
This line of research attempts to leverage advances in the field of cognitive neuroscience to further our understanding of persistent maladaptive choices of individuals with AN, in the hope that such advances will help in the development of novel treatments for this potentially fatal disorder. […] A better understanding of the neural underpinnings of AN may help to develop novel treatments and improve outcomes for these severely ill individuals. […] The findings described above demonstrate that the salient behavioral disturbance of individuals with AN is the selection of low-calorie foods in a remarkably stereotyped fashion that promotes persistence of illness. […] A logical and important next step is to ask what drives this behavior neurobiologically. […] The functioning of reward systems in AN is likely impacted by both food restriction and adolescence itself.
#97 A treatment for anorexia nervosa? | Channels – McGill University
https://www.mcgill.ca/channels/channels/news/treatment-anorexia-nervosa-357901
A McGill University-led research team working in collaboration with a French team (CNRS, INSERM and Sorbonne university) believes it has identified both the neurological mechanism underlying anorexia nervosa as well as a possible cure. […] Working with mice, the researchers discovered that a deficit in the acetylcholine, a neurotransmitter in an area of the brain called the striatum, which is associated with the reward system, can lead to excessive habit formation and precipitate the compulsive self-starvation seen in people who suffer from anorexia nervosa. […] We found that it fully reversed the anorexia-like behaviour in mice, and we believe that it could potentially offer the first mechanism-based treatment of anorexia nervosa.
#98 A treatment for anorexia nervosa? | Channels – McGill University
https://www.mcgill.ca/channels/channels/news/treatment-anorexia-nervosa-357901
A McGill University-led research team working in collaboration with a French team (CNRS, INSERM and Sorbonne university) believes it has identified both the neurological mechanism underlying anorexia nervosa as well as a possible cure. […] Working with mice, the researchers discovered that a deficit in the acetylcholine, a neurotransmitter in an area of the brain called the striatum, which is associated with the reward system, can lead to excessive habit formation and precipitate the compulsive self-starvation seen in people who suffer from anorexia nervosa. […] We found that it fully reversed the anorexia-like behaviour in mice, and we believe that it could potentially offer the first mechanism-based treatment of anorexia nervosa.
#99 Possible role of the gut microbiota in the pathogenesis of anorexia nervosa | BioPsychoSocial Medicine | Full Text
https://bpsmedicine.biomedcentral.com/articles/10.1186/s13030-021-00228-9
The theory of autointoxication, which states that toxins generated in the gut exert a negative impact on brain function, inducing depression, anxiety, and other mental diseases, was long regarded as an irrational concept. […] Further developments in this field could elucidate the role of gut microbes in the pathogenesis of eating disorders and further provide a strong rationale for probiotic intervention as a treatment for patients with AN.
#100 Pharmacological Management of Treatment-Resistant Anorexia Nervosa
https://www.psychiatrictimes.com/view/pharmacological-management-of-treatment-resistant-anorexia-nervosa
What may account for this possible difference between olanzapine and aripiprazole in AN? Olanzapine as well as most other current atypical antipsychotics, including quetiapine and risperidone is a 5-HT2A/D2 antagonist. Aripiprazole, in contrast, is a D2 and 5-HT1A partial agonist, meaning it acts differently at dopamine and serotonin receptors. Theoretical arguments have addressed how use of aripiprazole at lower doses (typically, 1-5 mg/d, with occasional titration up to 10 mg/d) may facilitate learning and behavior change in individuals with AN. […] Moreover, neurobiological research suggests that AN is associated with heightened responsiveness in brain reward circuits, which may be due to a hypersensitive dopamine system. Aripiprazole may downregulate D2 receptor activity, which may improve brain function, reduce anxiety, and aid in the psychotherapeutic process.
#101 The Pathophysiology of Anorexia Nervosa in Hypothalamic Endocrine Function and Bone Metabolism
https://pmc.ncbi.nlm.nih.gov/articles/PMC8776521/
Estrogen reduces the activity of the receptor activator of nuclear factor k-B ligand (RANKL) and limits the release of proinflammatory cytokines through increasing osteoprotegerin (OPG). […] Higher sclerostin levels are related to increased bone turnover indicators in controls but this association is interrupted in AN. […] Nutritional rehabilitation and behavioral support for bodyweight maintenance are essential and should be the cornerstones of AN treatment. […] AN is a primary psychiatric disorder characterized by severe endocrine disorders and severe bone loss. […] Currently, there are no FDA-approved medications for low BMD treatment in anorexia nervosa; therefore, weight gain and menstruation recovery remain the most effective strategy to increase BMD.
#102 What Is Anorexia Nervosa? | Eating Disorders Victoria
https://eatingdisorders.org.au/eating-disorders-a-z/anorexia-nervosa/
The cultural emphasis on thinness or smaller bodies as a moral and health imperative, along with the normalisation of intentional dieting, contributes to the valuation of individuals based on outward appearance. […] Anorexia nervosa can affect the functioning of the entire body. […] One of the defining features of anorexia nervosa is often a belief that behaviors, such as restricting food intake or engaging in excessive exercise, are rational and necessary. […] Treatment for anorexia nervosa is rarely a one-size-fits-all approach. It can involve working with a range of health professionals and trying several different approaches. […] Accessing treatment requires navigating different parts of the health care system. Treatment options are available in both the public and private health system.