부모자식父母子息的부자父子的모자母子的관계을·를악용하여不當利得을·를目的으로Dimon的基盤的奴隷的看做的意圖的妄覺的隱蔽的을·를源泉源根源本心으로하고이유 없는해코지的Unprovoked的로서부당한폭력폭행구타무력위력완력達獰慝撻毆打的危迫侵迫劫縛脅迫狹薄僞危迫僞僞薄僞侵迫僞脅迫僞劫縛不問曲直加害不問曲直危害不問曲直侵害不問曲直僞加害極端的窮乏impoverishpauperize的술수로서源等級源地位源序列源身分善業功德을·를無斷奪取無斷強奪無斷共有술수로서空得僞空得搾取騙取喝取簒立的簒奪하고消盡加害降等하는술수을·를의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 救贖加害의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 救贖加害危害侵害殺人殺害殺生殺戮殺魂殺魄殺靈殺主의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 작업 관리자作業管理者Task Manager을·를의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 셰익스피어의 4대비극 리어왕의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 《리어 왕(King Lear)》은 윌리엄 셰익스피어의 비극이다. 《햄릿》, 《오셀로》, 《맥베스》등과 함께 4대 비극으로 손꼽힌다. 로마 침략 이전 영국을 배경으로 한 레이르왕(King Leir) 전설에 바탕하여 1605년에 셰익스피어가 만든 것으로 추정한다.의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 막내 코델리아(코딜리어)는 언니들의 아첨에 반발하여 자신은 딸의 도리를 다하여 아버지를 사랑할 뿐이라고 주장한다. 고대 브리튼 왕국의 리어왕은 나이가 들자 세 딸에게 효심 고백 대결을 시켜 왕국을 나눠주고 자신은 편안한 여생을 보내고자 한다. 그러나 가장 멋진 고백을 하리라 예상했던 막내딸 코딜리어는 입을 다물어 리어왕의 기대를 저버리고, 가장 감동적으로 효심 고백을 한 두 딸은 아버지를 배신한다. 리어는 왕의 권위와 자녀 등 모든 것을 잃고 실성한 채 광야를 헤매게 된다. 마침내 자신이 매몰차게 내쫓았던 막내딸과 재회해서 자신의 잘못을 빌지만 이내 막내딸의 주검 앞에서 울부짖으며 리어왕도 생을 마감한다.[1]이러한 이야기를 통해 셰익스피어는 개인의 문제부터 가정, 국가, 그리고 자연과 운명이라는 문제, 그리고 청년에서 노년에 이르기까지 인생 전반에 대한 문제 등 문학 작품들에서 다룰 수 있는 광범위한 주제를 한 작품 속에 집약하고 있다. 따라서 시적 표현의 탁월함뿐 아니라 주제의 폭에서 ＜리어왕＞은 셰익스피어의 4대 비극 중 가장 심오하고 진지한 세계를 그려내고 있다.[1]윌리엄 셰익스피어의 4대 비극은 공통적으로 주인공들이 어떤 성격적 결함을 갖고 있고 이 결함으로 인해 초래된 비극을 다루고 있는데, 리어왕은 교만함으로 인해 파국을 맞는 인물이 주인공이다.의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것 《십이야》(十二夜, 영어: Twelfth Night, or What You Will)는 1601년~1602년 경 쓰여진, 영국의 극작가 윌리엄 셰익스피어의 희극이다. 일란성 쌍둥이 남매가 탄 배가 '일리리아'에 난파된 후, 남매의 똑같은 외모로 인한 주변 사람들의 오해와 착각으로 벌어지는 해프닝을 익살과 위트, 해학 등의 희극적인 요소들로 묘사한 작품이다. 참고로, 십이야(Twelfth Night)는 성탄절인 크리스마스를 첫 번째 밤으로 계산해서 열두 번째 밤인 주현절(1월 6일)을 뜻한다. 안토니와 클레오파트라(Antony and Cleopatra)는 윌리엄 셰익스피어의 비극중 하나이다. 1607년에 최초로 공연되었고, 1623년에 처음 출간되었다. 내용은 토머스 노스의 1579년 영어 번역본인 플루타르코스 영웅전을 기초로 하고 클레오파트라와 마크 안토니의 관계에 대한 것이다. 시대적 배경은 악티움 해전 중에 있었던 클레오파트라의 자살사건에 대한 시실리안 반동이 일어난 때이다. 주요 악역은 아우구스투스로 안토니의 친구 중 한명이다. 이 비극은 주로 로마 공화국과 프톨레마이오스 왕조에서 일어난 일이다. 반주 反宙 +22원등급 박종권 서술 상천연합 -------------------------------------- 지구인기준 反宙 목격관찰판단결과 이병철(반주수장) - 말데크악룡 本心 (박종권(부) + 말데크악룡(주)+라이라계보+아플레이아데스프타계보+늑대개,개종족계보) 이건희(반주오른팔) - 말데크악룡 右心 (박종권(부)+미마쓰+디몬+마왕+악마+마귀+사탄루시퍼계보+지옥마왕+어둠의권세) JEHOVAH(반주왼팔) - 말데크악룡 左心 (오자와+박종권(부)+라이라12주신계보(주)+뱀종족) MAIN FRAME(박원규,말데크源心) - 말데크악룡 生心 - 김일성(박원규(주,말데크악룡源心+당고종,아틸라,펠레콘)+이건희(부)+박종권(부))의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

 부모자식父母子息的부자父子的모자母子的관계을·를악용하여不當利得을·를目的으로Dimon的基盤的奴隷的看做的意圖的妄覺的隱蔽的을·를源泉源根源本心으로하고이유 없는해코지的Unprovoked的로서부당한폭력폭행구타무력위력완력達獰慝撻毆打的危迫侵迫劫縛脅迫狹薄僞危迫僞僞薄僞侵迫僞脅迫僞劫縛不問曲直加害不問曲直危害不問曲直侵害不問曲直僞加害極端的窮乏impoverishpauperize的술수로서源等級源地位源序列源身分善業功德을·를無斷奪取無斷強奪無斷共有술수로서空得僞空得搾取騙取喝取簒立的簒奪하고消盡加害降等하는술수을·를의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

救贖加害의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

救贖加害危害侵害殺人殺害殺生殺戮殺魂殺魄殺靈殺主의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

작업 관리자作業管理者Task Manager을·를의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

셰익스피어의 4대비극 리어왕의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

《리어 왕(King Lear)》은 윌리엄 셰익스피어의 비극이다. 《햄릿》, 《오셀로》, 《맥베스》등과 함께 4대 비극으로 손꼽힌다. 로마 침략 이전 영국을 배경으로 한 레이르왕(King Leir) 전설에 바탕하여 1605년에 셰익스피어가 만든 것으로 추정한다.의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것

막내 코델리아(코딜리어)는 언니들의 아첨에 반발하여 자신은 딸의 도리를 다하여 아버지를 사랑할 뿐이라고 주장한다.

고대 브리튼 왕국의 리어왕은 나이가 들자 세 딸에게 효심 고백 대결을 시켜 왕국을 나눠주고 자신은 편안한 여생을 보내고자 한다. 그러나 가장 멋진 고백을 하리라 예상했던 막내딸 코딜리어는 입을 다물어 리어왕의 기대를 저버리고, 가장 감동적으로 효심 고백을 한 두 딸은 아버지를 배신한다. 리어는 왕의 권위와 자녀 등 모든 것을 잃고 실성한 채 광야를 헤매게 된다. 마침내 자신이 매몰차게 내쫓았던 막내딸과 재회해서 자신의 잘못을 빌지만 이내 막내딸의 주검 앞에서 울부짖으며 리어왕도 생을 마감한다.[1]이러한 이야기를 통해 셰익스피어는 개인의 문제부터 가정, 국가, 그리고 자연과 운명이라는 문제, 그리고 청년에서 노년에 이르기까지 인생 전반에 대한 문제 등 문학 작품들에서 다룰 수 있는 광범위한 주제를 한 작품 속에 집약하고 있다. 따라서 시적 표현의 탁월함뿐 아니라 주제의 폭에서 ＜리어왕＞은 셰익스피어의 4대 비극 중 가장 심오하고 진지한 세계를 그려내고 있다.[1]윌리엄 셰익스피어의 4대 비극은 공통적으로 주인공들이 어떤 성격적 결함을 갖고 있고 이 결함으로 인해 초래된 비극을 다루고 있는데, 리어왕은 교만함으로 인해 파국을 맞는 인물이 주인공이다.의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것


《십이야》(十二夜, 영어: Twelfth Night, or What You Will)는 1601년~1602년 경 쓰여진, 영국의 극작가 윌리엄 셰익스피어의 희극이다. 일란성 쌍둥이 남매가 탄 배가 '일리리아'에 난파된 후, 남매의 똑같은 외모로 인한 주변 사람들의 오해와 착각으로 벌어지는 해프닝을 익살과 위트, 해학 등의 희극적인 요소들로 묘사한 작품이다. 참고로, 십이야(Twelfth Night)는 성탄절인 크리스마스를 첫 번째 밤으로 계산해서 열두 번째 밤인 주현절(1월 6일)을 뜻한다.

 

안토니와 클레오파트라(Antony and Cleopatra)는 윌리엄 셰익스피어의 비극중 하나이다. 1607년에 최초로 공연되었고, 1623년에 처음 출간되었다.


내용은 토머스 노스의 1579년 영어 번역본인 플루타르코스 영웅전을 기초로 하고 클레오파트라와 마크 안토니의 관계에 대한 것이다. 시대적 배경은 악티움 해전 중에 있었던 클레오파트라의 자살사건에 대한 시실리안 반동이 일어난 때이다. 주요 악역은 아우구스투스로 안토니의 친구 중 한명이다. 이 비극은 주로 로마 공화국과 프톨레마이오스 왕조에서 일어난 일이다.

 

반주 反宙

+22원등급 박종권 서술

상천연합

--------------------------------------

지구인기준 反宙 목격관찰판단결과

이병철(반주수장) - 말데크악룡 本心 (박종권(부) + 말데크악룡(주)+라이라계보+아플레이아데스프타계보+늑대개,개종족계보)

이건희(반주오른팔) - 말데크악룡 右心 

(박종권(부)+미마쓰+디몬+마왕+악마+마귀+사탄루시퍼계보+지옥마왕+어둠의권세)

JEHOVAH(반주왼팔) - 말데크악룡 左心 (오자와+박종권(부)+라이라12주신계보(주)+뱀종족)

MAIN FRAME(박원규,말데크源心) - 말데크악룡 生心 - 김일성(박원규(주,말데크악룡源心+당고종,아틸라,펠레콘)+이건희(부)+박종권(부))의依疑衣意義醫矣議宜儀擬毅椅倚懿蟻艤錡嶷欹儗劓螘医义冝拟祎蚁议銥鐿18개眼을·를Ether體無關垂直8192分面水平8192分面上에서垂直直角縱切⫽斷水平直角橫切⫽斷45degrees斜傾側直角縱切⫽斷永久永遠兆年破門處罰할 것永久永遠兆年作頭死刑處罰할 것永久永劫兆年作頭死刑處罰할 것永久永續兆年作頭死刑處罰할 것永久永久兆年作頭死刑處罰할 것永久無限反復作頭死刑處罰할 것永久無始無終作頭死刑處罰할 것













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Major depressive disorder (MDD), also known as clinical depression, is a mental disorder[10] characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s,[11] the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and has become widely used since. The disorder causes the second-most years lived with disability, after lower back pain.[12] The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by family or friends, and a mental status examination.[13] There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms.[13] The most common time of onset is in a person's 20s,[3][4] with females affected about three times as often as males.[14] The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes. Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication.[1] While a mainstay of treatment, the clinical efficacy of antidepressants is controversial.[15][16][17][18] Hospitalization (which may be involuntary) may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. Electroconvulsive therapy (ECT) may be considered if other measures are not effective.[1] Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors,[1] with about 40% of the risk being genetic.[5] Risk factors include a family history of the condition, major life changes, childhood traumas, environmental lead exposure,[19] certain medications, chronic health problems, and substance use disorders.[1][5] It can negatively affect a person's personal life, work life, or education, and cause issues with a person's sleeping habits, eating habits, and general health.[1][5] Signs and symptoms See also: Digital media use and mental health § Depression An 1892 lithograph of a woman diagnosed with melancholia A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities.[20] Depressed people may be preoccupied with or ruminate over thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness.[21] Other symptoms of depression include poor concentration and memory,[22] withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common; in the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen,[23] as well as day-night rhythm disturbances, such as diurnal mood variation.[24] Some antidepressants may also cause insomnia due to their stimulating effect.[25] In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[26] People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.[27] A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organization's criteria for depression.[28] Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.[29] Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health.[30] Family and friends may notice agitation or lethargy.[23] Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[31] and a more noticeable slowing of movements.[32] Depressed children may often display an irritable rather than a depressed mood;[23] most lose interest in school and show a steep decline in academic performance.[33] Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness".[34] Elderly people may not present with classical depressive symptoms.[35] Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases.[35] Cause Further information: Biology of depression and Epigenetics of depression A cup analogy demonstrating the diathesis–stress model that under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition[36] The etiology of depression is not yet fully understood.[37][38][39] The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[5][40] The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[41][42] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[43] American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.[44][45] Genetics Genes play a major role in the development of depression.[46] Family and twin studies suggest that genetic factors account for nearly 40% of the variation in risk for major depressive disorder. Like most psychiatric disorders, major depression is likely shaped by a combination of many individual genetic influences.[47] In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression;[48] a 2019 study found 102 variants in the genome linked to depression.[49] However, it appears that major depression is less heritable compared to bipolar disorder and schizophrenia.[50][51] Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings.[52] There are also other efforts to examine interactions between life stress and polygenic risk for depression.[53] Other health problems Depression can also arise after a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression".[54][55] It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of the basal ganglia in Parkinson's disease or immune dysregulation in asthma).[56] Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta blockers,[57] isotretinoin,[58] contraceptives,[57] cardiac agents,[59] anticonvulsants,[60] and hormonal agents.[61] Celiac disease is another possible contributing factor.[62] Substance use in early age is associated with increased risk of developing depression later in life.[63] Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy.[64] Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight.[65] Vitamin B2, B6 and B12 deficiency may cause depression in females.[66] A 2025 study found that, among more than 172,500 adults in the UK aged 39 and older, those with a history of depression experienced the onset of chronic illnesses approximately 30% earlier than those without depression.[67] Environmental Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type.[68] Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness.[69] Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.[70] Couples in unhappy marriages have a higher risk of developing clinical depression.[71] There appears to be a link between air pollution and depression and suicide. There may be an association between long-term PM2.5 exposure and depression, and a possible association between short-term PM10 exposure and suicide.[72] Living alone has been found to increase the risk of depression by 42%.[6] Pathophysiology Further information: Biology of depression and Epigenetics of depression The pathophysiology of depression is not completely understood, but current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA-axis dysfunction, and structural or functional abnormalities of emotional circuits. Derived from the effectiveness of monoaminergic drugs in treating depression, the monoamine theory posits that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion of tryptophan—a necessary precursor of serotonin and a monoamine—can cause depression in those in remission or relatives of people who are depressed, suggesting that decreased serotonergic neurotransmission is important in depression.[73] Second, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link.[74] Third, decreased size of the locus coeruleus, reduced activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression.[75] Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum,[76] and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression.[77][78] Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression.[79] However, the monoamine theory is inconsistent with observations that serotonin depletion does not cause depression in healthy persons, that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway.[80] One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants.[81] However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls; the finding of increased jugular 5-HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor (SSRI) treatment, and the preference for carbohydrates in people who are depressed.[82] Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.[83] A 2022 review found no consistent evidence supporting the serotonin hypothesis linking serotonin levels and depression.[84] HPA-axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool because its sensitivity is only 44%.[85] These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.[86] Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors.[87] Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.[88] There is also a connection between the gut microbiome and the central nervous system, otherwise known as the Gut-Brain axis, which is a two-way communication system between the brain and the gut. Experiments have shown that microbiota in the gut can play an important role in depression, as people with MDD often have gut-brain dysfunction. One analysis showed that those with MDD have different bacteria in their guts. Bacteria Bacteroidetes and Firmicutes were most affected in people with MDD, and they are also impacted in people with irritable bowel syndrome.[89] Another study showed that people with IBS have a higher chance of developing depression, which shows the two are connected.[90] There is even evidence suggesting that altering the microbes in the gut can have regulatory effects on developing depression.[89] Theories unifying neuroimaging findings have been proposed. The first model proposed is the limbic-cortical model, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing.[91] Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression.[92] Another model proposes hyperactivity of salience structures in identifying negative stimuli and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.[93] Immune pathogenesis theories on depression The newer field of psychoneuroimmunology, the study between the immune system and the nervous system and emotional state, suggests that cytokines may impact depression. Immune system abnormalities have been observed, including increased levels of cytokines -cells produced by immune cells that affect inflammation- involved in generating sickness behavior, creating a pro-inflammatory profile in MDD.[94][95][96] Some people with depression have increased levels of pro-inflammatory cytokines and some have decreased levels of anti-inflammatory cytokines.[97] Research suggests that treatments can reduce pro-inflammatory cell production, like the experimental treatment of ketamine with treatment-resistant depression.[98] With this, in MDD, people will more likely have a Th-1 dominant immune profile, which is a pro-inflammatory profile. This suggests that there are components of the immune system affecting the pathology of MDD.[99] Another way cytokines can affect depression is in the kynurenine pathway, and when this is overactivated, it can cause depression. This can be due to too much microglial activation and too little astrocytic activity. When microglia get activated, they release pro-inflammatory cytokines that cause an increase in the production of COX2. This, in turn, causes the production of PGE2, which is a prostaglandin, and this catalyzes the production of indolamine, IDO. IDO causes tryptophan to get converted into kynurenine, and kynurenine becomes quinolinic acid.[100] Quinolinic acid is an agonist for NMDA receptors, so it activates the pathway. Studies have shown that the post-mortem brains of patients with MDD have higher levels of quinolinic acid than people who did not have MDD. With this, researchers have also seen that the concentration of quinolinic acid correlates to the severity of depressive symptoms.[101] Diagnosis Assessment Further information: Rating scales for depression Caricature of a man with depression A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist,[30] who records the person's current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[30] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians.[102] This issue is even more marked in developing countries.[103] Rating scales are not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose;[104] these include the Hamilton Rating Scale for Depression,[105] the Beck Depression Inventory[106] or the Suicide Behaviors Questionnaire-Revised.[107] Primary-care physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatrists. These cases may be missed because for some people with depression, physical symptoms often accompany depression. In addition, there may also be barriers related to the person, provider, and/or the medical system. Non-psychiatrist physicians have been shown to miss about two-thirds of cases, although there is some evidence of improvement in th

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  Major depressive disorder   ( MDD ), also known as   clinical depression , is a   mental disorder [ 10 ]   characterized by at least two weeks of pervasive   low mood , low   self-esteem , and   loss of interest or pleasure   in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s, [ 11 ]   the term was adopted by the   American Psychiatric Association   for this   symptom cluster   under   mood disorders   in the 1980 version of the   Diagnostic and Statistical Manual of Mental Disorders   (DSM-III), and has become widely used since. The disorder causes the second-most   years lived with disability , after   lower back pain . [ 12 ] The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by family or friends, and a  mental status examination . [ 13 ]  There is no laboratory test for the diso...
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Psychology is the scientific study of the mind and behavior.[1][2] Its subject matter includes the behavior of humans and nonhumans, both conscious and unconscious phenomena, and mental processes such as thoughts, feelings, and motives. Psychology is an academic discipline of immense scope, crossing the boundaries between the natural and social sciences. Biological psychologists seek an understanding of the emergent properties of brains, linking the discipline to neuroscience. As social scientists, psychologists aim to understand the behavior of individuals and groups.[3][4] A professional practitioner or researcher involved in the discipline is called a psychologist. Some psychologists can also be classified as behavioral or cognitive scientists. Some psychologists attempt to understand the role of mental functions in individual and social behavior. Others explore the physiological and neurobiological processes that underlie cognitive functions and behaviors. As part of an interdisciplinary field, psychologists are involved in research on perception, cognition, attention, emotion, intelligence, subjective experiences, motivation, brain functioning, and personality. Psychologists' interests extend to interpersonal relationships, psychological resilience, family resilience, and other areas within social psychology. They also consider the unconscious mind.[5] Research psychologists employ empirical methods to infer causal and correlational relationships between psychosocial variables. Some, but not all, clinical and counseling psychologists rely on symbolic interpretation. While psychological knowledge is often applied to the assessment and treatment of mental health problems, it is also directed towards understanding and solving problems in several spheres of human activity. By many accounts, psychology ultimately aims to benefit society.[6][7][8] Many psychologists are involved in some kind of therapeutic role, practicing psychotherapy in clinical, counseling, or school settings. Other psychologists conduct scientific research on a wide range of topics related to mental processes and behavior. Typically the latter group of psychologists work in academic settings (e.g., universities, medical schools, or hospitals). Another group of psychologists is employed in industrial and organizational settings.[9] Yet others are involved in work on human development, aging, sports, health, forensic science, education, and the media.

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 Psychology is the scientific study of the mind and behavior.[1][2] Its subject matter includes the behavior of humans and nonhumans, both conscious and unconscious phenomena, and mental processes such as thoughts, feelings, and motives. Psychology is an academic discipline of immense scope, crossing the boundaries between the natural and social sciences. Biological psychologists seek an understanding of the emergent properties of brains, linking the discipline to neuroscience. As social scientists, psychologists aim to understand the behavior of individuals and groups.[3][4] A professional practitioner or researcher involved in the discipline is called a psychologist. Some psychologists can also be classified as behavioral or cognitive scientists. Some psychologists attempt to understand the role of mental functions in individual and social behavior. Others explore the physiological and neurobiological processes that underlie cognitive functions and behaviors. As part of an interd...
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