韓国人固有の遺伝子変異の圧倒的大部分はヒトの精神に関連している

要 旨

①2014年事実上はアメリカ政府食品医薬品局（ＦＤＡ）が執筆した朝鮮人を対象として分析した集団遺伝学論文の付属資料にて、地理的に近い日本人、北方系中国人が有さず、朝鮮人のみが有する固有の遺伝子変異 が生じている遺伝子リストがエクセルファイル形式で公表されています。

記事筆者が、長時間かけて、個別に手作業で調べたところ、朝鮮人固有の遺伝子変異のほぼ全てが、 何んらかの精神疾患（うつ病等）・パーソナリティー障害(間欠性爆発障害)などの 疾患感受性遺伝子であり、一言で言えば、ヒトの精神に関連する遺伝子変異でした。

イントロダクション

韓国は、金大中氏がノーベル平和賞を受賞した以外にはノーベル賞受賞者ゼロであることは良く知られています。しかし、記事筆者が、2018年に調べたところ、ノーベル賞はいうまでもなく、 ガウス賞（数学）、ボルツマン賞（物理学）、ロベルト・コッホ賞(医学)等々全63もの国際的に有名な自然科学関連賞について、韓国には受賞者がただの一人もいないことを発見しました。
この疑いようもない客観的事実は、記事筆者をして、朝鮮人（注①）は、日本人・中国人とは異なり精神面でかなり特異な人々ではなかろうか？との疑念を生じせしめ、（注②）朝鮮人ＤＮＡに関する集団遺伝学論文を調べるきっかけとなりました。 そして、韓国人集団遺伝学者が引用したがらない下記のアメリカ政府食品医薬品局（ＦＤＡ）が執筆した論文を見つけ出しました。 英文を読める方は、methods以外の部分を是非ご自身で直接読まれることを心よりお願い申し上げます。（論文であり、機械翻訳では読めません。とにかくご自分で読まれることがなによりも重要です。それで「彼らの本質」が分かります）

Whole genome sequencing of 35 individuals provides insights into the genetic architecture of Korean population



上記ＦＤＡ論文にて、エクセル形式で朝鮮人固有の遺伝子変異が生じているリストが付属資料として公開されています

記事筆者は、上記の朝鮮人固有の遺伝子変異が生じている遺伝子について、NCBI (The National Center for Biotechnology Information )で表示されてくる論文を参照しつつ、基本的には手作業でGoogle論文検索で長時間かけて調べました。 具体的には、CSMD1（遺伝子名）＋mental、CSMD1（遺伝子名）＋GWAS、CSMD1（遺伝子名）＋cognitive等々でグーグルの論文検索をする方法です。

結 果

additional_file_7.xlsx中から朝鮮人固有の遺伝子変異の数が300以上又は特筆すべき遺伝子に限定して個々の遺伝子を手作業で調べた結果が下記の通りです。

(1)DNA中で韓国人固有の変異が生じている遺伝子の圧倒的大部分が、何らかの精神疾患、パーソナリティー障害の疾患感受性遺伝子候補でした。 ただし、記事筆者が調べた範囲では、統合失調症とうつ病については、韓国の生涯有病率は日本と明確な差はないように思えます。（うつ病については論文により数値が異なり、統合失調症に関してはほぼ確実に日本と同様です。）

また、韓国人の場合、現生人類だけが有しているNOTCH2NL遺伝子に代表されるようにヒトの頭脳全般（ヒトの精神面での進化）に関連する遺伝子について 変異が数量ベースで見れば明確に集中していました。

下記に掲げた遺伝子について、韓国人は、地理的に近い日本人・北方系中国人が有していない韓国人固有の、韓国人だけの変異を有しているのだという点をご理解ください。

(2)ただし、病理遺伝学論文は、Ａという論文で、遺伝子名〇〇〇が疾病名〇〇〇と関連がありそうだとする病理遺伝学論文が出された後、 しばらくすると、関連性は薄いという別の論文が出されるケースが多い点にはくれぐれもご留意ください。

(3)RBFOX1遺伝子（paper[125]）及びPTPRD遺伝子（paper[127]）について、韓国人はサンプル数35名でそれぞれ1,272及び1,084の韓国人固有の変異を大量に有しています。
paper[125]及びpaper[127]が、正しいのであれば、韓国人固有の変異は、ほぼすべてが何らかの精神疾患・パーソナリティー障害の疾患感受性遺伝子候補であるにとどまらず、 脳のシナプス及びその接着状態(synaptic adhesion)そのものが、他の民族集団とは異なるようです。 脳のシナプスは、一般的には放出される神経伝達物質の種類の違いにより，興奮性と抑制性の2種類に大別されると思われますが、ほとんど未解明であり今後の研究の進展により数百年後には、明らかになるかもしれません。

(4)論文名は、この記事最下部に記載しています

①＝遺伝子名
②＝FDA論文が抽出した韓国人に固有の遺伝子変異数(additional_file_7.xlsx中のSNV1)
③＝知的障害、精神疾患、パーソナリティー障害等の名称

なお、paper[144] の付属資料中の遺伝子リストにより、遺伝子の長さ（単位：bp）≒遺伝子の塩基数と韓国人固有の変異数（塩基数）が比例関係にないことは確認済みです
（例）PRIM2遺伝子は、長さ4,668(bp)、5033の韓国人固有の変異、MAGI2遺伝子は、長さ31,624(bp)で506の韓国人固有の変異

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①	②	③
PRIM2	5033	DNAプライマーゼをコードしている （NCBI） 不眠症 paper[86] 統合失調症 paper[103]
CSMD1 最重要 100% 確実 SNV35＝1	1786	統合失調症 paper[9] paper[52] paper[115] paper[116] paper[141] paper[142] paper[148] paper[165] paper[170] 170のサンプルは日本人 双極性障害 paper[66] paper[148] paper[165] 健常者男性知的機能全般 rs10503253置換変異 paper[116] 抜粋メモはこのページ 自閉症 paper[137] 高齢健常者の認知能力 paper[138] 脳の扁桃体（社会的・感情的な行動）rs10105357変異 paper[139] rs10503253 ①統合失調症（患者）②健常者の場合には記憶・学習能力 paper[140]
snoU13 =snoRNA	1731	うつ病, 不眠症？ paper[43] snoU13　1989年発見
PDE4DIP	1374	精神障害全般 paper[4] うつ病, paper[91] （脳の神経細胞間）シナプスへの影響 paper[173]
RBFOX1 重要 100％ 確実	1272	知能 paper[168] 168論文はサンプル数30万以上GWAS論文 paper[169] 不眠症 paper[161] 自閉症 paper[165] 怒り、他者への攻撃性、行為障害、自閉症 paper[100] 統合失調症、精神機能全般 paper[5] paper[167] うつ病、統合失調症、神経症傾向 paper[121] パーソナリティー、アルコール依存症（攻撃性については否定） paper[122] 注意欠陥多動性障害 paper[123] 攻撃的な行動 paper[124] 統合失調症 (the neuronspecific RNA splicing regulator) paper[125]極めて重要な抜粋メモ その他関連論文多数
PTPRN2	1224	間欠性爆発障害 paper[99] うつ病 paper[6] 統合失調症、注意欠陥多動性障害 paper[126]
KMT2C	1091	知能 paper[159] 双極性障害 paper[7] paper[130] 統合失調症 paper[128]   うつ病 paper[129]
PTPRD 重要 100％確実	1084	不眠症 paper[161] 知能 paper[159] paper[168] 注意欠陥多動性障害 paper[165] 双極性障害 paper[165] 強迫性障害 paper[8] paper[165] paper[127] 統合失調症　synaptic adhesion paper[125] 脳細胞の結合＝シナプスの態様決定。例示的に、知的障害・不安症・強迫性障害 paper[127] 自閉症 paper[137] 強迫性障害 paper[143]
LINC00842	1008	該当なし 非コード領域
CNTNAP2	940	知的障害、自閉症 paper[109] 統合失調症 paper[10] paper[165] 精神障害全般、言語発達障害 paper[131]
ROBO2	932	統合失調症 うつ病 paper [13] 自閉症 paper [117]
ZNF717	859	知的障害 paper[14] 精神神経症候群  paper[93] 頭脳 paper[94] 自閉症 paper[132]
CROCC	844	該当なし
AF146191	800	不眠症 paper[101]
LSAMP	800	不眠症 paper[161] 自殺傾向 paper[15] 双極性障害 paper[165]
WWOX	797	精神薄弱 paper[81] 自閉症 paper[165]
DLG2	789	統合失調症 paper[5]
GUSBP1	760	該当なし
EYS	759	統合失調症 paper[5] 双極性障害 paper[160]
ANKRD30BL	730	該当なし
PCDHA1 ～ PCDHA14	710	統合失調症 paper[166]
MACROD2	693	知能 paper[168] paper[169] 自閉症 paper[165] 双極性障害 paper[5] うつ病 paper[158]
DPP6	681	神経発達症群 paper[89]
LRP1B	677	知能 paper[159] 認知機能 paper[5] 統合失調症 paper[165]
TPTE	664	知能 paper[159] うつ病リスク paper[110]
ANKRD36C	653	該当なし アルツハイマー病のみあり。＝ＭＲＩ診断＝精神疾患扱いではない paper[112]
PCDH15	645	認知機能(知的機能) paper[114] 統合失調症・自閉症 paper[82]
FHIT	642	統合失調症 paper[5] paper[165]
LINC00969	640	統合失調症 paper[57]
KCNJ12	626	うつ病 paper[113]
BAGE2	618	該当なし。アルツハイマー病のみあり paper[146]
UPK3B	608	該当なし
CTNNA3	605	統合失調症 paper[165] 自閉症 paper[79] 衝動的行動 paper[172] 抗うつ剤の有効性 paper[98]
NRXN3	602	神経精神疾患 paper[80] 自閉症 paper[117]
CDH13	600	自閉症・統合失調症・双極性障害・うつ病・注意欠陥多動性障害 paper[16] paper[64] 統合失調症・注意欠陥多動性障害 paper[165]
SGCZ	582	知能 paper[168] うつ病的傾向 paper[73]
CNTN5	568	自殺傾向 paper[74]
PARK2	568	知能 paper[159] 知的障害・自閉症 paper[109] パーソナリティー paper[75]
MAP2K3	564	精神疾患全般 paper[76] 自閉症 paper[146]
CCSER1	564	該当なし、アルコール依存症 paper[77]
GRID2	561	心的ストレス paper[78]
CTNNA2	553	知能 paper[168] 教育達成度 paper[5] 衝動的行動 paper[172]
DAB1	528	不眠症 paper[161] 精神薄弱 paper[44] 統合失調症 paper[165]
GPC5	527	知能 paper[159] 認知機能 paper[45]
NAALADL2	519	自閉症 paper[46]
MAGI2	506	統合失調症・うつ病 [paper[47] パーソナリティー [paper[75] 統合失調症、synaptic adhesion paper[125] paper[165]
DPP10	505	注意欠陥多動性障害 paper[48]
PDE4D	503	知能 paper[168] paper[169] 強迫性障害 paper[49] （脳の神経細胞間）シナプスへの影響 paper[173]
KCNIP4	497	パーソナリティー障害・注意欠陥多動性障害 paper[50]
CNTN4	485	知的障害・自閉症 paper[109] 統合失調症 paper[40] paper[165] 自閉症 paper[137] 双極性障害 paper[160]
TBC1D5	478	paper[51] 双極性障害
AGBL4	474	paper[52] 認知能力
ASIC2	471	paper[52] 統合失調症
CADM2	471	知能指数、rs17518584 paper[118]詳細はここにメモ paper[168] 精神疾患全般 paper[38] 認知機能 paper[88]
CDH12	469	統合失調症・双極性障害・うつ病 paper[24]
ZDHHC11	468	知能 paper[159]
ADARB2	468	自閉症 paper[53]
DCC	467	知能 paper[135] paper[168] paper[169] 不眠症 paper[161] 認知機能全般 paper[5] 注意欠陥多動症、うつ病 paper[134] 詳細メモはこの日 paper[162] 自閉症 paper[162] うつ病 paper[136] paper[137]→サンプル数約37万SNPs数は53を特定（論文メモこの日） paper[174] 統合失調症 paper[162] 衝動的行動 paper[171] paper[172] 脳容量 paper[164]
GALNTL6	459	知能 paper[159]
ANKRD36	458	該当なし アルコール依存症 paper[54]
CDH4	457	知能 paper[168] 統合失調症 paper[25]
PRR4	457	統合失調症 paper[55]
LRRC4C	448	知能 paper[159] 拒食症 paper[5] 統合失調症synaptic adhesion paper[125]
MIR44351HG	445	該当なし
LINC00960	443	統合失調症 paper[56]
SLC9B1P4	442	0
PTPRT	434	知能 paper[168] paper[169] 知的障害 paper[58] 自閉症 paper[165]
SDK1	431	不眠症 paper[161] 幼児虐待 paper[59]
PARD3B	430	知能 paper[159] パーソナリティー障害 paper[60]
SLC9B1P1	425	該当なし
TAS2R14	421	該当なし
RUNX1	420	精神薄弱 paper[61]
AUTS2	420	知能 paper[168] paper[169] 知的障害 自閉症 paper[111]　メモはこのページ 統合失調症・自閉症 paper [42],[53]
CSMD3	418	自閉症 paper[62]
NRXN1	418	知能 paper[159] 知的障害 自閉症 paper[109] 自閉症・統合失調症 paper[35] paper[95] 自閉症 paper[117] 統合失調症　synaptic adhesion paper[125] 精神障害全般・言語発達障害・統合失調症・自閉症 paper[131] paper[167]
LINC00955	418	該当なし
ZNF385D	418	統合失調症 paper[63]
PRKG1	417	注意欠陥多動性障害 paper[64] 衝動的行動 paper[172]
CAMTA1	416	知能 paper[159] paper[169] 記憶能力 paper[65]
SPAG16	414	双極性障害 paper[66] paper[156]
TMEM132D	410	知能 paper[159] パニック障害 paper[67] 不安症 paper[165]
ROBO1	409	数学及び言語に関する能力 paper[68]
GPC6	408	自閉症 paper[69] paper[137]
NBPF1	407	脳容量 paper[92]
LRRTM4	406	該当なし トゥレット症候群 paper[70]
NOTCH2NL ヒト固有	405	脳容量 ppaper[71] ヒトの頭脳の進化 paper[105]
NCOR1P2	402	該当なし(血圧)
TTC34	400	該当なし
NKAIN2	398	知能 paper[72] 統合失調症 paper[72]
SMYD3	397	精神薄弱 paper[41]
RPTOR	395	知能 paper[159] 統合失調症 paper[40]
AC090044.1	394	該当なし
OPCML	390	統合失調症 paper[37] paper[165]
SNX29	390	知能 paper[168] paper[169] 不眠症 paper[161] 教育達成度 paper[5] 自閉症 paper[26]
NRG1	388	注意欠陥多動性障害 paper[2] 双極性障害 paper[104] 統合失調症 paper[11]paper[87] 統合失調症synaptic plasticityrelated genes paper[125]
ERBB4	387	知能 paper[159] 統合失調症 paper[36] 自閉症 paper[117]
ERC2	386	自閉症,統合失調症 paper[35] 統合失調症・注意欠陥多動性障害 paper[126]
NTM	385	不眠症 paper[161] 知能指数 paper[34]
SRGAP2B	383	頭脳の発達 paper[83]
SLC9B1P3	383	該当なし
CNTNAP3B	379	認知障害 paper[39] Appendix 4
GRM7	379	双極性障害 paper[33]
CACNA2D3	379	統合失調症 paper[32] 統合失調症　ion channel genes paper[125]
MIR663A	376	該当なし
SNTG1	376	大脳皮質 paper[163]
SUMF1	374	精神薄弱 paper[31]
SORCS2	373	双極性障害, paper[30] paper[165]
DMD	373	自閉症 paper[117]
HYDIN	372	脳容量 paper[85]
DGKB	372	認知機能 paper[29]
NRG3	371	統合失調症 paper[28] 統合失調症　synaptic plasticityrelated genes paper[125]
FAM182B	369	該当なし
TEKT4P2	368	該当なし
DIP2C	367	精神疾患全般 paper[27]
AGBL1	366	自閉症 paper[26]
CDH18	364	統合失調症,双極性障害,うつ病 paper[24]
HERC2P3	364	注意欠陥多動性障害 paper[23]
FRG2C	363	注意欠陥多動性障害 paper[23]
TRPM3	359	知的障害 paper[22]
TRAPPC9	358	精神薄弱 paper[21] 知的障害 paper[133] 詳細はこの日にメモ
ERICH1AS1	357	統合失調症 paper[5]
DLGAP1	355	統合失調症 paper[20]
HDAC9	354	統合失調症 paper[19]
CTNND2	354	知能 paper[159] 知的障害 paper[18]
C10orf11	351	大脳皮質 paper[163]
ASTN2	348	脳容量 paper[164] 統合失調症、双極性障害、自閉症 paper[165]
CNTNAP5	340	双極性障害 paper[160]
PCDH9	330	知的障害、 自閉症 paper[109]
SHANK2	322	知的障害、自閉症 paper[109] 詳細このページメモ
SHANK2 精神疾患関連論文が極めて多数あり。	322	知的障害、自閉症 paper[109] paper[151] paper[152] paper[153] paper[154] うつ病 paper[129] paper[157] 自閉症、注意欠陥多動性障害 paper[149] 神経精神障害 paper[150] 注意欠陥多動症 paper[155]
FIP1L1	320	大脳皮質 paper[163]
EXOC4	320	知能 paper[147] paper[135] paper[168] paper[169]
DPYD	319	ボーダーラインパーソナリティー障害 paper[97] 自閉症 paper[117] 知能 paper[159] paper[168]
LARGE	317	知能 paper[159] paper[168]
NEGR1	312	不眠症 paper[161] 知能 paper[135] paper[147] paper[168] paper[169] うつ病 paper[158]
CALN1	311	知能 paper[159] paper[168] paper[169]
NPAS3	309	不眠症 paper[161] 知能 paper[159] 統合失調症 paper[165]
THSD7B	306	知能 paper[159]
AGAP1	303	知能 paper[159] paper[168] paper[169]
CACNA1C	302	統合失調症 paper[95] paper[141] paper[148] paper[166]
THOC3	285	知能 paper[159] SNV35＝35
DDAH1	285	双極性障害 paper[160] SNV35＝75 重要
ZNF806	270	SNV35=117。該当なし、アルツハイマー病のみ paper[146]
KIRREL3	245	知的障害、自閉症 paper[109]
FOXP1	244	知的障害（SNV35=1） paper[108]
AFF3	265	非症候性知的障害 paper[106] 知的障害 paper[107]
ARHGAP15	231	知能 paper[135]
CACNA1B	220	統合失調症　SNV35=26 paper[96]
SCAPER	176	知的障害 paper[133] 詳細はこの日にメモ
TRIO	169	知的障害 paper[108]
OR4C3 SNV35=48	163	注意欠陥多動症、うつ病 paper[134] 詳細メモはこの日 NCBIでは嗅覚受容体
OR4C5 SNV35=49	155	統合失調症 ppaper[90] 注意欠陥多動症、うつ病 paper[134] 詳細メモはこの日 NCBIでは嗅覚受容体
ARID1B	146	知的障害 paper[108]
MED13L	119	知的障害 paper[108] 詳細このページメモ
DYSF	110	知能　SNV35＝1 paper[135]

検証＝現実と一致しているか？

①上に掲げた朝鮮人固有の遺伝子変異の中で、最も多いPRIM2遺伝子は不眠症と関連しているとの論文が存在し、また、RBFOX1遺伝子等々について、非常にサンプル数の多い正確な分析論文（Nature掲載論文）paper[161]にて不眠症との関連が明確に指摘されている。（不眠症は、うつ病や自殺傾向と複合的に生ずるものです。韓国人はRBFOX1遺伝子等について、ＦＤＡ論文のサンプル35名全員が共有するする変異を有しています）

韓国における不眠症の状況について、日本のＮＨＫに相当するイギリスのＢＢＣ は、下記のような記事を配信し、韓国人が「眠ることと格闘」している状況を活写しており、完全に一致します。
 
②不眠症及び不眠症に確実に関連している憤怒調節障害（間欠性爆発障害 Intermittent explosive disorder）こそ朝鮮民族固有の精神面での「民族病」であると確信をもって断言します。なお、極めて多くの場合、MDD（ Major Depressive Disorder＝うつ病）の症状の一つが不眠であり、韓国の自殺率の高さの一つの要因である可能性も否定しきれない

不眠症と朝鮮人の憤怒調節障害

①RBFOX1遺伝子と不眠症

韓国人は、RBFOX1遺伝子において、サンプル数35名で1272と大量に韓国人固有の変異を有しています。この遺伝子が、現生人類の精神的形質と関連していることは、paper[161]paper[125] paper[100]等々、及び、NCBIでの検索結果からみて100%確実です。

特に、paper[161]は非常に多いサンプル数に基づく正確な分析であり、朝鮮人の民族病ともいうべき不眠症とこのRBFOX1遺伝子は確実に関連しています。

ヒトの場合、髪の毛の色、肌の色の濃淡、瞳の色、耳垢の乾湿など身体的特徴の多くが単一遺伝子によって決定されるのに対し、精神面での形質は、複数の遺伝子の変異と遺伝子中の配列の繰り返し数の相違などが複雑に関与しているため、単一の遺伝子によって決定されるものではないことは言うまでもないのですが、RBFOX1遺伝子が、ヒトの精神及び不眠症に関連することはほぼ確実です。

②PTPRN2遺伝子と憤怒調節障害

「朝鮮事情」　C・ダレ　第12章　国民性
P269 成長した後は、男も女も見境のないほどの怒りを絶え間なく爆発させるようになる。

韓国人はPTPRN2遺伝子について、1224と6番目に多く韓国人固有の変異を有している。下記論文では、憤怒調節障害（＝間欠性爆発障害）について、健常者とパーソナリティー障害者の比較分析結果として、PTPRN2遺伝子を抽出している。

GenomeWide DNA Methylation Changes Associated with Intermittent Explosive Disorder: A GeneBased Functional Enrichment Analysis
Janitza L MontalvoOrtiz, PhD et.al
Published: 02 November 2017

韓国人の「制御不能な怒りの爆発」という奇妙な現象は、李氏朝鮮時代に限らず、現在においても多くの識者が等しく指摘するところであり、疑う余地が全くない韓国人の民族性である。

「悪しき半島国家韓国の結末」 宮家邦彦（元外務省勤務）
ｐ32 民族性と言えば、昔から「韓国人は正気を失うほど激しく怒る」とか「韓国人は自分の感情をコントロールするすべをあまりにも知らなさすぎる」といった批判が聞かれる。また民族性として、「狭量、千篇一律、自惚れ、横柄、肉体労働を蔑む間違った自尊心、利己的個人主義」も指摘されてきた

ｐ67 個人的にはコリア人の性格はイラク人に似ていると思う。 幸か不幸か、筆者はこのバクダッドに2回赴任している。コリア半島と同様、イラク人も激しやすく、時に暴力的で、外国人には扱い難い人々であった

③CSMD1遺伝子と統合失調症

韓国人は、CSMD1遺伝子において、2番目に多い1,786もの韓国人固有の変異を有している。

上に掲げたグーグル論文検索結果では、圧倒的にCSMD1遺伝子と統合失調症の関係を示している、King of Mental desease（精神疾患の王様）とも呼ぶべき統合失調症であるからして当然の結果であると思われます。しかし、統合失調症の生涯有病率は欧米人が1％程度（100人に一人）であるに対し、東アジア人（中国人・韓国人・日本人）は、0.1%強=1000人に一人程度です。韓国人固有の変異の多さから見て、CSMD1遺伝子は統合失調症以外の韓国人固有の精神的形質に関連していると考えられます

CSMD1遺伝子はヒトの知能全般に関連する可能性が極めて高いです。このことは、 全63もの国際的に有名な自然科学関連賞について、韓国には受賞者がただの一人もいない結果と完全に合致すると記事筆者は見做しています。恐らくは、これらの遺伝子に生じた朝鮮人固有の遺伝子変異が 上記の異常な結果を引き起こした主原因でしょう。（韓国の自然科学系の研究環境及び論文発表数からみて、前記結果は絶対にありえず、極めて異常な現象である。）

なお、下記に画像化したように、韓国人サンプル35名全員が共通して有する非同義変異が最も多い遺伝子はOR4C5遺伝子です。 この遺伝子については、統合失調症と注意欠陥多動性障害の疾患感受性遺伝子候補である旨の論文が各１本ありますが、NCBIでの検索結果は、 OR4C5遺伝子は嗅覚に関連する受容体（レセプター）である旨を示しています。

結論

①世界中の集団遺伝学研究者は、韓国人集団遺伝学者がほとんど引用しないため、読まれることが少く引用数も少ないが、事実上はアメリカ政府食品医薬品局（ＦＤＡ）毒物研究センターが執筆した論文を読むべきである。
②日本人の病理遺伝学研究者は、ＦＤＡ論文にて抽出された朝鮮人固有の遺伝子変異リストに基づき、研究を進めるべきである。現状では、このリストは、日本で全く知られていない。 また、精神科医は、在日韓国・朝鮮人及び帰化済み朝鮮人への投薬時には、特段の配慮が必要である
③日本の文化人類学者は、韓国社会の異様性・病身性を徹底的に分析するべきである。その際には、ＤＮＡが朝鮮人である者の協力を絶対に求めるべきではない。
④日本人の起源を探求している研究者は、ＤＮＡが朝鮮人である者を研究グループから絶対に排除するべきである。

記事筆者は、アメリカ政府食品医薬品局（ＦＤＡ）毒物研究センターが執筆した論文及び同論文にて抽出された韓国人固有の遺伝子変異リストと上記の結果からみて、韓国人は精神面から見た場合には、完全なDNA異常集団であると絶対の自信をもって言い切る。

そして、韓国人の精神面でのDNAの異常性こそ、全63もの国際的な科学関連賞の受賞者がただの一人もいないという客観的事実に完全に合致し、かつ、韓国の合計特殊出生率の異常を極めた低下（2022年で0.78）が端的に示すように病身国家韓国を生み出した主原因である


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＊論文名一覧
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Rare coding variants in 10 genes confer substantial risk for schizophrenia.
Singh TJ et al.
Nature. April 6, 2022

paper[2]
an intriguing therapeutic target for neurodevelopmental disorders
Liang Shi & Clare M. Bergson
Nature Published: 16 June 2020

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An interaction network of mental disorder proteins in neural stem cells
M J Moen et al,
Nature Published: 04 April 2017

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Association between SNPs and gene expression in multiple regions of the human brain
S Kim et al,
Nature Published: 08 May 2012

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Identification of pleiotropy at the gene level between psychiatric disorders and related traits
Tatiana Polushina et al,
Nature Published: 29 July 2021

[cited from the above paper]
Here, we aimed to identify genetic overlaps at the gene level between 7 mental disorders (schizophrenia, autism spectrum disorder, major depressive disorder, anorexia nervosa, ADHD, bipolar disorder and anxiety), 8 brain morphometric traits, 2 cognitive traits (educational attainment and general cognitive function) and 9 personality traits (subjective wellbeing, depressive symptoms, neuroticism, extraversion, openness to experience, agreeableness and conscientiousness, children’s aggressive behaviour, loneliness) based on publicly available GWASs.

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A Genomewide Linkage Scan of Cocaine Dependence and Major Depressive Episode in Two Populations
BaoZhu Yang et ai.
Nature Published: 17 August 2011

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Exome sequencing for bipolar disorder points to roles of de novo lossoffunction and proteinaltering mutations
M Kataoka et al.
Nature Published: 24 May 2016

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Genomewide association study in obsessivecompulsive disorder: results from the OCGAS
M Mattheisen
Nature Published: 13 May 2014

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The SchizophreniaAssociated Gene, CSMD1,Encodes a BrainSpecific Complement Inhibitor
Matthew L Baum
Harvard Libraly

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CNTNAP2 gene dosage variation is associated with schizophrenia and epilepsy
J I Friedman et al.
Nature Published: 24 July 2007

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The molecular genetics of schizophrenia: new findings promise new insights M J Owen et al.
Nature Published: 28 October 2003

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A genomewide investigation into parentoforigin effects in autism spectrum disorder identifies previously associated genes including SHANK3
Siobhan Connolly et al.
Nature Published: 23 November 2016


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Convergence of evidence from a methylomewide CpGSNP association study and GWAS of major depressive disorder
Karolina A. Aberg et al.
Nature Published: 22 August 2018

[cited from the above paper]
ROBO2 (roundabout, axon guidance receptor, homolog 2) is critical for the maintenance of inhibitory synapses in the adult ventral tegmental area, a brain region important for the production of dopamine[41], and has been implicated in schizophrenia[42],[43],[44] and bipolar depression[45].

paper[14]
Identification of 11 potentially relevant gene mutations involved in growth retardation, intellectual disability, joint contracture, and hepatopathy
Hongyan Diao et al.
Published online 2018 Nov 16

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Association of limbic systemassociated membrane protein (LSAMP) to male completed suicide
Anne Must et al.
Published: 23 April 2008

[cited from above paper]
According to the results of the current study, there might be a chance that variations in LSAMP gene play a role in pathoaetiology of suicidal behaviour.

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The role of cadherin genes in five major psychiatric disorders: A literature update
Ziarih Hawi et al.
published: 18 September 2017

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Andreas Tzschach et al.
Nature Published: 21 October 2009

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CTNND2— a candidate gene for reading problems and mild intellectual disability
Wolfgang Hofmeister et al.
February 3, 2015

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HDAC9 is implicated in schizophrenia and expressed specifically in postmitotic neurons but not in adult neural stem cells
Bing Lang et al.
Published online 2011 Aug 18.

paper[20]
Genetic analysis of the DLGAP1 gene as a candidate gene for schizophrenia
JunMing Liet al
30 January 2013

paper[21]
Identification of Mutations in TRAPPC9, which Encodes the NIK and IKKβBinding Protein, in Nonsyndromic AutosomalRecessive Mental Retardation
Asif Mir et al.
11 December 2009

paper[22]
Diseaseassociated mutations in the human TRPM3 render the channel overactive via two distinct mechanisms
Siyuan Zhao et al.
eLife 2020

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De novo and inherited CNVs in MZ twin pairs selected for discordance and concordance on Attention Problems
Erik A Ehli et al.
Nature Published: 11 April 2012

paper[24]
A novel relationship for schizophrenia, bipolar and major depressive disorder Part 5: a hint from chromosome 5 high density association screen
Xing Chen et al.
Published online 2017 May 15.


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Neuronal cell adhesion genes Key players in risk for schizophrenia, bipolar disorder and other neurodevelopmental brain disorders?
Aiden P. Corvin
01 Oct 2010

paper[26]
Genomewide association analysis of autism identified multiple loci that have been reported as strong signals for neuropsychiatric disorders
Lu Xia et al.
published: 24 October 2019

paper[27]
Integrated multiomics reveal epigenomic disturbance of assisted reproductive technologies in human offspring
WeiChen et al.
Volume 61, November 2020

paper[28]
Neuregulin 3 (NRG3) as a susceptibility gene in a schizophrenia subtype with florid delusions and relatively spared cognition
B Morar et al.
Nature
Published: 15 June 2010

paper[29]
Genetic Basis of a Cognitive Complexity Metric
Narell K. Hansell et al.
Published: April 10, 2015

[cited from the above paper] Abstract
Relational complexity (RC) is a metric reflecting capacity limitation in relational processing. It plays a crucial role in higher cognitive processes and is an endophenotype for several disorders. However, the genetic underpinnings of complex relational processing have not been investigated. Using the classical twin model, we estimated the heritability of RC and genetic overlap with intelligence (IQ), reasoning, and working memory in a twin and sibling sample aged 1529 years (N = 787). Further, in an exploratory search for genetic loci contributing to RC, we examined associated genetic markers and genes in our Discovery sample and selected loci for replication in four independent samples (ALSPAC, LBC1936, NTR, NCNG), followed by metaanalysis (N>6500) at the single marker level. Twin modelling showed RC is highly heritable (67%), has considerable genetic overlap with IQ (59%), and is a major component of genetic covariation between reasoning and working memory (72%). At the molecular level, we found preliminary support for four singlemarker loci (one in the gene DGKB), and at a genebased level for the NPS gene, having influence on cognition. These results indicate that genetic sources influencing relational processing are a key component of the genetic architecture of broader cognitive abilities. Further, they suggest a genetic cascade, whereby genetic factors influencing capacity limitation in relational processing have a flowon effect to more complex cognitive traits, including reasoning and working memory, and ultimately, IQ.

paper[30]
SorCS2 is required for BDNFdependent plasticity in the hippocampus
S Glerup el al.
Nature Published: 26 July 2016

paper[31]
Candidate genes for recessive nonsyndromic mental retardation on chromosome 3p (MRT2A)*
JJ Higgins et al
published: 18 May 2004

paper[32]
Genetic Evaluation of Schizophrenia Using the Illumina HumanExome Chip
Tim Moons et al.
March 30, 2016

paper[33]
Allelic Association, DNA Resequencing and Copy Number Variation at the Metabotropic Glutamate Receptor GRM7 Gene Locus in Bipolar Disorder
Radhika Kandaswamy et al.
Accepted: 14 April 2014

paper[34]
NTM and NR3C2 polymorphisms influencing intelligence: Familybased association studies
Yue Pan et al.
Progress in NeuroPsychopharmacology & Biological Psychiatry 35 (2011) 154–160

paper[35]
CNTNAP2 and NRXN1 Are Mutated in AutosomalRecessive PittHopkinslike Mental Retardation and Determine the Level of a Common Synaptic Protein in Drosophila
ChristianeZweier et al
13 November 2009,

paper[36]
Schizophrenia Candidate Gene ERBB4: Covert Routes of Vulnerability to Psychosis Detected at the Population Level
Nicholas C. Stefanis
March 2013

paper[37]
OPCML Gene as a Schizophrenia Susceptibility Locus in Thai Population
Benjaporn Panichareon
Published: 21 July 2011

paper[38]
Genetic variation in CADM2 as a link between psychological traits and obesity
Julia Morris et al
Nature Published: 14 May 2019

paper[39]
Ancient Migrations The first complete genome assembly, annotation and variants of the 2 ZoroastrianParsi community of India
Naseer Pasha et al
February 17, 2021

paper[40]
Altered DNA methylation associated with a translocation linked to major mental illness
Daniel L. McCartney et al.
Nature Published: 19 March 2018

[cited from the above paper] Twentytwo of the DMRs identified were within the major histocompatibility complex (MHC; Fig. 3), which has been implicated in the pathogenesis of SZ through a largescale GWAS.16 In addition, we identified DMRs within two additional genes (IGSF9B, CNTN4) that showed genomewide association with SZ in the same study.
Two additional DMRs were identified within genes associated with SZ at the genomewide significant level by the SZ Working Group of the Psychiatric Genomics Consortium (PGC).16 These were within the genes IGSF9B and CNTN4, both of which function as cell adhesion molecules. Two largescale epigenomewide association studies of SZ have recently been reported.12,13 These studies reported significant differential methylation in RPTOR: a gene in which we identified a DMR. RPTOR is a key component of mTOR signalling, which has been implicated in synaptic plasticity.36

paper[41]
Derivative chromosome 1 and GLUT1 deficiency syndrome in a sibling pair
Dilek Aktas et al.
Published: 28 May 2010

paper[42]
Rare structural variants found in attentiondeficit hyperactivity disorder are preferentially associated with neurodevelopmental genes
J Elia et al
Nature Published: 23 June 2009


paper[43]
GWAS MetaAnalysis Reveals Shared Genes and Biological Pathways between Major Depressive Disorder and Insomnia
YiSian Lin
Published: 26 September 2021

paper[44]
The Gene Encoding Disabled1 (DAB1), the Intracellular Adaptor of the Reelin Pathway, Reveals Unusual Complexity in Human and Mouse*
Isabelle Bar et al.
FEBRUARY 2003


paper[45]
Postaxial polydactyly type A2, overgrowth and autistic traits associated with a chromosome 13q31.3 microduplication encompassing miR1792 and GPC5
P.Kannu et al.
8, August 2013

paper[46]
GenomeWide Association Study for Autism Spectrum Disorder in Taiwanese Han Population
PoHsiu Kuo et al.
2015 Sep 23

paper[47]
Genetic Dissection of Temperament Personality Traits in Italian Isolates Maria Pina Concas et al. 21 December 2021

paper[48]
Attention, cognitive control and motivation in ADHD: Linking eventrelated brain potentials and DNA methylation patterns in boys at early school age
Hartmut Heinrich et al
. Published: 19 June 2017

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Association study of the PDE4D gene and obsessivecompulsive disorder in a Chinese Han population
Huang, Xing et al.
December 2019

paper[50]
KCNIP4 as a candidate gene for personality disorders and adult ADHD
LenaWeißflog et al. 2012.07.017

paper[51]
Implication of synapserelated genes in bipolar disorder by linkage and gene expression analyses
Catalina Lopez de Lara
2010 Jul 29

paper[52]
EpigenomeWide Association Study of Cognitive Functioning in MiddleAged Monozygotic Twins
Anna Starnawskal et al
12 December 2017

paper[52]
Host genetics influences the relationship between the gut microbiome and psychiatric disorders
ThaisMartinsSilva
2 March 2021

paper[53]
Identification of a functional rare variant in autism using genomewide screen for monoallelic expression
Eyal BenDavid et al
15 September 2011

paper[54]
Genomewide association study for maximum number of alcohol drinks in European Americans and African Americans
Ke Xu et al
2015 Jun 3

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Sex differences in schizophrenia: a longitudinal methylome analysis
Christopher Adanty et al
Published: 30 December 2021

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Long noncoding RNAassociated competing endogenous RNA axes in the olfactory epithelium in schizophrenia: a bioinformatics analysis
Hani Sabaie et al.
Nature Published: 30 December 2021

paper[57]
GenomeWide Search for SNP Interactions in GWAS Data: Algorithm, Feasibility, Replication Using Schizophrenia Datasets
KwanYeung Lee et al.
Nature 28 August 2020

paper[58]
Modeling del(17)(p11.2p11.2) and dup(17)(p11.2p11.2) Contiguous Gene Syndromes by Chromosome Engineering in Mice: Phenotypic Consequences of Gene Dosage Imbalance
Katherina Walz 2003 May

paper[58]
Identification of pathogenic gene variants in small families with intellectually disabled siblings by exome sequencing
Janneke H M SchuursHoeijmakers et al
February 13, 2014

paper[59]
Exposure to childhood abuse is associated with human sperm DNA methylation
Andrea L. Roberts et al.
Nature Published: 02 October 2018

paper[60]
LENS: webbased lens for enrichment and network studies of human proteins
Adam Handen et al
Published: 09 December 2015

paper[61]
Syndromic Mental Retardation With Thrombocytopenia Due to 21q22.11q22.12 Deletion:Report of Three Patients
Eleni Katzaki et al
Accepted 3 March 2010


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Two patients with balanced translocations and autistic disorder: CSMD3 as a candidate gene for autism found in their common 8q23 breakpoint area
Chiara Floris et al
Nature Published: 13 February 2008

paper[63]
BCL9 and C9orf5 Are Associated with Negative Symptoms in Schizophrenia: MetaAnalysis of Two GenomeWide Association Studies
Chun Xu etal.
Published: January 29, 2013

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CaseControl GenomeWide Association of AttentionDeficit / Hyperactivity Disorder
Benjamin M. Neale et al
Published online 2010 Aug 5

paper[65]
Calmodulinbinding transcription activator 1 ( CAMTA1 ) alleles predispose human episodic memory performance
Matthew J. Huentelman et al.
Published: 30 April 2007

paper[66]
Genomewide association study of bipolar disorder in Canadian and UK populations corroborates disease loci including SYNE1 and CSMD1
Wei Xu et al.
Published: 04 January 2014

paper[67]
Replication and metaanalysis of TMEM132D gene variants in panic disorder A Erhardt et al Nature Published: 04 September 2012

paper[68]
KIAA0319 and ROBO1: evidence on association with reading and pleiotropic effects on language and mathematics abilities in developmental dyslexia
Sara Mascheretti et al
Nature Published: 16 January 2014

paper[69]
Postaxial polydactyly type A2, overgrowth and autistic traits associated with a chromosome 13q31.3 microduplication encompassing miR1792 and GPC5 P.Kannu et al Issue 8, August 2013

paper[70]
LRRTM4 Terminal Exon Duplicated in Family with Tourette Syndrome, Autism and ADHD
Raymond A. Clarke et al.
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paper[71]
HumanSpecific Genes, Cortical Progenitor Cells,and Microcephaly
Michael Heide
Published: 15 May 2021

paper[72]
Metaanalysis of Positive and Negative Symptoms Reveals Schizophrenia Modifier Genes
Alexis C. Edwards
Published: 27 August 2015

paper[73]
Genetic underpinnings of affective temperaments: a pilot GWAS investigation identifies a new genomewide significant SNP for anxious temperament in ADGRB3 gene Xenia Gonda et al. Nature Published: 01 June 2021
[cited from above paper] Suggestively significant findings in SNPbased tests for depressive temperament
In case of depressive temperament, genomewide SNPbased tests yielded a genomic inflation factor of λ = 1.00172. For the QQ plot, see Supplementary Fig. S3. No SNP survived Bonferroni correction for multiple testing, but five SNPs showed a suggestive significance, one of which resides in the SGCZ gene, whereas the rest are intergenic (Fig. 2 IC and Table 1).

paper[74]
Identification of novel genomewide associations for suicidality in UK Biobank, genetic correlation with psychiatric disorders and polygenic association with completed suicide
Rona J.Strawbridge
March 2019

paper[75]
Genetic Dissection of Temperament Personality Traits in Italian Isolates
Maria Pina Concas et al.
Published: 21 December 2021

paper[76]
Hippocampal overexpression of NOS1AP promotes endophenotypes related to mental disorders
FlorianFreudenberg et al.
September 2021

paper[77]
Ancestryspecific and sexspecific risk alleles identified in a genomewide geneby alcohol dependence interaction study of risky sexual behaviors
Renato Polimanti et al.
Published online 2017 Oct 9

paper[78]
Genetic mapping of habitual substance use, obesityrelated traits, responses to mental and physical stress, and heart rate and blood pressure measurements reveals shared genes that are overrepresented in the neural synapse
Majid Nikpay
Nature Published: 02 February 2012
[cited]
Links between substance use habits, obesity, stress and the related cardiovascular outcomes can be, in part, because of loci with pleiotropic effects. To investigate this hypothesis, we performed genomewide mapping in 119 multigenerational families from a population in the SaguenayLacStJean region with a known founder effect using 58 000 singlenucleotide polymorphisms and 437 microsatellite markers to identify genetic components of the following factors: habitual alcohol, tobacco and coffee use; response to mental and physical stress; obesityrelated traits; and heart rate (HR) and blood pressure (BP) measures. Habitual alcohol and/or tobacco users had attenuated HR responses to mental stress compared with nonusers, whereas hypertensive individuals had stronger HR and systolic BP responses to mental stress and a higher obesity index than normotensives. Genetic mappings uncovered numerous shared genes among substance use, stress response, obesity and hemodynamic traits, including CAMK4, CNTN4, DLG2, FHIT, GRID2, ITPR2, NOVA1 and PRKCE, forming network of interacting proteins, sharing synaptic function and display higher and patterned expression profiles in brainrelated tissues; moreover, pathway analysis of shared genes pointed to longterm potentiation.

paper[79]
An integrated analysis of rare CNV and exome variation in Autism Spectrum Disorder using the Infinium PsychArray
Elena Bacchelli
Nature Published: 21 February 2020

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A rare exonic NRXN3 deletion segregating with neurodevelopmental and neuropsychiatric conditions in a threegeneration Chinese family
Haiming Yuan et al.
2018 Aug 4

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The tumour suppressor gene WWOX is mutated in autosomal recessive cerebellar ataxia with epilepsy and mental retardation
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Issue 2, February 2014

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Ewoud R. E. Schmidt et al.
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Jorge I. Vélez et al.
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[cited from the above paper]
OR4C5 is a gene predicted by GDI to be highly damaging.

[notes]
# of SNVs in SNV1/ns is 21.
"# of SNVs in SNV35/ns" is 11.

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ただし、2016年の中国人による論文では、rs10503253置換変異と統合失調症の関係を否定している。P > 0.05と論文要旨で明言
サンプルは中国人のみである
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重要論文。23andMeの協力を得て、主にオランダの大学の研究者によるバカでかいサンプル数の分析。
筆頭著者の日本人女性は、アムステルダム自由大学所属でまだ若い。このような若い日本人研究者に一刻も早く韓国人ＤＮＡの精神面での完全な異常性に気づいて欲しい。





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paper[166]論文付属のtable4から。統合失調症の最大規模ＧＷＡＳ分析論文
Biological Insights From 108 Schizophrenia-Associated Genetic Loci
Schizophrenia Working Group of the Psychiatric Genomics Consortium
Nature. 2014 Jul 24

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