Video Metzitzah B’Peh – Mechanisms, immediate and long-term consequences, and the purpose

In 1909, Rabbi Moshe Mordechai Epstein from Slabodka, Lithuania, attempted to justify mouth-penis-wound-sucking with its monstrosity:

Since sucking blood and placing the bloody penis in one’s mouth are so repulsive, how can anyone be so dense as to presume that this process was instituted without it being an essential part of the mitzvah?”.

The content of the video is based on Chapter “Jewish circumcision for conquests with epidemics ” from the Book “The Jubilee Murders – Originators and Methods of Mass Murders” by Wolff Geisler, Verlag Wolff Geisler 2014.

Video Metzitzah B’Peh – Keystone of Judaism

Jewish people are in part more than ten times more likely to develop breast cancer, prostate cancer, colon cancer, ovarian cancer, pancreatic cancer, and affected by more than 160 exotic forms of dysregulation and “hereditary disease” than Non-Jewish persons; they are also a hundred times more likely to lack the CCR5 gene 32-basepair.

The homozygous removal of CCR5 32bp can protect those affected from plague, smallpox, tuberculosis, syphilis, and immunodeficiency (e.g. AIDS). It has had this effect for 4,000 years and is the reason why Jewish ritual circumcision is still performed today.

The content of the video is based on Chapter “Jewish circumcision for conquests with epidemics ” from the Book “The Jubilee Murders – Originators and Methods of Mass Murders” by Wolff Geisler, Verlag Wolff Geisler 2014.


Sources cited in video:

„Traditional Jewish Circumcision“ (uncut version) / Quick Clips Word Blips / youtube.com/watch?v=xTxD6l-8ppw / Camerawork: Michael Cohen, ©2012-13 ClipsNBlips, Jerusalem

Ariel Yosef Fenigstein Brit Talmon Tevet 5770 / Elad Fenigstein / youtube.com/watch?v=sYwQlfqDJLg

Brit Mila Eliav David / Raphael Seneor / youtube.com/watch?v=he9lH00E37A

Benzion’s Bris / Chaya Clayman / youtube.com/watch?v=NX1uLOd5uGs

Continue reading “Video Metzitzah B’Peh – Keystone of Judaism”

Genetic changes by Metzitza b’Peh

Genetic changes of many Jewish people by Metzitza b’Peh

The only genetic group attributes that are – relatively speaking – more common in Jewish people than in Non-Jewish persons are CCR5 gene 32-basepair deletion and probably also CCR2-64i and SDF1-S’A.

CCR5 gene 32-basepair deletion in one or both gene strands in the human genome most commonly occurs in groups of Jewish people: 25.9% of Lithuanian Jewish persons in Israel[1], 20.93% of Ashkenazi Jewish persons[2], 20.9% of Jewish people in Poland[3], and 19.5% of East European Jewish persons in Australia[4].

CCR 2-64i primarily came into being among Sephardic Jewish persons[5], who spread it throughout Dutch colonies, for example in south-east Asia. CCR5 gene 32-basepair deletion affects up to 18.4% (Goslar, Germany)[6], 18% (Dagö/Hiiumaa island, Estonia[7]), 16.8% (Azores[8]), 16.8% (Hawaiian Islands, Caucasians[9]), 16.6% (St. Petersburg[10]), 16% (Helsinki, Finland; Mordovia, Russia[11]), 14.8% (Estonia[12]), 14.6% (Iceland[13]), and 14.3% (France; referred to as “Germany”[14]) of people not classified as Jewish.

Congenital deletion of the 32-basepair in the CCR5 gene occurs in the descendants “of a single person[15] who lived “a few thousand years ago[16], “more than 2,500 years ago[17], “recent origin[18], “in historic times[19].

“… its recent emergence [is] consistent with a historic strong selective event (e.g. an epidemic of a pathogen that, like HIV-1, utilizes CCR5), driving its frequency upward in ancestral Caucasian populations”[20] (those “selected” survived, while the “non-selected” majority was killed). “The [CCR5Δ32] mutation has been under intense positive selection[21] (normal gene carriers were killed en masse).

99% of humans have the complete CCR5 gene 32-basepair, i.e. two strands with CCR5 p32. About 1% of humans have just one CCR5 p32 gene, while approx. 0.1% are deficient of both[22].

All people in Africa, Asia, Oceania, America who were not affected by Jewish migration or European conquests have the complete CCR5 gene 32-basepair.

The only way in which this genetic anomaly could spread through the Jewish population was through Jewish ritual circumcision with Metzitza b’Peh (cf. section 2.2).

2.1.1.1 CCR5 Deletion p32 of pharaohs?

For all people without a 32-basepair in the CCR5 gene (“CCR5 gene 32-basepair deletion”) to have descended from one person, as is assuredly the case, the 32-basepair must have been removed from one of the CCR5 gene strands and this hereditary anomaly passed on by descendants who had incestuous intercourse. The histories of Pharaoh Amenhotep III (c. 1403 – 1353 BC), who married his daughters Sitamu and Isis, Pharaoh Amenhotep IV (later Akhenaton, 1353 – 1336 BC), who descended from one of these marriages and fathered a son, Tutankhaton (later Tutankhamun, 1342 – 1323 BC) on one of his sisters or daughters, and Tutankhamun himself, who had two stillborn daughters with his sister Ankhesenaton (later Ankhesenamun), all provide examples of how such an event might have occurred.

 

The birth of Akhenaton corresponds to the story in the Jewish bible of how Yahweh created men and women[23], i.e. by shaping a man from the dust of the ground and blowing the breath of life into his nostrils[24]. Yahweh then put this man to sleep and took a rib from his body, from which he made a woman[25].

Various people around the biblical figure Abraham also fulfilled the requirements for the incestuous spread of CCR5 gene 32-basepair deletion. The year after Abraham was circumcised at the age of 99 (i.e. endowed with CCR5 gene 32-basepair deletion – author’s note), he produced his son Isaac. Isaac’s mother was the 90-year-old, hitherto childless Sarah, granddaughter of Abraham’s father Terah[26]. The conception was said to have been initiated by Yahweh and two angels.

The incest continued, despite normally being tabooed by the Jewish religion (cf. the stories of Lot’s daughters). Goodman confirms that there was a high degree of consanguinity among the direct descendants of Abraham and Sarah[27]. The Talmud propagates marriage between first cousins and between uncles and nieces[28]. In 1900, intermarriage between the 100,000 Jewish persons in Berlin was four times as common (2.3%) as between the 1.8 million Non-Jewish persons (0.6%)[29].

A CCR5 gene 32-basepair deletion that originated under Pharaoh Akhenaton could have been introduced to a Jewish family, then been passed on genetically and then tenthousandfold by Metzitza b’Peh.


Note: This is an excerpt from the book “The Jubilee Murders – Originators and Methods of Mass Murders”. This book can you buy in my shop.


[1] Lucotte G, Smets P. CCR5-Δ32 Allele Frequencies in Ashkenazi Jews. Gen Test Apr 7, 2003:333-7

[2] Martinson JJ, Chapman NH, Rees DC et al. Global distribution of the CCR5 gene 32-basepair deletion. Nat Genet 1997;16:100-3

[3] Lucotte G, Smets P. CCR5-Δ32 Allele Frequencies in Ashkenazi Jews. Gen Test Apr 7, 2003:333-7

[4] Buhler MM. Genetics of the immune cell receptors TCRB and CCR5 in human disease. Diss Univ of Sydney. Mar 27, 2006.

[5] Maayan S, Zhang L, Shinar E, et al. Evidence for recent selection of the CCR5-delta 32 deletion from differences in ist frequency between Ashkenazi and Sephardi Jews. Genes Immun, 2000 Aug;1(6):358-61

[6] Hummel S, Schmidt D, Kremeyer B, et al. Detection of the CCR5-Delta3 HIV resistance gene in Bronze Age skeletons. Gen Immun 6,2005:371-374

[7] Kalev I, Mikelsaar AV, Beckman L et al. High frequency of the HIV-1 protective CCR5 delta 32 deletion in native Estonians. Eur J Epidemiol 16(12), 2000:1107-9

[8] Freitas T, Brehm A, Fernandes AT. Frequency of the CCR5-delta 32 mutation in the Atlantic island populations of Madeira, the Azores, Cabo Verde, and Sao Tome e Principe. Hum Biol 78(6), 2006:697-703

[9] Lu Y, Nerurkar VR, Dashwood WM et al. Genotype and allele frequency of a 32-base pair deletion mutation in the CCR5 gene in various ethnic groups: Absence of mutation among Asians and Pacific Islanders. Int J Inf Dis, vol 3, 1999:186-91

[10] Magierowska M. Lepage V, Boubnova L et al. Distribution of the CCR5 gene 32 base pair deletion and SDF1-3’A variant. Immunogenetics 48, 1998:417

[11] Ferrari M, Ferrec C, Rosatelli C et al. The Δccr5 mutation conferring protection against HIV-1 in Caucasian populations has a single and recent origin in Northeastern Europe. Hum Mol Gen, vol 7(3), 1998:339-406(8).

[12] Kalev I, Mikelsaar AV, Beckman L et al. High frequency of the HIV-1 protective CCR5 delta 32 deletion in native Estonians. Eur J Epidemiol 16(12), 2000:1107-9

[13] Martinson JJ, Chapman NH, Rees DC et al. Global distribution of the CCR5 gene 32-basepair deletion. Nat Genet 1997;16:100-3

[14] Lucotte G, Smets P. CCR5-Δ32 Allele Frequencies in Ashkenazi Jews. Gen Test 7,4.2003:333-7. Muehlhausen/Mulhouse in Alsace, France, is incorrectly denoted as Mulheim, Germany – author’s note.

[15] Libert F, Cochaux P, Beckmann G, et al. The Δccr5 mutation conferring protection against HIV-1 in Caucasian populations has a single and recent origin in Northeastern Europe. Hum Mol Gen V7,3,1998:399-406

[16] Libert F. 1998

[17] Ducan SR. 2005

[18] Ferrari M. 1998

[19] Hummel S. 2005

[20] Stephens JC. 1998

[21] Galvani A. 2005; Novembre J, 2005

[22] Goupta A, Padh H. The global distribution of CCR5delta32 polymorphism: role in HIV-1 protection. BMC Infect Dis 2012;12:016

[23] Genesis 26-29

[24] Exodus 27

[25] Exodus 21-22

[26] Genesis 20:12

[27] Goodman:13

[28] Yebanot 62b; Sanhedrin 76b

[29] Singer 1904:22