If the throwing of children into the fire was the practice of the Khazars, said to be a sacrifice to Molech, the question raised would be, is Tay-Sachs disease the root of such extreme behaviour?
Just before we enter this arena, we should consider it possible that the Ashkenazi are the unwitting prisoners of the Sephardic Jews who have combined with the real power behind Rome the Empire. I present this here because what is not generally presented when it comes to the division within Jewry is the fact, the first Jews to be honoured in the Rothschild’s United Kingdom were Sephardic. Of course the other side to that coin would present the capture of the Sephardic by the Ashkenazi…. The Jury is out.
One reality that is known is how the Sabbatean cults undermined Jewry by killing Christian children and laying the blame on the resident Jewish communities. This kept up the division which drives the siege mentality within both communities, and as if such was not bad enough, both camps at almost all times, would end up turning to the perpetrators of the initial horror for support. It is therefore a reasonable suggestion to make that we have a third and secret hand ensuring the siege mentality for all camps remains a live act.
Tay-sachs disease is said by some to be related to blood libel, or, the Jewish practice of drinking (mostly young) blood. This is carried out at the point of circumcision when the practitioner will place his mouth on the fresh cut to take the blood. It affects mostly Ashkenazi Jews (1 in 27 carries the gene) and it’s a progressive degenerative neurological disorder causing death of brain cells and destroying the central nervous system.
The consequence of this disease that Ashkenazi have to interbreed in order to survive, they require blood from outside their gene pool. Today it’s treated with cord blood transplant, a very expensive procedure which requires a lot of baby blood.
This is perhaps the real origins of the idea of human vampirism.
As the world frantically looks for scapegoats, serious study must be had as it relates to what is fantasy and what is real.
Tay-Sachs disease (TSD) is a fatal genetic disorder, most commonly occurring in children, that results in progressive destruction of the nervous system. Tay-Sachs is caused by the absence of a vital enzyme called hexosaminidase-A (Hex-A). Without Hex-A, a fatty substance, or lipid, called GM2 ganglioside accumulates abnormally in cells, especially in the nerve cells of the brain. This ongoing accumulation causes progressive damage to the cells.
In children, the destructive process begins in the foetus early in pregnancy. However, a baby with Tay-Sachs disease appears normal until about six months of age when its development slows. By about two years of age, most children experience recurrent seizures and diminishing mental function. The infant gradually regresses, and is eventually unable to crawl, turn over, sit or reach out. Eventually, the child becomes blind, cognitively impaired, paralysed and non-responsive. By the time a child with Tay-Sachs is three or four years old, the nervous system is so badly affected that death usually results by age five.
A much rarer form of Tay-Sachs, late-onset Tay-Sachs disease, affects adults and causes neurological and intellectual impairment. Only recently identified, the disease has not been extensively described. As for the childhood form of Tay-Sachs, there is no cure. Treatment involves managing the symptoms of the disease.
Defect in Hex-A Gene Causes Tay-Sachs :
Tay-Sachs disease results from defects in a gene on chromosome 15 that codes for production of the enzyme Hex-A. We all have two copies of this gene. If either or both Hex-A genes are active, the body produces enough of the enzyme to prevent the abnormal build-up of the GM2 ganglioside lipid. Carriers of Tay-Sachs – people who have one copy of the inactive gene along with one copy of the active gene — are healthy. They do not have Tay-Sachs disease but they may pass on the faulty gene to their children.
Carriers have a 50 percent chance of passing on the defective gene to their children. A child who inherits one inactive gene is a Tay-Sachs carrier like the parent. If both parents are carriers and their child inherits the defective Hex-A gene from each of them, the child will have Tay-Sachs disease. When both parents are carriers of the defective Tay-Sachs gene, each child has a 25 percent chance of having Tay-Sachs disease and a 50 percent chance of being a carrier.
Eastern European (Ashkenazi) Jews at Greater Risk for Tay-Sachs Disease:
While anyone can be a carrier of Tay-Sachs, the incidence of the disease is significantly higher among people of eastern European (Ashkenazi) Jewish descent. Approximately one in every 27 Jews in the United States is a carrier of the Tay-Sachs disease gene. Non-Jewish French Canadians living near the St. Lawrence River and in the Cajun community of Louisiana also have a higher incidence of Tay-Sachs. For the general population, about one in 250 people are carriers.
There is no cure or effective treatment for Tay-Sachs disease. However, researchers are pursuing several approaches to finding a cure. Scientists are exploring enzyme replacement therapy to provide the Hex-A that is lacking in babies with Tay-Sachs. Bone marrow transplantation has been attempted also, but to date has not been successful in reversing or slowing damage to the central nervous system in babies with Tay-Sachs. Another avenue of research is gene therapy in which scientists transfer a normal gene into cells to replace an abnormal gene. This approach holds great promise for future Tay-Sachs patients.