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http://www.geneticstesting.com/lab_testing/jewish_disease.html

Genetics and Ashkenazi Jewish Populations

Individuals of Ashkenazi Jewish ancestry (Jews from Eastern Europe), like other ethnic populations, are at increased risk to develop certain genetic diseases and cancers.

Why are Ashkenazi Jewish individuals at higher risk for developing certain genetic conditions?

Every ethnic population has its own set of genetic predispositions to certain diseases and cancers. Just as sickle cell anemia tends to occur in African-Americans and thalassemia, another blood disorder, occurs more commonly in individuals of Mediterranean or South-East Asian descent, certain genetic conditions occur more frequently in Ashkenazi (Eastern European) Jewish individuals than in other groups. This excess happens for several reasons.

Long ago, by chance, a genetic change occurred that predisposed a person to a particular condition, and the genetic change was passed from one generation to the next until the present day. Since the Jewish populations of the past were relatively small compared to their neighboring populations, individuals with a genetic change made up a significant percentage of the Jewish population. Therefore, the genetic changes they carried had a great impact on the "gene pool" of the time. Second, when just a few individuals split off from a larger group (such as when Ashkenazi Jews migrated from one country to another), the genetic changes that those migrants carried became common and seen with higher frequency in the new migrant group than in the original community. Third, since Ashkenazi Jews tend to marry other Ashkenazi Jews (just like African-Americans tend to marry other African-Americans), the genetic changes that are carried by one partner are more likely to be carried by the other partner, since they are both of the same ancestry. Since many of the genetic conditions that Ashkenazi Jews and other ethnic populations are at higher risk for result from inheriting a particular genetic change from both parents (this is known as recessive), a child born to two parents of the same ancestry (regardless of what that ancestry is) is more likely to be at risk for genetic conditions than a child born with mixed ancestry. Other inherited conditions, such as inherited breast and/or ovarian cancer predisposition, are called dominant conditions. Dominant means that one changed copy of a gene is sufficient to cause the condition. If just one parent has the condition, the child may inherit it.

What are the genetic conditions that are more commonly found in Ashkenazi Jewish individuals?

As more research is done, knowledge about conditions other than those listed here may become apparent. Some additional conditions may be seen to occur more commonly in a particular ethnic group, and perhaps in the Ashkenazi Jewish population.

Bloom syndrome is an inherited disorder caused by a gene that does not function properly. A syndrome is a collection of characteristics that, when seen together in an individual, may signal a more complex underlying condition. Individuals with Bloom syndrome have short stature, a "narrow" face with a prominent nose, skin color changes in the face becoming more noticeable after sunlight exposure, a high-pitched voice, an increased susceptibility to infections and respiratory illness, and an increased susceptibility to cancer and leukemia. Some individuals with Bloom syndrome also have mental retardation. The syndrome also affects how chromosomes are copied and can lead to many breaks along the chromosomes. Although Bloom syndrome may occur in any nationality and ethnic group, it is most common in Jews of Eastern European descent (Ashkenazi Jews). At least one in 100 Ashkenazi Jews is a carrier for Bloom syndrome. Carriers do not have Bloom syndrome but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Bloom syndrome have a child together, each child has a 25% chance of having Bloom syndrome.

Canavan disease is caused by the lack of an enzyme in the body called aspartoacylase (ASPA) which breaks down a substance called NAA. The enzyme is particularly important in the part of the brain where nerve impulses are sent to other parts of the brain and to the spinal cord. When ASPA is missing from the body, NAA builds up and causes brain damage, mental retardation, a large head, tremors, and an inability to move muscles. Canavan disease may also cause blindness (due to problems with nerves from the eye to the brain), feeding difficulties, poor weight gain, and problems with swallowing. Although Canavan disease may occur in any nationality and ethnic group, it is most common in Jews of Eastern European descent (Ashkenazi Jews). An estimated one in 40 Ashkenazi Jews is a carrier for Canavan disease. Carriers do not have Canavan disease but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Canavan disease have a child together, each child has a 25% chance of having Canavan disease.

Cystic fibrosis (CF) is an inherited disorder that causes problems with breathing and digestion. Persons with cystic fibrosis have a problem with the way that a certain substance called chloride travels through the body. This causes the glands that produce mucus, saliva, and intestinal fluids to function improperly. The fluid in the lungs becomes thick and accumulates, leading to infections and breathing problems. Enzymes important for digestion are not properly secreted in the intestine, causing poor nutrition. Cystic fibrosis may occur in any nationality and ethnic group. An estimated one in 25 Caucasians in the United States is a carrier for cystic fibrosis. Carriers do not have cystic fibrosis but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for cystic fibrosis have a child together, each child has a 25% chance of having cystic fibrosis. Actually, Ashkenazi Jews are at a lower risk of being carriers for cystic fibrosis compared to non-Ashkenazi Jews or other ethnic populations (an estimated one in 29 Ashkenazi Jews is a carrier for cystic fibrosis). However, the specific gene change that is found in Ashkenazi Jews causes a more severe outcome than most of the other gene changes that have been identified in other populations, and cystic fibrosis is easily tested for in the Ashkenazi Jewish population.

Familial dysautonomia (FD) is a failure to properly control the autonomic and sensory nervous systems of the body. The autonomic and sensory nervous systems control involuntary body functions that we usually don't think about. Problems with swallowing, temperature regulation, blood pressure regulation, feeding, sensation to pain, seizures, a lack of tear production in the eyes, and pneumonia can develop. FD may also cause excessive sweating, delayed walking and speech, spine curvature, red puffy hands, red patches of skin after excitement or feeding, and a lack of taste buds. The cause of FD is unknown, but it is undoubtedly an inherited, genetic condition. Although FD may occur in any nationality and ethnic group, it is most common in Jews of Eastern European descent (Ashkenazi Jews). An estimated one in 30 Ashkenazi Jews is a carrier for FD. Carriers do not have FD but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for FD have a child together, each child has a 25% chance of having FD.

Fanconi anemia in an inherited condition characterized by a reduced production of all types of blood cells in the body. Individuals with Fanconi anemia often have a brown coloring to their skin, short stature, sometimes absent bones in their limbs, and an increased risk for cancer and leukemia. The syndrome also affects how chromosomes are copied and can lead to many breaks along the chromosomes. Although Fanconi anemia may occur in any nationality and ethnic group, one particular gene change is responsible for approximately 83% of cases of Fanconi anemia in Jews of Eastern European descent (Ashkenazi Jews). An estimated one in 89 Ashkenazi Jews is a carrier for Fanconi anemia. Carriers do not have Fanconi anemia but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Fanconi anemia have a child together, each child has a 25% chance of having Fanconi anemia.

Gaucher disease (pronounced "Go-Shay") is an inherited disorder caused by a change in the gene responsible for making an enzyme called glucocerebrosidase that the body needs to break down a particular kind of fat (called glucocerebroside). In people with Gaucher disease, the body is not able to properly produce this enzyme, and the fat cannot be broken down. The fat then accumulates in the liver, spleen, and bone marrow. Gaucher disease may occur among every nationality and ethnic group, but it is most common among Jews of Eastern European descent (Ashkenazi Jews). Type 1 Gaucher disease, in fact, is the most common genetic disorder among Jews. An estimated one in 10 Ashkenazi Jews is a carrier for Gaucher disease. Carriers do not have Gaucher disease but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Gaucher disease have a child together, each child has a 25% chance of having Gaucher disease. Types 2 and 3, however, are not more prevalent among the Jewish population.

Hereditary deafness may account for more than 60% of all cases of hearing impairment. Up to 100 genes are known to be involved in deafness. However, gene changes in one particular gene called called connexin 26 (also known as Cx26 or GJB2) may account for half of all early-onset cases of isolated deafness. Connexin 26 primarily functions in several structures that line the cochlear duct of the ear. Its role is to maintain the flow of substances through the components of the ear that are related to the process of hearing. One specific gene change, known as 30delG (or 35delG), accounts for 2/3 of the detectable gene changes in the connexin 26 gene. Hereditary deafness may occur in any nationality and ethnic group, but there is a higher incidence of this particular 30delG (or 35delG) gene change in the connexin 26 gene in individuals from Israel, Spain, and Italy who have hearing impairment. Another gene change, known as 167delT, is also found more commonly in individuals of Jewish ancestry. About 1 in 8 individuals is a carrier for one of the many different genes that cause hereditary deafness. About 1 in 30 individuals are symptom-free carriers of 30delG (or 35delG), and 1 in 20 to 1 in 25 individuals are carriers for any gene change in the connexin 26 gene. Carriers do not have hearing impairment but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for connexin 26 gene changes have a child together, each child has a 25% chance of having hearing impairment.

Niemann-Pick disease (Type A) is caused by the lack of a substance (called acid sphingomyelinase, or ASM) in the body. ASM normally breaks down a substance called sphingomyelin. When ASM is absent from the body, sphingomyelin builds up in certain cells and causes damage to the central nervous system, liver, and lungs. Problems including developmental delay, progressive spasticity, blindness, an enlarged liver and/or spleen, and a "cherry-red spot" in the eye (visible by a special eye exam) usually become apparent at 3 to 6 months of age. Niemann-Pick disease may also include jaundice (a yellow color of the skin) in infancy and progressive liver failure. Although Niemann-Pick disease may occur in any nationality and ethnic group, Niemann-Pick disease type A is most common in Jews of Eastern European descent (Ashkenazi Jews). An estimated one in 100 Ashkenazi Jews is a carrier for Niemann-Pick disease. Carriers do not have Niemann-Pick disease but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Niemann-Pick disease have a child together, each child has a 25% chance of having Niemann-Pick disease.

Tay-Sachs disease is caused by the lack of a substance (called hexosaminidase A or hex A) in the body. This substance usually breaks down a type of fat called GM2-ganglioside. When hex A is missing from the body it cannot break down this fat, and the fat accumulates to toxic levels in the body. The most damage is done to the cells of the brain and nervous system. Symptoms include severe mental and developmental delays as well as seizures during the first few months of life. A characteristic sign of Tay-Sachs disease is a "cherry-red" spot in the retina of the eye observed by a special eye exam. Although Tay-Sachs disease may occur in any nationality and ethnic group, it is most common in Jews of Eastern European descent (Ashkenazi Jews) and in some French-Canadian populations. An estimated one in 31 Ashkenazi Jews is a carrier for Tay-Sachs disease. Carriers do not have Tay-Sachs disease but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Tay-Sachs disease have a child together, each child has a 25% chance of having Tay-Sachs disease.

Torsion dystonia is a condition characterized by involuntary muscle movements leading to sustained muscle contractions. These muscle contractions result in unusual posture. Torsion dystonia may be due to a brain disorder, a reaction to a drug, or may signal the presence of a genetic disorder. Symptoms of genetic torsion dystonia, such as involuntary muscle twitches, usually occur beginning in childhood, but sometimes may not occur until later in life. Although torsion dystonia may occur in any nationality and ethnic group, one of three inherited forms is found mostly in Jews of Eastern European descent (Ashkenazi Jews). Between one in 6,000 and one in 2,000 Ashkenazi Jews has the gene change for torsion dystonia, but only about 30% of those individuals with the gene change will go on to develop the condition. If an individual with the gene change for torsion dystonia has a child, each child has a 50% chance of having the gene change for torsion dystonia.

Von Gierke disease (glycogen storage disease type 1a) is an inherited disorder caused by the lack of a substance in the body called glucose-6-phoshatase (or G6Pase). G6Pase is critical for its role in the production of glucose (a type of sugar) by the liver. When G6Pase is missing in the body, glycogen accumulates in the liver, kidney, and intestines. Von Gierke disease presents during the first year of life. Symptoms include low blood sugar levels, large livers, slow growth and very short stature, predisposition to bleeding episodes, increased types of fats and acids in the blood, and delayed onset of puberty. There is a characteristic "doll-like" facial appearance and a short, "stocky" body build in individuals with Von Gierke disease, due to an atypical distribution of fat tissue in the body. Long-term complications of Von Gierke disease include gout, tumors of the liver, osteoporosis, kidney stones, and other kidney problems (including kidney failure). Von Gierke disease may occur in any nationality and ethnic group, but it is more common in Jewish individuals. More than 26 gene changes have been identified in the G6Pase gene that cause Von Gierke disease, and several of these gene changes occur with greater frequency in specific ethnic groups. It is known yet known what percentage of individuals of Ashkenazi Jewish ancestry are carriers for Von Gierke disease. Carriers do not have hearing impairment but are capable of passing it on to their children if the other parent is also a carrier. If two carriers for Von Gierke disease have a child together, each child has a 25% chance of having Von Gierke disease.

Hereditary breast and/or ovarian cancer predisposition is an inherited condition that causes an increased risk of developing breast, ovarian, and certain other cancers. Between 5% and 10% of all breast and ovarian cancer cases are hereditary, meaning that they are due to a gene change that may be passed on through the family. Females with certain gene changes are at an increased risk to develop breast and cancer ovarian cancer, and males with these gene changes are more susceptible to colon, prostate, pancreas, thyroid, and breast cancers. Although these gene changes may occur in any nationality and ethnic group, an estimated one in 40 Jews of Eastern European descent (Ashkenazi Jews) carries one of three specific gene changes in one of two genes that are involved in hereditary breast and/or ovarian cancer predisposition.

Familial colorectal cancer (FCC) is an inherited condition, caused by a gene change that can be passed on through a family, that causes individuals to have an increased risk of developing colon cancer and rectal cancer. FCC is believed to be the most common form of inherited colon and rectal ("colorectal") cancer, with about 15% of all colroectal cancers being of this hereditary form called FCC. Although these gene changes may occur in any nationality and ethnic group, an estimated one in 16 Jews of Eastern European descent (Ashkenazi Jews) carries a specific gene change that causes FCC. Not all individuals with the gene change go on to develop colorectal cancer. Individuals with the gene change that causes FCC have a 20-30% lifetime chance of developing colorectal cancer (compared to the 5% general population risk of developing colorectal cancer and the 10% general risk in Ashkenazi Jews (before testing)).

If you are interested in an appointment for screening, call 713-790-1990

 

TRAITOR McCain

jewn McCain

ASSASSIN of JFK, Patton, many other Whites

killed 264 MILLION Christians in WWII

killed 64 million Christians in Russia

holocaust denier extraordinaire--denying the Armenian holocaust

millions dead in the Middle East

tens of millions of dead Christians

LOST $1.2 TRILLION in Pentagon
spearheaded torture & sodomy of all non-jews
millions dead in Iraq

42 dead, mass murderer Goldman LOVED by jews

serial killer of 13 Christians

the REAL terrorists--not a single one is an Arab

serial killers are all jews

framed Christians for anti-semitism, got caught
left 350 firemen behind to die in WTC

legally insane debarred lawyer CENSORED free speech

mother of all fnazis, certified mentally ill

10,000 Whites DEAD from one jew LIE

moser HATED by jews: he followed the law

f.ck Jesus--from a "news" person!!

1000 fold the child of perdition

 

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Modified Saturday, March 11, 2017

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