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PubMed1980

Genetic studies on Cochin Jews in Israel: 1. Population data, blood groups, isoenzymes, and HLA determinants.

The period in which Jews were first associated with Cochin and the Malabar coast was by tradition, after the destruction of the First Temple (586 BCE). Yet, the earliest evidence of Jewish settlements is from the tenth century CE. The largest group of Cochin Jews are the "Black Jews," of whom about 4,000 live in Israel. A high frequency of consanguineous marriages prevailed among Cochin Jews. Their mean height and weight were low when they came to Israel in 1954; an increase in both was observed 20 years later. Some of the allele frequencies of blood groups, isoenzymes, and HLA antigens were similar to those in other Jewish communities. In the high O, M, cde, and HLA-A28 and the low cDE allele frequencies Cochin Jews resembled Yemenite Jews. A few allele frequencies, the high Fya, AK2 and the low Jka and Hp1, were similar to those observed in indigenous southern Indian populations. In most HLA antigen and haplotype frequencies the Cochin Jews showed a distribution similar to that observed in other Jews and Caucasoids. No comparable HLA data on southern Indian populations were available. The results indicate that Cochin Jews have similarities with Jews, in particular Yemenite Jews, and with the indigenous populations of southern India.

Anthropometry↗
PubMed1980

Gm and Inv [Km] allotypes among Libyan and Ashkenazi jews, and Armenians living in Israel.

Serum samples from Armenians, and from Libyan and Ashkenazi Jews living in Israel were tested for Gm (1, 2, 3, 5, 6, 10, 11, 13, 14, 17, 21, 24, 26) and for Inv(1) [Km (1)]. The Gm data indicate that all three populations have Negroid and Mongoloid admixture. The minimum amount of admixture varies from 3.1% (Armenians) to 5.5% (Libyan Jews). This admixture had not been detected by the study of other polymorphisms, thus once again underlining the sensitivity of the Gm system. The haplotype frequencies among the Libyan Jews are markedly different from those among the Ashkenazi Jews. Surprisingly (coincidentally?) the haplotype frequencies among the Ashkenazi Jews and the Armenians are similar. The Libyan Jews have a significantly higher frequency of Inv1 than to the Ashkenazi Jews and among the latter, Inv1 is at least twice as frequent among Polish Jews as it is among Russian Jews.

Armenia↗
PubMed2004

Cancer in Jews: introduction and overview.

This article is based upon a literature overview of cancer in Jews. It involves a comparison of variation in incidence and prevalence rates between Jews and non-Jews. However, the reader must exercise a certain amount of skepticism when considering secular changes in cancer incidence and prevalence and the public health implications of such cancer variation. Ashkenazi Jews have a lifetime CRC risk of 9--15%. This elevated CRC risk is similar to that of individuals in the "familial risk'' category, and differs strikingly from the 5-6% CRC risk for non-Ashkenazi members of general Western populations. A MedLine search tested the hypothesis that site-specific and/or all-cancer incidence and mortality rates are either higher or lower than expected in Ashkenazi Jews worldwide, when compared with reference populations. Results showed that all cancer incidence and mortality is not higher in Ashkenazi Jews when compared to North American non-Hispanic whites. Indeed, rates for some cancers, such as carcinoma of the lung in Ashkenazi males, are low; this example is likely attributable in large part to decreased tobacco use. Carcinoma of the ovary, pancreas, stomach, and non-Hodgkin's lymphoma have a higher incidence rate in Ashkenazi. Even though BRCA1 and BRCA2 founder mutations which predispose to carcinoma of the breast and ovary appear increased in Ashkenazi breast cancer affected women, there was no evidence supporting an elevated risk of breast cancer among Ashkenazi women. Our primary concern, however, is that Ashkenazi Jews may have one of the highest lifetime CRC risks of any ethnic group in the world, a risk that diverges significantly from that of the general population; therein, it logically calls for more intensive CRC screening guidelines. We have emphasized that the reader use caution in the interpretation of statistics which portray variation in incidence and prevalence figures for cancer in any racial, ethnic, or religious group, inclusive, of course, of Jews. Clearly, more research will be required in the interest of accuracy in the understanding of these cancer variations, since they portend the need for special cancer control strategies. A lesser degree of attention can then be given to carcinoma of the penis and uterine cervix, which occur very infrequently in Jews. We urge our colleagues to continue to probe further into these statistical differences in cancer's incidence and prevalence in order to garner a better understanding of cancer's etiology and pathogenesis.

Breast Neoplasms↗
PubMed2004

A bridge between hearts: mutual organ donation by Arabs and Jews in Israel.

BACKGROUND: The availability of organ transplants depends largely on the will of the donor families. Given the current state of affairs in Israel, the authors evaluated the stance of Jews and Arabs toward mutual organ donations. METHODS: Between October 1997 and December 1999, there were 4.8 million Jews and 1.09 million Arabs living in Israel. Data gathered from 22 general hospitals for this period yielded 373 potential organ donors and 171 families (45.8%) that consented to the procedure. Actual donation was obtained from 157 patients. The authors examined the characteristics of the potential organ donors and organ recipients and the reasons (religious and nonreligious) for familial consent or refusal. Donation made since onset of the Intifada (armed Palestinian resistance) was also reviewed to determine whether any changes took place. RESULTS: Consent was obtained from 48.9% of the Jewish families approached, 30.7% of the Muslim Arabs, and 66.6% of the Christian Arabs. For the whole sample, altruism was the main reason for consenting. The percentages of Arabs and Jews (per population) on the waiting list for a heart (Jews, 90%; Arabs, 10%) or liver (Jews, 78.66%; Arabs, 21.34%) and who received a heart (Jews, 90%; Arabs, 10%) or liver (Jews, 78.36%; Arabs, 21.64%) were similar. There were relatively more Arab recipients of kidney transplants (waiting list, 11%; recipients, 18.6%) because of the higher percentage of children in the Arab group who were given priority. Since September 2000 (start of the Intifada), there has been a trend toward an increasing rate of refusal to donate among Arabs (consent obtained in 52.9% of Jewish families approached vs. 27.9% of the Muslim Arabs), mainly because of fear of rejection by the community for cooperating with Jews. CONCLUSIONS: The rate of organ donations among Arabs and Jews in Israel is proportional to their representation in the general population. The main reason for donating organs is altruism. Apparently, altruism cuts across the boundaries of religion and ethnic groups, even in a country where conflict prevails. We trust that progress in the international arena will bring the current cycle of violence to an end and allow humanitarian values to take preference over politics.

Adult↗
PubMed1997

The two common mutations causing factor XI deficiency in Jews stem from distinct founders: one of ancient Middle Eastern origin and another of more recent European origin.

Previous studies showed that factor XI (FXI) deficiency commonly observed in Ashkenazi Jews is caused by two similarly frequent mutations, type II (Glu117stop) and type III (Phe283Leu) with allele frequencies of 0.0217 and 0.0254, respectively. In Iraqi Jews, who represent the ancient gene pool of Jews, only the type II mutation was observed with an allele frequency of 0.0167. In this study we sought founder effects for each mutation by examination of four FXI gene polymorphisms enabling haplotype analysis in affected Jewish patients of Ashkenazi, Iraqi, and other origins and in Arab patients. Initial population surveys of 387 Middle Eastern Jews (excluding Iraqi Jews), 560 North African/Sephardic Jews, and 382 Arabs revealed allele frequencies for the type II mutation of 0.0026, 0.0027, and 0.0065, respectively. In contrast, the type III mutation was not detected in any of these populations. All 60 independent chromosomes bearing the type III mutation were solely observed in Ashkenazi Jewish patients and were characterized by a relatively rare haplotype. All 103 independent chromosomes bearing the type II mutation in patients of Ashkenazi, Iraqi, Yemenite, Syrian, and Moroccan Jewish origin and of Arab origin were characterized by another distinct haplotype that was rare among normal Ashkenazi Jewish, Iraqi Jewish, and Arab chromosomes. These findings constitute the first example of a mutation common to Ashkenazi Jews, non-Ashkenazi Jews, and Arabs and are consistent with the origin of type II mutation in a founder before the divergence of the major segments of Jews. Our findings also indicate that the type III mutation arose more recently in an Ashkenazi Jewish individual.

Africa, Northern↗
PubMed1999

Prevalence of the I1307K APC gene variant in Israeli Jews of differing ethnic origin and risk for colorectal cancer.

BACKGROUND & AIMS: Israeli Jews of European birth, i.e., Ashkenazim, have the highest colorectal cancer incidence of any Israeli ethnic group. The I1307K APC gene variant was found in 6.1% of American Jews, 28% of their familial colorectal cancer cases, but not in non-Jews. We assessed the I1307K prevalence in Israeli Jews of differing ethnic origin and risk for colorectal cancer. METHODS: DNA samples from 500 unrelated Jews of European or non-European origin, with or without a personal and/or family history of neoplasia, were examined for the I1307K variant by the allele-specific oligonucleotide (ASO) method. RESULTS: In persons at average risk for colorectal cancer, I1307K was found in 5.0% of 120 European and 1.6% of 188 non-European Jews (P = 0.08). It occurred in 15.4% of 52 Ashkenazi Israelis with familial cancer (P = 0.02) and was not detected in 51 non-European Jews at increased cancer risk. Colorectal neoplasia occurred personally or in the families of 13 of 20 Ashkenazi I1307K carriers, 8 of whom also had a personal or family history of noncolonic neoplasia. CONCLUSIONS: The I1307K APC variant may represent a susceptibility gene for colorectal, or other, cancers in Ashkenazi Jews, and partially explains the higher incidence of colorectal cancer in European Israelis.

Adenomatous Polyposis Coli Protein↗
PubMed1998

High frequency of a common Bloom syndrome Ashkenazi mutation among Jews of Polish origin.

Bloom syndrome (BS) is an autosomal recessive disorder characterized by small stature, immunodeficiency, chromosomal instability, and a predisposition to different types of cancer. Although extremely rare in the general population, BS is seen in about 1 in 48,000 Ashkenazi Jews. Mutation analysis of seven Ashkenazi BS probands has shown that all were homozygous for the same mutation in the BLM gene: 2281delATCTGAinsTAGATTC, also known as blmAsh. This finding, along with the increased incidence of BS among Ashkenazi Jews, suggests a founder effect for BS in this population. The purpose of this study was to determine the frequency of blmAsh mutation carriers in a randomly sampled Ashkenazi Jewish population in Israel. The initial study group included 1,613 Ashkenazi Jews who were referred for routine DNA screening tests (cystic fibrosis, Gaucher, Canavan, fragile X). None had a family history of BS. A group of 552 non-Ashkenazi Jews served as controls. Mutation analysis was performed by PCR amplification followed by analysis of a specific BstN1 restriction site, created by the blmAsh mutation. All positive carriers were confirmed by direct sequencing. Sixteen blmAsh carriers were detected among 1,613 Ashkenazi Jews (1 in 101), compared to none among 552 non-Ashkenazi individuals. In this study, Ashkenazi Jews of biparental Polish descent had a significantly higher proportion of the blmAsh mutation (1 in 37) compared to Ashkenazi Jews of non-Polish descent. These results provide further evidence that a founder effect is responsible for the increased incidence of Bloom syndrome among Ashkenazi Jews, particularly those of Polish descent.

Adenosine Triphosphatases↗
PubMed1989

Bulgarian Jews in Israel: genetic blood markers. Red-cell antigens, serum proteins and red-cell isozymes.

Two hundred and sixteen unrelated Bulgarian Jews were typed for the following genetic systems: ABO, MNS, Rh, Kell and Duffy of the blood groups; ADA, AK1, ACP1, ESD, GLO, PGD, PGM1 and PGM2 of the red-cell enzymes, and for the serum proteins HP, GC and PI. A comparison of observed gene frequencies with those of two other Sephardi Jewish groups, from Libya and Morocco, disclosed significant heterogeneity in several systems. This was mostly due to Moroccan Jews differing from Bulgarian or from both the Libyan and Bulgarian Jews. A comparison of gene frequencies in Bulgarian Jews with those in Oriental Jews from Iraq and in Ashkenazi Jews from Poland disclosed a similarity between the three groups in Rh, ADA, GLO, PGM1 and HP. The frequencies for the above systems in the three groups were closer to those of Middle Easterners than to those of Europeans. A different pattern was observed for GC and PI, in which Bulgarian resembled Polish Jews and differed significantly from Iraqi Jews. This probably reflects an outcome of convergent adaptive processes.

Adult↗
PubMed2001

Do Ashkenazi Jews have a higher than expected cancer burden? Implications for cancer control prioritization efforts.

BACKGROUND: Recent genetic susceptibility findings in Jews of Eastern European descent, commonly called Ashkenazi Jews, have led to concerns that they may be stigmatized as being more cancer prone than other groups. OBJECTIVE: To examine the hypothesis that site-specific or all-cancer incidence and mortality rates are higher than expected in Ashkenazi Jews worldwide when compared with referent populations. METHODS: A MEDLINE search was performed using keywords "Jews," "cancer," "incidence" and "mortality" to identify studies directly relevant to the primary study question. RESULTS: Little evidence suggested that all-cancer incidence or mortality is higher in Ashkenazi Jews than in North American non-Hispanic whites. Ashkenazi Jewish men appear to have relatively low cancer rates, which may be due to lower tobacco use. Colorectal cancer was shown to disproportionately overburden Ashkenazi Jews, who may also be at increased risk for ovarian, pancreatic and stomach cancer, and non-Hodgkin's lymphoma. Little evidence was found supporting an elevated risk of breast cancer in Ashkenazi Jewish women. Rates of lung, cervical, penile and prostate cancers appear low in this population. Rate disparities were generally attributed to lifestyle differences, particularly diet and tobacco use, rather than to genetic predisposition. CONCLUSIONS: Ashkenazi Jews do not appear to have a higher total cancer burden than comparable North American populations. Any cancer rate differentials in this group are more likely to be related to lifestyle and dietary factors than to genetics. However, colorectal cancer rates in Ashkenazi Jews may be the highest of any ethnic group in the world and cancer controllers should consider this when developing future screening, diagnostic and policy strategies.

Humans↗
PubMed2003

A novel NOD2/CARD15 haplotype conferring risk for Crohn disease in Ashkenazi Jews.

Crohn disease (CD) exhibits a 2-4-fold increased frequency in Jews as compared with other ethnic/racial groups. Three coding variants of the NOD2/CARD15 have been reported as independent disease-predisposing mutations (DPMs), but these were found in only 30%-40% of patients with CD and could not account for all the linkage between CD and the IBD1 locus. The aim of the present study was to explore whether additional DPMs at the IBD1 locus exist in the high-risk Jewish group. Sixty-four Ashkenazi Jewish and 147 non-Jewish white families were studied. Six microsatellite markers spanning IBD1 were genotyped for linkage analysis in subgroups stratified on NOD2/CARD15 DPM status. SNPs in NOD2/CARD15 (R702W, G908R, 1007fs, and S268P) were then genotyped in family and independent case-control samples. On the basis of initial results, sequencing was done on NOD2/CARD15-translated regions in 12 Jewish individuals. Subsequently, a new NOD2/CARD15 variant was genotyped and analyzed. After excluding the influence of the three DPMs, significant linkage of IBD1 to CD in Jews remained with two peaks at D16S403 (mean allele sharing [MAS] = 0.70] and D16S411 (MAS = 0.59). Further, we observed an increased frequency of a haplotype carrying only the 268S variant in Jewish patients (OR = 3.13, P=.0023) but not in non-Jews, suggesting the existence of a Jewish-specific additional disease-predisposing factor on this haplotype. Sequencing of this haplotype revealed a new variant (IVS8+158; JW1). The 268S-JW1 combination exhibited a further increased risk (OR = 5.75, P=.0005) and the highest population-attributable risk (15.1%) for CD among reported DPMs in Jews. In Ashkenazi Jews, unrecognized population-specific predisposing factor(s) exist on the 268S-JW1 haplotype at the IBD1 locus. This factor may contribute to the higher risk for CD in Ashkenazi Jews as compared with non-Jews.

Amino Acid Substitution↗
PubMed1999

Mendelian diseases among Roman Jews: implications for the origins of disease alleles.

The Roman Jewish community has been historically continuous in Rome since pre-Christian times and may have been progenitor to the Ashkenazi Jewish community. Despite a history of endogamy over the past 2000 yr, the historical record suggests that there was admixture with Ashkenazi and Sephardic Jews during the Middle Ages. To determine whether Roman and Ashkenazi Jews shared common signature mutations, we tested a group of 107 Roman Jews, representing 176 haploid sets of chromosomes. No mutations were found for Bloom syndrome, BRCA1, BRCA2, Canavan disease, Fanconi anemia complementation group C, or Tay-Sachs disease. Two unrelated individuals were positive for the 3849 + 10C->T cystic fibrosis mutation; one carried the N370S Gaucher disease mutation, and one carried the connexin 26 167delT mutation. Each of these was shown to be associated with the same haplotype of tightly linked microsatellite markers as that found among Ashkenazi Jews. In addition, 14 individuals had mutations in the familial Mediterranean fever gene and three unrelated individuals carried the factor XI type III mutation previously observed exclusively among Ashkenazi Jews. These findings suggest that the Gaucher, connexin 26, and familial Mediterranean fever mutations are over 2000 yr old, that the cystic fibrosis 3849 + 10kb C->T and factor XI type III mutations had a common origin in Ashkenazi and Roman Jews, and that other mutations prevalent among Ashkenazi Jews are of more recent origin.

Alleles↗
PubMed1984

Social locations and interpretations: how Jews define alcoholism.

A study of 88 Jews in central New York State, in which respondents were encouraged to discuss their opinions on alcoholism in depth through open-ended verbal questions, revealed differences between the various Jewish denominational affiliations. Orthodox Jews tend to offer disease definitions of alcoholism and their major response to suspected alcoholics is fear, whereas Reform and nonpracticing Jews define alcoholism in terms of psychological dependency and view suspected alcoholics with condemnation and blame. The groups' experiences with drinking and alcoholism also differ. The Orthodox Jews drink on special and sacramental occasions and report not having known any heavy drinkers; Reform and nonpracticing Jews integrate drinking into their daily social interactions and have known persons considered to be alcoholics. Conservative Jews discuss definitions and experiences of drinking and alcoholism with a lack of clarity and their views are midway between those of the Orthodox and those of the Reform and nonpracticing Jews. It is suggested that the places of groups within society and in networks of related groups parallel the interpretations that members hold concerning social phenomena.

Adolescent↗
PubMed1981

Genetic polymorphisms among Iranian Jews in Israel.

Iranian Jews represent a very ancient Jewish community with a high frequency of inbreeding. A sample of Iranian Jews, mainly unrelated students, was tested for genetic markers of red blood cells and serum. The frequency of glucose-6-phosphate dehydrogenase deficiency was not uniform among Jews who had lived in different areas of Iran; it was lower among those from central Iran (6.7%) than in those from southern and western Iran (16.7% and 20.6%, respectively). The frequencies of B, CDe, cDE, S, and K alleles were among the highest recorded in Jewish ethnic groups. Iranian Jews were similar to Iraqi Jews with respect to the frequencies of the blood markers B, CDe, cde, cDe, ACP, PGM1, ADA, and Hp; however, the B and CDe markers occur with similar frequencies among indigenous Iranians. The presence of the cDe allele and the Gm1,5,13,14,17 haplotype in low frequencies indicates black admixture. Mongoloid admixture is indicated by the polymorphism of the Gm1,13,15,16,17 haplotype. The very rare phenotype Gm(3,5,13,14,17) was observed in 4.8% of 167 individuals tested. This phenotype has not been previously observed among Jews.

Blood Group Antigens↗
PubMed2002

Male breast carcinoma in Israel: higher incident but possibly prognosis in Ashkenazi Jews.

BACKGROUND: Little information is available regarding male breast carcinoma. However, cumulative data have suggested a propensity for the disease among Ashkenazi Jews. Because Ashkenazi Jews comprise one of the major ethnic groups in Israel, the authors conducted a local study to shed more light on the features of this rare disease. METHODS: From 1960 to 2000, 131 men with breast carcinoma were treated at the Rabin Medical Center or the Rambam Medical Center, and, from 1980 to 1997, 470 patients with this diagnosis were recorded in the Israel Cancer Registry. These two data bases were used to analyze the epidemiologic and clinicopathologic characteristics of male breast carcinoma in Israel. RESULTS: Seventy-eight percent of the 131 Jewish patients were Ashkenazi. Most of their clinical characteristics were similar to those of their Sephardic counterparts. However, there was a statistically significant difference in the pattern of comorbidity between these groups (P = 0.000), and there was a trend toward a younger age at onset and more advanced tumor stage at the time of diagnosis for the Sephardim. It also was found that Sephardic origin was associated with poorer outcome (P = 0.03). Analysis of the Cancer Registry data base revealed an 80% increase in the risk of the disease for Ashkenazi Jews compared with Sephardic Jews (odds ratio, 1.8; 95% confidence interval, 1.4-2.3; P = 0.001). Survival analysis from this source suggested a poorer outcome for Sephardic Jews compared with Ashkenazi Jews (62% vs. 64.3% estimated 5-year survival rates, respectively; P = 0.08). CONCLUSIONS: Analyses of two independent data bases, patient charts, and a cancer registry indicate that breast carcinoma seems to be more prevalent among Ashkenazi Jewish men. At the same time, affected Ashkenazi patients may have a more favorable outcome than their Sephardic counterparts.

Adenocarcinoma↗
PubMed2003

Constitutively increased neutrophil surface expression of beta2-integrin in Yemenite Jews.

The aim of this study was to analyze surface expression of neutrophil adhesion molecules in Yemenite Jews as compared to other ethnic populations in Israel. The constitutive neutrophil expression of CD11b and L-selectin (LS), as well as their expression in response to an in vitro chemoattractant and growth factor stimulation were studied by flow cytometry. Mean surface expression of CD11b molecule was statistically significantly increased among the Yemenite Jews tested compared to the non-Yemenite Jews (327.1 +/- 129.2 vs. 237.0 +/- 133.1; p = 0.002), with no significant correlation to their absolute neutrophil count. LS expression was similar in the two study groups. In vitro analysis of CD11b and LS expression induced by chemoattractant and G-CSF showed no difference between neutrophils of Yemenite versus non-Yemenite Jews. The study results suggest that in Yemenite Jews, circulating neutrophils display significantly increased expression of beta2-integrin molecules on their surface compared to non-Yemenite Jews.

Adult↗
PubMed1997

Cystic fibrosis in Jews: frequency and mutation distribution.

The incidence of cystic fibrosis and the frequency of disease causing mutations varies among different ethnic groups and geographical regions around the world. The Jewish population is comprised of two major ethnic groups. Ashkenazi and Non-Ashkenazi. The latter is further classified according to country of origin. An extreme variability in the disease frequency (from 1:2400-1:39,000) was found among the different Jewish ethnic groups. In the entire Jewish CF population, only 12 mutations were identified that altogether enable the identification of 91% of the CF chromosomes. However, in each Jewish ethnic group, the disease is caused by a different repertoire of a small number of mutations. In several ethnic groups, there is a major CFTR mutation that accounts for at least 48% of the CF chromosomes. High proportion of the CF chromosomes can be identified in Ashkenazi Jews (95%), Jews originating from Tunisia (100%), Libya (91%), Turkey (90%), and Georgia (88%). High frequencies of CFTR mutations were found among infertile males with CBAVD who might not have additional CF clinical characteristics. Of the Jewish males with CBAVD, 77% carried at least one CFTR mutation. The 5T mutation is the major mutation in Jewish CBAVD affecteds accounting for 32% of the chromosomes among Ashkenazi Jews and 36% among the non-Ashkenazi Jews. Five additional CFTR mutations, W1282X (12%), delta F508 (9%), N1303K (3%), D1152H, (5%)), and R117H (1%) were identified among Ashkenazi Jews with CBAVD. Only two mutations, delta F508 and R117H, were found among non-Ashkenazi males with CBAVD. An increased frequency of the 5T allele was also found among Jewish patients with atypical CF presentation, 18% in Ashkenazi, and 10% in non-Ashkenazi Jews. In summary, we present the required information for genetic counseling of Jewish families with typical and atypical CF and for carrier screening of healthy Jewish individuals.

Alleles↗
PubMed2000

The power and limits of ethnonationalism: Palestinians and Eastern Jews in Israel, 1974-1991.

The relative standings of four ethnic groups - Muslim Palestinians, Christian Palestinians, Asian-African Jews, European Jews -were compared, using mobility data from 1974 and 1991. The findings show that despite the lack of government support and the prevalence of inexorable discrimination against Israeli Palestinians, they have narrowed the gap with Asian-African Jews in both education and occupational prestige. This finding demonstrates that ideological and political hegemony is not always effective in improving the socio-economic standing of preferred minorities (Asian-African Jews), and that social and economic structures may counterbalance the anti-Palestinian nationalist ideology. The analysis suggests that residential and educational segregation of Palestinians protects them from direct competition with European Jews, whereas Asian-African Jews have to compete with this dominant group in schools, as well as in the labour market.

Adolescent↗
PubMed2001

The IBD1 locus for susceptibility to Crohn's disease has a greater impact in Ashkenazi Jews with early onset disease.

OBJECTIVE: Recent studies have suggested that a susceptibility gene located on chromosome 16 and designated IBD1 may contribute to the development of Crohn's disease (CD). However, these findings were observed in predominantly non-Jewish populations; in the three studies where Ashkenazi Jews were included for analysis, the results have been widely divergent. Because Ashkenazi Jews are known to have a higher incidence of the disease than non-Jews, we sought to determine whether this previously reported linkage could be extended to the Ashkenazi population. In addition, we examined whether Ashkenazi Jewish patients with an early age of onset (< or = 21 yr) showed greater evidence of linkage to this locus. METHODS: Linkage analysis for the IBD1 region was performed on 123 Ashkenazi Jewish CD patients distributed among 53 families. Only patients with four Jewish grandparents were considered to be Jewish. Of the 123 Ashkenazi Jewish patients, 75 (61%) had an age of onset < or = 21 yr. RESULTS: Ashkenazi Jews showed only modest evidence of linkage (nonparametric linkage 1.63, p = 0.05) to the IBD1 locus. However, when the Ashkenazi population was subdivided on the basis of age of onset, there was a striking increase in linkage in families where affected individuals had an age of onset < or = 21 yr (nonparametric linkage 3.02, p = 0.002). In contrast, there was no evidence of linkage in the Jewish families where all affected individuals had an age of onset > 21 yr. CONCLUSIONS: The IBD1 gene plays a greater role in conferring susceptibility to CD in Jews with early onset disease than in Jews with late onset disease.

Adult↗