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Affective disorders among Jews: a historical review and meta-analysis.

Descriptions of affective disorders among Jews date back to biblical times. For over a century the psychiatric literature has debated whether Jews are more vulnerable to affective disorders. To ascertain the validity of this finding we undertook a meta-analysis of data extracted from the literature published to date. Forty-three studies were identified that could be analysed statistically using Cohen's d and a Mantel-Haenszel summary odds ratio. An increased, but weak overall risk was found for males. Possible biases of the literature are discussed, including differential help-seeking patterns, lack of accounting for readmission rates, failure to control for confounding variables, and an anti-Semetic orientation on the part of researchers. Reasons for why Jews have higher rates of affective disorders than non-Jews are explored.

Europe↗

Oculopharyngeal MD among Bukhara Jews is due to a founder (GCG)9 mutation in the PABP2 gene.

OBJECTIVE: To determine whether all cases of oculopharyngeal muscular dystrophy (OPMD) among Bukhara Jews share the same founder mutation. BACKGROUND: Autosomal dominant OPMD is caused by a (GCG)8-13 repeat expansion in the polyadenylation binding protein 2 (PABP2) gene. The disease has a worldwide distribution but is particularly prevalent in Bukhara Jews and in French Canadians, in whom it was introduced by three sisters in 1648. METHODS: We established the size of the PABP2 mutation in 23 Bukhara Jewish patients belonging to eight unrelated families. In all families, we constructed haplotypes for the carrying chromosomes composed of the alleles for eight chromosome 14q polymorphic markers. RESULTS: All patients share a (GCG)9 PABP2 mutation and a four-marker haplotype. Furthermore, a shared intron single nucleotide polymorphism (SNP) in the PABP2 gene 2.6Kb from the mutation was not observed in 22 families with (GCG)9 mutations from nine different countries. The smaller size of the chromosomal region in linkage disequilibrium around the mutation in Bukhara Jews, as compared with French Canadians, suggests a founder effect that occurred more than 350 years ago. Based on the Luria-Delbrück corrected "genetic clock," we estimate that the mutation appeared or was introduced once in the Bukhara Jewish population between AD 872 and 1512 (mean, AD 1243). CONCLUSION: OPMD among Bukhara Jews is the result of a shared, historically distinct, PABP2 (GCG)9 mutation that likely arose or was introduced in this population at the time they first settled in Bukhara and Samarkand during the 13th or 14th centuries.

Genetic Linkage↗

[Tuberculosis among Jews and blacks in the US: the medical-anthropological debate on racial differences in predisposition to a disease, 1850-1920].

This article analyses historic models of the susceptibility to tuberculosis among American Jews and African Americans. Both medical and anthropological accounts from the period studied (1850-1920) reflect a very low TB rate among Jews, while attributing a very high disease rate to African Americans. Explanations for this difference between the two ethnic groups varied over the passing decades, reflecting changing conceptions of the 'anthropological nature' of Jews and African Americans. This article attempts to show the extent to which the medical and anthropological disciplines were interconnected and mutually influential. Firstly, Jews and African Americans were considered to be 'other' because they exhibited specific nosological behaviour. In addition, white Gentile doctors attributed different disease susceptibilities to these groups because they appeared to constitute a 'peculiar type'.

Black or African American↗

The I1307K adenomatous polyposis coli gene variant does not contribute in the assessment of the risk for colorectal cancer in Ashkenazi Jews.

Ashkenazi Jews with the I1307K adenomatous polyposis coli gene variant were suggested to confer a higher risk for colorectal cancer (CRC). We assessed the clinical importance of this polymorphism in Israeli Jews at average and elevated risk for CRC. Among 1,370 consecutive subjects that were examined, 975 Ashkenazi Jews were stratified into those at average risk (no personal or family history of colorectal neoplasia) and those at high risk. DNA was obtained from peripheral leukocytes and amplified by PCR, with primers designed to detect the I1307K variant. Overall, I1307K polymorphism was found in 7.1% (9.1% among Ashkenazi and 1.7% among non-Ashkenazi Jews). The carrier rate was 8.3 and 9.3% in average and high-risk Ashkenazim, respectively (P = 0.65). The overall odds ratio for neoplasia in carriers was 1.43 (95% confidence interval, 0.89-2.30). Age, gender, and the histopathological features of adenomas and cancers did not differ between carriers and noncarriers. No interaction on the CRC risk was found between I1307K variant and lifestyle modifiers (such as cigarette smoking, alcohol consumption, high body mass index, low physical activity, and vitamins/antioxidant intake). The I1307K adenomatous polyposis coli gene variant is not an important marker for increased risk for CRC. It confirms previous reports of a slight nonsignificant increase (OR, 1.4) in the risk of CRC in these carriers. There is no interaction effect on the risk of colorectal neoplasia between the I1307K variant and various lifestyle risk factors. The usual recommended screening and surveillance strategies should be used for carriers of this polymorphism.

Adenomatous Polyposis Coli Protein↗

The gene for familial Mediterranean fever in both Armenians and non-Ashkenazi Jews is linked to the alpha-globin complex on 16p: evidence for locus homogeneity.

Familial Mediterranean fever (FMF) is a recurrent inflammatory disorder characterized by short episodes of fever, peritonitis, pleuritis, and arthritis. While FMF has been shown to be inherited in an autosomal recessive fashion in both non-Ashkenazi Jews and Armenian families, clinical differences have raised the possibility of genetic heterogeneity. As its pathogenesis is unknown, mapping of the gene for FMF may provide the first objective method for early and accurate diagnosis of this disease. After excluding 45% of the entire human genome, we studied 14 Armenian and 9 non-Ashkenazi Jewish families with FMF and tested linkage with the alpha-globin locus on chromosome 16. Analysis of the PvuII length polymorphism of the 3' HVR (hypervariable region) probe showed significant linkage with the FMF gene (maximum lod score [lodmax] = 9.76 at maximum recombination fraction [theta] = .076). In the Armenians, the lodmax = 3.61 at theta = .10; and for the non-Ashkenazi Jews, lodmax = 6.28 at theta = .06. There was no evidence for genetic heterogeneity between the Armenians and the non-Ashkenazi Jews (chi 2 = 1.28; P = .26) or within either ethnic group (chi 2 = .00; P = .50). Thus, the gene for FMF is linked to the alpha-globin complex on chromosome 16p in both non-Ashkenazi Jews and Armenians.

Armenia↗

Familial leukopenia among Yemenite Jews.

Benign familial leukopenia was found in 75 of 200 healthy Yemenite Jews examined. The leukopenia was not a constant finding and was not associated with a tendency toward infection. HLA typing showed no significant differences in the frequency of the various HLA antigens between the subjects with and without leukopenia. No similarity was found between the HLA of the Yemenite Jews with leukopenia and that reported in black Africans with benign familial leukopenia. The suggestion of a genetic contribution from African blacks to Yemenite Jews is not supported by these results. The question remains to be answered whether the familial leukopenia in Yemenite Jews and black Africans is the result of a mutation.

Adolescent↗

Ala244Val is a common, probably ancient mutation causing factor VII deficiency in Moroccan and Iranian Jews.

We investigated the molecular basis for factor VII (FVII) deficiency in Israel and found that 13 patients were homozygous and 10 heterozygous for a C to T substitution at nucleotide 10648 of the FVII gene. This predicted an Ala244Val change and was associated with decreased FVII activity and antigen level. Of the 36 Ala244Val positive alleles, 20 were observed in patients of Moroccan origin, 10 in Iranian-Jewish patients and 6 in patients of other origins. A computer model of the serine protease domain of FVII suggested that the Ala244Val substitution may cause distortion of the entire protein structure. Intragenic polymorphic sites analyses disclosed a founder effect for the Moroccan and Iranian-Jewish patients. A survey of the Ala244Val mutation revealed an allele frequency of 1:42.5 in Moroccan Jews and 1:40 in Iranian Jews. As Moroccan Jews have been separated from Iranian Jews for more than two millennia, the data suggest that the Ala244Val mutation occurred in ancient times.

Alanine↗

Changing patterns of internal migration 1970-1990: a comparative analysis of Jews and whites in the United States.

Independently conducted yet complementary sets of data from the 1970/1971 and 1990 National Jewish Population Surveys and the U.S. censuses of the same years were used to analyze changes in the internal migration of Jews and whites during the periods 1965-1970(1971) and 1985-1990. Interstate lifetime and five-year migration rates among Jews increased to levels significantly surpassing those of whites. Adjusting Jewish migration rates for the educational achievement of their white counterparts did not have much of an effect on lifetime migration or on the recent migration of the 1970/1971 Jewish population; however, it accounted meaningfully for the migration propensities of Jews in the period 1985-1990. These findings suggest that socioeconomic status has begun to play a larger role in promoting different migration patterns than in promoting ethnic group differences. Further, the direction of Jewish migrations followed those of whites (i.e., from the North-east and Midwest to the South and West): and due to their higher migration rates, Jews have considerably narrowed the regional distribution differences between themselves and whites. I interpret these results as evidence of the weakening role of ethnicity in present-day America.

Acculturation↗

Water-soluble viscous substance of Jew's mellow leaves lowers serum and liver cholesterol concentrations and increases fecal steroid excretion in rats fed a high cholesterol diet.

The effect of Jew's mellow leaf powder and its water soluble viscous substance on cholesterol metabolism in rats fed a high cholesterol diet was examined. When compared to the controls, total serum and liver cholesterol concentrations were significantly decreased or tended to decrease in the groups given dry powder of fresh Jew's mellow leaves, dry powder purchased from the market or residual powder after extracting with ethanol, whereas no difference was observed in those given residual powder after extracting with water. There were significant increases or increasing tendencies in the fecal excretion of bile acids, total neutral sterols and cholesterol in those fed the experimental diets when compared to the control group. Rats fed a diet containing a water-soluble viscous substance (1.7%, about 1% as dietary fiber) obtained from the dry powder of Jew's mellow leaves showed significant decreases in serum and liver cholesterol concentrations and increases in fecal excretions of bile acids and neutral sterols. Based on the above, the component of dry powder of Jew's mellow leaves that is effective in decreasing serum and liver cholesterol concentrations was found to be a soluble dietary fiber, and the mechanism was assumed to be largely due to the increased excretion of bile acids and neutral sterols.

Animals↗

Tay-Sachs disease and HEXA mutations among Moroccan Jews.

Moroccan Jewry (N>750,000) is the only non-Ashkenazi Jewish community in which Tay-Sachs disease (TSD) is not extremely rare. Previous studies among Moroccan Jewish TSD families identified three HEXA mutations. In this study, extended to enzyme-defined and new obilgate TSD carriers, we found four additional mutations. One of them is a novel, IVS5-2(A-->G) substitution, resulting in exon skipping, and it was found only among enzyme-defined carriers. The seven HEXA identified mutations among Moroccan Jews are: deltaF(304/305), R170Q, IVS-2(A-->G), Y180X, E482K, 1278+TATC, and IVS12+1(G-->C). Their respective distribution among 51 unrelated enzyme-defined and obligate carriers is 22:19:6:1:1:1:1. The mutation(s) remain unknown in only three enzyme-defined carriers. Five of the seven Moroccan mutations, including the three most common ones, were not found among Ashkenazi Jews. Compared with the much larger and relatively homogeneous Ashkenazi population, the finding among Moroccan Jews probably reflects their much longer history.

Heterozygote↗

Prevalence of Lithuanian mutation among St. Petersburg Jews with familial hypercholesterolemia.

We used polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis to detect LDL receptor gene defects in the St. Petersburg population. We have found a deltaG197 mutation in several patients of Jewish origin. The mutation named is shown to be responsible for one-third (7/23) of familial hypercholesterolemia (FH) cases in St. Petersburg Jews and absent in patients of Russian descent. The prevalence of a deltaG197 mutation in St. Petersburg Jews is consistent with its origin in Lithuania or Poland. The deltaG197 mutation can be easily detected in polyacrylamide minigels because of formation of specific heteroduplexes during PCR with DNA of heterozygous patients. Taken together with high prevalence of the mutation in St. Petersburg Jews, this observation provides an opportunity for DNA diagnostics of FH in this ethnic group.

DNA Mutational Analysis↗

High frequency of congenital adrenal hyperplasia (classic 11 beta-hydroxylase deficiency) among Jews from Morocco.

Steroid 11 beta-hydroxylase deficiency is relatively frequent in Israel among North African Jews. Over a 39-year period, 38 affected individuals from 25 families were diagnosed. Nineteen families came from Morocco, and in another 2, one parent came from Morocco (80% of all parents). Demographic studies showed that most of their grandparents were born in the region of the Atlas Mountains. In Israel, the overall incidence of the disorder is estimated between 1 in 30,000 to 1 in 40,000 births, but in offspring of Moroccan Jews the ratio is 1 in 5,000 to 1 in 7,000, with an allele frequency of 1 in 70 to 1 in 84 and a carrier frequency of 1 in 35 to 1 in 42. The clinical expression is characterized by a wide range of variability in the signs of androgen and mineralocorticoid excess. Virilization in the female ranged from enlarged clitoris in the mildest forms, to markedly hypertrophied clitoris with penile urethra and fused labial-scrotal folds in the most severe forms. Hypertension causing vascular accidents and death was observed in both severe and mildly virilized patients, whereas masculinized females were sometimes normotensive. Based on historical evidence, the origin of the ancestors, and the onomastic analysis of the families surnames, we propose that the mutation of 11 beta-hydroxylase deficiency in Jews from Morocco may have originated in either the ancient Jewish settlers or the native Berber tribes who lived in the region of the Atlas Mountains in the southern region of Morocco before the destruction of the Second Temple by the Romans, in the year 70 C.E.

Adrenal Hyperplasia, Congenital↗

Hereditary disorders among Iranian Jews.

Iranian Jews represent an ancient community with a very high degree of inbreeding. Although the community remained relatively isolated, it had strong ties with Babylonian Jewry in Iraq. Several genetic disorders have been reported to be frequent among Iranian Jews, in particular, corticosterone methyloxydase deficiency type II, polyglandular syndrome, and rimmed vacuole myopathy. Based on the data collected in our clinic, recessive and dominant deafness also appear to be frequent. Other diseases, such as beta-thalassemia, achromatopsia, colobomatous microphthalmia, Dubin-Johnson syndrome, and congenital myasthenia gravis, were frequent in both the Iranian and Iraqi Jewish communities. The place of origin of the families within Iran and the results of molecular studies suggest some reason(s) for the high frequency of these disorders among Iranian Jews. While the high frequency of some of the disorders, such as corticosterone methyloxydase deficiency type II, represents a founder effect, in other diseases (such as beta-thalassemia) it was secondary to heterozygote advantage.

Gene Frequency↗

Ethnic communities in Israel: the genetic blood markers of the Moroccan Jews.

One hundred and ninety-six Moroccan Jews now settled in Israel were typed for 7 blood groups, 12 red cell enzymes and 2 plasma protein systems. Their blood group picture is in agreement with results previously obtained on different samples of Moroccan Jews: rather high B in ABO, somewhat elevated frequencies of cDe and cDE in Rh and K in Kell. Differences in various blood markers exist between them and other North African Jewish communities. This fact, together with data on disease distribution and HLA frequencies, supports our assumption that Jews in the North African diaspora lived as small secluded isolates even within the same geographical zones. Comparisons with meager data on the neighboring non-Jewish populations do not disclose any resemblance to either Arab or Berber inhabitants of Morocco.

Blood Group Antigens↗

Human T-cell lymphotropic virus type I in Iranian-born Mashhadi Jews: genetic and phylogenetic evidence for common source of infection.

High prevalence of human T-cell lymphotropic virus type I (HTLV-I) infection and disease has been identified among Iranian-born Mashhadi Jews, an ethnically segregated, highly inbred population. To determine the origin and genetic diversity of HTLV-I in this group, 1,039 bp spanning selected regions of the HTLV-I gag, pol, env and pX genes were enzymatically amplified and sequenced directly from DNA of five Mashhadi Jews (three with spastic myelopathy and two asymptomatic carriers). Alignment and comparison of these sequences with cosmopolitan and Australo-Melanesian topotypes of HTLV-I indicated that the HTLV-I strains from Mashhadi Jews, which were > or = 99.9% identical among themselves, exhibited considerable sequence similarity (> or = 99%) to HTLV-I strains from southern India, suggesting a common source of infection. Phylogenetic analysis, using the maximum parsimony method, was consistent with a single-source introduction of HTLV-I into the Mashhadi Jewish community.

Adult↗

Dating the origin of the V170M mutation causing non-type I cystinuria in Libyan Jews by linkage disequilibrium and physical mapping of the SLC7A9 gene.

Cystinuria is an autosomal recessive disorder of the transepithelial transport of amino acids, clinically manifested by the development of kidney stones. Mutations in the gene encoding rBAT (SLC3A1, on chromosome 2p16.3) are linked to type I cystinuria, while the SLC7A9 locus (19q13.1), expressing b0,+ AT protein, is involved in non-type I cystinuria, which is very common among Libyan Jews. Applying two methods for linkage disequilibrium analysis to haplotype data spanning six 19q12-q13.1 polymorphic markers, and relying on the physical distances between the markers and the recently mapped SLC7A9 (CSNU3) locus, the age of the founder missense V170M mutation causing non-type I cystinuria in Jews of Libyan ancestry is calculated to be approximately 14 to 15 generations (g) (95% confidence interval: 9-20 g) or slightly more. The estimated age dates the most recent common ancestor of the mutation-bearing chromosomes back to the time (or some decades before) Jewish families settled in Libya following their expulsion from the Iberian Peninsula. This finding makes the molecular population genetics of cystinuria understandable in the context of the Libyan Jews' history.

Amino Acid Substitution↗

Lung cancer histology in major ethnic groups among the Jews. Israel, 1962-1982.

Lung cancer rates in Israel are lower than in other Western countries, not explainable by smoking habits. Due to the different relation of Squamous cell carcinoma (SqCC) and Adenocarcinoma (AC) with smoking it was of interest to study the histologic distribution in Israel. A total of 7508 histologically confirmed lung cancer cases among Jews were studied in the period 1962-82. SqCC was the leading tumor-type in Jewish men and AC in Jewish women. European-American born males in the last study period showed a decrease in SqCC rate while Asian-African born males showed a steep increase in SqCC rate, most prominent among the younger age-groups. Rates of AC increased in both, European-American and Asian-African males, but more steeply in the latter in most age-groups. Only for Large cell carcinoma were the overall rates higher in Asian-African than in European-American born males. SqCC increased in European-American born females and also steeply increased in the over 55 years old Asian-African born females. AC increased in European-American born females (both young and old), but only in the young Asian-African born females (decreasing in the older). European-American born Jews still have higher rates of both, more and less smoking related lung cancer histological types, than Asian-African born Jews. The steep increase in rates of some of the histological types in the latter with the pronounced increased in the younger age-groups is expected to cause a change in the ethnic rate-ratio which has already been demonstrated for the overall lung cancer rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

The polyglandular deficiency syndrome: a new variant in Persian Jews.

Five Persian Jews were detected with the polyglandular deficiency syndrome (PDS). Primary hypoparathyroidism and hypogonadism were present in each, adrenal insufficiency in two, and insulin-dependent diabetes mellitus and latent hypothyroidism in single subjects. The percentage of T and B cells, and the mononuclear cell response to phytohemagglutinin and Concanavalin A were normal in all five. IgG and IgA levels and the OKT4+/OKT8+ cell ratio were low in one subject. Antinuclear and antithyroid antibodies were present in one subject. HLA-DR5 was present in 4/4, HLA-24 and B5 (B51) in 3/4 subjects. A single case of isolated hypoparathyroidism (IHP) was detected among 12 first degree relatives. HLA antigens B8, DR3, were absent in all of these subjects. Seven non-Iranian Jews with IHP were also examined. HLA A26 or A25 were present in all seven. Persian Jews appear to have a unique variant of PDS.

Adolescent↗