ISSN:1042-0533    

DOI:10.1002/ajhb.1310050402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractIt has long been recognized that the prevalence of many, possibly most diseases differs among different ethnic groups, and it is further known that cultural differences among people affect the acceptability of measures to prevent or ameliorate a given disease process. Major public health challenges of our time are the delineation and understanding of how these differences in prevalence arise, and the fashioning of acceptable and effective intervention strategies. The web of causation is undoubtedly complex and in the unraveling there will be a need to examine new paradigms, new models of how genes and environments interact in the evolution of disease. These models must recognize the levels within the disease process where interactions can occur. This will demand a holistic rather than the reductionist approach that has obtained in the past. However, there are promising developments at the molecular and cellular levels, and the methods of data analysis grow progressively more sophisticated. This presentation briefly describes the methods of and problems confronted by genetic epidemiology in the context of studies of ethnic differences in disease. © 1993 Wiley‐Liss, I

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractEthnic variations in health present a useful paradigm for the study of disease etiology. The knowledge base in this area has expanded dramatically in recent years, both as a result of research across cultures and studies within multiethnic societies. The growth in descriptive information, however, has not always been paralleled by an increase in causal explanations. At both the theoretical and practical levels confounding remains an unsolved problem. Because of the frequent correlation between ethnicity, socioeconomic status, and risk exposures it is often difficult to isolate the relative impact of genetics and external risk factors. The importance of variation in allele frequencies in determining ethnic diesease patterns is further complicated by the difficulty in providing precise ethnic group designations. Inference regarding causal relationships becomes particularly challenging for polygenic disorders like hypertension and non–insulin‐dependent diabetes mellitus, where good candidate genes are not available. At the same time, exposures are often known before the genetic basis of susceptibility has been identified and provide a practical basis for prevention. Prevention campaigns should be merged with etiologic research whenever possible and close collaboration among scientists working in public health and epidemiology and those based in genetics and biology would facilitate development of an appropriately balanced strategy. © 1993 Wiley‐Lis

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractConsiderable ethnic variation in the prevalence of non–insulin‐dependent diabetes mellitus (NIDDM) is recognized around the world and provides an interesting case study in the interaction of genetic and environmental factors in disease causation and distribution. Over the past one half century, numerous studies have shown that Native Americans, with some exceptions such as Arctic Eskimos and subarctic Athapaskan Indians, are generally a high risk group for NIDDM. There are, however, regional differences, reflecting the differential effects of genetic susceptibility, level of acculturation, and the contributions of specific risk factors such as physical activity, diet, and obesity. This paper reviews the extensive epidemiological, clinical, and anthropological literature on NIDDM among Native Americans in Canada and the United States. It discusses the extent and magnitude of the problem, etiology and risk factors, the public health impact of its serious complications, strategies for prevention and control, and current attempts to explain the prominence of this metabolic disorder among the indigenous inhabitants of the New World. © 1993 Wiley‐Lis

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractNon–insulin‐dependent mellitus (NIDDM) is a common, multifactorial disease with a significant genetic component to disease susceptibility. Biometrical analysis of family data has consistently found evidence of the action of a major gene in determining susceptibility to NIDDM in families. However, the identity of the gene or genes that contribute to NIDDM in the general population is still not known. Recent advances in molecular biology have given investigators access to a number of plausible candidate genes for NIDDM and these have been used as test loci in association and linkage studies with inconsistent results. A review of the candidate gene studies in NIDDM suggests that the failure of these studies to identify specific loci involved in conferring susceptibility to NIDDM is, in part, due to failure to incorporate a number of biological features of the disease. The frequency of NIDDM in the population suggests that the alleles involved in NIDDM are common and their individual impact too small to be detected by simple single locus methods of analysis. Studies of other phenotypic forms of diabetes mellitus suggest that susceptibility to NIDDM is probably determined by alleles at more than one locus acting independently or in concert. The evolutionary history of certain populations may have isolated alleles conferring susceptibility to NIDDM in ethnically defined populations at high risk of NIDDM. These populations may provide a unique opportunity to identify specific genes involved in the complex etiology of NIDDM. © 1993 Wiley‐Lis

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050406

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractThis paper reviews recent data concerning the role of inherited differences in body fat content. The heritability of percent body fat or fat mass reaches about 25% of the age and gender adjusted phenotypic variance. One study has reported a significant major gene effect accounting for almost one half of the variance in body fat content. Experimental overfeeding studies suggest that body weight and fat gains are influenced by undefined genetic characteristics. Significant heritability estimates have been reported for major determinants of body fat content, including fat content of the diet, resting metabolic rate, thermic response to food, and level of habitual physical activity. Animal genetic studies and other experimental approaches indicate that the number of genes affecting body fat content, and associated with the susceptibility to obesity, is likely to be high. Currently available research strategies along with more extensive intermediate phenotyping will advance our knowledge about the genetic basis of human obesity. © 1993 Wiley‐Liss, I

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050407

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractCardiovascular risk factors associated with underlying coronary artery and hypertensive disease develop during childhood. Race‐ and sex‐specific observations from childhood to young adulthood provide clues to the clinical presentation of cardiovascular disease risk later in life. Of particular interest are observations on distributions of levels, tracking, and determinants of lipoproteins and blood pressure, and the impact of obesity on cardiovascular risk during transition periods of growth and maturation. Mean levels of serum lipids and lipoproteins reach adult levels by 2 years of age. After a slight decline during puberty, low‐density lipoprotein cholesterol (LDL‐C) rises rapidly in young adulthood while high‐density lipoprotein cholesterol (HDL‐C) declines during adolescence to reach adult levels, particularly for White males. Both systolic and diastolic blood pressures tend to increase with growth until adult stature is reached with somewhat higher levels seen in Blacks. Significant consistency in ranks over time (tracking) is noted. The single best predictor of young adult levels is the level during childhood. Obesity and lifestyles influence lipoprotein levels early in life with risk factor variables clustering just as in adults. Autopsy studies reveal a significant relation of coronary artery lesions to adverse lipoprotein profiles, blood pressure and obesity, especially in males, underlying the importance of multiple risk factors. These observations emphasize the need for developing preventive approaches to adult cardiovascular disease beginning in childhood. © 1993 Wil

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050408

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractMany genes are hypothesized to be involved in determining an individual's risk for coronary artery disease (CAD). Recent efforts have focused on the genetic architecture of quantitative traits related to risk for CAD. Studies relating genetic variation in the structural gene for apolipoprotein E to plasma levels of apolipoprotein E illustrate strategies to begin to understand the genetic architecture of plasma levels of apolipoprotein E. Studies using a measured gene approach suggest that variability in the isoforms of apolipoprotein E explain some, but not all, of the variability in plasma levels of apolipoprotein E. Products of other genes may be associated with plasma apolipoprotein E variability. No studies to date have presented findings from an unmeasured gene approach to plasma levels of apolipoprotein E. Models most often used in the unmeasured gene approach are not appropriate for studies of plasma levels of apolipoprotein E and perhaps are inappropriate for the study of other traits. Variations of the models are suggested to ask if a single unmeasured gene is the same gene defined by the apolipoprotein E isoforms. Another model can be used to ask if there is evidence for genes influencing levels of apolipoprotein E after accounting for the effects of the isoforms. Both the measured gene and unmeasured gene strategies have limitations. The failure of most models to allow for the complexity of genotype‐phenotype relationships or the heterogeneity of genetic causes will slow the progress to understand the genetic architecture of quantitative traits associated with risk for CAD. © 1993 Wiley‐Liss,

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050409

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractMortality rates among adult men and women, inhabitants of the city of Wrocław, were studied within 5‐year age classes between 20 and 64 years of age relative to two social variables: education and marital status of the deceased. Age‐ and sex‐specific mortality rates reveal a systematic social gradient. They are highest among persons with primary or “basic vocational” school education, lower among those with secondary school education, and lowest among those with college education. This gradient consistently appears in each of the age classes of males and females, although it is more pronounced among males. In both sexes, married persons have lower rates of mortality than those who have never married or were divorced or widowed. Among females, marital status appears to have a stronger effect on age‐specific rates of mortality than educational status; the reverse is the case among males. © 1993 Wi

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050410

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractCraniometric data have been collected from published and unpublished reports of numerous authors on 961 male and 439 female crania from various sites in Subsaharan Africa spanning the last 100 ka. All data available in the literature, irrespective of their “racial” affinities, were used to cover the prehistoric and early historic times (up to 400 a BP). Samples covering the last 400 years do not include European colonists and consist of skeletons exavated at archeological sites, collected by early European travelers and derived from anatomical collections. Cranial capacity, depending on the mode of its calculation, has decreased by 95–165 cm3among males and by 74–106 cm3among females between the Late Stone Age (30‐2 ka BP) and modern times (last 200 years). Values of the cranial index did not show any trend over time and their averages remained in the dolichocephalic category. The decrease in cranial capacity in Subsaharan Africa is similar to that previously found in Europe, West Asia, and North Africa, but, unlike the latter, it is not accompanied by brachycephalization. © 1993 Wiley

ISSN:1042-0533    

DOI:10.1002/ajhb.1310050411

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY