Disease In African Americans Research Articles

STROKE IN AFRICAN AMERICANS

There is an excess burden of cerebrovascular disease in African Americans. This article will define possible reasons for excess stroke risk, review racial differences in stroke subtype and stroke prevention programs in the African American Community, and delineate sequelae of stroke. The authors provide insights about stroke prevention in African Americans and highlight challenges to reduce the burden of cerebrovascular disease in this high-risk group.

APOE [formula omitted] and [formula omitted] genotypes are important risk factors for Alzheimer's disease in African Americans

APOE [formula omitted] and [formula omitted] genotypes are important risk factors for Alzheimer's disease in African Americans

Childhood rural residence is a risk factor for incident Alzheimer's disease in African Americans

Childhood rural residence is a risk factor for incident Alzheimer's disease in African Americans

The human leukocyte antigen HLA DRB3*020/DQA1*0501 haplotype is associated with Graves' disease in African Americans.

Information on genetic susceptibility to Graves' disease in African Americans is limited. We studied DRB1, DQB1, DRB3 subtypes, DQA1*0501, DQA1*0201, and CTLA-4 polymorphisms in 49 African American patients with adult onset Graves' disease and 47 racially-matched controls using PCR-based sequence-specific priming methods. There were no significant differences in DRB1 or DQB1 allelic frequencies or CTLA-4 polymorphisms between patients and controls. However, we found that the frequency of DRB3 was significantly increased in the patients (75.5% vs. 57.4%, P = 0.006, X2 = 3.52), especially for the DRB3*0202 subtype (53.1% vs. 23.4, P = 0.003, X2 = 8.91). In this one respect, the finding was in concordance with our previous observations in Caucasian patients with adult-onset Graves' disease. In addition, whereas the frequency of DQA1*0501 was increased (P = 0.018, X2 = 5.63) in our patients, the haplotype of DRB3/DQA1*0501, or DRB3*0202/DQA1*0501 was found to be more strongly associated (P = 0.008, X2 = 7.0; P = 0.0008, X2 = 11.34, respectively). These data suggest that DRB3*0202, particularly when found with DQA1*0501 in a haplotype is a susceptible gene(s) for Graves' disease in adult African Americans. Considering these data with those in Caucasian patients, our results would suggest that the primary Graves susceptible locus is likely DRB3 and not DRB1.

Rising Levels of Cardiovascular Mortality in Mississippi, 1979-1995

Background: Cardiovascular disease rates are improving in the United States, but not for certain subgroups, especially some African Americans. The objective of the study is to assess current levels and trends in cardiovascular disease mortality in Mississippi. Methods: Mortality statistics from the U.S. vital statistics system for the period 1979-95 were used. Comparison of age-adjusted mortality rates in Mississippi with the other states for the year 1995 and with the nation as a whole over the period of 1979-95 was performed. Results: Mississippians had the highest age-adjusted cardiovascular disease morality rates in the nation in 1995. Overall, the cardiovascular rates in Mississippi were 37% higher than for the U.S. African American men and women from Mississippi had especially high cardiovascular mortality rates, approximately 50% and 70% higher than their white counterparts, respectively. The higher burden of cardiovascular disease in African Americans from Mississippi was especially marked in the younger age groups. Since about 1984-85, cardiovascular mortality rates in Mississippi have been increasing for African Americans, whereas nationally they have been decreasing. In contrast, cardiovascular mortality rates for whites in Mississippi have been declining, but at a much slower rate than seen nationally. The wide divergence in trends for African American and white men and women over that period in Mississippi has lead to an estimated 19,400 excess cardiovascular deaths. Virtually identical trends were found for heart disease. Conclusions: Cardiovascular diseases are a major public health problem in Mississippi that is especially severe in African American residents, and the problem is growing worse each year. It is important to identify the determinants of and solutions for this enormous public health problem in Mississippi

Rising levels of cardiovascular mortality in Mississippi, 1979-1995.

Cardiovascular disease rates are improving in the United States, but not for certain subgroups, especially some African Americans. The objective of the study is to assess current levels and trends in cardiovascular disease mortality in Mississippi. Mortality statistics from the U.S. vital statistics system for the period 1979-95 were used. Comparison of age-adjusted mortality rates in Mississippi with the other states for the year 1995 and with the nation as a whole over the period of 1979-95 was performed. Mississippians had the highest age-adjusted cardiovascular disease morality rates in the nation in 1995. Overall, the cardiovascular rates in Mississippi were 37% higher than for the U.S. African American men and women from Mississippi had especially high cardiovascular mortality rates, approximately 50% and 70% higher than their white counterparts, respectively. The higher burden of cardiovascular disease in African Americans from Mississippi was especially marked in the younger age groups. Since about 1984-85, cardiovascular mortality rates in Mississippi have been increasing for African Americans, whereas nationally they have been decreasing. In contrast, cardiovascular mortality rates for whites in Mississippi have been declining, but at a much slower rate than seen nationally. The wide divergence in trends for African American and white men and women over that period in Mississippi has lead to an estimated 19,400 excess cardiovascular deaths. Virtually identical trends were found for heart disease. Cardiovascular diseases are a major public health problem in Mississippi that is especially severe in African American residents, and the problem is growing worse each year. It is important to identify the determinants of and solutions for this enormous public health problem in Mississippi.

Atypical parkinsonism in Afro-Caribbean and Indian origin immigrants to the UK.

This article reviews evidence for the occurrence of atypical parkinsonism in Afro-Caribbean and Indian ethnic minority subjects living in western countries, particularly the UK. Current information on the frequency, pattern, and prevalence of Parkinson's disease and parkinsonism in these communities is unclear and controversial. While several workers have suggested that there is a low prevalence of Parkinson's disease in populations of African origin, other workers have suggested a higher prevalence of Parkinson's disease in African Americans. Furthermore, little information is available in relation to the pattern of parkinsonism in these subjects. A recent phenomenologic study of parkinsonism in the French West Indies by Caparros-Lefebvre and colleagues has indicated a significantly increased frequency of atypical parkinsonism in local non-white subjects. Since 1995, we have been studying the pattern and frequency of parkinsonism in Afro-Caribbean and Indian (originating from the Indian subcontinent) patients living in the UK, with London serving as the coordinating center. Our results indicate that there is a three- to fourfold increase in the frequency of occurrence of sporadic atypical parkinsonism characterized by levodopa hyporesponsiveness, bradykinesia-dominant disease, and early cognitive dysfunction in these patients even after exclusion of patients with clinically probable multiple system atrophy, progressive supranuclear palsy, and Lewy body dementia. These findings are similar to observations made in the French West Indies. Ongoing studies in India suggest that atypical parkinsonism also affects local patients, and the pattern of parkinsonism tends to differ from Afro-Caribbean subjects in the UK. Studies are currently underway to unravel the mechanism of increased frequency of atypical parkinsonism in these ethnic groups and include genetic studies addressing polymorphisms of enzymes metabolizing levodopa, dietary neurotoxin screen and functional imaging studies of the striatum using positron emission tomography. Furthermore, the contribution of diabetes mellitus and hypertension, commonly seen in these ethnic groups, is also being examined.

Hypertensive cardiovascular disease in African Americans.

Hypertension is the most common public health challenge in the United States because of its prevalence and associated increase in comorbid cardiovascular diseases. Yearly expenses related directly or indirectly to the treatment and detection of hypertension in the United States are approximately $10 billion, excluding the enormous yearly financial burden of $259 billion and the social burden from heart disease and stroke, which remain the first and third leading causes of death, respectively, in the United States. Despite the importance of these observations, blood pressure is poorly controlled in the United States.

Insulin sensitivity in subjects with type 2 diabetes. Relationship to cardiovascular risk factors: the Insulin Resistance Atherosclerosis Study.

Among nondiabetic subjects, insulin resistance has been associated with increased cardiovascular risk factors, including dyslipidemia, hypertension, impaired fibrinolysis, and coagulation. Less is known about the relationship between insulin resistance and cardiovascular risk factors in subjects with type 2 diabetes. To examine this issue, we determined insulin sensitivity (SI) in 479 type 2 diabetic subjects by minimal model analyses of frequently sampled intravenous glucose tolerance tests in the Insulin Resistance Atherosclerosis Study (IRAS), a large multicenter study of insulin sensitivity and cardiovascular disease in African-Americans, Hispanics, and non-Hispanic whites. We defined insulin-sensitive subjects as having SI > or = 1.61 x 10(-4) min-1.microU-1.ml-1 (above median in nondiabetic subjects of all ethnic groups in the IRAS). Using this definition, only 37 type 2 diabetic subjects were insulin sensitive, and the remaining 442 were insulin resistant. After adjustment for age, sex, ethnicity, and clinic, insulin resistance was significantly correlated with total triglycerides, VLDL cholesterol, VLDL triglyceride, fibrinogen, PAI-1, and fasting glucose, and was inversely correlated with HDL cholesterol level and LDL size. Carotid intimal-medial thickness was greater in insulin-resistant than in insulin-sensitive subjects, but this difference was not statistically significant. After further adjustment for waist circumference (marker of visceral adiposity), insulin-resistant subjects continued to have higher plasminogen activator inhibitor 1 and VLDL triglyceride levels, lower HDL cholesterol levels, and smaller LDL particle size than did insulin-sensitive subjects. After further adjustment for fasting glucose levels, these results were very similar. We conclude that insulin-resistant type 2 diabetic subjects have more atherogenic cardiovascular risk factor profiles than insulin-sensitive type 2 diabetic subjects and that this is only partially related to increased obesity and an adverse body fat distribution.

The Role of Hypertension, Obesity, and Diabetes in Causing Renal Vascular Disease

The Jackson Heart Study will be an epidemiological study of African Americans in Jackson, Mississippi, to identify risk factors for development and progression of cardiovascular disease. One of the potential risk factors to be assessed in this study is renal vascular disease. Atherosclerotic renal vascular disease is a disease of the elderly, is predominantly seen in white people, and is strongly associated with diffuse atherosclerotic disease and high-grade hypertensive retinopathy. Patients with ischemic nephropathy may constitute up to 16% of new dialysis patients and die more quickly while on renal replacement therapy. Although often not present, hypertension is a commonly observed consequence (but probably not a cause) of renal vascular disease, and the control of blood pressure may not halt the progression of the disease. Approximately 2025% of patients with moderate to severe renal artery stenosis will be diabetic. Diabetic patients fair less well with intervention and have a higher progression to end-stage renal disease or death. Obesity is not commonly seen in patients with renal vascular disease. The Jackson Heart Study may be able to assess the true incidence of atherosclerotic renal vascular disease in African Americans and its impact of cardiovascular morbidity and mortality.

The role of hypertension, obesity, and diabetes in causing renal vascular disease.

The Jackson Heart Study will be an epidemiological study of African Americans in Jackson, Mississippi, to identify risk factors for development and progression of cardiovascular disease. One of the potential risk factors to be assessed in this study is renal vascular disease. Atherosclerotic renal vascular disease is a disease of the elderly, is predominantly seen in white people, and is strongly associated with diffuse atherosclerotic disease and high-grade hypertensive retinopathy. Patients with ischemic nephropathy may constitute up to 16% of new dialysis patients and die more quickly while on renal replacement therapy. Although often not present, hypertension is a commonly observed consequence (but probably not a cause) of renal vascular disease, and the control of blood pressure may not halt the progression of the disease. Approximately 20-25% of patients with moderate to severe renal artery stenosis will be diabetic. Diabetic patients fair less well with intervention and have a higher progression to end-stage renal disease or death. Obesity is not commonly seen in patients with renal vascular disease. The Jackson Heart Study may be able to assess the true incidence of atherosclerotic renal vascular disease in African Americans and its impact of cardiovascular morbidity and mortality.

The role of genetic and environmental factors in cardiovascular disease in African Americans.

Considerable interest has been focused over the years on estimating the relative importance of genetic and environmental factors on differences in rates of cardiovascular disease in blacks and whites. However, recent advances in molecular science have helped to illuminate the underlying complexity of this problem. Attempts to impute the genetic component from "what was left over" after control for a limited set of environmental exposures is increasingly recognized as naive. The requirements for a model that could account for interactions between genetic and environmental factors far exceeds the precision of our measurements. Although it is obvious that blacks experience not only unique environmental exposures, such as white racism, but more intense exposure to common factors, such as obesity, current methods make it very difficult to summarize these effects. Simpler models, using data from large samples, could provide greater precision and might illuminate the exposure-outcome relationships common to all groups. Meanwhile, efforts to identify genetic underpinnings of complex disorders will have to reach a much higher level of development before useful conclusions can be reached about the magnitude and variation of effects between racial and ethnic groups.

The Role of Genetic and Environmental Factors in Cardiovascular Disease in African Americans

Considerable interest has been focused over the years on estimating the relative importance of genetic and environmental factors on differences in rates of cardiovascular disease in blacks and whites. However, recent advances in molecular science have helped to illuminate the underlying complexity of this problem. Attempts to impute the genetic component from “what was left over” after control for a limited set of environmental exposures is increasingly recognized as naive. The requirements for a model that could account for interactions between genetic and environmental factors far exceeds the precision of our measurements. Although it is obvious that blacks experience not only unique environmental exposures, such as white racism, but more intense exposure to common factors, such as obesity, current methods make it very difficult to summarize these effects. Simpler models, using data from large samples, could provide greater precision and might illuminate the exposure-outcome relationships common to all groups. Meanwhile, efforts to identify genetic underpinnings of complex disorders will have to reach a much higher level of development before useful conclusions can be reached about the magnitude and variation of effects between racial and ethnic groups.

Cerebrovascular disease in African Americans.

It was an honor to be selected as the first lecturer for the American Heart Association (AHA) Presidential Symposium in conjunction with the 23rd International Joint Conference on Stroke and Cerebral Circulation. I wish to thank Dr Martha Hill, the AHA President, for the invitation to participate. Dr Hill has had a longstanding interest in cardiovascular health issues in the African American community. I also wish to thank Drs Edward Cooper and Jacqueline Washington, who served as panel discussants for the symposium. Since 1981, I have been carrying out epidemiological studies of stroke in African Americans. The studies have included both observational ones and clinical trials. At the present time, we are completing a secondary stroke prevention trial: the African American Antiplatelet Stroke Prevention Study (AAASPS). I now provide an overview of cerebrovascular disease in African Americans. I begin my discussion with a brief review of the constructs race and ethnicity. Williams has critically examined the scientific consensus on the conceptualization of race.1 The United States government recognizes four racial groups—white, black, Asian or Pacific Islander, and American Indian or Alaskan Native—and one ethnic category, Hispanic. The distinction between race and ethnicity may be obscured, however, as some Hispanics may prefer to refer to themselves as a racial category.1 In the social science literature, the early definitions of race used the term to capture “physical” or “biological” characteristics that differentiated human populations. The term was then extended to encompass biological and social interaction. More recent definitions of race have discredited the early definition that included physical or biological characteristics because in general, phenotypic characteristics do not correlate well with biochemical or other genetic characteristics, and there may be more genetic variation …

Genetic susceptibility to lupus nephritis.

Although cumulative evidence suggests that a genetic predisposition plays a major role in development of systemic lupus erythematosus (SLE) and/or lupus nephritis (LN), the susceptibility genes are mostly unknown. The difficulty in identifying susceptibility genes is due in part to multiple genes with variable genetic effects and the diverse genetic backgrounds of human populations. In human SLE, genes of early components of complements as well as many polymorphic genes (including the MHC class II and class III, FcgammaR, mannose-binding protein, IL-6, Bcl-2, and IL-10 genes) have been associated with SLE or LN by population-based case-control or within-case studies. The contribution of some of these disease-associated genes to the presence or absence of clinical manifestations has been further tested in mice with targeted disruption of the specific candidate gene. In addition to SLE susceptibility genes, there may be a separate set of nephropathy susceptibility genes predisposing to LN as suggested by the familial clustering of end-stage renal disease in African-Americans with LN. The availability of densely mapped genetic markers spanning the entire genome has enabled the identification of chromosomal regions linked to disease susceptibility genes without prior knowledge of the gene function. Our group has used known murine lupus susceptibility loci as a guide, and conducted linkage analysis of genetic markers located within a specific, possibly syntenic human chromosomal region. Evidence for linkage of a chromosome 1q41-42 region was observed in SLE-affected sib pairs from multiple ethnic groups. More recently, several groups have reported results of genome scans of SLE-affected sib pairs or pedigrees. These exciting recent developments in delineating the genetic basis of SLE or LN are summarized in this review.

Race and hypertension: science and nescience.

Although race is widely used in hypertension research as a marker of increased risk, its meaning as an etiologic quantity is obscure.1 2 3 4 5 Because of its importance as a social category in American life, separating what we “know” about race through socialization from what can be known on the basis of scientific inquiry is difficult.6 This dilemma represents a specific example of how social influences impact the conduct of science. While the process by which evidence is gathered and evaluated is usually constrained by an existing theoretical model (the “hypothetico-deductive process”), hypotheses arise more informally from the interplay of “inspiration” and “intuition.”7 Although hypothesis generation is at the core of scientific activity, it is peculiarly vulnerable to the influences of ideology. Contemporary perspectives on science as a practical human activity thus acknowledge that inspiration and intuition are the products of imagination and, as such, are derived from the investigator’s experience—both inside and outside the laboratory.8 While it is necessary to take account of the assumptions about race that are generated by our participation in a racially stratified society, it is also necessary to define exactly what we can know about race through the conduct of science. In this discussion, we are interested in moving beyond concerns about social influences on hypothesis generation and will attempt to address the logic of studies that use race comparisons to examine causal relationships. Specifically, we ask the question, “Can available statistical adjustment methods lead to valid inferences when race is regarded as an etiologic quantity, rather than a broad indicator of risk factor status?” Despite the popularity of racial hypotheses, we argue that comparative studies based on observations of broad phenotypes—such as high blood pressure, obesity, or glucose intolerance—have little potential to contribute new knowledge. The attempt …

Inflammatory bowel disease in African-American children living in Georgia.

We describe the clinical characteristics of inflammatory bowel disease (IBD) African-American compared with non-African-American children. We identified 172 children with IBD; forty-nine (29%) were African-American. Median symptom duration before IBD diagnosis in African-American children (6 months) was shorter than that of non-African-American children (10 months). The most frequent presenting symptom was hematochezia (ulcerative colitis) and abdominal pain (Crohn's disease) in both racial groups. The estimated incidence of Crohn's disease in African-Americans ranged from 7 per 100,000 to 12 per 100,000, whereas the observed incidence in those with ulcerative colitis was between 5 and 7 per 100,000 during the 10 years of the study. Our pilot study suggests that IBD may be more common in African-American children than previously reported. Prospective population-based studies would be useful to determine whether inheritable factors linked with ethnicity are associated with IBD.

Dupuytren's disease in African-Americans

Seventeen African-American patients were operated on for Dupuytren's contracture over a 14-year period. Six-month minimum follow-up was available for 16 patients. The initial deformity, and results of surgical release of Dupuytren's contracture in this population was similar to that described in North Europeans.

Myocardial Infarction With and Without Coronary Artery Disease in African Americans

Myocardial Infarction With and Without Coronary Artery Disease in African Americans

Myocardial infarction with and without coronary artery disease in African Americans

Myocardial infarction with and without coronary artery disease in African Americans