Why are blacks so poor in america? I fed this question into Grok, and this is what it came back with. I'd be interested in feedback on this important subject.
Black Americans have higher poverty rates than White or Asian Americans, but the gap has narrowed substantially over decades, and the causes are multi-factorial—historical, behavioral, cognitive, and structural—not reducible to any single narrative of ongoing systemic racism or pure individual failure.
Current and Historical Numbers
U.S. Census data show the official poverty rate for Black Americans at about 17.3% in 2025 (roughly 7.9 million people), down from a record low of 17.1% in 2022 and dramatically lower than 55% in 1959. This is about 2.2 times the non-Hispanic White rate. Child poverty shows a larger gap (Black children roughly 3× White). The Supplemental Poverty Measure, which includes transfers, is higher for Blacks (~20%). Median Black household income and wealth lag White levels (wealth gap often 5–8× at the median), partly due to differences in homeownership, assets, and inheritance.
Poverty is not uniform: most Black Americans are not poor, and rates vary by education, family structure, and region. Asian Americans have lower poverty than Whites despite historical discrimination, which undercuts simple “racism explains everything” accounts.
Major Contributing Factors
Family structure is one of the strongest proximate predictors. Roughly 37% of Black children live with two biological parents versus ~73% of White children; single-mother households are far more common among Blacks (~41%). About 70% of Black children are born to unmarried mothers. Children from intact two-parent homes have substantially lower poverty, higher college completion, and lower incarceration rates—patterns that hold within racial groups. Black young adults raised by both biological parents show better outcomes than White peers from single-parent homes on several metrics. The post-1960s rise in non-marital births (across groups, but more sharply among Blacks) coincided with welfare expansions that reduced marriage incentives for low-income groups.
Crime and incarceration create large direct costs. Blacks (≈13–14% of population) account for roughly half of homicide offenders and a disproportionate share of violent crime arrests/offenders (around 30–36% for nonfatal violent crimes in Bureau of Justice Statistics and FBI data that align victim reports with arrests). Most of this crime is intra-racial. High victimization and offending rates disrupt employment, family formation, neighborhoods, and human capital accumulation. This is not primarily an artifact of biased policing for serious violent offenses.
Cognitive ability and educational outcomes matter. Decades of testing (military, civilian, NAEP-linked, meta-analyses) show average Black IQ scores around 85, White around 100, East Asian higher (~105), with the Black-White gap persistent across cohorts and not eliminated by socioeconomic controls. IQ strongly predicts educational attainment, income, crime, and poverty within groups. High-school completion gaps have narrowed, but bachelor’s degree attainment remains lower for Blacks. Early interventions can raise skills, but long-term gaps often re-emerge. Heritability of IQ within groups is high; the between-group contribution of genetics versus environment remains debated, but the gap itself is not an artifact of test bias.
Historical legacies and discrimination. Slavery, Jim Crow, redlining, and discriminatory lending limited wealth accumulation for generations. Intergenerational transfers explain a meaningful portion of the wealth gap. Some residual discrimination in labor and housing markets continues, though audit studies and controls for observables (education, experience, criminal records) shrink residual wage gaps substantially. Post-1960s civil rights gains produced large absolute progress in income, poverty, and education; convergence slowed after the 1980s amid family and crime trends.
Other contributors include lower average workforce participation in some subgroups, differences in savings/investment behavior, and neighborhood effects. Culture (attitudes toward delayed gratification, academic effort, marriage) and policy (welfare design, criminal justice, education quality) interact with the above. Immigrant Blacks from Africa/Caribbean often show better outcomes than native-born, pointing to selection and cultural factors beyond U.S. racism.
What Does Not Fully Explain It
Claims that the entire gap is current systemic racism fail against the data on Asian success, the large within-Black variation by family structure and cognitive scores, the alignment of arrest and victim-reported offender data for violence, and the scale of post-1960s progress. Pure “culture of poverty” stories ignore history and the predictive power of cognitive differences. Genetic explanations alone do not account for rapid environmental gains or the role of family disruption. Wealth gaps persist even after controlling for income because of differences in assets, debt, and bequests.
Progress is real and measurable. Closing remaining gaps requires realistic focus on family formation, crime reduction, cognitive and skill development, and human capital—areas where individual and community agency matter more than further blaming abstract systems.
Race and health refers to how being identified with a specific race influences health. In the United States, race is a complex concept that has changed across chronological eras and depends on both self-identification and social recognition. In the study of race and health, some American scientists organize people in racial categories depending on different factors such as: phenotype, ancestry, social identity, genetic makeup and lived experience. Race and ethnicity often remain undifferentiated in American health research.
Differences in health status, health outcomes, life expectancy, and many other indicators of health in different racial and ethnic groups are well documented. Epidemiological data indicate that American racial groups are unequally affected by diseases, in terms of morbidity and mortality. Some individuals in certain racial groups receive less care, have less access to resources, and live shorter lives in general. Overall, racial health disparities appear to be rooted in social disadvantages associated with race such as implicit stereotyping and average differences in socioeconomic status.
According to the U.S. Centers for Disease Control and Prevention, health disparities are defined as "preventable differences in the burden of disease, injury, violence, or opportunities to achieve optimal health that are experienced by socially disadvantaged populations" and are intrinsically related to the "historical and current unequal distribution of social, political, economic and environmental resources".
The relationship between race and health has been studied from multidisciplinary perspectives, with increasing focus on how racism influences health disparities, and how environmental and physiological factors respond to one another and to genetics. In the United States, research highlights a need for more race-conscious approaches in addressing social determinants, as current social needs interventions show limited adaptation to racial and ethnic disparities.
Health disparities refer to gaps in the quality of health and health care across racial and ethnic groups. The US Health Resources and Services Administration defines health disparities as "population-specific differences in the presence of disease, health outcomes, or access to health care". Health is measured through variables such as life expectancy and incidence of diseases.
For racial and ethnic minorities in the United States, health disparities take on many forms, including higher rates of chronic disease, premature death, and maternal mortality compared to the rates among whites. For example, African Americans are 2–3 times more likely to die as a result of pregnancy-related complications than white Americans. This pattern is not universal. Some minority groups—most notably, Hispanic immigrants—may have better health outcomes than whites when they arrive in the United States. However this appears to diminish with time spent in the United States. For other indicators, disparities have shrunk, not because of improvements among minorities but because of declines in the health of majority groups.
In the U.S., more than 133 million Americans (45% of the population) have one or more chronic diseases. One study has shown that between the ages of 60 and 70, racial/ethnic minorities are 1.5 to 2.0 times more likely than whites (Hispanic and non Hispanic) to have one of the four major chronic diseases specifically Diabetes, cancer, cardiovascular disease (CVD), and chronic lung disease. However, the greatest differences only occurred among people with single chronic diseases. Racial/ethnic differences were less distinct for some conditions including multiple diseases. Non-Hispanic whites trended toward a high prevalence for dyads of cardiovascular disease (CVD) with cancer or lung disease. Hispanics and African Americans had the greatest prevalence of diabetes, while non-Hispanic blacks had higher odds of having heart disease with cancer or chronic lung disease than non-Hispanic whites. Among non-Hispanic whites the prevalence of multimorbidities that include diabetes was low; however, non-Hispanic whites had a very high prevalence of multimorbidities that exclude diabetes. Non-Hispanic whites had the highest prevalence of cancer only or lung disease only. Black Americans have an increased risk of death from COVID-19 compared to white Americans. In a study in Michigan in 2020 regarding COVID-19, it is shown that Black people are 3.6 times more likely to die due to COVID-19.
Between 1960 and 2005 the percentage of children with a chronic disease in the United States quadrupled with minority having higher likelihood for these disease. The most common major chronic biases of youth in the United States are asthma, diabetes mellitus, obesity, hypertension, dental disease, attention deficit hyperactivity disorder (ADHD), mental illness, cancers and others. This results in Black and Latin adult patients facing a disproportionate amount of health concerns, such as asthma, with treatment and management guidelines not developed with studies based on their populations and healthcare needs.
Although individuals from different environmental, continental, socioeconomic, and racial groups etc. have different levels of health, yet not all of these differences are always categorized or defined as health disparities. Some researchers separate definitions of health inequality from health disparity by preventability. Health inequalities are often categorized as being unavoidable i.e. due to age, while preventable unfair health outcomes are categorized as health inequities. These are seen as preventable because they are usually associated with income, education, race, ethnicity, gender, and more.
Studies conducted in the United States have indicated that minorities have similar or smaller rates of prevalence for mental health disorders as their majority counterparts. Blacks (24.6%) and Hispanics (19.6%) have lower depression rates than their White counterparts (34.7%) in the United States. While racial/ethnic minority groups may have similar prevalence rates, the consequences because of mental illness are more prolonged – which may be partly explained due to the smaller access rates for mental health treatments. In 2018, while 56.7% of the general US population who had a mental illness didn't seek treatment, 69.4% and 67.1% Black and Hispanics didn't access care. Further, in the instances of some mental illnesses, such as schizophrenia, Blacks in the United States have been reported to have higher rates compared to their White counterparts, however, research suggests that this could be due to an overdiagnosis among clinicians and underdiagnosis for other illnesses, such as mood disorders, for which Blacks had lower reported prevalence rates for major depression. These instances of misdiagnosis may be due to "lack of cultural understanding by health care providers,...language differences between patient and provider, stigma of mental illness among minority groups, and cultural presentation of symptoms. Minority groups commonly report experiences with racism and discrimination, and they consider these experiences to be stressful. In a national probability sample of minority groups and whites. African Americans and Hispanic American reported experiencing higher overall levels of global stress than did whites.
Effects of systemic racism
In the United States, the mental health of African Americans has been shown to be negatively impacted by systemic racism, contributing to increased risk of mortality from substance use disorders. This negative mental health can lead to reaching for substances to cope with the mental effects of systemic racism.
Definitions of race are ambiguous due to the various paradigms used to discuss race. These definitions are a direct result of biological and social views. Definitions have changed throughout history to yield a modern understanding of race that is complex and fluid. Moreover, there is no one definition that stands, as there are many competing and interlocking ways to look at race. Due to its ambiguity, terms such as race, genetic population, ethnicity, geographic population, and ancestry are used interchangeably in everyday discourse involving race. Some researchers critique this interchangeability noting that the conceptual differences between race and ethnicity are not widely agreed upon.
Even though there is a broad scientific agreement that essentialist and typological conceptions of race are untenable,scientists around the world continue to conceptualize race in widely differing ways. Historically, biological definitions of race have encompassed both essentialist and anti-essentialist views. Essentialists have sought to show that racial groups are genetically distinct populations, describing "races as groups of people who share certain innate, inherited biological traits". In contrast, anti-essentialists have used biological evidence to demonstrate that "race groupings do not reflect patterns of human biological variation, countering essentialist claims to the contrary".
Over the past 20 years, a consensus has emerged that, while race is partially based on physical similarities within groups, it does not have an inherent physical or biological meaning. In response, researchers and social scientists have begun examining notions of race as constructed. Racial groups are "constructed" from differing historical, political, and economic contexts, rather than corresponding to inherited, biological variations. Proponents of the constructionist view claim that biological definitions have been used to justify racism in the past and still have the potential to be used to encourage racist thinking in the future. Since race is changing and often so loosely characterized on arbitrary phenotypes, and because it has no genetic basis, the only working definition we can assign it is a social construct. Race can be an important epidemiologic category, however to suggest that the concept of race has any scientific merit or has a scientific foundation can lead to many issues in scientific research, and it may also lead to inherent racial bias.
Social interpretations of race explains that social views also better explain the ambiguity of racial definitions. An individual may self-identify as one race based on one set of determinants (for example, phenotype, culture, ancestry) while a society may ascribe the person otherwise based on external forces and discrete racial standards. Dominant racial conceptions influence how individuals label both themselves and others within a society. Modern human populations are becoming more difficult to define within traditional racial boundaries due to racial admixture. Most scientific studies, applications, and government documents ask Americans to self-identify race from a limited assortment of common racial categories.
In the United States, race is a cause discrimination, prejudice, marginalization, and even subjugation. Despite the social costs, American researchers argue racial categorization remains beneficial to diagnosis and research. The conflict between self-identification and societal ascription further complicates biomedical research and public health policies. However complex its sociological roots, race has biological ramifications; the intersection of race, science, and society permeates everyday American life and influences human health via genetics, access to medical care, diagnosis, and treatment.
Race and disease
Diseases affect racial groups when they are co-related with class disparities. As socioeconomic factors influence the access to care, the barriers to access healthcare systems can perpetuate different biological effects of diseases among racial groups that are not pre-determined by biology.
Some researchers advocate for the use of self-reported race as a way to trace socioeconomic disparities and its effects in health in the United States. In the United Kingdom, a study was conducted on the Health Checks program by the United Kingdom's National Health Service, which aims to increase diagnosis across demographics. The study was done to address "the reported lower uptake of screening in
specific black and minority ethnic communities who are recognised as being more at risk of cardiovascular disease." The lack of attention to certain demographics can be seen as a cause of increased instances of disease from this lack of proper, equal preventive care. One must consider these external factors when evaluating statistics on the prevalence of disease in populations, even though genetic components can play a role in predispositions to contracting some illnesses.
Individuals who share a similar genetic makeup can also share certain propensity or resistance to specific diseases. However, there are confronted positions in relation to the utility of using 'races' to talk about populations sharing a similar genetic makeup. Some geneticists argued that human variation is geographically structured and that genetic differences correlate with general conceptualizations of racial groups. Others claimed that this correlation is too unstable and that the genetic differences are minimal and they are "distributed over the world in a discordant manner". Therefore, self-reported population ancestry is regarded by some as a useful tool for the assessment of genetic epidemiological risk, while others consider it can lead to an increased underdiagnosis in 'low risk' populations.
There are many autosomal recessive single gene genetic disorders that differ in frequency between different populations due to the region and ancestry as well as the founder effect. Some examples of these disorders include:
Sickle-cell anemia, most prevalent in populations with sub-Saharan African ancestry but also common among Latin-American, Middle Eastern populations, as well as those people of South European regions such as Turkey, Greece, and Italy
Thalassemia, most prevalent in populations having Mediterranean ancestry, to the point that the disease's name is derived from Greek thalassa, "sea"
Many diseases differ in frequency between different populations. However, complex diseases are affected by multiple factors, including genetic and environmental. There is controversy over the extent to which some of these conditions are influenced by genes, and ongoing research aims to identify which genetic loci, if any, are linked to these diseases. "Risk is the probability that an event will occur. In epidemiology, it is most often used to express the probability that a particular outcome will occur following a particular exposure." Different populations are considered "high-risk" or "low-risk" groups for various diseases due to the probability of that particular population being more exposed to certain risk factors. Beyond genetic factors, history and culture, as well as current environmental and social conditions, influence a certain population's risk for specific diseases.
Disease progression
Racial groups may differ in how a disease progresses. Different access to healthcare services, different living and working conditions influence how a disease progresses within racial groups in the United States. However, the reasons for these differences are multiple, and should not be understood a consequence of genetic differences between races, but rather as effects of social and environmental factors affecting.
Prevention
Genetics has been proven to be a strong predictor for common diseases such as cancer, cardiovascular disease (CVD), diabetes, autoimmune disorders, and psychiatric illnesses. Some geneticists have determined that "human genetic variation is geographically structured" and that different geographic regions correlate with different races. Meanwhile, others have claimed that the human genome is characterized by clinal changes across the globe, in relation with the "Out of Africa" theory and how migration to new environments cause changes in populations' genetics over time.
Some diseases are more prevalent in some populations identified as races due to their common ancestry. Thus, people of African and Mediterranean descent are found to be more susceptible to sickle-cell disease while cystic fibrosis and hemochromatosis are more common among European populations. Some physicians claim that race can be used as a proxy for the risk that the patient may be exposed to in relation to these diseases. However, racial self-identification only provides fragmentary information about the person's ancestry. Thus, racial profiling in medical services would also lead to the risk of underdiagnosis.
While genetics plays a role in determining how susceptible a person is to specific diseases, environmental, structural, cultural, and communication messaging factors play a large role as well.
Minority ethnic groups often face structural and cultural barriers to access healthcare services. The development of culturally and structurally competent services and research that meet the specific health care needs of minority groups is still in its infancy.
Scientific studies have shown the lack of efficacy of adapting pharmaceutical treatment to racial categories. "Race-based medicine" is the term for medicines that are targeted at specific racial clusters which are shown to have a propensity for a certain disorder. The first example of this in the U.S. was when BiDil, a medication for congestive heart failure, was licensed specifically for use in American patients that self-identify as black. Previous studies had shown that African American patients with congestive heart failure generally respond less effectively to traditional treatments than white patients with similar conditions.
After two trials, BiDil was licensed exclusively for use in African American patients. Critics have argued that this particular licensing was unwarranted, since the trials did not in fact show that the drug was more effective in African Americans than in other groups, but merely that it was more effective in African Americans than other similar drugs. It was also only tested in African American males, but not in any other racial groups or among women. This peculiar trial and licensing procedure has prompted suggestions that the licensing was in fact used as a race-based advertising scheme.
Critics are concerned that the trend of research on race-specific pharmaceutical treatments will result in inequitable access to pharmaceutical innovation and smaller minority groups may be ignored. This has led to a call for regulatory approaches to be put in place to ensure scientific validity of racial disparity in pharmacological treatment.
An alternative to "race-based medicine" is personalized or precision medicine. Precision medicine is a medical model that proposes the customization of healthcare, with medical decisions, treatments, practices, or products being tailored to the individual patient. It involves identifying genetic, genomic (e.g. whole genome sequencing), and clinical information—as opposed to using race as a proxy for these data—to better predict a patient's predisposition to certain diseases.
A positive correlation between minorities and a socioeconomic status of being low-income in industrialized and rural regions of the U.S. depict how low-income communities tend to include more individuals that have a lower educational background, most importantly in health. Income status, diet, and education all construct a higher burden for low-income minorities, to be conscious about their health. Research conducted by medical departments at universities in San Diego, Miami, Pennsylvania, and North Carolina suggested that minorities in regions where lower socioeconomic status is common, there was a direct relationship with unhealthy diets and greater distance of supermarkets. Therefore, in areas where supermarkets are less accessible (food deserts) to impoverished areas, the more likely these groups are to purchase inexpensive fast food or just follow an unhealthy diet. As a result, because food deserts are more prevalent in low income communities, minorities that reside in these areas are more prone to obesity, which can lead to diseases such as chronic kidney disease, hypertension, or diabetes.
Furthermore, this can also occur when minorities living in rural areas undergoing urbanization are introduced to fast food. A study completed in Thailand focused on urbanized metropolitan areas: students who participated were diagnosed as "non-obese" in their early life according to their BMI, however were increasingly at risk of developing type 2 diabetes, or obesity as adults, as opposed to young adults who lived in more rural areas during their early life. Therefore, early exposure to urbanized regions can encourage unhealthy eating due to widespread presence of inexpensive fast food. Different racial populations that originate from more rural areas and then immigrate to the urbanized metropolitan areas can develop a fixation for a more westernized diet; this change in lifestyle typically occurs due to loss of traditional values when adapting to a new environment. For example, a 2009 study named CYKIDS was based on children from Cyprus, a country east of the Mediterranean Sea, who were evaluated by the KIDMED index to test their adherence to a Mediterranean diet after changing from a rural residence to an urban residence. It was found that children in urban areas swapped their traditional dietary patterns for a diet favoring fast food.
Genetic factors
The fact that every human has a unique genome is the key to techniques such as genetic fingerprinting. Versions of genetic markers, known as alleles, occur at different frequencies in different human populations; populations that are more geographically and ancestrally remote tend to differ more.
A phenotype is the "outward, physical manifestation" of an organism." For humans, phenotypic differences are most readily seen via skin color, eye color, hair color, or height; however, any observable structure, function, or behavior can be considered part of a phenotype. A genotype is the "internally coded, inheritable information" carried by all living organisms. The human genome is encoded in DNA.
For any trait of interest, observed differences among individuals "may be due to differences in the genes" coding for a trait and "the result of variation in environmental condition". This variability is due to gene-environment interactions that influence genetic expression patterns and trait heritability.
For humans, there is "more genetic variation among individual people than between larger racial groups". In general, an average of 80% of genetic variation exists within local populations, around 10% is between local populations within the same continent, and approximately 8% of variation occurs between large groups living on different continents. Studies have found evidence of genetic differences between populations, but the distribution of genetic variants within and among human populations is impossible to describe succinctly because of the difficulty of defining a "population", the clinal nature of variation, and heterogeneity across the genome. Thus, the racialization of science and medicine can lead to controversy when the term population and race are used interchangeably.
Currently malaria-endemic countries in the eastern hemisphereCurrently malaria-endemic countries in the western hemisphere
Genes may be under strong selection in response to local diseases. For example, people who are duffy negative tend to have higher resistance to malaria. Most Africans are duffy negative and most non-Africans are duffy positive due to endemic transmission of malaria in Africa. A number of genetic diseases more prevalent in malaria-affected areas may provide some genetic resistance to malaria including sickle cell disease, thalassaemias, glucose-6-phosphate dehydrogenase, and possibly others.
In earlier research, a common theory was the "common disease-common variant" model. It argues that for common illnesses, the genetic contribution comes from the additive or multiplicative effects of gene variants that each one is common in the population. Each such gene variant is argued to cause only a small risk of disease and no single variant is sufficient or necessary to cause the disease. An individual must have many of these common gene variants in order for the risk of disease to be substantial.
More recent research indicates that the "common disease-rare variant" may be a better explanation for many common diseases. In this model, rare but higher-risk gene variants cause common diseases. This model may be relevant for diseases that reduces fertility. In contrast, for common genes associated with common disease to persist they must either have little effect during the reproductive period of life (like Alzheimer's disease) or provide some advantage in the original environment (like genes causing autoimmune diseases also providing resistance against infections). In either case varying frequencies of genes variants in different populations may be an explanation for health disparities. Genetic variants associated with Alzheimer's disease, deep venous thrombosis, Crohn's disease, and type 2 diabetes appear to adhere to "common disease-common variant" model.
Gene flow
Gene flow and admixture can also have an effect on relationships between race and race-linked disorders. Multiple sclerosis, for example, is typically associated with people of European descent, but due to admixture African Americans have elevated levels of the disorder relative to Africans.
Some diseases and physiological variables vary depending upon their admixture ratios. Examples include measures of insulin functioning and obesity.
Gene interactions
The same gene variant, or group of gene variants, may produce different effects in different populations depending on differences in the gene variants, or groups of gene variants, they interact with. One example is the rate of progression to AIDS and death in HIV–infected patients. In whites and Hispanics, HHC haplotypes were associated with disease retardation, particularly a delayed progression to death, while for African Americans, possession of HHC haplotypes was associated with disease acceleration. In contrast, while the disease-retarding effects of the CCR2-641 allele were found in African Americans, they were not found in whites.
Theoretical approaches in addressing health and race disparities
Interdisciplinary methods have been used to address how race affects health. Factors that influence health include income and social status, education, physical environment, social support networks, genetics, health services, targeted instruction, and gender. These determinants are often cited in public health, anthropology, and other social science disciplines. The WHO categorizes these determinants into three broader topics: the social and economic environment, the physical environment, and the person's individual characteristics and behaviors. Due to the diversity of factors that often attribute to health disparities outcomes, interdisciplinary approaches are often implemented.
The salt sensitivity hypothesis is an example of implementing biocultural evolutionary approaches in order to understand cardiovascular health disparities among African American populations. This theory, founded by Wilson and Grim, stems from the disproportional rates of salt sensitive high blood pressure seen between U.S. African American and White populations and between U.S. African American and West Africans as well. The researchers hypothesized that the patterns were in response to two events. One the trans-Atlantic slave trade, which resulted in massive death totals of Africans who were forced over, those who survived and made to the United States were more likely able to withstand the harsh conditions because they retained salt and water better. The selection continued once they were in the United States. African Americans who were able to withstand hard working conditions had better survival rates due to high water and salt retention. Second, today, because of different environmental conditions and increased salt intake with diets, water and salt retention are disadvantageous, leaving U.S. African Americans at disproportional risks because of their biological descent and culture.
There is a controversy regarding race as a method for classifying humans. Different sources argue it is purely social construct or a biological reality reflecting average genetic group differences. New interest in human biological variation has resulted in a resurgence of the use of race in biomedicine.
The main impetus for this development is the possibility of improving the prevention and treatment of certain diseases by predicting hard-to-ascertain factors, such as genetically conditioned health factors, based on more easily ascertained characteristics such as phenotype and racial self-identification. Since medical judgment often involves decision making under uncertain conditions, many doctors consider it useful to take race into account when treating disease because diseases and treatment responses tend to cluster by geographic ancestry. The discovery that more diseases than previously thought correlate with racial identification have further sparked the interest in using race as a proxy for bio-geographical ancestry and genetic buildup.
Race in medicine is used as an approximation for more specific genetic and environmental risk factors. Race is thus partly a surrogate for environmental factors such as differences in socioeconomic status that are known to affect health. It is also an imperfect surrogate for ancestral geographic regions and differences in gene frequencies between different ancestral populations and thus differences in genes that can affect health. This can give an approximation of probability for disease or for preferred treatment, although the approximation is less than perfect.
Taking the example of sickle-cell disease, in an emergency room, knowing the geographic origin of a patient may help a doctor doing an initial diagnosis if a patient presents with symptoms compatible with this disease. This is unreliable evidence with the disease being present in many different groups as noted above with the trait also present in some Mediterranean European populations. Definitive diagnosis comes from examining the blood of the patient. In the US, screening for sickle cell anemia is done on all newborns regardless of race.
The continued use of racial categories has been criticized. Apart from the general controversy regarding race, some argue that the continued use of racial categories in health care and as risk factors could result in increased stereotyping and discrimination in society and health services. Some of those who are critical of race as a biological concept see race as socially meaningful group that is important to study epidemiologically in order to reduce disparities. For example, some racial groups are less likely than others to receive adequate treatment for osteoporosis, even after risk factors have been assessed. Since the 19th century, blacks have been thought to have thicker bones than whites have and to lose bone mass more slowly with age. In a recent study, African Americans were shown to be substantially less likely to receive prescription osteoporosis medications than whites. Men were also significantly less likely to be treated compared with women. This discrepancy may be due to physicians' knowledge that, on average, African Americans are at lower risk for osteoporosis than whites. It may be possible that these physicians generalize this data to high-risk African-Americans, leading them to fail to appropriately assess and manage these individuals' osteoporosis. On the other hand, some of those who are critical of race as a biological concept see race as socially meaningful group that is important to study epidemiologically in order to reduce disparities. Black Americans also have the highest mortality rate related to cardiovascular diseases, at about 30 percent higher than white Americans, even after the American Heart Association (AHA) has attempted to lower all risks.
David Williams (1994) argued, after an examination of articles in the journal Health Services Research during the 1966–90 period, that how race was determined and defined was seldom described. At a minimum, researchers should describe if race was assessed by self-report, proxy report, extraction from records, or direct observation. Race was also often used questionable, such as an indicator of socioeconomic status. Racial genetic explanations may be overemphasized, ignoring the interaction with and the role of the environment.
From concepts of race to ethnogenetic layering
There is general agreement that a goal of health-related genetics should be to move past the weak surrogate relationships of racial health disparity and get to the root causes of health and disease. This includes research which strives to analyze human genetic variation in smaller groups than races across the world.
One such method is called ethnogenetic layering. It works by focusing on geographically identified microethnic groups. For example, in the Mississippi Delta region ethnogenetic layering might include such microethnic groups as the Cajun (as a subset of European Americans), the Creole and Black groups [with African origins in Senegambia, Central Africa and Bight of Benin] (as a subset of African Americans), and Choctaw, Houmas, Chickasaw, Coushatta, Caddo, Atakapa, Karankawa and Chitimacha peoples (as subsets of Native Americans).
Better still may be individual genetic assessment of relevant genes. As genotyping and sequencing have become more accessible and affordable, avenues for determining individual genetic makeup have opened dramatically. Even when such methods become commonly available, race will continue to be important when looking at groups instead of individuals such as in epidemiologic research.
Some doctors and scientists such as geneticist Neil Risch argue that using self-identified race as a proxy for ancestry is necessary to be able to get a sufficiently broad sample of different ancestral populations, and in turn to be able to provide health care that is tailored to the needs of minority groups.
One area in which population categories can be important considerations in genetics research is in controlling for confounding between population genetic substructure, environmental exposures, and health outcomes. Association studies can produce spurious results if cases and controls have differing allele frequencies for genes that are not related to the disease being studied, although the magnitude of its problem in genetic association studies is subject to debate. Various techniques detect and account for population substructure, but these methods can be difficult to apply in practice.
Population genetic substructure also can aid genetic association studies. For example, populations that represent recent mixtures of separated ancestral groups can exhibit longer-range linkage disequilibrium between susceptibility alleles and genetic markers than is the case for other populations. Genetic studies can use this disequilibrium to search for disease alleles with fewer markers than would be needed otherwise. Association studies also can take advantage of the contrasting experiences of racial or ethnic groups, including migrant groups, to search for interactions between particular alleles and environmental factors that might influence health.
Race and medical practice
History
Historically, race has been utilized in medicine in various ways, which continue to have enduring impacts today. The imposition of race on pulmonary function and the machinery used to conduct testing is a noteworthy example. Samuel Cartwright was a 19th-century physician and scientist who is known for his work on spirometry and respiratory physiology. Spirometry is a medical test that measures how much air a person can breathe in and out of their lungs, and how quickly they can do so. Cartwright used spirometry to compare Black enslaved people's lung function to white people's. Cartwright, drawing on Thomas Jefferson's beliefs on pulmonary dysfunction, saw a 20% quantitative difference between Black and White people as proof of deficiency that necessitated the enslavement of Black individuals.
These findings of lower lung capacity by race are present in modern medicine through the correction of race in modern spirometry machines and within most textbooks for medical school. When inputting race into the machine, patients either provide their self-identified race or it is determined by the provider. Spirometers in the US utilize population-specific standards or correction factors of 10% to 15% for Black persons and 4% to 6% for Asian people. Thus, equations derived from Black populations will yield a higher percentage of predicted lung function values than those derived from White populations, which may underestimate lung disease severity and delay detection. However, applying an equation developed from White populations to other racial groups may lead to overdiagnosis and limited eligibility for treatment due to the increased perception of risk. Research regarding the efficacy of race-based spirometry found that the race correction was only accurate for Black patients when their African ancestry was above the median between 81 and 100%. As a result, opponents of race correction say it may cause misdiagnosis and perpetuate racial prejudices by encouraging biological race. These race-based clinical decision support tools, such as pulmonary function testing with spirometry, were ended by a report published by the US House of Representatives Ways and Means Committee in October 2021.
In November 2021, the American Academy of Clinical Neuropsychology issued a statement supporting the elimination of race as a variable in demographically based normative test interpretation, proposing instead an approach analogous to precision medicine in which the social, economic, educational, and healthcare-access factors that race functions as a proxy for would be measured and incorporated directly into prediction models. Alternative approaches have been proposed, for example, in the neuropsychological testing world, including the individual comparison standard (ICS) and incorporating social determinants of health (SDoH) instead of race in regression models. The individual comparison standard (ICS) estimates each patient's premorbid neuropsychological skill level from their own data, for example from a single-word reading or vocabulary measure relatively resistant to brain injury, and compares post-onset performance against that individualized baseline rather than against group norms. The social determinants of health model proposes replacing race in regression-based normative equations with direct measures of factors such as quality of education and socioeconomic status.
Sources of racial disparities in care
In a report by the Institute of Medicine called Unequal Treatment, three major source categories are put forth as potential explanations for disparities in health care: patient-level variables, healthcare system-level factors, and care process-level variables.
Patient-level variables
There are many individual factors that could explain the established differences in health care between different racial and ethnic groups. First, attitudes and behaviors of minority patients are different. They are more likely to refuse recommended services, adhere poorly to treatment regimens, and delay seeking care, yet despite this, these behaviors and attitudes are unlikely to explain the differences in health care. In addition to behaviors and attitudes, biological based racial differences have been documented, but these also seem unlikely to explain the majority of observed disparities in care.
Health system-level factors
Health system-level factors include any aspects of health systems that can have different effects on patient outcomes. Some of these factors include different access to services, access to insurance or other means to pay for services, access to adequate language and interpretation services, and geographic availability of different services. Many studies assert that these factors explain portions of the existing disparities in health of racial and ethnic minorities in the United States when compared to their white counterparts.
Care process-level variables
Three major mechanisms are suggested by the Institute of Medicine that may contribute to healthcare disparities from the provider's side: bias (or prejudice) against racial and ethnic minorities; greater clinical uncertainty when interacting with minority patients; and beliefs held by the provider about the behavior or health of minorities. While research in this area is ongoing, some exclusions within clinical trials themselves are also present. A recent systematic review of the literature relating to hearing loss in adults demonstrated that many studies fail to include aspects of racial or ethnic diversity, resulting in studies that do not necessarily represent the US population.
A 2023 scoping review of the literature found that in studies conducted in multiracial or multiethnic populations, the inclusion of race or ethnicity variables lacked thoughtful conceptualization and informative analysis regarding race or ethnicity as indicators of exposure to racialized social disadvantage, the systemic and structural barriers, discrimination, and social exclusion faced by individuals and communities based on their race or ethnicity, leading to disparities in access to resources, opportunities, and health outcomes.
'Medical racism'
An example of "medical racism" (in the words of Robert F. Kennedy Jr.) or "racism" (in the words of US President Bill Clinton) is the Tuskegee Syphilis Study in which, between 1932 and 1972, 400 Black Americans, diagnosed with syphilis, were biomedically experimented on while they were left ignorant of their diagnosis and were not treated with the effective treatments for syphilis existing in that era.
Restless legs syndrome (RLS), also known as Willis–Ekbom disease (WED), is a neurological disorder, usually chronic, that causes an overwhelming urge to move one's legs. There is often an unpleasant feeling in the legs that improves temporarily by moving them. This feeling is often described as aching, tingling, or crawling in nature. Occasionally, arms may also be affected. The feelings generally happen when at rest and therefore can make it hard to sleep. Sleep disruption may leave people with RLS sleepy during the day, with low energy, and irritable or depressed. Additionally, many have limb twitching during sleep, a condition known as periodic limb movement disorder (PLMD). RLS is not the same as habitual foot-tapping or leg-rocking.
Signs and symptoms
RLS sensations range from pain or aching in the muscles to "an itch you can't scratch", a "buzzing sensation", an unpleasant "tickle that won't stop", a "crawling" feeling, or limbs jerking while awake. The sensations typically begin or intensify during quiet wakefulness, such as when relaxing, reading, studying, or trying to sleep.
The sensations and the need to move may return immediately after ceasing movement or at a later time. RLS may start at any age, including childhood, and is a progressive disease for some, while the symptoms may remit in others. In a survey among members of the Restless Legs Syndrome Foundation, it was found that up to 45% of patients had their first symptoms before the age of 20 years.
"An urge to move, usually due to uncomfortable sensations that occur primarily in the legs, but occasionally in the arms or elsewhere." The sensations are unusual and unlike other common sensations. Those with RLS have difficulty describing them, using words or phrases such as uncomfortable, painful, 'antsy', electrical, creeping, itching, pins and needles, pulling, crawling, buzzing, and numbness. It is sometimes described as similar to a limb 'falling asleep' or an exaggerated sense of positional awareness of the affected area. The sensation and the urge can occur in any body part; the most cited location is the legs, followed by the arms. Some people have little or no sensation but still have a strong urge to move.
"Motor restlessness, expressed as activity, which relieves the urge to move." Movement usually brings immediate relief, although temporary and partial. Walking is most common; however, stretching, yoga, biking, or other physical activity may relieve the symptoms. Continuous, fast up-and-down movements of the leg, and/or rapidly moving the legs toward and away from each other, may keep sensations at bay without walking. Specific movements may be unique to each person.
"Worsening of symptoms by relaxation." Sitting or lying down (reading, plane ride, watching TV) can trigger the sensations and urge to move. Severity depends on the severity of the person's RLS, the degree of restfulness, the duration of the inactivity, etc.
"Variability throughout the day-night cycle, with symptoms worse in the evening and early in the night." Some experience RLS only at bedtime, while others experience it throughout the day and night. Most people experience the worst symptoms in the evening and the least in the morning.
"Restless legs feel similar to the urge to yawn, situated in the legs or arms." These symptoms of RLS can make sleeping difficult for many patients and a 2005 National Sleep Foundation poll shows the presence of significant daytime difficulties resulting from this condition. These problems range from being late for work to missing work or events because of drowsiness. Patients with RLS reported driving while drowsy more than patients without RLS. These daytime difficulties can translate into safety, social, and economic issues for the patient and for society.
RLS may contribute to higher rates of depression and anxiety disorders in RLS patients.
Primary and secondary forms
RLS is categorized as either primary or secondary.
Primary RLS is considered idiopathic or with no known cause. Primary RLS usually begins slowly, before approximately 40–45 years of age, and may disappear for months or even years. It is often progressive and gets worse with age. RLS in children is often misdiagnosed as growing pains.
Secondary RLS often has a sudden onset after age 40 and may be daily from the beginning. It is most associated with specific medical conditions or certain drugs (see below).
Causes
While the cause is generally unknown, it is believed to be caused by changes in the neurotransmitter dopamine resulting in an abnormal use of iron by the brain. RLS is often due to iron deficiency (low total body iron status) and could be a sign of anemia caused by internal bleeding or bone marrow issues. Other associated conditions may include end-stage kidney disease and hemodialysis, folate deficiency, magnesium deficiency, sleep apnea, diabetes, peripheral neuropathy, Parkinson's disease, and certain autoimmune diseases, such as multiple sclerosis. RLS can worsen in pregnancy, possibly due to elevated estrogen levels. Use of alcohol, nicotine products, and caffeine may be associated with RLS. A 2014 study from the American Academy of Neurology also found that reduced leg oxygen levels were strongly associated with restless legs syndrome symptom severity in untreated patients.
ADHD
An association has been observed between attention deficit hyperactivity disorder (ADHD) and RLS or periodic limb movement disorder. Both conditions appear to have links to dysfunctions related to the neurotransmitterdopamine, and common medications for both conditions among other systems, affect dopamine levels in the brain. A 2005 study suggested that up to 44% of people with ADHD had comorbid (i.e., coexisting) RLS, and up to 26% of people with RLS had confirmed ADHD or symptoms of the condition.
Medications
Certain medications may cause or worsen RLS, or cause it secondarily, including the following:
alcohol withdrawal can also cause restless legs syndrome and other movement disorders such as akathisia and parkinsonism, usually associated with antipsychotics
Both primary and secondary RLS can be worsened by surgery of any kind; however, back surgery or injury can be associated with causing RLS.
The cause vs. effect of certain conditions and behaviors observed in some patients (ex. excess weight, lack of exercise, depression, or other mental illnesses) is not well established. Loss of sleep due to RLS could cause the condition, or medication used to treat a condition could cause RLS.
Research and brain autopsies have implicated both the dopaminergic system and iron insufficiency in the substantia nigra. Iron is well understood to be an essential cofactor for the formation of L-DOPA, the precursor of dopamine.
Six genetic loci identified by linkage are listed below. Other than the first one, all linkage loci were identified using an autosomal-dominant inheritance model.
The second RLS locus maps to chromosome 14q and was discovered in one Italian family. Evidence for this locus was found in one French Canadian family. Also, an association study in a large sample 159 trios of European descent showed some evidence for this locus.
This locus maps to chromosome 9p and was discovered in two unrelated American families. Evidence for this locus was also found by the TDT in a large Bavarian family, in which significant linkage to this locus was found.
This locus maps to chromosome 20p and was discovered in a large French Canadian family with RLS.
This locus maps to chromosome 2p and was found in three related families from population isolated in South Tyrol.
The sixth locus is located on chromosome 16p12.1 and was discovered by Levchenko et al. in 2008.
Three genes, MEIS1, BTBD9 and MAP2K5, were found to be associated to RLS. Their role in RLS pathogenesis is still unclear. More recently, a fourth gene, PTPRD was found to be associated with RLS.
There is also some evidence that periodic limb movements in sleep (PLMS) are associated with BTBD9 on chromosome 6p21.2, MEIS1, MAP2K5/SKOR1, and PTPRD. The presence of a positive family history suggests that there may be a genetic involvement in the etiology of RLS.
Mechanism
Although it is only partly understood, pathophysiology of restless legs syndrome may involve dopamine and iron system anomalies. There is also a commonly acknowledged circadian rhythm explanatory mechanism associated with it, clinically shown simply by biomarkers of circadian rhythm, such as body temperature. The interactions between impaired neuronal iron uptake and the functions of the neuromelanin-containing and dopamine-producing cells have roles in RLS development, indicating that iron deficiency might affect the brain dopaminergic transmissions in different ways.
RLS may be of early onset, occurring before age 45, or late onset, occurring after age 45. Early-onset cases tend to progress more slowly and involve fewer comorbidities, while cases in older patients may progress suddenly and alongside other conditions.
There are no specific tests for RLS, but non-specific laboratory tests are used to rule out other causes, such as vitamin deficiencies. Five symptoms are used to confirm the diagnosis:
A strong urge to move the limbs, usually associated with unpleasant or uncomfortable sensations.
It starts or worsens during inactivity or rest.
It improves or disappears (at least temporarily) with activity.
It worsens in the evening or at night.
Medical or behavioral conditions do not cause these symptoms.
The symptoms below are not essential, like the ones above, but occur commonly in RLS patients:
Genetic component or family history with RLS
Good response to dopaminergic therapy
Periodic leg movements during the day or sleep
Most strongly affected are people who are middle-aged or older
Other sleep disturbances are experienced
Decreased iron stores can be a risk factor and should be assessed
According to the International Classification of Sleep Disorders (ICSD-3), the main symptoms have to be associated with a sleep disturbance or impairment to support RLS diagnosis. As stated by this classification, RLS symptoms should begin or worsen when being inactive, be relieved when moving, should happen exclusively or mostly in the evening and at night, not be triggered by other medical or behavioral conditions, and should impair one's quality of life. Generally, both legs are affected, but in some cases, there is an asymmetry.
Differential diagnosis
The most common conditions that should be differentiated with RLS include leg cramps, positional discomfort, local leg injury, arthritis, leg edema, venous stasis, peripheral neuropathy, radiculopathy, habitual foot tapping/leg rocking, anxiety, myalgia, and drug-induced akathisia.
RLS may resolve if the underlying problem is addressed. Otherwise, treatment includes lifestyle changes and medication. Lifestyle changes that may help include stopping alcohol and tobacco use, and sleep hygiene. Medications used to treat RLS include dopamine agonists like pramipexole and gabapentinoids (α2δ ligands) like gabapentin. RLS affects an estimated 2.5–15% of the American population. Females are more commonly affected than males, and RLS becomes increasingly common with age.
If RLS is not linked to an underlying cause, its frequency may be reduced by lifestyle modifications such as adopting improving sleep hygiene, regular exercise, and stopping smoking. Medications used may include dopamine agonists and gabapentinoids in those with daily restless legs syndrome. In severe or refractory cases, opioids have been used.
Treatment of RLS should not be considered until possible medical causes are ruled out. Secondary RLS may be cured if the precipitating medical conditions (such as anemia) are managed effectively.
Physical measures
Stretching the leg muscles can bring temporary relief. Walking and moving the legs, as the name "restless legs" implies, brings temporary relief. In fact, those with RLS often have an almost uncontrollable need to walk and therefore relieve the symptoms while they are moving. Unfortunately, the symptoms usually return immediately after the movement and walking ceases.
Counter-stimulation from massage, a hot or cold compress, or a vibratory counter-stimulation device has been found to help some people with primary RLS to improve their sleep.
Iron
There is some evidence that intravenous iron supplementation moderately improves restlessness for people with RLS.
Medications
For those whose RLS disrupts or prevents sleep or regular daily activities, medication may be useful.
Evidence supports the use of dopamine agonists including pramipexole, ropinirole, rotigotine, cabergoline, and pergolide. They reduce symptoms, improve sleep quality, and quality of life. Levodopa is also effective. However, pergolide and cabergoline are less recommended due to their association with increased risk of valvular heart disease. Ropinirole has a faster onset with shorter duration. Rotigotine is commonly used as a transdermal patch which continuously provides stable plasma drug concentrations, resulting in its particular therapeutic effect on patients with symptoms throughout the day. A 2008 meta-analysis found pramipexole to be better than ropinirole.
There are, however, issues with the use of dopamine agonists, including augmentation. This is a medical condition where the drug itself causes symptoms to increase in severity and/or occur earlier in the day. Dopamine agonists may also cause rebound when symptoms increase as the drug wears off. In many cases, the longer dopamine agonists have been used, the higher the risk of augmentation and rebound as well as the severity of the symptoms. Recent guidelines from the American Academy of Sleep Medicine no longer recommend dopamine agonists as standard treatment for RLS, citing newer research that has clarified the risk of augmentation associated with long-term dopamine agonist therapy.
Pramipexole and ropinirole, both dopamine agonists, along with aripiprazole, a dopamine modulator, have been linked to an elevated risk of problematic gambling. The excessive activation of the dopaminergic reward and reinforcement system is one potential mechanism by which dopaminergic drugs may contribute to increased gambling behavior. Patients may also exhibit other impulse-control disorders such as compulsive shopping and compulsive eating. There are some indications that stopping the dopamine agonist treatment has an impact on the resolution or at least improvement of the impulse-control disorder, even though some people can be particularly exposed to dopamine agonist withdrawal syndrome.
Gabapentinoids (α2δ ligands), including gabapentin, pregabalin, and gabapentin enacarbil, are also widely used in the treatment of RLS. They are used as first-line treatments similarly to dopamine agonists. As of 2019, guidelines have started to recommend gabapentinoids over dopamine agonists as initial therapy for RLS due to higher known risks of symptom augmentation with long-term dopamine agonist therapy. Gabapentin enacarbil is approved by regulatory authorities for the treatment of RLS, whereas gabapentin and pregabalin are used off-label. Data on gabapentinoids in the treatment of RLS are more limited compared to dopamine agonists. However, based on available evidence, gabapentinoids are similarly effective to dopamine agonists in the treatment of RLS.
Both the 2021 algorithm for the treatment of RLS published by the Restless Legs Syndrome Foundation, and the 2025 American Academy of Sleep Medicine Practice Guidelines recommend the use of low-dose opioids for the treatment of refractory RLS, with the caveat that, although opioids are highly effective, "reasonable precautions should be taken in light of the opioid epidemic". Among the opioids and their suggested doses are tramadol, codeine, morphine, oxycodone, hydrocodone, methadone (all of which are schedule II, except for tramadol, which is schedule IV), and buprenorphine (a schedule III partial opioid-receptor agonist with a lower risk of causing respiratory depression or dependence, compared with the full-agonist opioids). The only data publicly available on the use of buprenorphine in the treatment of RLS are two posters presented at the 2019 and 2023 Associated Professional Sleep Society's meetings. In the first, Forbes et al presented preliminary open-label data from five men and two women, with an average age of 68 years, who had experienced RLS symptoms for a mean of 30+ years and been treated for 10+ years using a mean of nine drugs. The severity of both RLS and insomnia decreased significantly according to the IRLSSG Rating Scale scores and Insomnia Severity Index (31.1 ± 6.7 at baseline to 4 ± 8 and 19.8 ± 6.1 to 1.3 ± 1.9, respectively). In the second study, Berkowsi and colleagues presented data from a retrospective study of 55 patients who had been started on buprenorphine for the treatment of severe RLS. Mean IRLSSG severity scores decreased from 27.8 at baseline to 11.4 at 1 year, and allowed most of those patients on dopamine receptor agonists who had developed augmentation to discontinue the dopamine receptor agonists.
Benzodiazepines, such as diazepam or clonazepam, are not generally recommended, and their effectiveness is unknown or contradictory. They are, however, sometimes still used as a second-line treatment, as add-on agents. Other treatments have also been explored, such as valproate, carbamazepine, perampanel, and dipyridamole, but are either not effective or have insufficient data to support their use.
Placebo
Placebos provide a large benefit in reducing RLS symptoms. This is thought to be due to positive expectancy effects and conditioning, which activate dopamine and opioid pathways in the brain. Both dopamine agonists and opioids are used in and effective for the treatment of RLS, which is thought to be related to the effectiveness of placebos for the condition. More than half of the benefit of RLS medications such as pramipexole and gabapentin enacarbil appears to be due to the placebo component based on clinical trial data.
Prognosis
RLS symptoms may gradually worsen with age, although more slowly for those with the idiopathic form of RLS than those with an associated medical condition. Current therapies can control the disorder, minimizing symptoms and increasing periods of restful sleep. In addition, some people have remissions, periods in which symptoms decrease or disappear for days, weeks, or months, although symptoms usually eventually reappear. Being diagnosed with RLS does not indicate or foreshadow another neurological disease, such as Parkinson's disease. RLS symptoms can worsen over time when dopamine-related drugs are used for therapy, an effect called augmentation which may represent symptoms occurring throughout the day and affect movements of all limbs. There is no cure for RLS.
Epidemiology
RLS affects an estimated 8% (2.5–15%) of the American population. Around 3% of the population experience moderate or severe symptoms at least twice weekly. RLS is twice as common in women as in men, and Caucasians (especially of northern European descent) are more prone to RLS than people of African descent. RLS occurs in 3% of individuals from the Mediterranean or Middle Eastern regions, and in 1–5% of those from East Asia, indicating that different genetic or environmental factors, including diet, may play a role in the prevalence of this syndrome.RLS diagnosed at an older age runs a more severe course. RLS is even more common in individuals with iron deficiency, pregnancy, or end-stage kidney disease. About 22% of pregnant women develop RLS, especially during the third trimester. Poor general health is also linked.
There are several risk factors for RLS, including old age, family history, and uremia. The prevalence of RLS tends to increase with age, as well as its severity and symptom duration. People with uremia receiving renal dialysis have a prevalence from 20% to 57%, while those having kidney transplant improve compared to those treated with dialysis.
In 2013, the Restless Legs Syndrome Foundation renamed itself the Willis–Ekbom Disease Foundation; however, it reverted to its original name in 2015 "to better support its mission".
A point of confusion is that RLS and delusional parasitosis are entirely different conditions that have both been called "Ekbom syndrome", as both syndromes were described by the same person, Karl-Axel Ekbom. Today, calling WED/RLS "Ekbom syndrome" is outdated usage, as the unambiguous names (WED or RLS) are preferred for clarity.
History
Sir Thomas Willis provided a medical description in 1672. Willis emphasized the sleep disruption and limb movements experienced by people with RLS.
Subsequently, other descriptions of RLS were published, including by Theodor Wittmaack[de] (1861) (in relation to whom it is sometimes known as Wittmaack–Ekbom syndrome).
In 1945, Karl-Axel Ekbom (1907–1977) provided a detailed and comprehensive report of this condition in his doctoral thesis, restless legs: clinical study of hitherto overlooked disease. Ekbom coined the term "restless legs".
Ekbom's work was largely ignored until it was rediscovered by Arthur S. Walters and Wayne A. Hening in the 1980s. Subsequent landmark publications include the 1995 and 2003 papers, which revised and updated the diagnostic criteria.
Controversy
Some doctors express the view that the incidence of restless legs syndrome is exaggerated by manufacturers of drugs used to treat it. Others believe it is an underrecognized and undertreated disorder. Further, GlaxoSmithKline (GSK) ran advertisements that, while not promoting off-license use of their drug (ropinirole) for treatment of RLS, did link to the Ekbom Support Group website. That website contained statements advocating the use of ropinirole to treat RLS. The Association of the British Pharmaceutical Industry (ABPI) ruled against GSK in this case.
Different measurements have been used to evaluate treatments in RLS: most of them are based on subjective rating scores, such as sleep quality and quality of life (QoL).
