Everyone Is African (12 page)

News stories, public protests, a documentary film, a class-action lawsuit, blogs, and books have made Whiteclay, Nebraska, infamous for alcohol abuse. As is the case on several reservations, alcohol cannot be sold on the Pine Ridge Indian Reservation, which is located immediately north of Whiteclay across the Nebraska–South Dakota border. Chris Hedges and Joe Sacco, in their book
Days of Destruction, Days of Revolt
, offer a stark description of the town:

Whiteclay, an unincorporated village that exists for only a block and a half before vanishing into the flatlands of the surrounding prairie, has only five or six permanent residents. It exists to sell beer and malt liquor. It has no town hall, no fire department, no police department, no garbage collection, no municipal water, no town sewer system, no parks, no benches, no public restrooms, no schools, no church, no ambulance service, no civic organizations, and no library…. The liquor stores dispense the equivalent of 4.5 million 12-ounce cans of beer or malt liquor a year, or 13,500 cans a day…. Whiteclay's clients, however, are some of the poorest people in the country. They are Native Americans from the Pine Ridge reservation that is less than 200 feet away, just over the state line in South Dakota.
¹⁷

That social issues—such as poverty, unemployment, discrimination, substandard health care, poor living conditions, and diminished educational opportunities—contribute to alcohol dependence on reservations is beyond question. However, is there evidence that genetic variants inherent to Native Americans confer increased susceptibility to alcohol dependence? Thus far, genetic analysis of several variants in alcohol-metabolizing genes among Native Americans who reside on reservations shows some statistically reliable correlations of alcohol dependence with certain variants. In some cases, the association is negative; the derived variants
protect
against alcohol dependence.
¹⁸
Other research suggests that alcohol dependence may be associated less with alcohol-metabolizing genes and more with variants in other genes that confer a generalized craving for addictive substances, including alcohol, methamphetamines, and cocaine.
¹⁹
The correlations identified thus far, however, are relatively mild. The evidence collectively indicates that,
although genetic constitution may contribute some degree of either predisposition or protection, deplorable social and economic conditions on reservations are the overriding factors responsible for the rampant abuse of alcohol and other addictive substances.

Many of the variants we've examined so far arose from mutations that originated less than twenty thousand years ago in localized populations and have spread beyond their regions of origin more recently. However, even the most ancient variation that arose in Africa and is retained in people worldwide is associated with geographic differences in health.

One of the best-studied examples is the
AGT
gene, which regulates blood pressure. A derived variant is associated with lower blood pressure, which confers lower incidence of heart disease in people alive today. This variant is very old, having first appeared in Africa before the ancient out-of-Africa migrations. Both variants are now present in populations throughout the world but are distributed unevenly. The ancestral variant is more common in Africa, as well as in some regions of the world outside Africa. The derived variant bears the marks of a selective sweep in several places where it is more prevalent, outside Africa.
²⁰
One possible explanation for the uneven distribution is natural selection for salt regulation. This gene regulates the amount of salt retained by the body, and the ancestral variant tends to cause salt retention, a trait that was advantageous in parts of the world where dietary salt was in short supply, which was the case in much of Africa. Other parts of the world have abundant salt, however, and in these regions, salt retention can be a liability because excess salt increases blood pressure. Ancient diets probably varied in the amount of salt they had, resulting in different effects of natural selection.

These examples of health issues are just a very small sampling of hundreds associated with variants in DNA dispersed among the world's people. Ancient African variants as well as more recent variants are distributed unevenly throughout the world's human population, and the incidence of diseases influenced by these variants is often correlated with geographic ancestry. A combination of factors is responsible for this nonuniform distribution of variants, including where and when mutations originated, emigration and settlement patterns of ancient humans, historic mating and cultural practices, geographic
barriers and topography, climate, random fluctuations in variant frequencies from one generation to the next, and the influence of natural selection.

Throughout much of human history—including recent history, right up to the present—false assumptions about the relationship of race, ancestry, health, and inheritance have abounded. In some cases, racist misconceptions reinforced these false assumptions. Perhaps nowhere is this more evident than with the history of sickle-cell disease in the United States. Sickle-cell anemia has been known as a specific disease for little more than a century, first identified in 1910 in an African Caribbean young man who was a student in the United States.
²¹
In the ensuing years, additional cases of sickled cells in blood were identified, some associated with outward symptoms of sickle-cell anemia but most without symptoms (the genetic distinction between sickle-cell trait and anemia remained unknown until 1949), which contributed to a plethora of false assumptions prior to that time.
²²
According to two physicians writing in 1930 about what later was identified as sickle-cell trait, “the sickler who presents even mild anemia is a subnormal individual and even though he may not be regarded as an active case of sickle cell anemia, he is still ill equipped to withstand the vicissitudes of life.”
²³

At first, all cases of sickled cells were identified exclusively among African Americans, and the disease became widely characterized as a “Negro disease.” Although a few cases were identified in people of European, Middle Eastern, and south Asian ancestry, they were often attributed to supposed undocumented African ancestry under the flawed assumption that the genetic factor causing sickled cells could only be African in origin. By the 1940s, scientists were in the midst of a concerted effort to determine the extent of cell sickling in Africa. They found high prevalence of people with sickled cells but apparently few cases of sickle-cell anemia. Most physicians working in Africa ascribed this observation to three factors: 1) inadequate diagnosis, 2) high mortality rates in Africa for children with sickle-cell anemia, and 3) difficulties distinguishing the symptoms of sickle-cell anemia from those of malaria. However, others attributed the supposed higher prevalence of sickle-cell anemia in African Americans to so-called racial mixing in their ancestry.

It was well known at the time that most African Americans had some European ancestry, as is now well documented by modern genetic evidence.
²⁴
This
was, in large part, a result of sexual abuse by slave owners and masters, abundantly recorded in the dictated recollections of former slaves.
²⁵
African Americans, therefore, were viewed during the middle of the twentieth century as a mixed or hybrid race, as opposed to native people who resided in Africa. In 1950, A. B. Raper published an extensive review of the scientific literature available at the time. Referring to this supposed higher incidence of sickle-cell anemia in African Americans when compared to native Africans, he wrote that “some factor imported by marriage with white persons, is especially liable to bring out the haemolytic [anemic] aspect of the disease, while the anomaly remains a harmless one in the communities in which it originated.”
²⁶
This view, widely held at the time, supposedly justified the assertion that African Americans were members of a genetically inferior mixed race, inferior both to “pure” Europeans and “pure” Africans. It further lent erroneous support to the notion of white supremacy, and laws mandating antimiscegenation and racial segregation.

Scientific research later dispelled these fallacies. Sickle-cell anemia was indeed present in Africa, with symptoms as severe as elsewhere. It also appeared in people with no African ancestry, particularly in the Arabian Peninsula, south Asia, and the Mediterranean region, areas where malaria was prevalent. And the notion of so-called pure races had no support in genetic data. Nonetheless, dogmatically held opinions regarding white supremacy, the supposed inherent inferiority of African Americans, and the presumption that racial purity was essential remained strong well into the 1960s and ‘70s, and even to the present, often fallaciously supported through inaccurate suppositions about sickle-cell disease.

As the civil rights movement gained momentum in the late 1960s, political agendas to improve racial equality in the United States emphasized sickle-cell anemia as a priority for research and treatment. Prior to that time, genetic conditions that were more common in European Americans had received the lion's share of governmental and philanthropic research funding. Robert B. Scott, a physician and professor at the Howard University College of Medicine in Washington, DC, was one of the strongest and most vocal advocates for increasing research funding on the biological basis of and treatment for sickle-cell anemia. In an influential 1970 article, he lamented the broad neglect of sickle-cell anemia and the lack of funding to support research and treatment:

In 1967 there were an estimated 1,155 new cases of SCA [sickle-cell anemia], 1,206 of cystic fibrosis, 813 of muscular dystrophy, and 350 of phenylketonuria. Yet volunteer organizations raised $1.9 million for cystic fibrosis, $7.9 million for muscular dystrophy, but less than $100,000 for SCA. National Institutes of Health grants for many less common hereditary illnesses exceed those for SCA.
²⁷

Underfunding for sickle-cell anemia was more a political issue than a scientific or medical one. Sickle-cell anemia was medically more serious than many less prevalent diseases yet was not a high priority for government or philanthropic support. According to Melbourne Tapper, writing in retrospect in 1999, “African Americans sought to increase funding for sickling research by turning to telethons, modeled on those for cystic fibrosis, muscular dystrophy, and cerebral palsy. These telethons were unsuccessful not because of the clinical nature of sickling, but because they were unable to neutralize the historical difference of the population in which sickling was primarily found—African Americans.”
²⁸

A biochemical test that could accurately diagnose both sickle-cell anemia and sickle-cell trait had been available since 1949.
²⁹
Several states implemented testing programs—voluntary in some cases, mandatory in others—targeting the African American population, often with well-documented instances of racism in the administration of these tests. Against this backdrop, President Richard M. Nixon proposed increased funding for sickle-cell research, and Congress responded by passing the National Sickle Cell Anemia Control Act (the word
Control
was later changed to
Prevention
), which Nixon signed into law in 1972. Although testing was encouraged, it was voluntary, partially overcoming some of the earlier claims of racist coercion associated with mandatory testing.

The purpose of testing was to inform potential parents who both were heterozygous carriers (in other words, who both had sickle-cell trait) of the possibility of having a child with sickle-cell anemia. As envisioned by Scott, “Whether a young couple will decide to have no children, or plan a limited family size, or disregard the risk would be entirely their own decision.”
³⁰

Despite its lofty goals, the impact of this act quickly faded. Congress
failed to appropriate sufficient funding for it, and the act expired three years after it was signed into law. Several clinics established under it had to be closed for lack of funds. Federal funding for sickle-cell anemia was later incorporated into funding for genetic diseases in general, so it once again had to compete with diseases that were most prevalent among European Americans, such as cystic fibrosis and muscular dystrophy.
³¹

Research in 1986 showed that early intervention with treatments for infants with sickle-cell anemia could significantly improve their lifelong outlook for health. This finding offered an impetus for mandatory newborn screening. Newborns identified with sickle-cell anemia could be immediately identified and provided treatment, thereby increasing their lifetime outlook for health. Over the next twenty years, states began implementing sickle-cell testing for newborns, with universal testing in all fifty states and the District of Columbia by 2006. With the support of sickle-cell organizations, healthcare professionals, and the National Association for the Advancement of Colored People (NAACP), Congress passed the Sickle Cell Treatment Act of 2003, which President George W. Bush signed into law. The act provided federal funding for research, counseling, education, matching funds for Medicaid to assist with treatment, and establishment of sickle-cell centers throughout the United States.

Sickle-cell disease is, without doubt, the most prominent example of how health, inheritance, and ancestry have become entangled with racial tensions. Those tensions have persisted for more than a century and are still with us, as the latest controversy regarding testing athletes for sickle-cell trait attests. There are other examples as well. Although perhaps not as well known, they, too, illustrate how ignorance of scientific information can result in discrimination, whether intended or not.

An example is lactose intolerance—the inability to fully digest dairy products, especially fresh milk—which is common throughout the world, affecting more than 65 percent of the world's population. In fact, it is the original ancestral state of humanity. Mammals, including humans, consume milk during infancy, then are weaned from milk as they begin consuming other foods. The principal sugar in milk is lactose, and the body must break it down into other sugars to digest it. A single gene in our DNA, called
LCT
, encodes a protein
called lactase, which carries out the first step of lactose metabolism. This gene is active during infancy but, in many people, is genetically programmed to shut down after weaning because anciently, before humans domesticated milk-producing animals, the gene was no longer needed in children who were weaned. Some people carry a derived variant that disrupts this shutdown, retaining
LCT
gene activity into adulthood and allowing them to continue consuming milk, a condition known as
lactase persistence
. Several derived variants that confer lactase persistence have arisen independently in humans, and they are mostly found in people whose ancestry traces to populations that relied on domesticated animals for milk, such as cattle, sheep, and goats.