I’m watching Mystery Diagnosis right now, and I heard the narrator say that lupus is three times more common in African Americans than Caucasian Americans. (The woman was black.) So let’s look into it.
Lupus is a long-term autoimmune disease where the body’s immune system becomes hyperactive and attacks healthy tissue. It can damage any part of the body, skin cells, joints, organs. Many symptoms of lupus exist, like kidney inflammation, swelling, and damage to the blood, heart, joints, and lungs. No cure exists for lupus, though there are ways to minimize inflammation through diet and lifestyle.
Lupus is two to three times more likely to occur in women of color—blacks, Hispanics/Latinos, Native Americans, and others—compared to white Americans. Somers et al (2014) state that lupus affects 1 in 537 black women, “with black patients experiencing earlier age at diagnosis, >2-fold increases in SLE incidence and prevalence, and increased proportions of renal disease and progression to ESRD as compared to white patients.” However, Somers et al (2016) note that medical records may be poor or missing while the reliability of diagnosis is low for non-whites and non-blacks. They also note that race and ethny data in the US is based on self-ID for the parents and child on the birth certificate, but self-ID has almost a perfect relationship with geographic ancestry (i.e., race) (Tang et al, 2005).
Guillermo et al (2017: 7) write that:
Ethnicity is a biological and social construct, including not only genetic ancestry, but also cultural characteristics (language, religion, values, social behaviors, country of origin) yet it is an arbitrary definition . Race is oftentimes used interchangeable with ethnicity but it mainly refers to the biological features of groups of people. Given that there are differences in the clinical characteristics and prognosis among different populations, it is worth evaluating the impact of race/ethnicity in SLE. Genetic ancestry influences the risk for the incidence of SLE; for example, Amerindian ancestry is associated with an increased number of risk alleles for SLE , and also with an early age at onset , Amerindian and African ancestry are associated with a higher risk for kidney involvement [122,123] and European ancestry with a lower risk .
First, let’s look at ref , which is McKenzie and Crowcroft (1994), who Guillermo et al (2017) cite as saying that ethnicity is “an arbitrary definition.” They note that some researchers use Blumenbach’s terms (see Spencer, 2014). They claim that modern definitions class Asians as Caucasian or black … what? They state that modern definitions classify Asians as black because “all disadvantaged groups [are] “black populations,”
[since] the experience of racism is paramount.” This is ridiculous on so many levels.
In any case, Southern Europeans are more likely to have a higher risk of renal involvement, and antibody production but along with that a lower risk of discoid rash whereas Western Europeans while Ashkenazi Jews “seem to be protected from neurologic manifestations” (see Richman et al, 2009). Asians and Native Americans in Canada are less likely to have manifestations than Africans; a type of lupus known as cutaneous vasculitis is more common in Native Americans from Canada, while Asians from Canada had a lower rate of serotisis and arthritis compared to Caucasians, Native Americans and African descendants (Peschken et al, 2015). However, Peschken et al (2015) note that while ethnicity was not that strong a predictor of damage accrual, low income was.
Kidney involvement is a major factor in the development of lupus (Bagamant and Fu, 2009), while it is more frequent in “Hispanics”, African-descendants, and Asians. Further, “Hispanics” and blacks are more likely to have end-stage renal failure than whites (Ricardo et al, 2015). When it comes to lupus nephritis—inflammation of the kidneys caused by lupus—“Hispanics” also have a better response to mycophenolate mofetil, which is an immunosuppressive drug that prevents organ rejection (Appel et al, 2009). After the onset of the disease, the disease declines slowly in “Hispanics”, then Africans, and finally fastest in whites. There also seems to be an SES factor in the aetiology of the disease. Sule and Petri (2005) write that “Socioeconomic status can have a major impact on SLE disease manifestations and mortality, independent of ethnicity“, while saying that association with SES is all over the place, with there being no relationship with SES and lupus acquisition.
Vila et al (2003) studied “Hispanics” from Texas and Puerto Rico. They noted that those from Texas accrued more damage than those from Puerto Rico. This is not surprising. “Hispanics” are not a homogenous group (they are a socialrace with no minimalist correlate, they have differing admixture from all over; “Hispanics” can be of any race. Vila et al (2007: 362) note that:
This diversity appears to be areflection of the great variability that exists between these populations with regards to their genetic, environmental and sociodemographic backgrounds.
“Hispanics” from the southeast part of America are different ethnically than those from the southeast.
Blacks and “Hispanics” have a higher rate of mortality than whites, but these differences disappear once SES is accounted for (Ward, Pyun, and Studenski, 1995; Kasitanon, Magder, and Petri, 2006; Fernandez et al, 2007). There could be some genetic differences between races/ethnies that contribute to disease differences between them. But as Kampourakis (2017: 19) notes in his book Making Sense of Genes:
… genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin.
In sum, there is a wide range of differences between races and ethnies when it comes to lupus. Is the main cause environmental or genetic? Neither, as genes and environment interact to form disease (and any other) phenotypes. So if one at-risk minority group has a low SES, that may be a risk factor. The fact that there are ethnic differences in response to autoimmune drugs when it comes to certain forms of lupus is interesting. The wide range of ethnic differences in the acquisition of the disease is interesting, with Ashkenazi Jews seemingly protected from the disease. In any case, there are racial/ethnic differences in the acquisition of this disease and to better treat those with this disease—and any other—we need to be realists about race, whether it’s biological or social, since there are very real disease and mortality outcomes between them.