Unexpectedly Intriguing!
August 13, 2008

"What does not kill you makes you stronger."

That observation was communicated to us more than once by e-mail after we found that blacks over the age of 80 are living longer than whites of the same age. And to be honest, there's a uplifting kind of logic about it. If an individual can overcome adversity in their life, the logic goes, they're much more likely to have developed the skills and the strength needed to cope with other adversities in the future and thus, be able to prevail over them as well.

But where the human biology is involved, things generally don't work that way.

Consider the chickenpox virus (varicella zoster), which is behind a relatively common childhood disease in the United States. Once a child has chickenpox, they're immune from having it again for the rest of their life. But rather than developing a stronger, healthier immune system, the virus instead lies dormant for years until it activates when the body is stressed from other conditions. Then the virus may re-emerge to only affect adults who have previously had chickenpox, but now in its more sinister form, shingles (herpes zoster.)

What does not kill you does not necessarily make you stronger. In biology, more often than not, what doesn't kill you instead softens you up for what will, or as is more often the case, what might protect you from a particular kind of harm (a blessing) also makes you more vulnerable to whatever it might be that will eventually kill you (a curse).

That insight will come into play again and again as we consider why people whose ancestors originate in sub-Saharan Africa are so much more vulnerable to so many different diseases than those whose ancestors originated in other parts of the world.

And as we'll soon see, African blessings and African curses are tightly intertwined.

The Challenges of Sub-Saharan Africa

Worldwide Malaria Endemic Zones Compared to just about everywhere else in the world, sub-Saharan Africa presents some of the greatest challenges to human health. Parasitic infections such as malaria and tuberculosis cause millions of deaths each year, while other lesser known infections such as shistosomiasis and onchoceriasis (river blindness), are endemic throughout most of the region and severely affect the health of millions of people.

Likewise, the highest concentrations of several virus-borne diseases anywhere in the world, such as HIV may found in sub-Saharan Africa.

The most vulnerable victims of the parasitic infections are children. The magnitude of infant and child mortality between birth and five years old from these kinds of conditions in sub-Saharan Africa is astronomical. In the following chart, we've incorporated the percentage of survivors by age for sub-Saharan African populations developed by the Givewell charitable organization with that for the African American population in the United States:

Percentage of Survivors by Age and Origin, Out of 100,000 Born Alive

We see that the number of lives claimed by malaria, respiratory infections, diarrhea, perinatal conditions, measles and HIV/AIDS, as only 90% of those born alive survive to reach Age 5. Excepting under-5 deaths caused by these conditions, almost 96% of sub-Saharan Africans would reach their fifth birthday. Both figures are compared to the roughly 99% of African Americans who do reach Age 5.

We also see the gap between the percentage of people who reach any given age between sub-Saharan African and the black population of the United States opens wider and wider before beginning to narrow at Age 60, which roughly 28% of the sub-Saharan population reach as compared to nearly 65% of African Americans. The last comparison point for data is for Age 80, the age to which some 12% of sub-Saharan Africans survive, as compared to 41% of African Americans for every 100,000 born alive of each group.

Blessings and Curses

Surviving Malaria, Greater HIV Vulnerability

Plasmodium falciparum vector Longtime readers of Political Calculations may recall that we've previously created tools to assist in better targeting malaria prevention efforts in the regions of the world where it is endemic and kills more than 700,000 people a year. As such, there's no better place for us to begin showing how better biological defenses that developed to protect against one health condition opens up weaknesses against others.

Given the massive exposure to the various parasites of the Plasmodium family that cause various forms of malaria in sub-Saharan Africa over several thousand years of history, it may not be surprising to learn that surviving sub-Saharan Africans have developed genetic defenses against many of them. In research led by Weijing He that was just published in July 2008, Duffy Antigen Receptor for Chemokines Mediates trans-Infection of HIV-1 from Red Blood Cells to Target Cells and Affects HIV-AIDS Susceptibility, it would appear that a genetic mutation that served to protect sub-Saharan Africans from the form of a now nearly-extinct form of malaria caused by the Plasmodium vivax parasite greatly increases the likelihood that they will contract the HIV-1 virus if exposed to it. The authors of the study estimate that roughly 11% of the HIV burden in Africa is directly linked to the greater vulnerability created by this particular adaptation.

For African Americans, that translates to a 40% greater risk of acquiring the HIV-1 virus if exposed compared to those who lack the genetic mutation that once protected their ancestors from malaria, which might go a very long way to explaining why the black population of the U.S. is so much more likely to have HIV/AIDS. The good news, if you could consider it that, is that the genetic adaptation would also seem to slow the progression of the disease compared to those who do not have it. Additional research has already begun to confirm these basic findings.

HIV/AIDS and Parasitic Worms

As a side note, the adaptation that defeats P. vivax-driven malaria isn't the only correlation between parasitic infections and increased vulnerability to HIV/AIDS. Newly published research led by Agnès-Laurence Chenine, Acute Shistosoma mansoni Infection Increases Susceptibility to Systemic SHIV Clade C Infection in Rhesus Macaques after Mucosal Virus Exposure, suggests the same parasitic worms behind shistosomiasis may also expose those infected to greater vulnerability in contracting HIV. With sub-Saharan Africa being an endemic region for human infection by the parasites, this study may help explain why HIV/AIDS has become so prevalent among the human populations of the region compared to other areas in the world.

In this case, the infections generated by the parasitic worms would seem to soften up the body's first-line defenses against basic infection with HIV through heterosexual transmission, sharply reducing the quantity of the virus needed to establish itself within a host. That, in turn, would largely account for the greater incidence of HIV/AIDS in sub-Saharan Africa than anywhere else in the world.

Melanin and Tuberculosis

Tuberculosis Incidence Map, 2004 With much of sub-Saharan Africa lying in the tropics, where direct sun exposure may be found at its highest levels anywhere in the world, one of the great adaptations that has developed over the millenia among the peoples who live there is increased levels of melanin, which is the substance that gives hair and skin their pigmentation. Here, those with greater levels of melanin in their skin, which corresponds with darker skin color, are much better able to tolerate long hours of exposure to direct sunlight and ultraviolet rays, than those with lower levels of melanin in their skin, who are at much greater risk of sunburn in the short term and skin cancer with repeated, prolonged exposure over the long term.

That enhanced protection comes with a very recently discovered price. Tuberculosis is a disease caused by the pathogen Mycobacterium tuberculosis, which infects roughly eight million people annually and kills some two million people worldwide, primarily in sub-Saharan Africa. According to research led by Philip T. Liu published in February 2006, Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response, the increased levels of melanin found in peoples of African descent accounts for the much lower levels of Vitamin D produced through sunlight exposure, which corresponds to greater vulnerability to infection by the M. tuberculosis microbe.

Since UV-B radiation from direct sunlight stimulates the production of Vitamin D in humans through natural chemical reactions, people with increased levels of melanin in their skin produce much lower levels of the vitamin than those with lower levels of melanin, as those whose skin contains higher levels of melanin absorb more of the sun's ultraviolet radiation, thereby limiting the amount of the vitamin produced through this particular mechanism.

This turns out to be vitally important as Vitamin D plays an essential role in the immune system's response to infections. Low levels of Vitamin D in the bloodstream result in the production of much lower levels of cathelicidin when a microbe invades the body, as compared to when high levels of Vitamin D are present. Cathelicidin acts as a microbicide, an agent that kills infectious microbes like the agent behind tuberculosis, M. tuberculosis, which in turn accounts for why peoples of African descent are so much more vulnerable to becoming infected with, and dying from, tuberculosis.

Although both infections and deaths from tuberculosis in the United States are rare and almost non-existent, African Americans are roughly 8 times as likely as other racial/ethnic groups to become infected with tuberculosis if exposed. The researchers conducted laboratory tests to evaluate the effect of increasing the level of Vitamin D in African American blood serum to levels typical of those found in the white population of the United States.

Increasing the level of Vitamin D increased the level of cathelicidin produced within the African American blood samples. This result suggests that Vitamin D dietary supplementation could make for a remarkably effective method for reducing the infection rate of tuberculosis in peoples of African descent. Clinical trials for tuberculosis endemic regions in both Africa and Asia have been proposed to test if these laboratory results can be replicated on a larger scale and to verify if lower rates of the incidence of tuberculosis would result.

A Simple Vitamin Deficiency?

This latter bit of science points to a tantalizing solution to the problem of the racial life expectancy gap in America - could a deficiency of Vitamin D explain why African Americans are more likely to die of a wide variety of chronic diseases than the members of the white population in the United States? And could the gap be closed by addressing the vitamin deficiency within the black population of the U.S.?

As we'll show you tomorrow, that might just be the case. And then we'll also show you that the solution is not quite as simple as you might think....

All the Posts in the Series

For reference, here are all of the posts in our series covering the racial disparity between the life expectancies in the United States:

Blacks Living Longer Than Whites

The post that started the whole thing! We were surprised to find that blacks over the age of 80 had longer remaining life expectancies than whites of the same ages in the U.S. We also used the opportunity to ridicule some pretty blatant rent-seeking behavior on the part of researchers seeking funding for their work.

Erasing the Gap in Racial Life Expectancies

We revisited the life expectancy figures between blacks and whites and took a closer look at the underlying data, which allowed us to reject racism as an explanation for what we observed. We also began asking "why this, but not this?" in comparing not just the survivorship of the black and white populations of the United States, but urban vs rural blacks, immigrant vs native-born blacks, and the effect of older vs younger mothers for African American infant mortality.

The Disproportionate Killers

You can't address racial disparities in life expectancies unless you know what chronic health conditions disproportionately affect the black population of the United States compared to other racial or ethic groups.

African Blessings, African Curses

Chronic diseases often have a very strong genetic or heredity component in determining who is vulnerable to them. In this post, we explored the idea that what doesn't kill you either softens you up for what will or makes you more vulnerable to other health hazards in comparing the black population of the United States to sub-Saharan Africans who share much the same genetic anthropology, while also discovering very recent research whose results potentially explain why all peoples of African descent are more vulnerable to the things that disproportionately kill African Americans.

A Seemingly Simple Solution

Does a chronic vitamin deficiency explain why the disparities between black and white life expectancies in the U.S.? We explore this possibility and why it may not as easy to address as you might think on first glance, as well as how individual African Americans might do so successfully.

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