African-Americans consume substantially less than the recommended daily intake
of calcium and yet have the densest bone mass of any American ethnic group, and
are at the lowest risk of osteoporosis, fragile bone disease and other calcium
deficiency disorders. Studies have shown that this occurs because blacks have
higher rates of calcium retention and greater calcium utilization efficiency
than other ethnicities. So what public health message is given to black
parents? It is that their children suffer from calcium deficiency and
should therefore be fed more dairy products in order to prevent osteoporosis.
But what might the implications be of pushing high sodium, high fat dairy
products on a population that is not in need of supplemental calcium but that
is suffering from skyrocketing rates of juvenile obesity and salt-sensitive
hypertension? The medical response is that those ailments are probably
caused by a calcium-deficiency as well.
The greatest danger in perceiving all ethnicities to be biological carbon
copies of Northern Europeans is that such an unacknowledged paradigm blocks
group testing of its underlying assumptions. For instance, the public
health model employed by researchers in the United States is one
based on the concept of "Northern European universality.”
It operates from the unexamined premise that whatever nutritional
guidelines and health messages are most beneficial for mainstream Americans,
who are predominantly of Northern European ancestry, are ipso facto deemed
best for all ethnicities and population groups. Thus the Food and Drug
Administration offers a one-size-fits all set of nutritional guidelines
for food labeling.
The Eurocentric
Paradigm
But how do we tell when a paradigm does not conform to a universal biological
standard? It will only be when too many paradoxes in the research
findings pile atop one another. In fact, African-Americans are suffering
from growing health disparities at a time when the larger society is making its
greatest health strides. In 2010, The American Public Health Association
issued an ongoing progress analysis entitled “Black-White Health Disparities in
the United States and Chicago.” It noted: “With more than 15 years of
time and effort spent at the national and local level to reduce disparities the
impact remains negligible.”([1])
Blacks are not getting poorer. But they are getting sicker and the anomalies
are stacking up in a wobbling heap of file folders stamped with a “?”
However, a clarification is in order. Even though the subject of this
article is “ethnicity,” it repudiates 19th century pseudo-scientific
racial classifications as bogus. Because over the past fifty thousand
years, the human species has migrated and adapted to new climactic, nutritional
and epidemiological environments, biogeneticists have shown that there are an
infinite number of ways to parse micro-populations. For example,
convergent evolution has allowed African-Americans to share dark pigmentation
with East Indians of Dravidian ancestry, the sickle-cell gene with southern
Mediterranean populations, Saudi Arabians and East Indians because of the
presence of malaria.([2])
East and Southern Africans share lactase persistence with Northern Europeans
because of their dairy-farming food culture.([3])
African-Americans share salt-sensitivity with Yamamoto Indians of the Brazilian
rain forest because both groups originated in sodium-deficient tropical regions
far from the coast.[4])
In spite of these adaptations, the human species has in common 99.9
percent of all its biological traits.([5])
However, in a multi-ethnic society like the United States, the small margin of
genetic variants that are environmentally influenced must be identified
and addressed in their own right. It becomes the responsibility of
the dominant ethnicity to ensure that it does not universalize its own medical
standards and pathologize any differing biological norms observed in minority
ethnicities. If the medical and public health system does not rise to the
challenge of establishing different sets of standards for diverse populations
when needed, it is inevitable that the majority demographic will see health
improvements over time. However, those minority ethnicities whose
nutritional or other medical norms are at greatest deviance from those of the
majority will see a deterioration in health no matter how well intentioned
government efforts might be at rectifying disparities.
One illustration of this potential problem has already arisen in regards to
ethnic differentials in nutritional standards for daily sodium intake. Growing
medical evidence points to African-Americans being at greater risk of
salt-sensitive hypertension and also of dying from end stage renal failure at
3.5 times the rate of whites.([6])
Studies have consistently shown that an exceptional sodium retention
capacity in the kidneys of many black Americans compared to whites is caused by
the longer length of time it takes to excrete a sodium load and higher red
blood cell sodium levels.([7])
The reasons may relate to the biological adaptations of their ancestors, who
were forced to survive sweltering tropical climates, which were geologically
deficient in sodium (being far inland from the salt-rich coastal areas).([8])
The Institute of Medicine has therefore come to recommend that healthy
African-Americans reduce their daily sodium intake to 1500 mg./daily, which is
a full 800 mg. less than the federally-recommended intake for the American
public.([9])
However recent studies by Scandinavian researchers have called into question
the 2300 mg. federal standard, even claiming that it is too low.([10])
The popular media has widely reported this medical report under such headlines
as “Sodium Intake Guidelines are Too Low.” ([11])
While this debate may indeed hold validity for people of Northern
European ancestry, not a single medical journal disputes the dangers of a
high-sodium diet for African-Americans.([12])
And yet, blacks have no way of knowing that they are placing themselves at
higher risk of end-stage-renal-failure unless they ignore FDA nutritional
labels as well as the popular media and start poring through medical journals.
Whose Calcium
Deficiency?
However, the clearest evidence of the Eurocentric paradigm’s blindspot
regarding biological differences in nutritional values has been the medical
community’s preoccupation with correcting calcium deficiency in blacks. ([13])
The focus on this issue began with an article that appeared in a 2005 issue
of The Journal of the American College of Nutrition entitled:
“The Myth of Increased Lactose Intolerance in African-Americans. Its authors
asserted:
The 'African-American
diet' is more likely to be low in a variety of vitamins and minerals, including
calcium. African-Americans consume low amounts of dairy foods and do not meet
recommended intakes of a variety of vitamins and minerals, including calcium.
Low intake of calcium and other nutrients put African-Americans at an increased
risk for chronic diseases. . . Research has shown that
lactose maldigesters, including African-American maldigesters, can consume at
least one cup (8 oz) of milk without experiencing symptoms, and that tolerance
can be improved by consuming the milk with a meal, choosing yogurt or hard
cheeses, or using products that aid in the digestion of lactose such as lactase
supplements or lactose-reduced milks. ([14])
However lactase
non-persistence, commonly referred to in the United States as lactose
intolerance is not a disorder. It is an ethnic trait, like skin
color. It is most commonly seen in populations of non-dairy farming
ancestry. In fact, seventy-percent of the human species ceases after
weaning, to produce lactase, the enzyme required to metabolize the
dominant milk sugar, lactose. While less than five percent of Americans
being of Northern European ancestry carry this trait, eighty to one hundred
percent of American Indians do, seventy- five percent of African-Americans,
ninety-five percent of Asians, fifty to eighty percent of Hispanics, as well as
sixty to eighty percent of Ashkenazic Jews.([15])
In the U.S., because the mainstream population has inherited the gene mutation
that allows them to digest lactose, the medical community is generally
unfamiliar with lactase non-persistence. It is clinically defined as a
disorder, for which a range of medications, treatments, and dietary supplements
are offered to ameliorate the symptoms.([16])
However, a closer examination of the matter shows that lactose intolerance is
only a disorder (and one that can indeed prove fatal) for those members of
lactose tolerant ethnic populations, who are born with a congenital defect in
which the gene is missing or whose digestive organs have been damaged and thus
the enzyme cannot be produced. As for the lactose non-tolerant,
the same principles of genetic adaptation that protects Congolese people from
skin cancer, protects blacks and others of non-dairy farming ancestry from
needing the supplemental calcium that the bodies of lactose tolerant adults
have come to require for bone health.
Calcium Efficiency
More than two decades of research studies have confirmed that African-Americans
are not calcium deficient. The Third National Health and Nutrition Examination
Survey (NHANES) 1988-1991 documented the fact that blacks have lower calcium
intakes than whites but higher bone mass. ([17])
This finding was initially labeled a “paradox.”
However, since then, medical researchers have continued to study the phenomenon
in order to piece together the mechanism by which a non-dairy consuming
ethnicity would have a stronger skeletal mass and exhibit genetic protections
against osteoporosis and other fragile bone disorders. These subsequent
studies have revealed a highly efficient utilization mechanism for lower level
intakes of dietary calcium. Black adolescents were shown to have higher
rates of calcium absorption, increased net skeletal retention and lower urine
calcium than their white counterparts.([18]) Such processes occurring in childhood in addition
to relative resistance to the bone resorption of parathyroid hormone also
offer bone protections, which persist into old age.([19]-[20])
Nevertheless, in 2006, an article appeared in the Journal of
Nutrition asserting that healthy blacks were Vitamin D deficient and
that this condition, created by their dark skin complexions, put them at risk
of osteoporosis, cardiovascular disease, cancer, diabetes, and other serious
chronic conditions.([21])
A popular website cautioned African-Americans that they needed ten
times more sun exposure to produce the same amount of Vitamin D as a person
with pale skin.([22])
Fortunately, by 2013 a new study had appeared in theNew England
Journal of Medicine correcting the earlier report and asserting that
blacks had been misdiagnosed as Vitamin D deficient.([23])
Inversion Theories
These kinds of mistakes should be easily spotted. But the “Eurocentric
Paradigm” hides them behind easily-generated “inversion theories.”
They borrow the same data sets and research findings but switch symptoms.
An example of an inversion theory would be acknowledging that
blacks do not suffer from osteoporosis, fragile bones or other calcium
deficiency disorders common to whites. But the theory asserts that their
calcium deficiency symptoms merely manifest themselves in a different set of
disorders, which just so happen to be whatever disorders African-Americans are
at greatest risk of suffering. In this case the diseases are obesity,
high blood pressure, diabetes II and prostate cancer.([24])
No actual research is needed to tie these disorders to calcium,
since the data already exists both that blacks suffer a calcium deficiency and
that they suffer from this other range of disorders as well. This is a
classic case of falsely inferring causation from correlated but mismatched
data.
Worsening of Health
Disparities
A flawed Eurocentric Paradigm and the inversion theories it spawns cannot help
but worsen health disparities. This is because they carry
consequences. Vital clues are lost. Time and funding are frittered away
on quixotic journeys to cure phantom diseases. In the meantime, the real
disorders take lives that might have been saved had public health knowledge
identified a particular ethnicity’s biological signatures rather than founder
in undifferentiated data.
For example, African-American men have the highest rate of prostate cancer in
the world.([25])
A growing body of research has also pointed to the fact that overconsumption of
calcium increases the risk of prostate cancer, including in black males.
This rate of prostate cancer does not however extend to West African males, who
share the same genetic ancestry. But neither do the latter consume dairy
products. On the other hand, this has become a steadily increasing part
of the black American diet because of the public health focus on calcium
deficiency among blacks.
Over the past two decades, the prevalence of obesity among African-American
adolescents has nearly doubled, rising from 13.4 percent to 24.4 percent.([26])
Earlier studies appeared to show that dairy products might have a weight-loss
effect, but on whom? The primary dietary shift for black juveniles
has been the addition of high fat-dairy to their diets during this same period
and at the instigation of health experts concerned at possible calcium
deficiencies.
Also, if lactose
intolerant African-Americans are born with genetic advantages, which protect
them from osteoporosis and bone disease, through a mechanism of calcium
homeostasis, and which also reduces the amount of calcium intake required, is
it necessary or even safe for them to over-consume calcium? What might
happen if this homeostatic process is unbalanced?
There is an urgent need to establish micro-population/ethnic databases, so that
the most critical findings and medical advances that could be of special
relevance to target ethnic population do not vanish into the mainstream data
ocean. Such an undertaking would also require some effort at substituting
population genetics for antequated racial classifications. While ethnic
terminology can be a convenient shorthand, we must be careful. Most
American ethnicities, including black Americans are admixed populations,
meaning that genetic biomarkers, rather than self-identification will be
required to distinguish populations in research purporting to establish causes
and correlations. For example, the range of African-American ancestry
goes all the way from individuals with 100% West African ancestry to those who
might, for example, have 1% West African Ancestry, 97% European Ancestry, and
2% Native American ancestry. Thus studies looking for correlations
between disorders or traits common to West Africans but not to Europeans would
spoil their data findings without first having clarified the genetic admixture
of the test pool. If for instance a study showed that
African-Americans who drank milk also had lighter complexions, did the milk
lighten their complexions, or did darker blacks refrain from drinking milk
because of lactose intolerance, a trait that those having more European
ancestry had not inherited?
Conclusion
The Eurocentric Paradigm does not need to be jettisoned. It needs to be
seen for what it really is – a model and standard of excellence for what
general human biology and all ethnic medicine must become in the U.S. The
care and sophistication with which populations of Northern European ancestry
are being examined becomes a methodology for approaching genetic variants
identified in African-Americans, Latinos, Asian-Americans, Ashkenazic Jews,
Native-Americans and other ethnicities. This is an enormous challenge but it is
one worth embracing. For, it recognizes the unique position America may
hold for the biological future of the human species, as the wanderings of
50,000 years of global migrations find their way home.
([1])Orsi JM, Margellos-anast H, Whitman S. Black-White health
disparities in the United States and Chicago: a 15-year progress analysis. Am J
Public Health. 2010;100(2):349-56.
([2] ) El-Hazmi MA, Al-Hazmi AM, Warsy AS. Sickle cell
disease in Middle East Arab countries. Indian J Med Res.
2011;134(5):597-610.
([3])Catherine J. E. Ingram, C.J.E., Elamin, M.F.,
Mulcare, C.A., Weale, M.E., Tarekegn, A.,Raga, T.O., Bekele, B. Elamin,
F.M., Thomas, M.G., Bradman, N. A novel polymorphism associated with lactose
tolerance in Africa: multiple causes for lactase persistence? Human
Genetics. February 2007, Volume 120, Issue 6, pp 779-788
([4]) Gleiberman,L. Sodium, Blood Pressure, and Ethnicity: What
Have We Learned? American Journal of Human Biology. 2009;21:679-686
([5]) Shastry, B.S. SNP alleles in human disease and
evolution. Journal of Human Genetics. November 2002, Volume
47, Issue 11, pp 0561-0566
([6] ) Lipworth, L., Mumma, M.T., Cavanaugh, K.L., Edwards,
T.L., Ikizler, T.A., Tarone, R.E., McLaughlin, J.K., Blot, W.J.,
Incidence and Predictors of End Stage Renal Disease among Low-Income Blacks and
Whites. PLOS, Published: October 24, 2012.
([7]) Gleiberman,L. Sodium, Blood Pressure, and Ethnicity: What
Have We Learned? American Journal of Human Biology. 2009;21:679-686
([8]) Gleiberman,L. Sodium, Blood Pressure, and Ethnicity:
What Have We Learned? American Journal of Human Biology. 2009;21:679-686
([9] ) Available at:
http://www.iom.edu/Reports/2013/Sodium-Intake-in-Populations-Assessment-of-Evidence/Report-Brief051413.aspx.
Accessed June 30, 2014.
([10]) Graudal, N, Alderman, M.H. . Compared With Usual Sodium
Intake, Low- and Excessive Sodium Diets are Associated. American
Journal of Hypertension. Mar 20, 2014.
([11])Available at:
http://www.thehealthierlife.co.uk/natural-health-articles/nutrition/low-sodium-intake-myth/.
Accessed June 30, 2014.
([12] ) Appel, L.J., Frohlich, E.D., Hall, J.E.,
Pearson, T.A., Sacco, R.L., Seals, D.R., Sacks, F.M.
The Importance of
Population-Wide Sodium Reduction as a Means to Prevent Cardiovascular Disease
and Stroke; A Call to Action From the American Heart Association. Circulation.2011
(123) 1138-1143
([13])Heaney, R.P. Low Calcium Intake Among African Americans:
Effects on Bones and Body Weight.The Journal of Nutrition 136 (4)
1095-1098
([14]) Byers, K.G., Savaiano, D.A. The myth of increased
lactose intolerance in African-Americans. Journal of the American
College of Nutrition. 2005 Dec;24(6 Suppl):569S-73S.
(Accessed June 2014)
([16]) http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance/ (Accessed
June 2014)
([17]) Alaimo K, McDowell MA, Briefel RR, Bischof AM, Caughman
CR, Loria CM, Johnson CL. Dietary intake of vitamins, minerals, and fiber of
persons 2 months and over in the United States: Third National Health and
Nutrition Examination Survey, Phase 1, 1988–91. Advance data from vital and
health statistics; no. 258. Hyattsville, Maryland: National Center for Health
Statistics. 1994.
([18]) Bryant RJ, Wastney ME, Martin BR, Wood O, McCabe GP,
Morshidi M, Smith DL, Peacock M, Weaver CM: Racial differences in bone turnover
and calcium metabolism in adolescent females. J Clin Endocrinol Metab
88: 2003. 1043–1047.
([19])Heaney R P. Ethnicity, bone status, and the calcium
requirement. Nutritional Research. 2002;22:153–78.
([20]) Aloia JF, Mikhail M, Pagan CD, Arunachalan A, Yek JK,
Flaster E. Biochemical and hormonal variables in black and white women matched
for age and weight. J Lab Clin Med. 1998;132:383–9.
([21]) Harris, S.S. Vitamin D and African Americans. Journal
of Nutrition, 2006 Volume 136 (4) 1126-1129.
([22]) http://articles.mercola.com/sites/articles/archive/2014/05/28/vitamin-d-deficiency-signs-symptoms.aspx (Accessed June 2014)
([23]), Powe, C.E., Evans, M.K., Wenger, J., Zonderman, A.B.,
Berg, A.H. Nalls, M. Tamex, H. Zhang, D., Bhan, I. Karumanchi, S.A., Vitamin
D–Binding Protein and Vitamin D Status of Black Americans and White Americans New
England Journal of Medicine 2013; 369:1991-2000
([24]) Heaney, R.P. Low Calcium Intake Among African Americans:
Effects on Bones and Body Weight.The Journal of Nutrition 136 (4)
1095-1098
([25]) McIntosh, H. Why Do African- American Men Suffer
More Prostate Cancer? Why Do African- American Men Suffer More Prostate
Cancer? Journal of the National Cancer Institute. 89 (3): 1997
Prevalence and Trends
in Overweight Among US Children and Adolescents, 1999-2000. Journal of the
American Medical Association, 288(14): 1728-1732, 2002.
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