The Backbone Volume 2 Issue 1

The Backbone
The Official Journal of the

W. Montague Cobb Research Laboratory
Winter 2015 Spring 2016

Volume 2 Issue 1
Cover page credit: We thank Amanda D. Strong for access to this photo of a cadaver from the W. Montague Cobb Research Lab.
The Backbone
OFFICIAL JOURNAL OF THE W. MONTAGUE COBB RESEARCH LABORATORY, HOWARD UNIVERSITY
ISSN (Online): 2373-3934
ISBN (Print): 2373-3926
Editor-in-Chief: Fatimah Jackson, Ph.D.
Production Editor: Nicholas Guthrie
Copy Editor: Amanda D. Strong
The Backbone is published twice a year by the W. Montague Cobb Research Laboratory at Howard University. This
online, open-access journal accepts original articles, short biohistories, and recent abstracts on scientific considerations
of broad aspects of the African diaspora. Manuscripts for publication consideration, comments on the journal, and other
inquiries should be sent to: cobbresearchlab@howard.edu
Howard University All Rights Reserved
Contents
Editorial
Resilience Through Research and Publication
Fatimah L.C. Jackson
... 1
Full Articles
Chronic Kidney Disease and its Sequelae within the Cobb Collection: Osteological Manifestations
and Clinical Record of Evidence
Amanda D. Strong, Uzaomaka Nqaogwugwu, M.D., Christopher Cross, M.S., Fatimah Jackson, Ph.D.... 2
Analysis of Potential Treatments for Sickle-Cell Anemia, or Drepanocytosis, in Adults

Cameron D. Clarke . 10
Genetic Behavioral Evidence for Autism in the Cobb Collection

Jayla Harvey , Fatimah Jackson, Ph.D.... 16
A Review: Evolutionary Theories of the Pathogenesis of Schizophrenia

Nichelle Jackson...... 19
How might the genetic identification of mental disorders vary across geographical spaces, cross
culturally and though time?
Sedera Moore .. 26
Prevalence and Anatomical Evidence of Treponemal Infection in the Cobb Collection

Nicholas Guthrie .. 31
Biohistories
The Story of CC18
Theodore Meadough, Jermain E. Robertson .. 35
The Story of CC112

Turquoisia McNabb, Whitley Hatton . 39
The Story of CC312

Christine Okaro, Christopher Wilson .42
The Story of CC315

James M. Bryne III, Lopriela Seabrook ... 46
CobbResearchLab.com/TheBackbone
Winter 2015Spring 2016
Volume 02 Issue 01
The Backbone
CONTENTS
The Story of CC331

Jordan Mitchell, Jordan R. Howard .. 49
The Story of CC437

Rachel Davalos, Mariela A. Martnez .. 52
The Story of CC459

Jasmine Mack, Ambra Palushi . 55
Recent Abstracts from W. Montague Cobb Research

Laboratory
Validation of Cobb Collection Biohistories
Davlyn Hollie ... 58
How the Cobb Research Lab succeeds in increasing the number of STEM and STEM-affiliated
Students
Sherese Taylor .... 59
Investigation of the Cobb Collection, A Statistical Approach

Nicholas Guthrie .. 60
Overview of the Interface of the Cobb Research Laboratory and the Robert Wood
Johnson Summer Medical and Dental Education Program (SMDEP) at Howard University
Donna Grant-Mills, RDH, M.Ed., DDS . 61
Comparative Analysis of DNA Extraction Techniques on DNA yield from Ancient Teeth
Latifa Jackson Ph.D. 62
Geospatial Assessment o Residential and Work Sites for Cobb Collection Individuals
Hasan Jackson 63
Minimally Invasive Method to extract DNA from Dentition using Cobb Collection Human Skeletal
Remains
Alexis Payne, Christopher Cross, M.S., Latifa Jackson, Ph.D, John Harvey, D.D.D., Fatimah Jackson, Ph.D. . 64
Trends and Causes of African-American Osteoarthritis and Osteoporosis within the Cobb Collection
Sierra Williams . 65
Volume 02 Issue 01
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CONTENTS
Evidence for Arthritis and Specifically Osteoarthritis in the Cobb Collection

Maimouna Traore ... 66
Biohistorical Analysis od Cardiovascular Disease in the Cobb Collection

Jameshisa Alexander . 67
Historical Trends of Hypertension and Cardiovascular Disease within the Cobb Collection
Janet Mansaray ... 68
The Prevalence and Biohistory of Congestive Heart Failure in the Cobb Collection
Kayla Bedeau .. 69
The Correlations between African-American Life Experiences and Type 2 Diabetes

Whitney Griffith .... 70
Prevalence of Cerebrovascular Accident within African Americans of the Cobb Collection

Natalia Christian .. 71
Assessment on the Resurgence of Rickets and Scoliosis on African Americans

Khristian Ifill .. 72
Identifying the effects and treatment of Alzheimers disease in African Americans

Youngho Jung . 73
Lead in Teeth: Reconstructing Environmental Biohistory and Health at the New York African
Burial Ground Using Laser Ablation-Inductively Coupled Plasma-Mass Spectrometry (LA-ICP-MS)
Joseph L. Jones, Ph.D. .. 74
Profile and initial elemental determination of soil samples collected rom the New York African Burial
Ground Remains
Candice Duncan, Ph.D. ,,,.. 75
Analysis of Grave Soil Samples Found in the New York African Burial Ground
Keely Clinton 76
Enhancing Public Access to Recent Research on the African Burial Ground Materials: Grave Soil and
Oral Microbiome Analyses
Fatimah Jackson, Ph.D. . 77
Announcements/Advertisements
Volume 02 Issue 01
Editorial
Resilience through Research and Publication
Fatimah L.C. Jackson, Ph.D.
Resilience is the process of adapting well in the face of adversity, trauma,
tragedy, threats or significant sources of stress. Writing about African
American history, studying human biology, and interpreting the past are all
activities that can contribute to our resilience as individuals and as a nation.
We become vulnerable when we are unfamiliar with our past, when we
cannot reconstruct the successes of our ancestors, when we cannot learn
from their mistakes and misjudgments. Resilience is primarily a learned
attribute. Stress stimulates resilience to subsequently stressful episodes,
particularly when it is mild in magnitude and controllable by the individual
(Ashokan et al 2016) Research on African American health and lifeways can
provide a kind of stress inoculation by familiarizing us with what has occurred in the past and how it was
responded to. This, in turn can facilitate our psychological adaptations, social connections, life meaning and
planning, and ultimately physical wellness. Researching and writing about scientific aspects of the African
Diasporas, particularly its transatlantic components, can begin to heal the longstanding wounds of that
experience and its sequelae by changing the social context within which these historical facts are
understood. The social context is the third pillar linking individual genetic susceptibility, a traumatogenic
event, and the phenotypic expression of stress (see Auxmry, 2012).
This issue of The Backbone contains articles on various clinical conditions evident in the Cobb Collection as
well as theoretical papers on aspects of human evolutionary biology. As a new feature of The Backbone, we
feature a diverse set of short biohistories on specific individuals of the Cobb Collection. These were
researched and reconstructed by Summer Medical and Dental Educational Program (SMDEP) student
scholars during the summer 2015 research program held at the Cobb Research Laboratory (see Cobb
Research Lab News 2(3) Summer 2015). This issue concludes with a flurry of recent abstracts on a range of
scientific topics from the Cobb Research Laboratory. These abstracts include topics affiliated with our
research on ancient human DNA and our historical studies of health disparities. The abstracts will be given
as research papers on April 12, 2016 during a special symposium during Howard Universitys Research
Week 2016.
Ashokan A, Sivasubramanian M, Mitra R. 2016 Seeding Stress Resilience through Inoculation. Neural Plast. 2016;2016:4928081.
doi: 10.1155/2016/4928081. Epub 2016 Jan 5. Accessed February 10, 2016
Auxmry Y. 2012 [Posttraumatic stress disorder (PTSD) as a consequence of the interaction between an individual genetic
susceptibility, a traumatogenic event and a social context]. Encephale. 2012 Oct;38(5):373-80. (in French) doi: 10.1016/
j.encep.2011.12.003. Epub 2012 Jan 24. Accessed February 10, 2016.
Winter 2015Spring2016
Volume 02 Issue 01 11
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FULL ARTICLES
Chronic Kidney Disease and its Sequelae within the Cobb Collection
GENETICS & EPIDEMIOLOGY
Chronic Kidney Disease and its Sequelae within the Cobb

Collection: Osteological Manifestations and Clinical Record
of Evidence
Amanda D. Strong1,2
Uzoamaka Nwaogwugwu, M.D.3
Christopher Cross, M.S.,1,4 Fatimah Jackson, Ph.D.1,2
1W.
Montague Cobb Research Laboratory, Howard University

2Department of Biology, Howard University
3Department of Medicine, College of Medicine, Howard University
4Department of Anatomy, Howard University
Chronic Kidney Disease (CKD) has plagued the African American (AA) community as a frequent result of severe
hypertension and diabetes, both diseases that may be instigated by environmental factors or hereditary factors such
as genetics. CKD is an ailment that causes a dangerous imbalance of vital minerals and ions, and can cause waste to
build up throughout the major organs of the body. In contrast to its prevalence, there is an underrepresentation of
CKD when participating in cadaver dependent research; this is the result of major consequences of CKD, such as
cardiovascular or neurological symptoms being pronounced the cause of death. The Cobb Research Laboratorys (CRL)
investigation within chronic kidney disease will involve the examination of cadaver skeletons whose deaths have been
notably caused by CKD. With the information gathered from these investigations, the CRL team is optimistic for
anatomical clues left behind by the disease in the hopes of diagnosing other unknown cases within the Cobb
Collection for further research. With the findings of more cases it will be possible to examine the genes that are linked
to CKD as well as find explanations that could assist in research on the preventative progression of the disease.
Introduction
In the United States, the AA community constitutes
approximately 13% of the entire population, yet 32% of
all patients receiving treatment for kidney failure are
AA,1 this leads to an overall kidney failure rate that is
over three times larger than that of our Caucasian
counterparts. It has also been shown that AAs require
dialysis or transplantation at younger ages.6,7 Chronic
kidney disease most often leads to end-stage renal
disease (ESRD) in which the kidneys can no longer
function at the level necessary to remove all of the waste
and excess water from the body.2 AAs have greater
incidence rates of ESRD at each decade of life compared
with any other racial/ethnic group.6,7 The likelihood for
the development of chronic kidney disease is determined
by the relationship and interactions between genes and
FIGURE 1: RISK FACTORS FOR CKD5
the environment.3 It is key to understand both the

genetic and environmental factors so that novel
treatments and therapies can be developed. Most
importantly, understanding the underrepresentation of
CKD and why it plagues our community will aid in
developing the preventative measures needed to
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improve our statistical status on the matter. Socio-
those groups, AAs have, and have always
environmental, behavioral, biomedical, and predisposing
had, the highest rate of CKD incidents.
factors all work together towards particular health
African Americans and Native Americans share many
outcomes. Once all taken into consideration, real
social environmental stressors that may have aided in
progress can and will be made.
their correlation up until 1999. The quickly accelerating
Background Research
progression of the disease has often be attributed to risk

factors such as diabetes, hypertension and obesity;
As reported by the National Kidney and Urologic
however, this has not been able to explain the elevated
Diseases Information Clearinghouse (NKUDIC) and
rate of CKD progressing into ESRD among AAs and other
displayed in Figure 1, African-Americans (red circles)
groups with low socioeconomic status.8 Unfortunately,
have the highest occurrence of ESRD incidents and well
the consequences of the social environment is too often
as the highest exponential increase since the year of
over-looked as a contributing element. Through
1980. In second lead, incidents in Native Americans (blue
behavioral science studies, it has been established that

there are psychological and physiological consequences
dependent on the environment in which one works and
lives.9,10 Social environmental stressors such as poverty
and discrimination are proven to adverse the bodies
psychological functioning as well as prompt response in
regards to the nervous and vascular systems; these
complications place individuals at greater risk for
developing CKD and cause a lesser ability to prevent the
progression towards ESRD.8 From Figure 3, it can be seen
that social environmental factors are the beginning of a
FIGURE 2: INCIDENT RATES OF ESRD BY RACE4
chain of risk factors that can contribute to other high risk

factors such as psychosocial and behavioral that lead to
negative
effects
in
pathophysiological
mechanisms. Social issues such as economic struggle and

discrimination often lead to psychological manifests of
anxiety, depression and stress. Alone, the psychological
state can impact the physiological functions of the body;
however, the situation is heightened double-fold when
these psychological factors instigate poor habits such as
drug use, poor diet and lowered physical activity. Many

studies
FIGURE 3: CKD RISK FACTOR FLOW CHART8
have
focused
on
the
effect
of
racial
discrimination and institutionalized racism.

It has been suggested that the excess risks for chronic
diamonds) began to rise up until 1999 when a decrease
diseases such as CKD among groups such as African
began. Asians (yellow squares) and Caucasians (green
Americans (and Native Americans) are a function of
triangles) have shown the slightest increase in
economic deprivation. However, racial disparities in the
comparison with the others. Compared to the other
prevalence and progression of kidney disease continue
ethnic groups analyzed and to the overall average of
to persist even when the socioeconomic position at the
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individual and community level is improved and

11,12,13
stable.
with nondiabetic etiologies of ESRD, there was strong
The main concern given by Figure 1 is in
suggestive evidence for linkage on chromosome 10p,
regards to the continuation of an exponential rise in
specifically.3 Curiously, this is near the D10S1435 marker
ESRD in African-Americans that differentiates them from
that is confirmed to have a consistent presence in
others of same or lower socioeconomical status. These
diabetic families.19 For AA families with a history of type
results lead us to examine the genetic factors as the only
2 diabetic nephropathy, a genome wide scan on sibling
key to understanding why the difference among AAs
pairs showed evidence for linkage on chromosomes 3q,
have the highest risk
10q, and 18q.20 Notably, the type 1 diabetic nephropathy
associated with family history, as do Native Americans15
locus was at the 3q peak in the chromosome. 21 Studying
and Hispanic Americans;16 however, it is observed in case
the close proximity of these chromosomal markers and
studies across the United States that AAs are the only
loci may help to explain the continuous relation between
racial group to have a nine-fold higher risk of developing
diabetes and renal disease beyond the physiological level
ESRD if they already have a first degree family member
and allow for a genetic perspective. This information is
occurs. It is a fact that AAs
17
14
Some studies have concluded racially
extremely useful in determining the cause of CKD
variable susceptibility rate is due to familial clustering of
underrepresentation in the AA community. Essentially,
on dialysis.
those with CKD in certain racial groups, but other
there is a considerable amount of evidence that supports
research has indicated a correlation among AA
family history of renal disease, as well as familial
individuals who have a mutation at the location of the
clustering of ESRD, as contribution to the pathogenesis
From newer studies a positive correlation
of chronic kidney failure.3 Identification of causative
between similar genetic mutations and familial clustering
elements located within the genome may enlighten the
has been found, thus combining the two previous
development of innovative gene therapies.3
PKD1 gene.
3,18
theories.
In Kidney International studies, it was shown that the
location of the PKD1 gene mutation is directly correlated
with the severity of renal disease and the onset of
18
ESRD.
In studies regarding rodent renal failure a
correlation was noticed in the Rf-1 gene, the rodent

analog of the human chromosome10 To assess any
10
possible linkage between markers on chromosome and

ESRD potential, a linkage analysis was performed in
African American sibling-pairs. It was shown that in AAs
Osteopathic Research
According to Dr. Uzoamaka Nwaogwugwu, MD and
DaVita expert, renal osteodystrophy is the most common
bone disease associated with kidney failure. This disease
causes significant imbalances in calcium, parathyroid
hormone, phosphorus and activated vitamin D. The
condition further develops to affect the balance of
osteoclast
and
osteoblast
development
and
22
production. When the calcium levels in the blood begin

to drop a significant amount, the body begins to over
activate the parathyroid glands to produce the
parathyroid hormone. This hormone will begin to extract
calcium from the skeletal system and into the
bloodstream in order regain calcium equilibrium. As the
calcium is being stripped from the bones they begin to
weaken and the texture becomes chalky, rather than the
FIGURE 4: OSTEOMALACIA ON BONE23
natural sturdy form.22 Secondly, kidney disease causes an

extremely high amount of phosphorous levels in the
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blood. Because calcium and phosphorous share a
symbiotic relationship, the body will begin to draw

calcium from the bones into the blood to create
equilibrium between calcium and phosphorous.22 Of
course, this causes the same side effect of low blood
calcium and diminishes the bone. The kidneys serve an
ultimately vital function of activating the vitamin D that
courses through our blood to form calcitriol. Calcitriol is
acts to assist the body in absorbing calcium and
maintaining normal parathyroid hormone levels.22
Unfortunately, when the kidneys begin to fail, they are
no longer able to convert vitamin D into calcitriol and the
FIGURE 5: RENAL OSTEODYSTROPHY X-RAY24
body is no longer able to absorb dietary calcium

properly. Again, the body attempts to fulfill its calcium
need by stealing from within the bones.
The typical symptoms for degradation of the bone
include: bone and joint pain, bone deformation and
fractures, as well as poor mobility.22 In the case of this
research, bone deformation is the key component. When
having suffered from long-term renal failure or chronic
kidney disease, evidence of the disease is left behind on
the skeletal structure. Osteodystrophy, osteomalacia,
uremia and metabolic bone disease all alter the visual
integrity of the bone. Bone lesions, porousness, thinning
or thickening, and the abnormal curving of the bone are
FIGURE 6: EXAMPLE OF LYTIC BONE LESION25
all potential signs that the skeletal system was being

robbed of essential minerals and ions.
In Figure 4, the abnormal curvature and slight protrusion
towards the tips of the bone can be seen. When
describing osteomalacia, Dr. Nwaogwugwu described
how the bone matrix weakens and the bone begins to
flare up towards the joints, where majority of the
damage occurs. Figure 5 shows the lack of mineral

density near the joints when suffering from renal
osteodystrophy. Renal osteodystrophy has been viewed
using an X-ray, even when being viewed as a defleshed
cadaver. The symptoms most suitable for observation in
the laboratory are related to lesion formation. Lesions
can be seen on the bone without using tools, however,
this can cause an issue when attempting to differentiate
natural deterioration from mechanical damage due to
FIGURE 7: X-RAY OF BONE LESIONS26
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processing. Fortunately, an X-ray picture of the bone
lesions can reveal its true nature and will not be

confused with mechanical damage.
Methods and Procedures

Extensive research was done on what types of
osteological symptoms would be present in order to
truly piece together our analysis of cadaver skeletons
from the Cobb collection. The beginning step was to
completely review the digital Cobb Collection files, with
the assistance of our director, Dr. Fatimah Jackson, for all
patients whose cause of death was related to kidney

malfunction or kidney disease. The exact cause of death,
age, race and body number was noted. It was then that
FIGURE 9: JOINT (1) FROM #693
some of the noted bodies were pulled with guidance of

our assistant curator and student
of anatomy,
Christopher Cross. The entire anatomy of a carefully

chosen, defleshed cadaver was laid out on the laboratory
table and reconfigured for organization and easy access,
as shown in Figure 8.
Beginning with the bones that survive the most
tension and pressure through the lifetime, as well as the
highly sensitive joints, we attempted to find signs of
lesioning, porosity and abnormal morphology on the
femurs. This task became difficult as we faced questions
that had not yet posed an issue. During the retrieval of
many skeletons from the African Burial Ground (New
FIGURE 8: DEFLESHED CADAVER #693
FIGURE 10: JOINT (2) FROM #693
FIGURE 11: FEMURS FROM #693
6
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York), many of the bones were damaged through
biopsies will allow us to insure consistent results by
mechanical digging and treating.
confirming osteopathic symptoms that appear similar
As can be seen in Figure 9 and in Figure 10, it is difficult
also have similar chemical and molecular makeup. This
to categorize the damage on the bone under a specific
will be helpful in proving the exact mineral composition
cause. While it is possible that the damage to the bone
that results from these pathological processes. Along
could be the result of deterioration, it could also be
with Dr. Nwaogwugwu, we hope to make a connection
damage inflicted from machinery or rough handling
with
during transportation.
department in order to gain a more complete
the
Howard
University
Hospital
Pathology
Figure 11 is an example of how normal differences in
understanding of the bone pathologies in this focus. To
midsagittal skeletal structure can be mistaken for the
assist in differentiating what is appropriate for expected
thinning or improper curving of the bone.
The
anatomical difference in the bone versus significant bone
left femur, on the bottom of the figure, appears thinner
curvature or loss (Figure 11), the Howard University
with slightly more curvature than its left counter part. It
Hospital Osteology department will be able to analyze
is expected for the skeletal anatomy to differ slightly
measurements taken in the lab as well as photographs.
when analyzing midsagittal pieces. The question that
In the proceeding research, we will use the
arises is whether or not this difference is significant
information gain to find more cases of osteopathic
enough to note it as an osteopathic symptom. In the lab,
symptoms representing CKD in the Cobb Collection.
we also noticed a difference in the texture and color of
Specifically, we will do this by examining defleshed
the two bones, yet determination of the cause was not
cadavers that have causes of death most often
entirely
associated with CKD (i.e., diabetes, cardiovascular
clear.
All
fragments
in
question
were
photographically captured for future comparison.
disease, nuerological disorders). Not only will this add

more sources to our research, but will allow for the W.
Conclusion
Ultimately, we were not able to determine as much
as had been anticipated through the physical laboratory
analysis due to the uncertain observations; however, the
flaws in our expectations have been led us to new
venues, methods, and resources to continue our hunt for
answers. To eliminate misperception between natural
deterioration of bone and mechanical damage done to it,
we have proposed x-ray scanning. By using a
radiographically produced image (Figure 5 and Figure 7),
it would allow us to see beyond the outer surface of the
bone and deeper into its matrix; for example, dark areas
within the bone matrix will indicate significant
deterioration, as in renal osteodystrophy whereas patchlike spots on the bone will indicate bone lesions have
formed. Utilizing the Howard University Hospital Critical
Image and Photo department will allow the W.
Montague Cobb Research laboratory access to x-ray
machines as well as bone biopsy processes. Bone
Montague Cobb Research Laboratory to have a more

detailed record for causes of death. Having an extended
collection of defleshed cadavers specifically marked for
CKD would also allow us to collect DNA samples from a
variety of sources in order to analyze the genes and
attempt to find common markers and genetic clues.
Potentially, finding a common genetic factor amongst all
CKD cases in the Cobb Collection could allow for a
starting point for gene therapies. We can then extend
the research to verify whether CKD is prominent in a
certain sex, age or lifestyle (i.e., profession, family size)

within the AA community. By comparing location of
deaths, a crude idea of how the social environment
impacted
composed.
the
progression
of
CKD
can
be
Being that the Cobb Collection contains
African remains dating back to the 17th century, we also

hope to find a positive correlation between rising CKD
levels and time spent in what is now the United States.
We are hoping to find clues that will allow us to
7
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hypothesize in regards to why AA specifically have 6. Tareen N, Zadshir A, Martins D, et al. Chronic kidney disease
in African American and Mexican American populations.
developed predispositions for chronic disease that is not

common of our ancestry.
Kidney Int. 2005;68(supplement 97):S137S140.

7.
Bruce, Marino A., Bettina M. Beech, Mario Sims, Tony N.

Brown, Sharon B. Wyatt, Herman A. Taylor, David R.
Discussion
Williams, and Errol Crook. "Social Environmental Stressors,
In all, this research is guided towards to the awareness
Psychological Factors, and Kidney Disease." Journal of
and understanding of how and why chronic kidney disease
Investigative Medicine : The Official Publication of the
affects the African American population at an exponential
American Federation for Clinical Research. U.S. National
rate. Our research could potentially serve as a foundation
Library of Medicine, 18 Feb. 2010. Web.
of knowledge for a disease that is highly neglected on the 8. Fremont A, Bird C. Social and psychological factors,
physiological processes, and physical health. In: Bird C,
preventative and treatment level in our community. If we
Conrad P, Fremont A, editors. Handbook of Medical
improve our understanding of what factors place African
Sociology. Upper Saddle, NJ: Prentice Hall; 2000. pp. 334
Americans at risk for chronic kidney disease, we will be

better equipped to avoid those scenarios as preventative
measure.
Acknowledgements
I would like to thank our director, Dr. Fatimah Jackson,
PhD, for allowing us to be apart of the amazing experience
of the W. Montague Research Cobb Laboratory. We would
also like to thank our curator, Christopher Cross, MS, for
his helpful instruction when analyzing the anatomy of the

cadaver skeletons in the Cobb Collection. Finally, I would
352.
9.
Seeman T, Mcewan B. Impact of social environment

characteristics on neuroendocrine regulation. Psychosom
Med. 1996;58:459471.
10. Norris K, Nissenson AR. Race, gender, and socioeconomic

disparities in CKD in the United States. J Am Soc Nephrol.
2008;19(7):12611270.
11. Tarver-Carr ME, Powe NR, Eberhardt MS, et al. Excess risk of
chronic kidney disease among African Americans versus
white subjects in the united states: a population-based
study of potential explanatory factors. J Am Soc Nephrol.

2002;13:23632370.
like to thank Matthew Calhoun for his ideas and 12. Volkova N, McClellan W, Klein M, et al. Neighborhood
constructive conversation toward the research.
poverty and racial differences in ESRD incidence. J Am Soc
Nephrol. 2008;19(2):356364.
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Kidney Foundation. N.p., Apr. 2014. Web.
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Australian Institute of Health and Welfare. N.p., n.d. Web.
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13. Freedman, BI, Soucie, JM, McClellan, WM: Family history of

end-stage renal disease among incident dialysis patients. J
Am Soc Nephrol 1997 8:19421945.
14. Pettitt, DJ, Saad, MF, Bennett, PH, et al: Familial
predisposition to renal disease in two generations of Pima
Indians with type 2 (noninsulin-dependent) diabetes
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15. Pugh, J: Diabetic nephropathy and end-stage renal disease
in Mexican Americans. Blood Purif 1996 14:286292.
16. Freedman, BI, Spray, BJ, Tuttla, AB, Buckalew, VM: The
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Am J Kidney Dis 1993 21:387393.
17. Rosetti, S, Burton, S, Strmecki, L, et al: The position of the
polycystic kidney disease 1(PDK1) gene mutation correlates
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13:12301237, 10.1097/01.ASN.0000013300.11876.37.
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25. Museum of London - Cross Bones Burial Ground Photographs." Museum of London - Cross Bones Burial Ground:
Centre for Human Bioarchaeology. N.p., 2005. Web.

26. "Orthopedic Teaching: Bone Lesions Case 2 Answer." Bone
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School of Medicine, n.d. Web
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Potential Treatments for Sickle-Cell
Analysis of Potential Treatments for Sickle-Cell Anemia, or

Drepanocytosis, in Adults
Cameron D. Clarke1,2 ,3
1W.

3Department of Health, Human Performance and Leisure Studies,, Howard University
This research paper discusses the clinical and evolutionary history of sickle-cell disease, also known as sickle-cell anemia, or
drepanocytosis. It noted the genetic causes and physiological effects of sickle-cell disease, and the evolutionary and
environmental factors involved in the diseases emergence, finding that its proliferation was likely the result of a selective sweep
of an adaptation of the red blood cells that had a secondary protective effect against malaria in heterozygous individuals. This
also mentioned two of the possible treatment methods that could be used to eliminate or mitigate sickle-cell disease and its
symptoms. The first treatment method analyzed was therapy of a patient with sickle-cell disease to increase the production of
healthy red blood cells containing fetal hemoglobin. The second involved a bone marrow transplant to replace the defective bone
marrow. It was found that while both treatments are effective in reducing the severity of sickle-cell disease, only a bone marrow
transplant has been conclusively shown to be able to cure the condition, and even then, has only undergone trial testing amon g
children. However, there is currently preliminary clinical research being conducted on gene therapy to promote the bodys
continued production of fetal hemoglobin, preventing sickle-cell hemoglobin S from even developing, and curing sickle-cell disease
Clinical Background
Sickle cell disease, also known as sickle-cell anemia or

drepanocytosis, is a hereditary blood disorder,
characterized by a genetic mutation in the gene that
codes for hemoglobin in the red blood cells of the body.
Hemoglobin is an iron-based metalloprotein that binds
to molecules of oxygen in the capillaries of the lungs, and
then carries them through the bloodstream, releasing
the oxygen molecules into the somatic cells, and binding
to carbon dioxide, which is released back into the lungs
with each exhalation.1 This paper will discuss three (3)
distinct varieties of hemoglobin: Hemoglobin A (HbA),
the normal adult form of hemoglobin; hemoglobin S
(HbS), the diseased variety of hemoglobin; and
hemoglobin F (HbF), fetal hemoglobin. Sickle cell disease
occurs as a result of a mutation at a single nucleotide (A
to T) of the -globin gene, which results in glutamic acid
being substituted by valine at position 7 (position 6
under the historic nomenclature. This causes the protein
to form Hemoglobin S (HbS) in its final conformation,
instead of Hemoglobin A (HbA), normal adult
hemoglobin. Under normal conditions, the mutation is
generally benign, causing no apparent effects on the
secondary, tertiary, or quaternary structures of
hemoglobin in conditions of normal oxygen
concentration. Under conditions of low oxygen

concentration, however, this mutation allows for the
polymerization of the HbS itself. When HbS is in
conditions of low oxygen saturation, the hydrophobic
residues of the valine (formerly glutamic acid) at position
7 of the beta chain in hemoglobin are able to associate
with the hydrophobic patch, causing hemoglobin S
molecules to aggregate and form fibrous precipitates
(Figure 1). These precipitates form long, interlocking
strands within the blood cells, elongating and distorting
its shape, and causing them to take on the distinctive
malformed sickle-like shape that gives the condition its
name. These sickle cells are far less efficient in carrying
oxygen than the ordinary rounded cells, additionally,
after a cell is sickled, it loses much of its elasticity,
becoming much more inflexible. This rigidity makes the
cells much more likely to become trapped in the small
openings of the capillaries and narrow blood vessels. As
cells accumulate in the blocked vessels, they can cause
ischemia (oxygen deprivation) and cell death in the
affected areas, a complication called a sickle-cell crisis.
Sickle-cell crises are often extremely painful, and
potentially fatal if the obstruction occurs around a vital
organ and causes organ damage or failure. Additionally,
the deformation of the cells by the hemoglobin fibers
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present itself when the allele for sickle-cell disease is

passed from both parents during reproduction. In
individuals that are heterozygous for sickle-cell disease
(one copy of the diseased allele), also called carriers,
the sickle cell load is greatly reduced, and symptoms
generally only appear after prolonged oxygen
FIGURE 2: MALARIA DISTRIBUTION
FIGURE 1: DIAGRAM OF SICKLE CELLS CAUSING VASO-OCCLUSIVE

CRISIS
reduces the integrity of the cell membrane, making the

cells much more likely to lyse. This damage is severe, to
the extent that while healthy red blood cells may
typically function for 90120 days, sickled cells only last
1020 days before lysis.2 This rapidly accelerated rate of
hemolysis is from where the condition derives its
designation as an anemia; although the bone marrow
creates red blood cells at increased volume compared to
healthy humans, it is simply unable to compensate for
the rate of cell destruction. Patients are often left with
lower-than-normal levels of erythrocytes, and can
exhibit symptoms common to general anemia sufferers,
including feeling tired, weakness, shortness of breath, or
a poor ability to exercise.3
Evolutionary Background
Sickle-cell disease is an allelic disorder, located on the

chromosome 11, at 11p15. It has an autosomal recessive
pattern of inheritance, in that the condition will only
FIGURE 3: SICKLE-CELL DISTRIBUTION
deprivation, or severe dehydration. Evolutionarily, the

emergence and proliferation of the sickle-cell allele are
likely linked to the diseases protective effect against
malaria, a far more expansive and lethal disease, found
in a similar range (Figures 2 & 3).
This is due to the sickling of the cells interfering with
the complex lifecycle of the parasite that causes malaria,
Plasmodium malariae. Plasmodium reproduces within
the erythrocytes. In a carrier for sickle-cell disease, the
presence of the malaria parasite causes the red blood
cells with defective hemoglobin to ruptureprematurely,
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making the Plasmodium parasite unable to reproduce.

Further, the polymerization of the hemoglobin affects
the ability of the parasite to digest hemoglobin in the
first place. This reduced efficacy of Plasmodium leads to
shorter and less severe infections among sickle-cell
carriers. Therefore, in areas with endemic malaria,
chances of survival actually increase among
heterozygotes. However, this protective effect does not
extend to sickle cell homozygotes, or people with the
disease, since the premature lysis of infected cells is a
common cause of sickle-cell crises. The heterozygote
advantage, however, is enough to account for the
persistence of sickle-cell disease in areas with high
endemic malaria. Analysis of the diseases genetic
history via restriction endonuclease analysis found that it
most likely arose spontaneously in several different
areas, with a different variant of the mutation emerging
in each one. These variants are known as Cameroon,
Senegal, Benin, Bantu, and Saudi-Asian. This evidence
also supports the hypothesis that the mutation that
causes sickle cell arose and proliferated as a result of the
widespread malaria that is endemic to the regions.
Fetal Hemoglobin Treatment
begin producing adult hemoglobin (HbA) (Figure 4).In
most cases, the switch from fetal hemoglobin to adult

hemoglobin is relatively inconsequential. However, since
the structure and genetics of fetal hemoglobin differ
from those of adult hemoglobin, it is not affected by the
same genetic mutations that govern the production of
adult hemoglobin. When fetal hemoglobin production is
switched off after birth, normal children begin producing
adult hemoglobin (HbA). Children with sickle-cell disease
instead begin producing a defective form of hemoglobin
called hemoglobin S (Figure 5). However, among children
with the sickle-cell trait, where fetal hemoglobin remains

the predominant form of hemoglobin after birth, the
frequency and severity of sickle-cell crises decrease
FIGURE 4: HEMOGLOBIN A
In addition to corroborative evidence of evolutionary
pressure for the emergence of sickle cell, the restriction

endonuclease analysis of the disease also found that in
some regions, including Senegal and Saudi-Asia, the
sickle-cell mutation has variants that are correlated with
increased and persistent production of hemoglobin F,
also known as fetal hemoglobin (HbF).4,10 Fetal
hemoglobin is the type of hemoglobin that is produced
in the human fetus during the last seven months of

development
in
the
uterus.
Functionally,
fetal
hemoglobin differs little from adult hemoglobin, apart

from the fact that it has a slightly higher oxygen affinity,
and bonds more tightly, but still temporarily, to the
oxygen molecules in the capillaries of the lungs.5 This is
due to the mixture of oxygenated and deoxygenated
blood in the maternal blood that is delivered to the fetus
via the umbilical vein. Generally, within six months of
FIGURE 5: HEMOGLOBIN S
relative to those where fetal hemoglobin production has

ceased. This protective effect was observed in variants of
the sickle-cell mutation in Senegal and Saudi-Asia, where
it is believed to be a secondary adaptation, blunting
some of the acute complications of sickle cell disease.
birth, humans stop producing fetal hemoglobin, and

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Fortunately, much progress has been made in a clinical
production of HbF in humans is feasible in order to more
application for this phenomenon.
permanently treat, or even cure, sickle-cell disease.
In a landmark study in the New England Journal of
Preliminary studies have already found that it is possible
Medicine, it was found that not only did treatment of
to completely cure mice of a variant of sickle-cell disease
patients with hydroxycarbamide (hydroxyurea), an
by using gene therapy, and studies in humans have
antineoplastic (tumor-inhibiting) drug, increase the
shown promising results, to the extent that gene therapy
quantity of fetal hemoglobin in erythrocytes, but that it
has moved on to the early stages of clinical trials as a
also appeared to break down cells that were likely to
permanent cure for sickle-cell disease.8,9,11
sickle, further decreasing the risk of vaso-occlusive sickle

-cell crises. Additionally, a second study discovered that
the treatment of sickle-cell disease with a combination
therapy
of
hydroxycarbamide
and
recombinant
erythropoietin (a hormone involved in red blood cell

synthesis) further increased levels of HbF, and further
reduced
the
frequency
of
acute
sickle-cell
complications.6 Even more significant, this treatment

method was found to have no major adverse side
effects, and so would likely significantly improve patient
outcomes and quality of life.
Important to note, however, is that the study was only
conducted on adults, so it is not currently clear how
much the success would translate to interventions in
children. Additionally, hydroxyurea treatment has only
been shown to reduce the frequency of sickle-cell crises,
not prevent them entirely. As such, it is only a partially
effective treatment, not a cure. It also has not been
tested in an attempt to resolve a currently occurring
sickle-cell crisis, and so cannot be recommended as an
emergency
intervention.
Finally,
the
researchers
involved with the study noted that there is concern that

long-term hydroxyurea therapy may be carcinogenic or
leukemogenic, because some other antineoplastic agents
have such effects.7 As with any medication, additional

research is necessary in order to more completely
understand the mechanism of hydroxyurea therapys
function in preventing crises, and its long-term effects on
individuals and their children. However, this treatment is
already in use in patients suffering from sickle-cell
disease, and so far has seen widespread success.
On the horizon, researchers have begun testing
whether
gene
therapy
to
stimulate
permanent
Hematopoietiec Stem Cell Transplantaion
For all of the promising research on the horizon,
however, a cure for sickle cell disease already exists.

Hematopoietic stem cell transplantation (HSCT), also
known as bone marrow transplantation, has been shown
to permanently cure children of sickle cell disease when
it is successful. Allogenic bone marrow transplants, the
type used in sickle-cell procedures, are a high-risk
procedure, usually involving two people: the (healthy)
donor and the recipient (patient). In the procedure, the
donor and the recipient must both be tested to
determine if they have similar or identical variants of the
human leukocyte antigen (HLA) system. This network of
genes is responsible for an individuals immune response

to foreign cells and molecules. If the two individuals are
incompatible, or too dissimilar, the transplantation will
fail, as the recipients immune system will either attack
the donors stem cells, or the donors stem cells will
cause an infection in the recipients tissues, a condition
called graft-versus-host disease . Even if the HLA patterns
of the individuals match, in order to minimize the
possibility of a rejection, the patient must be subjected
to immunosuppressant treatment to destroy their
immune response system. This immunosuppression is

part of what makes the procedure so high-risk; patients
with compromised immune systems are extremely
vulnerable to infection, such that even a relatively
mundane disease such as the common cold can be fatal.
Once the recipient is immunosuppressed, the donor is
placed under general anesthesia, and the hematopoietic
stem cells are removed from a large bone of the donor,
typically the pelvis, through a large needle that reaches
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Discussion
Of the methods described, as a practical solution for

patients with mild to moderate sickle-cell disease, with
only occasional, infrequent vaso-occlusive crises, the
combination therapy of hydroxyurea and recombinant
erythropoietin seems to be the ideal currently available
treatment, both in terms of relative safety and likelihood
of success, and in terms of effectiveness. Of course, as
elaborated, all of the treatments require further
research to conclusively determine their long-term
FIGURE 6: BONE MARROW HARVEST
health risks and benefits, but currently the risks of
the center of the bone. This technique is referred to as a
hydroxyurea are the most widely studied and well
bone marrow harvest (Figure 6). The cells are then
known. The most promising of the treatments, however,
implanted into the patients own bones, and after a few
remains gene therapy, which, unlike hydroxyurea
weeks to allow the cells to multiply, the patient is
therapy, promises to completely cure sickle-cell disease,
removed from immunosuppressants, and the procedure
and without the complex surgery and high-risk
is completed.
immunosuppression
of
hematopoietic
stem
cell
Although HSCT, due to its relatively high risk, is
transplantations. Unfortunately, as this method is still in
generally only attempted in people with conditions that
its earliest stages of clinical trial, it may be years before it
are extremely life-threatening, recent advances in the
becomes available to the average sickle-cell patient.

Sickle-cell disease is a stigmatized, misunderstood, and
safety and standardization of the procedure have made

it safe
life-altering condition, but it is no longer the death
enough to attempt in individuals with less-threatening
sentence it once was. Hopefully, with additional study,
conditions, such as sickle-cell anemia. In such cases,
evolutionary and clinical research, and public health
however, studies have only been conducted among
outreach, we can make sickle-cell disease no more than
children. A recent study by the New England Journal of
a nuisance, instead of a potentially debilitating condition.
Medicine found that of 22 patients upon whom bonemarrow transplants were performed, 20 survived the
procedure itself, and 16 were found to be free of sickle-
References
1.
Maton, Anthea; Jean Hopkins; Charles William

McLaughlin; Susan Johnson; Maryanna Quon Warner;
David LaHart; Jill D. Wright (1993). Human Biology and
Health. Englewood Cliffs, New Jersey, USA: Prentice Hall.
ISBN 0-13-981176-1.
2.
Maakaron, J. (2014). Sickle Cell Anemia. Medscape.

Retrieved April 14, 2015, from http://
emedicine.medscape.com/article/205926-overview
3.
Stedman's medical dictionary (28th ed. ed.). Philadelphia:

Lippincott Williams & Wilkins. 2006. p. Anemia. ISBN
9780781733908.
4.
Lanzkron S, Strouse JJ, Wilson R et al. (June 2008).

"Systematic review: Hydroxyurea for the treatment of
cell disease in the months following the procedure,

survival and event-free survival at four years of 91
percent and 73 percent, respectively. Although these

results are promising, a mortality rate of 9%, and with
only a 10% mortality likelihood by age 20 is clearly
unacceptable, so more advancements must be made,
both in the calculations of the likelihood of rejection, and
in
the
safety
hematopoietic
of
stem
the
cell
procedure
itself,
transplantation
before
can
be
considered a viable and efficacious treatment for sicklecell disease.

5
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FULL ARTICLES
adults with sickle cell disease". Annals of Internal

Medicine 148 (12): 93955. doi:10.7326/0003-4819-14812-200806170-00221. PMC 3256736. PMID 18458272
5.
Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition.

New York: W H Freeman; 2002. Section 10.2, Hemoglobin
Transports Oxygen Efficiently by Binding Oxygen
Cooperatively.
6.
Rodgers GP, Dover GJ, Uyesaka N, Noguchi CT, Schechter

AN, Nienhuis AW (January 1993). "Augmentation by
erythropoietin of the fetal-hemoglobin response to
hydroxyurea in sickle cell disease". The New England
Journal of Medicine 328 (2): 7380. doi:10.1056/
NEJM199301143280201. PMID 7677965.
7.
Charache S, Terrin ML, Moore RD et al. (May 1995).

"Effect of hydroxyurea on the frequency of painful crises
in sickle cell anemia. Investigators of the Multicenter
Study of Hydroxyurea in Sickle Cell Anemia". The New
England Journal of Medicine 332 (20): 131722.
doi:10.1056/NEJM199505183322001. PMID 7715639
8.
Pawliuk R, Westerman KA, Fabry ME, Payen E, Tighe R,

Bouhassira EE, Acharya SA, Ellis J, London IM, Eaves CJ,
Humphries RK, Beuzard Y, Nagel RL, Leboulch P (2001).
"Correction of Sickle Cell Disease in Transgenic Mouse
Models by Gene Therapy". Science 294 (5550): 236871.
doi:10.1126/science.1065806. PMID 11743206.
9.
Wilson, Jennifer Fisher (18 March 2002). "Murine Gene

Therapy Corrects Symptoms of Sickle Cell Disease". The
Scientist Magazine of the Life Sciences. Retrieved 17
December 2014.
10. Green NS, Fabry ME, Kaptue-Noche L, Nagel RL (Oct 1993).

"Senegal haplotype is associated with higher HbF than
Benin and Cameroon haplotypes in African children with
sickle cell anemia". Am. J. Hematol. 44 (2): 1456.
doi:10.1002/ajh.2830440214. ISSN 0361-8609. PMID
7505527.
11. St. Jude Children's Research Hospital (4 December 2008).
"Gene Therapy Corrects Sickle Cell Disease In Laboratory
Study". ScienceDaily. Retrieved 17 December 2014.
6
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The Backbone
Evidence for Autism in the CC
Genetic Behavioral Evidence for Autism in the

Cobb Collection
Jayla Harvey1,2
Fatimah Jackson, Ph.D.1,2
1W.

1 in 88 children in the United States are diagnosed with autism; this number has grown exponentially over the past couple of
years, primarily due to raised awareness of this disorder. The definition of autism as we know it today didnt come about until
1980. Prior to that, autism was defined as schizoid personality disorder attributed fundamentally to a lack of maternal
warmth. Mental health issues, in general, in African Americans have not been extensively studied and are frequently underdiagnosed. Differential expression of mental disease likely stems from the multi-generational inhumane effects of the
transatlantic slave trade, segregation, racism, and discrimination. As a result, the literature is scant on explicit descriptions of
autism for the African American population. However, new scientific advances are suggesting that autism is genetically linked by
clusters of DNA markers. Since African Americans rich diversity is not widely represented in either genetic or behavioral studies,
this research will search for evidence of mental disease in specific individuals within the Cobb Collection try to develop a bridge
between the behavioral expression of mental disease and the presence of genetic susceptibility genes for autism. This study will
focus on African American adults from the District of Columbia, Maryland, and Virginia area who died in the 1930s, 40s and 50s
and for whom clinical reports and other clinical and demographic clues suggest evidence of mental disease. Advanced
bioinformatic approaches will be expended to identify likely autism gene clusters in the targets of study.
Introduction
Methods and Results
Hospital in Washington, D.C between the decades of
various genes that have been linked to autism over the
1930s through 1950s were institutionalized because they
past couple years. The genes have been grouped into
Many of the patients confined at St. Elizabeths
The genes that will be studied in this experiment are
were unable to function in society. This inability to
three categories: mutated genes, deleted or copied
assimilate into the general public may be a consequence
genes, or genes with methylation changes.
of an undiagnosed mental illness. Autism Spectrum
Mutated
genes
either
show
single
nucleotide
Disorders (ASD) were not characterized separately from
polymorphisms (SNPs) or frameshift mutations. The
schizophrenia at this time, therefore it is possible that
mutated genes being studied are Dopamine Receptor D2
some patients that were being held at St. Elizabeths
(DRD2: Gene ID1813), Protein phosphate1, regulatory
Hospital because they didnt exhibit normal behavior
inhibitor subunit 1B (PPP1R1B: Gene ID 84152), and
14
Latest genetic research
Neuroligin4, X-linked (NLGN4X: Gene ID57502). DRD2
shows that ASD can be shown through a connection of
encodes for the D2 subtype of a dopamine receptor
and suffered from an ASD.

many mutated genes.
These mutations can be
which
has
roles
in
postsynaptic
neurons
and
dopamine
synthesis
and
etiologically effected by the environment the patient was
autorecpetor
subjected to. African-Americans of this time period
neurotransmission. The receptor inhibits adenylyl cyclase
would likely be more susceptible to these mutations due
activity, which catalyzes the conversion of ATP and cyclic
to the immense stressors of living in a time of
adenosine monophosphate (cAMP) and pyrophosphate.3
segregation, Jim Crow Laws, post slavery traumatic
cAMP is important because it is used in the intracellular
syndrome, and poverty.
signal transduction. In ASD, the DRD2 gene shows an
mediating
over transmission of the T allele, which causes the gene

1
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to be incorrectly, negatively effecting how cells send

4
incorporating the trust and empathy of in-groups with
signals to each other. The PPP1R1B gene encodes for
their suspicion and rejection of outsiders. In ASDs, there
DARPP-32, a bifunctional signal transduction molecule,
is reduced to no expression of the CD38 protein due the
expressed in dopaminoceptive neurons and mediates the
fact that the gene is mutated or deleted. The CADPS2
effects of D1 and D2 dopamine receptors. In ASDs, this
gene encodes for calcium binding proteins that play a
gene shows an over transmission of the C allele, which
major role in exocytosis of neurotransmitters and
can show decreased release of dopamine. Altered levels
neuropeptides into the synapse and of dense core
of the DARPP-32 molecule displays impaired reversal
vesicles in neuroendocrine cells.8
learning. Mutated DRD2 and PPP1R1B genes additively
regulates neurotrophin release from granule cells
predispose ASDs and are
only found in male
leading to regulate cell differentiation and survival during
patients. The decreased dopamine activity in the medial
cerebellar development. CADPS2 is deleted in ASD. The
This gene also
prefrontal cortex is also a sign of ASD. The NLGN4X gene
gene PCDH10 deals with the establishment and function
effects cell adhesion molecules localized at the CNS
of cell to cell connections in the brain at the
synapse. It is still being studied, about the exact
synapse. This is also one of the largest deletions in ASD.9
variation of this gene sequence that predisposes ASD,
The absence of this gene negatively affects the cells to
but it has been suggested that the defect in this gene
create synapses and communicate with each other.
12
negatively affects synaptogenesis. Therefore, when this

gene is mutated, neurons in the CNS have trouble
communicating with each other due to the fact that they are
unable to create proper synapses.
Certain genes have deleted or copied sequences that
cause either a lack of or overproduction of specific

proteins. The deleterious or copied genes in this study
are Fragile X mental Retardation 1 (FMR1: Gene ID2332),
CD38 molecule (CD38: Gene ID952), Ca2+-dependent
secretion activator 2 (CADPS2), and protocadherin alpha
cluster
10,
complex
locus
(PCDHA10:
Gene
ID56139). FMR1 is a very well studied gene that encodes

for the Fragile X mental retardation 1 protein. In the
brain, the protein may play a role in the development of
6
the connections between nerve cells at the synapse. The

protein also regulates synaptic plasticity.
Synaptic
plasticity is the ability of synapse to adapt over time in

response to experience.13 Synaptic plasticity plays a role
in learning and memory. In Fragile X syndrome, which
has features of ASD, 200+ CGG repeats causes the gene
to be unstable and in consequence to be silenced,

making little to no protein. Fragile X syndrome is a
precursor for Autism. The CD38 gene encodes for a
transmembrane protein, CD38, which regulates oxytocin
secretion. Oxytocin is described as the bonding
Methylation changes on a DNA sequence alters how

the gene or protein is expressed without changing the
actual sequence. The genes with epigenetic changes

that may predispose autism that are being studied in this
research are Nuclear Receptor Subfamily 3, group C,
Member 1 (NR3C1: Gene ID2908) and Methyl CpG
Binding Protein 2 (MECP2: Gene ID4204). NR3C1 gene
encodes for a glucocorticoid receptor that regulates
transcription factors. Glucocorticoids are involved in
inflammatory responses, cellular proliferation and
differentiation in target tissues. In ASD, it has been
found that suppressed methylation on hippocampal DNA
may be due to deprived maternal care during
infancy.10 This methylation suppression at the NR3C1
gene leads to a decreased number of the glucocorticoid
receptors needed to regulate transcription. The MECP2
gene encodes for the methyl-CpG binding protein 2. This
gene is located on the X chromosome at Xq28; it is an Xlinked dominant mutation that is only found in females,
due to the fact that it is lethal in males. MECP2 is
identified with Retts Syndrome, a precursor to autism.11
De novo mutations at CpG dinucleotide causes
epigenetic change of deacylation of core histones, which
changes the chromatin architecture and leads to
hormone.7 It also promotes ethnocentric behavior,

17
2
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transcriptional repression. This repression show low
5. Joe A Hettinger, X. L. (2012). DRD2 and PPP1R1B (DARPP32) polymorphisms independently confer increased risk
levels of gene transcription.
for autism spectrum disorders and additively predict

affected status in male-only affected sib-pair families.
Conclusion
Autism is a heterogeneous neuro-developmental
syndrome with a complex genetic etiology. Unifying

principles among cases of autism are likely to be at the
level of brain circuitry at the synapse. All of the genes in
this study effect the synaptic transmission of information
in some way. The idea that ASD can be affected or

caused by environmental factors is reinforced by the
Behavioral and Brain Functions.

6. U.S National Library of Medicine. (2012, August). FMR1
Gene. Retrieved from Genetics Home Reference: http://
ghr.nlm.nih.gov/gene/FMR1
7. Heon-Jin Lee, A. H. (2009). Oxytocin: the Great Facilitator
of Life. Progressive Neurobiology.
8. Declan J. James, a. T. (2013). CAPS and Munc13: CATCHRs
that SNARE Vesicles. Frontiers in Endocrinology, 817.
characteristic called synaptic plasticity, in which a
9. Eric M. Morrow, S.-Y. Y.-K.-S. (2008). Identifying Autism
synapse can change and adapt by either strengthening of
Loci and Genes by Tracing Recent Shared Ancestry.
weakening over time in response to increases or
Science.
decreases in activity or because of an alternation in the

number
of
neurotransmitter
receptors
on
the
synapse. Conclusively, ASD is likely to be a synaptic

disorder.
In the future we plan to extract DNA from the selected
specimen and first look for the group of genes that
would have been deleted or copied, then mutated
genes. Lastly, we will look for possible methylation
changes on the previously highlighted genes. If a patient
exhibits more than 3 mutated genetic factors then we
will pull their archived records and compare their
psychiatric records with genetic evidence found on their
genome
and
possibly,
tentatively
change
their
psychiatric records with genetic evidence found on their

genome and possibly, tentatively change their diagnoses
10.L J van der Knaap, H. R. (2014). Glucocorticoid receptor

gene (NR3C1) methylation following stressful events
between birth and adolescence. The TRAILS study.
Translational Psychiatry.
11. Lam CW, Y. W. (2000). Spectrum of mutations in the

MECP2. J Med Genet.
12.Jamain, S. (2003). Mutations of the X-linked genes
encoding neuroligins NLGN3 and NLGN4 are associated
with autism. Nature Genetics 34, 27-29.
13.Sarah R. Gilman, I. I. (2011). Rare De Novo Variants
Associated with Autism Implicate a Large Functional
Network of Genes Involved in Formation and Function of
Synapses. CellPress: Neuron, 898-907.
14.(2013). The Evolution of Autism. Retrieved from The

History of Autsim: http://ct-educationadvocates.com/
information/autism/the-evolution-of-autism/
to an ASD.
References
1. Barak Goodman, J. M. (Director). (2010). American
Experience: The Lobotomist [Motion Picture].
2. Geschwind, D. H. (2008). Autism: Many Genes, Common
Pathways. CellPress, 391-395.

3. NCBI. (2015, April 5). DRD2 dopamine receptor D2 [ Homo
sapiens (human) ]: Gene ID 1813. Retrieved from NCBI
Gene
Summary:
http://www.ncbi.nlm.nih.gov/gene?
cmd=Retrieve&dopt=full_report&list_uids=1813
4. J. Reece, N. C. (2002). Biology. San Francisco.
3
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Evolution of the Pathogenesis of Schizophrenia
A Review: Evolutionary Theories of the Pathogenesis of

Schizophrenia
Nichelle Jackson1,2
1W.

Evolutionary theories suggest schizophrenia, and other psychiatric disorders, are uniquely human disorders that coevolved during
evolution of the human brain. As brain size and complexity, relative to body mass increased, the energetic demand required for
advancements in cognition, language, and executive function increased. Currently, a variety of techniques using rodent models
and comparative genetics are used to investigate the pathophysiology and therapeutic targets of schizophrenia while simultaneously placing this disorder into an evolutionary perspective. Theories regarding the cause of schizophrenia range from geneenvironment interactions to differences in brain chemistry and structure. Much research has been done to identify the role of single gene mutations and neuronal mitochondrial dysfunction in the onset schizophrenia.
Introduction
Throughout
subjected to crude forms of therapy as researchers

history,
individuals
with
psychiatric
search for long-lasting antipsychotic medications.
disorders were stigmatized, dehumanized, and separated
Currently, schizophrenia is understood as a highly
from the community. During the Middle Ages, individuals
heritable and debilitating psychological disorder with a
afflicted by an illness were thought to be either
world-wide incidence of approximately 1%. Despite
possessed by demons or punished by gods. To cure
medical advancements, the cause of schizophrenia is still
these disorders, individuals were subjected to blood-
unknown. Many individuals afflicted with this disorder
lettings, exorcisms or burned at the stake. By the 19th
become dependent on family members and medical
century, psychiatric disorders were still not understood,
professionals and unable to live a normal life. Instead,
but illnesses were viewed as a sickness rather than an
these individuals are. The economic costs associated
evil or divine punishment. During this time, the mentally
with the symptoms of schizophrenia total an upwards of
ill were placed in asylums and prisons where they
$63 billion dollars in the United States alone.23 If the
received inhumane and insufficient care. Emil Kraepelin
suffering of patients and families is not enough
was the first to described the symptoms of schizophrenia
motivation to fund schizophrenia research, the economic
in 1896. Kraepelin used the term dementia praecox, to
burden should be.
characterize a distinct form of dementia marked by poor
Patients afflicted by schizophrenia exhibit a variety of
mental function in addition to reoccurring delusions and
positive, negative and cognitive symptoms that vary
hallucinations.
In 1911, Eugen Bleuler
renamed
among individuals. Positive symptoms are characterized
dementia praecox to schizophrenia (schizo=split;
by psychotic behaviors not seen in healthy individuals.
phren= mind) and further characterized the disorder by
Such symptoms include, hallucinations, delusions,
noting the incidence of positive and negative symptoms.
thought
Within the last century, knowledge of the neurological
blocking,
basis and associated therapies of schizophrenia have
(stereotyped movement, catatonia). Flat affect and lack
improved. Patients with schizophrenia are no longer
of pleasure in everyday life are considered negative
disorders
(disorganized
neoglisms)
and
thinking,
movement
thought
disorders
symptoms because they are qualities that disappear in

1
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individuals presented with the disorder. Finally, cognitive
connectedness coupled with decreased expression of
symptoms are characterized by a deficits in working
GABAergic interneurons. These structural changes are
19
correlated with deficits in the formation, maintenance
Symptoms of schizophrenia typically manifests during
and orchestration of synapses that disrupts normal brain
adolescence and early adulthood, between the ages of
function.
memory,
executive
functioning
and
attention.
16 and 30. Childhood onset of schizophrenia is rare, but,

does occur. However, symptoms of schizophrenia do not
manifest once middle age is reached. Sexual dimorphism
Genetic and Environmental Factors
Familial studies implicate a strong genetic component
of this disorder, exists as males tend to experience
to the susceptibility of schizophrenia, and several
symptoms sooner and more severely than females.
candidate genes have been identified. Disrupted-in-
Additionally, males are more likely to be diagnosed with
schzophrenia-1 (DISC1), Neuregulin (NRG1), Nuclear
schizophrenia while females are more likely to be
receptor related 1 protein (Nurr1), and Dystrobrevin
diagnosed with schizoaffective disorders.
binding protein 1 (DTNBP1) are a few of the top
Though the precise cause of schizophrenia is unknown,
candidate genes that display positive selection for genes
genetic and environmental factors have been found to
associated with schizophrenia.13,25 However, since the
play an important role in the incidence of schizophrenia.
risk of developing schizophrenia decreases as the degree
As previously mentioned, schizophrenia occurs in 1% of
of genetic relatedness decreases, and twins do not have
the general population. For second-degree relatives of
a 100% risk of developing the disorder if one twin is
individuals diagnosed with schizophrenia, the genetic
diagnosed, environmental insults have been suggested
risk is greater than 1% and for first-degree relatives, the
to exert some degree of influence on the susceptibility to
risk is around 10%. Identical twins have the highest risk
schizophrenia. Therefore, schizophrenia is theorized to
of developing schizophrenia if one twin has the disorder
be the result of genetic and environmental interactions.
19
However, since the risk of identical twins
Environmental factors such as maternal stress, social
developing schizophrenia is well below 100%, scientists
isolation, immune activation and pharmacological
believe there are environmental factors that contribute
interference have been found to mimic or exacerbate
to greater vulnerability to.
symptoms of schizophrenia when combined with
(40-65%).
Alternatively, differences in brain chemistry and

structure may play a role in schizophrenia. Schizophrenia
individuals predisposed with genetic risk factors.

DISC1, is among the most characterized gene
enlarged
implicated in schizophrenia. This gene was originally
ventricles, and an overall reduction in brain size
discovered in a Scottish family with a high prevalence of
especially in the hippocampus, thalamus, and frontal
schizophrenia and psychoaffective disorders including:
has
lobes.
been
21
consistently
associated
with
Neuroimaging and immunohistochemistry of
schizoaffective
disorder,
bipolar
disorder,
major
post-mortem brains of schizophrenic patients were
depression, adolescent conduct disorder and autism
marked by neurological abnormalities, particularly in the
spectrum disorders.13,18 Dysfunction of this scaffolding
hippocampus and neocortex, when compared to normal
protein is characterized by a balanced translocation
controls. Neurons in these regions were also smaller with
between chromosomes 1 and 11 that has been linked to
abnormal
synaptic
the development of psychosis. Additionally, DISC1
organization. Moreover, immunohistochemistry found a
interacts with other proteins important to functions of
marked decrease in biomarkers for GABAergic inhibitory
intracellular
dendritic
interneurons.
24
arborization
Taken
together,
and
this
disorder
is
signaling,
neurodevelopment
and
synaptogenesis.
characterized by a reduction in synaptic organization and

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The Backbone
Evolutionary Perspective of Schizophrenia
outgrowth, neurotransmitter package and release, and
Human evolution is predominantly characterized by
dendritic modeling.4 Comparative genomics suggests
the transition to bipedalism and the evolution of brain
mitochondrial genes coevolved with increased metabolic
size. The evolution of brain size led to increased
processes and neuronal activity. Mitochondria adapted
cognition and executive functioning, in addition to, more
to produce more efficient means of electron transport
complex forms of language. The increase in brain size
during oxidative phosphorylation thereby increasing
was marked by increased development of the neocortex,
energy levels necessary to maintain brain function. This
with a significant increase in size and complexity of the
is thought to have coevolved with increased gene-
prefrontal cortex (PFC). Increases of the PFC led to
expression levels of genes associated with energy
advantages in emotional processing, motor control, and
metabolism and synaptic connectivity in the human
regulation of behavior in response to environmental
neocortex compared to non-human primate relatives.10
stimuli.25 One theory suggests genetic changes that
Schizophrenia is thought to be a human specific disease
caused these enhancements occurred over 50,000 years
because its clinical symptoms indicate dysfunction
ago when Homo sapiens transitioned from precursor
among genes and/or pathways involved in human brain
hominid species. Additionally, these enhancements may
evolution.25 In particular, changes in metabolic pathways
have occurred when H. sapiens adapted to live in bigger
have been implicated in disorders like schizophrenia that
social groups forced to forage for sustenance. In these
impact cognitive abilities.
conditions, individuals evolved to cooperate, empathize

and access the emotional states of others with cognitive
adaptations.
12,7
In order to perform these energetically
demanding tasks, a balance between brain size and
Methods and Materials

Animal Models of Schizophrenia
To study schizophrenia, researchers must study the circuitry
energy demand was established. To meet the energetic
and molecular mechanisms of human brain. However, because
demands imposed by evolution of brain size, researchers
the organ is so vital to human life, obtaining the necessary
believe species could have increased energy intake and
samples is difficult and impractical. Tissue donated from post-
production and/or reduced the amount of energy used

by other bodily functions.
In order to obtain the energy necessary to maintain
basal function, the brain depends on oxidative
phosphorylation. At rest, the human brain uses
approximately 20% of total body oxygen consumption.
This can be compared to apes that use 13% and other
mortem
patients
has
led
to
several
advances
in
neuroanatomical differences observed in the disorder, but

physiological information cannot be obtained from dead
tissue. Additionally, studying post-mortem brains does not
provide insight needed to determine whether structural
changes are the cause or result of the disorder. Instead, animal
models are used because basic brain circuitry and molecular
mechanisms are conserved among many species throughout
vertebrate mammals that need 2-8%, but are considered
evolution.27 Traditionally, gene mutations identified from
to be less intelligent.16 The amount of total body oxygen
patient samples have been isolated and then genetically
consumed only increases when performing energetically
modified in mice. Mice exhibit validity if (1) there is a mutation
demanding tasks. Glucose metabolism is an important

source of energy within neuronal mitochondria that are
needed for oxidative phosphorylation and intracellular
Ca2+ regulation to maintain homeostasis. Moreover,
mitochondria that move within neurons are essential for
processes that contribute to neurogenesis and neural
plasticity including: neuronal differentiation, neurite
in the gene that has been supported by human literature, (2)

physical or behavioral phenotypes associated with the
disorder are displayed, and (3) mice exhibit similar phenotypic
response to therapy seen in humans. Despite construct
validity, caution must be used when interpreting results
because differences between human and rodent brains exist.
Therefore, some results may not translate to humans, which
may explain why some mouse therapies fail in preliminary
3
The Backbone
stages of clinical trials.
Comparative Genomics
A second strategy for investigating human evolution of
the brain and psychiatric disorders is the hypothesisgenerating approach. Collecting data for comparative
genomics, neuroanatomical features and behaviors in
human and non-human primates provides a library of
information on the evolution of the human brain. As
access to the fossils of archaic humans such as
Neanderthals and Denisovans increases, their genome
should be sequenced and included in comparative
analysis. Behavioral and some neuroanatomical features
unique to humans can be analyzed by visually observing
physical differences between species. However, nextgeneration sequencing techniques including, Illumina,
RNA-seq, chromatin immunoprecipitation coupled DNA
sequencing (ChIP-seq) and de novo genome assembly
can be used to identify specific genes and mutations
unique to human evolution. Genomic sequences can be
added to and/or downloaded from the genome-wide
association study (GWAS) to examine SNPs from
schizophrenia meta-analysis. GWAS allows for the

comparison highly conserved sequences within and
across species as well as an indication of genetic
expression levels. Once identified, the behavior of
human cells and humanized animals can be analyzed
and modified in order to target and develop novel
treatments for schizophrenia.
Results
Gene-Environment Models of Schizophrenia

Animal models have led to novel discoveries in the
pathophysiology and potential therapeutic targets of
schizophrenia. Transgenic DISC1 rodent models have
been created that express phenotypic symptoms of
schizophrenia seen in humans. DISC1 mice exhibit
negative symptoms including depression (as measured
by increased immobility in forced swim tests, as well as,
tail suspension tests) and anxiety (measured by
reductions in time spent in the open arms of elevated
FULL ARTICLES
plus mazes).9.13 Pre-pulse inhibition and startle assays
measured cognitive deficits in sensorimotor gating while

deficits in spatial and working memory were exhibited by
delayed matching to position/non-matching to position
tasks.9,14 [Li et al., 2007] Finally, positive symptoms were
noted by the hyperactive ambulation of males in the
open field assay.9 Phenotypes presented by DISC1
mutant mice were highly dependent on the strain of
mice used, translocation site of the mutation and the sex
of the animal.
Immunohistochemistry of brains from post-mortem
schizophrenic patients has indicated a reduction in

biomarkers, parvalbumin (PV) in GABAergic inhibitory
neurons in regions of the hippocampus, anterior
cingulate cortex, and the PFC.11,24,26 Other GABAergic
interneuron biomarkers, like calretinin (CR) exhibit
similar expression levels in schizophrenic and control
humans and animals. This is significant because though
comprising roughly 15% of neurons in the cortex, PV
GABAergic interneurons serve an essential role in the
maintenance and orchestration of normal brain function.
The maturation process of these neurons is not well
understood, but, accumulating evidence suggests Nmethyl-D-aspartate
receptor
(NMDAR)
signaling
influences the maturation of GABAergic interneurons.

Environmental stress was also found to influence the
pathogenesis of schizophrenia by
disrupting the
homeostatic physiological stress response modulated by

the hypothalamic-pituitary-adrenal (HPA) axis to increase
production
of
glucocorticoids.3 The
increase
in
glucocorticoid levels led to increased sensitivity to stress

as well as deficits in brain maturation. Due to this,
individuals in stressful environments are prone to the

development of a variety of mental disorders including
schizophrenia and depression. Previous studies have
examined
environmental
insults
of
psychological,
immune and pharmacological stressors in the form of

maternal separation, social isolation, social defeat, viral
infections and drug abuse. Restraint stress was shown to
impair working memory in rodents.8 The stress of social
isolation has been linked to deficits in sensorimotor
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The Backbone
gating, changes in the projections of dopaminergic
from these two hits synergistically combine to manifest
neurons, as well as, increases in despair and locomotor
symptoms of schizophrenia in adulthood.
20
activity. Finally, mice injected with viral constructs that

induce innate immune responses, showed deficits in
short-term
memory,
dependent
object
learning,
recognition,
social
context-
interaction
and
immunoreactivity of parvalbumin interneurons in the

PFC.11
Independently both genetics and the environment can
increase susceptibility to psychiatric disorders like
schizophrenia. However, those with the greatest risk of
being diagnosed with schizophrenia are individuals

exposed to genetic and/or environmental insults during
prenatal development and adolescence. Animal models
showed
that
predisposed
when
DISC1
combined
mice,
with
animals
genetically
faced
with
environmental stressors during adolescence exhibited

greater deficits in executive functioning, working
memory, and increased movement disorders compared
to wild-type, or DISC1/no stress cohorts.
20
Epigenetic experiments lend support to the twohit model of schizophrenia. The first hit occurs during
the perinatal period when the embryo is exposed to
genetic or environmental insults, which makes children
more vulnerable to psychiatric disorders. Prenatal
exogenous and endogenous environmental factors part
of the first hit include: maternal malnutrition, repeated
psychological stress, exposure to infection, obstetric
complications, gut microbiota and changes in prenatal
endocrine
function.
These
factors,
along
with
schizophrenic candidate genes, primes the brain for

neuropathological
disorders
by
(1)
increasing
neuroinflammation, (2) degenerating axons, myelin and

oligodendrocytes, in addition to, (3) altering brain
connectivity and morphology.
21,6
During adolescence, a
second round of environmental insults (exposure to

stress, drugs, trauma and infection) unmasks the
endophenotypic traits associated with schizophrenia by
activating the inflammatory, oxidative and nitrosative
stress pathways, mitochondrial dysfunction, apoptosis
and progressive brain changes. Together, the impacts
Coevolution of schizophrenia with the evolution of

increased brain size and complexity not a human specific
trait
Humans, ten species of non-human primates, thirtyone non-primate eutherian mammals, two marsupials
and one monotreme were used for the identification of
schizophrenia related orthologues. Of the forty-two
eutherian mammals, two marsupial and one monotreme
genomes analyzed from the gene-disease associations
compared by the Genetic Associated Database (GAD),
several orthologues associated with psychiatric disorders
were found.22 Orthologues were found for schizophrenia
genes, as well as, genes associated with autism, ADHD,
bipolar disorder, depression, anxiety, addiction, eating
disorders, Alzheimers, Parkinsons, migraine and stroke.
GAD revealed positive selection (as measured by dN/dS
mutation rates) of genes associated with schizophrenia.
Both human and non-human primates (particularly
catarrhines) showed similar ratios of positive selection.
Interestingly, when compared to other large brained

mammals, cetaceans like the bottle-nosed dolphins and
killer whales, showed higher average dN/dS ratios for
psychiatric disorder orthologues.22 Taken together, this
data suggests genes associated with schizophrenia are
not uniquely human; rather these genes were seen in
closely related apes, old world monkeys and some
toothed cetaceans. This information is not particularly
surprising
considering
since
compared
anthropoid
to
primates
other
and
mammals
odontocete
cetaceans show similar evolution rates to humans.

Primates and cetaceans shown a greater brain to body
mass ratio and greater variations in encephalization
quotients indicating a relaxation of evolutionary
constrains.1 Furthermore, of the 228 genes discovered to
be under positive selection in dolphins, twenty-seven
were found to be associated with processes of the
nervous system including synaptic plasticity, human
intellectual disorders and sleep.17 Additionally, increased
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selection was found on genes related to mitochondria
comparative genetics has led to many advancements in
expression and metabolism.
genes and pathways involved in the disorder. Future
An increase in brain mass must be compensated by an
research must continue to have a holistic approach while
increase in energetic demands. Increased energy may
investigating the pathogenesis of schizophrenia due to
come from an increase in metabolic turnover rate,
its polytypic nature. One theory of the development of
neuronal mitochondria, reallocation of energy from
schizophrenia if the two-hit model. Environmental or
other functions or a combination of events. A positive
genetic insults during natal development can prime the
correlation between brain mass and basal metabolic
brain to become more vulnerable to psychosis.
rates among primates indicates some species do
Furthermore
compensate for larger brains by increasing metabolic
exponentially if individuals that have been primed during
12
the
risk
of
pathogenesis
increases
turnover rates. When energetic demands are not met,
development are exposed to environmental stressors
deficits occur in working memory, executive functioning
during adolescence. If so, that individual is likely to
25
manifest symptoms associated with schizophrenia in
Humans with schizophrenia display abnormalities in
adulthood. A second, more evolutionary theory for the
glucose tolerance and increased insulin resistance. Since
pathogenesis of schizophrenia is related to the
glucose in the brain is metabolized in the brain,
mitochondrial dysfunction in the brain. Essentially, if
abnormalities
suggests
mitochondria are not meeting the energy demands
schizophrenia may be associated with mitochondrial
associated with increased cognition in the human brain,
and language and an increase in psychosis is observed.
25
in
glucose
metabolism
Additional support stems from lower
individuals are prone to psychiatric disorders like
metabolic rates and lower blood flow in the frontal brain
schizophrenia. However, moving forward, one area of
during cognitive tasks, altered levels of glycolic enzymes
focus should be on characterizing the influence of AMPA
and byproducts in the brain, reduced number of
and NMDA receptors at the molecular level and in the
mitochondria
context of evolution due to their direct influence on
dysfunction.
in
the
striatum
and
hypoplastic
mitochondria in oligodendrocytes in the caudate nucleus
learning and memory.
and PFC of schizophrenic individuals compared to

healthy controls. From these results, it becomes clear
how mitochondrial dysfunction can lead to deficits in
neurotransmission
and
synaptic
plasticity
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The Backbone
Mental Disorders Across Geographical Spaces
How might the genetic identification of mental disorders vary

across geographical spaces, cross culturally and through
time?
Sedera Moore1,2
1W.
Genetics are used to link and identify a variety of functions that occur in the body. Moreover, genetics can be utilized to analyze
ailments, such as the various mental disorders that people suffer from daily. While the diagnosis of mental disorders is not a rare
concept, there are dissimilarities in the causes of people being diagnosed. However, before discussing variations in the genetic
identification of mental disorders, it is important to have an understanding of what mental disorders are. This paper will
introduce the concept of mental disorders and provide several examples in regards to the variation of mental disorders across
geographical spaces, cross culturally, and through time relating to genetic identification, exposed environment, and specific
ethnic groups.
Introduction
Mental disorders are illnesses that stem from a malfunction
in the brain. For the purpose of simplification, we will first view
the term mental disorder as two separate entities. The word
mental relates to the mind and ones intellectual activity.
The term disorder conveys the presence of an irregularity or

disturbance. Combining these separate definitions, a mental
disorder is an irregularity or disturbance. How might the
genetic identification of mental disorders vary across
geographical spaces, cross culturally and through time?
Mental disorders are not uniformly dispersed across the
globe. The magnitude of people diagnosed with mental
disorders varies across geographical spaces, cross culturally,
and throughout generations. A prime example of this variation
in the genetic identification of mental disorders can be seen in
in an article titled, The role of the genetic variation in the
causation of mental illness: an evolution-informed framework.
Genetic Variation: An Evolution-Informed

Network
According to this article, mental illness usually begins to
emerge early in the reproductive age and is linked to a
considerable amount of procreative disadvantages. In theory,
these procreative disadvantages observed by mental illnesses
should lead to these disorders having strong negative selection
pressures. On the contrary, mental disorders appear to be a
common diagnosis; specifically in twin studies which show a

strong correlation between the diseases etiology and its
genetic contribution. This article discussed a proposed
hypothesis for identifying mental illness, suggesting that the
genetic contribution to mental illness results from geneenvironment interactions and rare genetic variants.
Depression and Gene-environment

Interactions
An example where mental disorders may be contributed
with certain environmental influences can be seen with
depression. Depression is a mental health condition that
underlies a mood disorder causing severe sadness and
affecting a persons normal daily functionings.
Recent
discoveries show that individuals with one or two short alleles

of the serotonin transporter gene promoter polymorphism (5-
HTTLPR) have an increased susceptibility to depression when

encountering stressful life events.15 These results appeared
when the 5-HTTLPR gene, stress, and depression were
observed simultaneously over a course of 5 years prior to the
onset of the depression. Depression severity displayed
episodes at an average duration of 24 months and were
associated with loss, threat, and humiliation. Overall, the
outcome of this study revealed that the depression most likely
stems from life events that occurred after the onset of the
disorder.
1
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Increased Life Expectancy and Alzheimers

Disease
Throughout time, life expectancy has increased globally.
According to the National Institute on Aging, The dramatic
increase in average life expectancy during the 20th century
ranks as one of societys greatest achievements. Although
most babies born in 1900 did not live past age 50, life
expectancy at birth now exceeds 83 years in Japanthe
current leaderand is at least 81 years in several other
countries. Less developed regions of the world have
experienced a steady increase in life expectancy since World
War II, although not all regions have shared in these
improvements. One notable exception is the fall in life

expectancy in many parts of Africa because of deaths caused
by the HIV/AIDS epidemic. The most dramatic and rapid gains
have occurred in East Asia, where life expectancy at birth
increased from less than 45 years in 1950 to more than 74
years today. There is possibly a positive correlation between
an increase in some mental disorders and higher life
expectancies.
As humans continue to live longer, they can be affected by
different mental disorders later on in life. This is seen in people
with Alzheimers disease. Alzheimers disease is a degenerative
brains neurons.
The targeted age group for Alzheimers
disease begins around age 65. A study done at Duke University

determined that there has been approximately a fourfold
increase in the rate of people being diagnosed with
Alzheimers: escalating from 35/1000 in 1991 to a striking
135/1000 in 1999. When isolating this data by racial group and
gender, the Alzheimers disease rate increased by a factor of
4.7 in African American women in comparison to a factor of
2.3 for White women. There is currently an estimated 5.1
million people living with Alzheimers disease in the United
States for 2015. Due to an increase in life expectancy through
time, this disease is expected to triple in its effect rising from
5.1 million to an anticipated 13.8 million by 2025.
Racial Health Disparities and Schizophrenia
counterparts. Schizophrenia is a severe brain disorder in which
people interpret reality abnormally. Moreover, schizophrenia

may result in some combination of hallucinations, delusions,
and extremely disordered thinking and behavior. A Child
Health and Development Study examined the schizophrenia
health disparity through study subjects conceived from black
and white women from a common area.
These women were enrolled during pregnancy at the
Alameda County Kaiser Permanente Medical Care Plan clinics
over the course of 6 years (1959-1966). During this time frame,
there were 19,044 live births and of these live births 12,094
progeny were selected to be observed in the study. These
offspring were charted for 16 years (1981-1997) with the
purpose of addressing if African Americans have higher rates
of schizophrenia than whites. In addition, the study looked
into whether this expected risk increase is arbitrated by the
socioeconomic status (SES) background of the offspring. The
title of this study was Race and risk of schizophrenia in a US
birth cohort: another example of health disparity?
An analytic sample of 2,128 African American women and
4,508 White women were used for the data comparison. The
fathers of these children were mainly the same race as the
mothers (98% for African Americans and 92% for Whites). The
remaining offspring were excluded from data analysis for
reasons including; death, adoption, loss to follow up, and

exclusion of sibling information. Thus, the resultant sample
consisted of 6,636 women; approximately 68% White and 32%
African American. From this sample 62 cases of schizophrenia
spectrum disorder (SSD) were diagnosed; 32 African
Americans (22 men and 10 women) and 30 Whites (20 men
and 10 women). Moreover, the study states that The
proportion of SSD cases diagnosed with schizophrenia was
higher among African Americans (23/32) than among whites
(15/30). Within diagnostic categories, the mean age at index
treatment was similar for African American and white cases
(22.5 and 23.9 years for schizophrenia, 26.3 and 26.8 years for
other SSDs, respectively).
When comparing these two groups, variation is present in
the magnitude of people affected by this mental disorder by
Similar to Alzheimers disease, variations are seen in the
race. Additionally, the socioeconomic status background of
diagnosis of mental illness when looking at a correlation
these diagnosed groups were observed. There was minimal
between race and the mental disorder schizophrenia.
correlation seen between in the higher percentage of African
Specifically, certain health disparities are observed between
Americans diagnosed with schizophrenia in comparison to
blacks and whites, in terms of schizophrenia, and studies show
whites and socioeconomic status. Prior to factoring in
that blacks are more likely to be diagnosed than their white
socioeconomic status (SES) African Americans were 3-fold
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more likely to get schizophrenia than whites; however,
CACNA1C gene is highly expressed in the brain. When tested
succeeding the SES factorization, African Americans were 2-
for genetic variation, it was proposed that the representative
fold more times as likely. Based on this information,
SNP (the rs2159100 for rs1006737) plays a role in the
socioeconomic status may partially coincide with race when
magnitude at which the CACNA1C gene is expressed.
observing increased risks of schizophrenia.
According to the results, carriers of the risk-associated

genotype (AA) had highest expression, with heterozygotes
Genetic Identification of the Five Spectrum

Disorders
(GA) having intermediate expression and the common allele

carriers (GG) having the lowest expression (P = .002 for linear
Furthermore, another study that looked into the genetic

identification of mental disorders focused on five specific
mental disorders; autism spectrum disorder, attention deficithyperactivity disorder, bipolar disorder, major depressive
disorder, and schizophrenia. This study analyzed singlenucleotide polymorphism (SNP) data for 61,220 people of
European ancestry; 33,332 cases and 27,888 controls, for the
purpose of characterizing the allelic contribution of each
disorder. Significant data was observed on a number of loci
theoretically linked to schizophrenia and bipolar disorder in
previous studies. The loci were located near MIR137
(microRNA 137), TCF4 (transcription factor 4), the MHC region
on chromosome 6, and SYNE1 (spectrin repeat containing,
nuclear envelope 1). Based on results from polygenic risk
scores the loci showed cross disorder associations; particularly
between adult-onset disorders.

Moreover, Genome Wide Association Studies (GWAS)
produced data that linked 4 SNPs to bipolar disorder
(rs937l601, rs10994397, rs4765914, and rs12576775) and 10
SNPs to schizophrenia (rs2021722, rs1625579, rs12966547,
rs7914558, rs11191580, rs7004633, rs10503253, rs17662626,
and rs17512836). Additionally, a meta-analysis done for the
five disorders revealed results for regions at a genome-wide
significance threshold (p<5108). The SNPs on chromosome 3
(rs2535629) and chromosome 10 (rs11191454 and rs2799573)
showed that these SNPs had a supported effect for all five of
the disorders (autism spectrum disorder, attention deficithyperactivity disorder, bipolar disorder, major depressive
disorder,
and
schizophrenia).
The
meta-analysis
for
chromosome 12 revealed the rs1024582 SNP specific to

bipolar disorder and schizophrenia.
Bipolar and Schizophrenia Disorder CANA1C

Gene
Likewise, a different study looked into a bipolar and
schizophrenia disorder risk gene CACNA1C: where the
regression analysis). Additionally, there was dissimilarity in

the CACNA1C gene expression in terms of race/ethnicity. This
was the case for whites and African Americans. The study
concluded that this variation is possibly a result of a difference
in minor allele frequency (26% for whites and 45%, for African
Americans). The risk associated alleles are associate with
increased levels of CACNA1C mRNA.
Furthermore, the study shows that calcium channel defects
may add to the genetic cause of bipolar disorder and
schizophrenia by changing the functional activity of the brains
electrical systems. This data corresponds to the COMT, GRM3,
BDNF, and DISC1 genes that have been associated with neural
circuitry diagnosis and pattern effects. The article states that,
Investigations of the N-back working memory task have
shown that patients with schizophrenia and their healthy
siblings have increased prefrontal cortical activity for a given
level of performance, suggesting that inefficiency in this

circuitry is heritable and a good intermediate phenotype
related to genetic risk for schizophrenia. Analogous studies
have been performed among patients with bipolar disorder
using neuroimaging tasks that target mood circuitry in the
temporal lobe. Other studies have targeted serotonin signaling
genes and have found that healthy subjects who are carriers of
the short allele of the serotonin transporter, the target of
drugs that treat the mood symptoms of bipolar disorder, have
higher ratings of anxiety and depression, and have greater
activation of the limbic circuitry, similar to this data.
These results indicate that there is a genetic factor in the

diagnosis of schizophrenia and bipolar disorder. Not only did
the patients already diagnosed with schizophrenia have
increased prefrontal cortical activity, so did their undiagnosed
healthy siblings. The association of this increased prefrontal
cortical activity between the patients and their siblings shows
that schizophrenia may be linked to a hereditary source.
Moreover, healthy people that carried the short allele of the
serotonin transporter (target of drugs that treat bipolar
disorder) showed increased levels of anxiety and depression.
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This is indicative of the short serotonin transporter allele
physical interaction was found between G72 and D-amino-acid
playing a role in bipolar disorder. Bipolar disorder displays
oxidase (DAO). DAO is expressed in the human brain, where it
symptoms of high anxiety and depression levels. Linking this to
oxidizes D-serine, a potent activator of NMDA glutamate
short allele builds a connection to the genetic identification of
receptor. Co-incubation of G72 and DAO in vitro revealed a
the bipolar disorder.
functional interaction with G72 enhancing the activity of DAO.
Bipolar and Schizophrenia Disorder at several

Genes
Another study looked into the genes responsible for
schizophrenia and bipolar to attribute them as implications of
psychiatric disease studies. The NRG1 gene has been linked to
schizophrenia following multiple studies that provided
evidence supporting this association. These studies include; a

systematic study of 8p21-22 and a multi-marker haplotype at
the 5 end of the NRG1 gene. The binding protein dysbindin
(DTNBP1) has also been implicated as being associated with
schizophrenia, however, studies of dysbindin in association
with bipolar disorder have not displayed significant results.
According to the article researchers, found no significant
associations in bi-polar disorder as a whole but found
modestly significant evidence for association in the subset of
bipolar cases with predominantly psychotic episodes of mood
disturbance with a similar pattern of findings to that seen by
this group in schizophrenia. His finding suggests that variation

in dysbindin confers risk to psychosis rather than to mood
disorders per se, although replication is required. The results
from the binding protein dysbindin shows the variation in the
genetic identification of mental disorders. Dysbindin marks
significant outcomes in terms of the mental disorder
schizophrenia however, it this is not the case for bipolar
disorder. This may be a consequence of different mechanisms
attributing to the mental disorders.
Similarly, the G72(DAOA)/G30 locus, which is best
associated with bipolar disorder, shows specific variants
connected to the disorder. Previous studies of the G72(DAOA)/
G30 locus were performed by association mapping in the
linkage region on chromosome 13q22-34. Similar results were
observed between French Canadian and Russian populations
at two genes; the G72 (D-amino acid oxidase activator) and the
G30 gene (DAOA antisense RNA 1). According to the study,
They found associations in French Canadian and Russian
populations in markers around two novel genes, G72 and G30,
which are overlapping but transcribed in opposite directions.
G72 is a primate-specific gene expressed in the caudate and
amygdala. Using yeast two-hybrid analysis, evidence for
Consequently,G72 has now been named D-amino-acid oxidase

activator
(DAOA)
Associations
between
DAOA
and
schizophrenia have subsequently been reported in samples

from Germany, China, Ashkenazi Jews, and both the United
States and South Africa, as well as a small sample of very early
onset psychosis subjects from the United States. There is no
consensus concerning the specific risk alleles or haplotypes
across studies.
Likewise, this study also looked at the effects of the DISC1
gene in schizophrenia. This gene was associated with broad
phenotypic results in connection to bipolar disorder,
schizophrenia, and recurrent depression. In a balanced
chromosomal translocation (1;11)(q42;q14.3), two DISC1
genes were disturbed (the DISC1 and the DISC2 gene) at
chromosome 1. The article states that, A small pedigree has
recently been reported in which a 4bp deletion in exon 12 of
DISC1 cosegregates with schizophrenia and schizoaffective
disorder. The final gene discussed in this article was the brain
derived neurotrophic factor gene (BDNF) in association with
mood disorders; specifically bipolar disorder. It states in the

text, Only one frequent, non-conservative polymorphism in
the human BDNF gene has been identified, a single nucleotide
polymorphism (SNP) at nucleotide 196 within the 5 pro-BDNF
sequence that causes an amino acid substitution of valine to
methionine at codon 66 (Val66Met) and may have a
functionally relevant effect by modifying the processing and
trafficking of BDNF. Three positive results were recorded in a
family based association study in conjunction with the BDNF
gene. The family was Caucasian of European-American origin
and consisted of two bipolar adults and one small onset child.
Each family member displayed an over-transmission of the

Val66Met allele. According to these results, this variant may
attribute to the susceptibility of bipolar disorder in certain
individuals.
Variant Genetic Identification of OCD

Correspondingly, another study looked into the genetic
identification of obsessive compulsive disorder (OCD). OCD is a
mental health disorder categorized by unreasonable thoughts
and fears (obsessions) that lead to repetitive behaviors
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(compulsions) sufficient enough to affect a persons normal
4.
"Living Longer." National Institute on Aging. US.

Department of Health and Human Services, Oct. 2011.
Web. 18 Apr. 2015. <http://www.nia.nih.gov/research/
publication/global-health-and-aging/living-longer>.
5.
"Alzheimer's Disease & Dementia | Alzheimer's

Association." Alzheimer's Disease & Dementia |
Alzheimer's Association. N.p., n.d. Web. 27 Apr. 2015.
6.
Taylor, Donald H., Jr., Frank A. Sloan, and Murali

Doraiswamy. "Marked Increase in Alzheimer's Disease
Identified in Medicare Claims Records Between 1991 and
1999." Marked Increase in Alzheimer's Disease Identified
in Medicare Claims Records Between 1991 and 1999. The
Geneological Society of America3, 3 Sept. 2003. Web. 26
Apr. 2015
7.
"Latest Alzheimer's Facts and Figures." Latest Facts &

Figures Report. Alzheimer's Association, 17 Sept. 2013.
Web. 26 Apr. 2015.
8.
"Schizophrenia." Definition. Mayo Clinic, 24 Jan. 2014.

Web. 22 Apr. 2015. <http://www.mayoclinic.org/diseasesconditions/schizophrenia/basics/definition/con20021077>.
9.
Bresnahan, M., M. D. Begg, A. Brown, C. Schaefer, N.

Sohler, B. Insel, L. Vella, and E. Susser. "Race and Risk of
Schizophrenia in a US Birth Cohort: Another Example of
Health Disparity?" International Journal of Epidemiology
36.4 (2007): 751-58. Web. 26 Apr. 2015.
daily functioning. The goal of this study was to determine the

role of genetic variation of SLC1A1 in OCD in a large casecontrol study and to better understand how SLC1A1 variation
affects functionality. This experiment consisted of 987
people; 325 obsessive compulsive disorder subjects and 662
ethnically and sex-matched controls. Significant results were
observed in association of 3 genetic markers (rs3087879,
rs301430, and rs7858819) in obsessive compulsive disorder
using haplotype analysis. A haplotype labeled H4 was nearly
twice more common in OCD cases than in the control cases;
the H4 OCD cases had a haplotype frequency of 9.4%
compared to the controls haplotype frequency of 5.1%. Also,
the rs393331 SNP was associated with an OCD-hoarding subphenotype as assessed by 2 independent, validated scales.
This correlates with SLC1A1 gene expression and shows the
association of the quantative trait loci with obsessivecompulsive disorder.
Conclusion
There is evident variation in the genetic identification of
mental disorders across geographical spaces, cross culturally,
and through time. Studies have shown that an abnormal
production of certain genes are recognized as a possibly cause
of increasing a persons susceptibility to some mental
disorders. Additionally, studies have presented variation in the
racial/ethnic groups affected by a mental illness. Specifically,
multiple studies have recognized African Americans as a
primary victims of schizophrenia. Moreover, the exposed
environment of individuals have been linked to their
predisposition to mental illness. Hopefully, future studies can
further target the mechanisms causing mental disorders and
acquire prevention techniques.
References
1.
Uher, R. "The Role of Genetic Variation in the Causation of

Mental Illness: An Evolution-informed Framework."
Molecular Psychiatry 14.12 (2009): 1072-082. 25 Aug.
2009. Web. 19 Apr. 2015.
2.
"Depression." NAMI: National Alliance on Mental Illness.

N.p., n.d. Web. 25 Apr. 2015.
3.
Monroe, Scott M., and Mark W. Reid. "Gene-Environment

Interactions
in
Depression
Research:
Genetic
Polymorphisms
and
Life-Stress
Polyprocedures."
Psychological Science 19.10 (2008): 947-48. Web. 25 Apr.
2015.
10. "Identification of Risk Loci with Shared Effects on Five

Major Psychiatric Disorders: A Genome-wide Analysis."
The Lancet 381.9875 (2013): 1371-379. Web. 25 Apr.
2015.
11. Bigos, K. L., V. S. Mattay, J. H. Callicott, R. E. Straub, R.
Vakkalanka, B. Kolachana, T. M. Hyde, B. K. Lipska, J. E.
Kleinman, and D. R. Weinberger. "Genetic Variation in
CACNA1C Affects Brain Circuitries Related to Mental
Illness." Archives of General Psychiatry 67.9 (2010): 93945. Web. 27 Apr. 2015.
12.
Craddock, N. "Genes for Schizophrenia and Bipolar

Disorder? Implications for Psychiatric Nosology."
Schizophrenia Bulletin 32.1 (2005): 9-16. Web
13. "Obsessive-compulsive Disorder (OCD)." - Mayo Clinic.

N.p., n.d. Web. 27 Apr. 2015.
14. Wendland, J. R., P. R. Moya, K. R. Timpano, A. P.
Anavitarte, M. R. Kruse, M. G. Wheaton, R. F. RenPatterson, and D. L. Murphy. "A Haplotype Containing
Quantitative Trait Loci for SLC1A1 Gene Expression and Its
Association With Obsessive-Compulsive Disorder."
Archives of General Psychiatry 66.4 (2009): 408-16. Web.
23 Apr. 2015.
15. Caspi, A., Sugden, K., Moffitt, T.E., Taylor, A., Craig,
I.W., Harrington, H., McClay, J., Mill, J., Martin,
J., Braithwaite, A., and Poulton, R. Influence of life stress
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The Backbone
Prevalence and Anatomical Evidence of Treponemal Infection

in the Cobb Collection
Nicholas Guthrie1,2
1W.

Understanding the health of our ancestors can give us a viewpoint to understand present-day health conditions. The
relationship of African American (AA) ancestry to infectious disease status has not been extensively studied. This study
aims to characterize AA health by osteologically investigating the microbial effects of Treponema palladium (TP)
bacteria on AAs who died in the greater DC metropolitan area from 1930 to 1969. The gram-negative, spiral shaped
bacteria has four pathogenic subspecies; pallidum, pertenue, endemicum, and carateum, causing syphilis, yaws,
endemic syphilis, and pinta, respectively. To confirm TP infection, we will use the Cobb Collection autopsy and clinical
records in conjunction with scientific methods of microscopic analysis, microbial analysis, and various imaging
techniques. Our expected results will yield better understanding of the pathology of TP and its contribution to AA
morbidity and mortality during the era of overt racial segregation to the present day.
Introduction
with significant clinical and autopsy data including age,
The W. Montague Cobb Research Laboratory is a rare

resource for research on a unique human skeletal and
bioarchaeological collection. The Cobb Collection is
named after the first African American biological
anthropologist
and
renowned
Chair
of
Howard
Universitys Anatomy Department, Dr. William Montague

Cobb. His research aimed to create a less racialized
perspective on human life and showed the impact race
could have on the heath of a person, showing that racism
in America had an impact on the health and livelihood of
African Americans.1 The Cobb collection contains
approximately 699 de-fleshed human cadavers that were
donated and collected for scientific purposes during the
majority of the 20th century, and is unique in that it is

the only skeletal collection residing at a historically black
university. The Cobb Collection has undergone very little
research and lends itself to novel insights about the lives
and deaths of Americans living in the Washington, D.C.
area. This affords this research a unique opportunity to
become a reference on African Americans from the late
19th to mid- 20th Century. Approximately 83% of the
Cobb Collection is African American and contains records
sex, place of death, cause(s) of death, and morbidity.2

Health disparities for African Americans include
differences in rates of cardiovascular diseases, diabetes,
periodontitis and life expectancy relative to whites. In
addition, populations living in poverty also exhibit health
issues including asthma attacks and obesity. Since a
greater percent of African-descendant people continue
to live below the poverty line, a duality of risk factors
exist for this population. Furthermore, previous research
hints at differences in health between Africandescendant people in Africa and the United States,
suggesting that variation in environment, such as slavery
and poverty, affects general health.3
Treponemes (TP) are helically coiled, corkscrewshaped cell with a double membrane system. The
spirochete has two flagella that originate at both ends of
the organism and point inward along its length, and are
contained in the periplasmic space between the inner
and outer membranes, which enable motility. The
pathogenic treponemes classification is based primarily
upon the clinical manifestations of the respective
diseases they cause: Treponema pallidum subsp.
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The Backbone
pallidum is the causative agent of venereal syphilis; T
pallidum subsp. Pertenue causes yaws; T pallidum subsp.

endemicum causes endemic syphilis; and T carateum is
associated with pinta. -These microbes are generally
transmitted by close non-venereal contact, with the
exception of venereal syphilis. DNA hybridization shows
high genetic relation between the species, but overall
understanding
of
the
pathogenesis
of
human
treponematoses is limited. The inability to grow these

spirochetes in vitro and limited viability in vivo requires
expensive
and
laboratory
difficult
animals.
ultrastructure
continual
Also,
permits
only
their
propagation
fragile
limited
in
cellular
FIGURE 5: RENAL OSTEODYSTROPHY X-RAY24
mechanical
manipulation of the pathogen, in order to preserve its

integrity and viability.7
Diagnosis of treponemal disease relies heavily on its
clinical manifestation. The patient's symptoms and signs,
in combination with knowledge of the epidemiological
context of human treponematoses aid in a positive
diagnosis. Treponemal disease manifests in three stages:
primary, secondary, and tertiary. In all stages, tissue
FIGURE 1: Rothschild figure showing superior view of the cranium and

lateral view of tibiae with prominent periosteal reactions and periosteal
striations23
damage is caused by both localized and systemic

inflammation. Primary infection produces mild, nondiagnostic lesions, secondary stage infection adds
osteitis, or inflammation of the inner structures of bone
FIGURE 6: EXAMPLE OF LYTIC BONE LESION25
(though it can heal spontaneously), and tertiary infection

shows distinctive skeletal lesions and osteomyelitis, an
infection originating in the marrow. Neurological affects
do occur but symptoms may not become apparent until
years after infection, though infection of the central
nervous system occurs relatively early. In the laboratory,
the available diagnostic tools for detection are direct
detection of treponemes in biological specimens,

through including molecular assays and serological tests
is desirable.4
Methods and Procedures

In order to screen the Cobb Collection for TP, the
database of medical records was evaluated for TP cause
of death. Three members of the collection, CC18, CC22,
CC109, were then inspected for TP bone lesions using
FIGURE 2: Rothschild figure showing lateral view of ulna and tibiae

with gummatous lesions but minimal periosteal striations
2
The Backbone
FIGURE 3: Lateral view of CC18 radius showing periosteal reactions

and prominent cortical thickening and periosteal striations
FULL ARTICLES
FIGURE 5: Lateral view of CC109 radius showing a large gummatous

lesion
Conclusion
Through screening, TP infection was visually
confirmed in the 3 subjects. While a sample size of 3
does not allow for many conclusions to be drawn about
the health conditions of the time period, additional
screening of the Cobb Collections can be conducted in
the future. The TP infection lesions are not unique to TP
infection. For example, Mycobacterium tuberculosis, the
causative agent of tuberculosis, is shown to cause bone
lesions in late stages of infection.5 Therefore, CC
members with similar bone degradation should be
screened for TP infection using DNA extraction and
molecular diagnosis.
FIGURE 4: Lateral view of CC22 radius showing a large gummatous
lesion
methods from Rothschild et al (1994).6 All surfaces of
References
1.
COBB." The Backbone 1.1 (2015): n. pag. Web. 10 Apr.
skeletal remains were visually examined to identify all

occurrences of bone alterations throughout each
Kamei, Yah. "THE LIFE OF DR. WILLIAM MONTAGUE

2015.
2.
Cross, Christopher N. "APPLYING NEXT GENERATION
skeleton and variation from normal smooth cortical
SCIENCE
surfaces was noted. Treponemal disease was specifically
LABORATORY." The Backbone 1.1 (2015): n. pag. RSS.
recognized on the basis of periosteal reaction and

osteitis.
STANDARDS
IN
THE
COBB
RESEARCH
Web. 10 Apr. 2015.

3.
Gomez, M. "USING THE CONTENTS OF THE COBB

RESEARCH LABORATORY TO UNDERSTAND TODAY'S
HEALTH DISPARITIES." The Backbone 1.1 (2015): n. pag.
3
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FULL ARTICLES
Web. 10 Apr. 2015.
4.
Harper, K. N., Zuckerman, M. K., Harper, M. L., Kingston, J.

D. and Armelagos, G. J. (2011), The origin and antiquity of
syphilis revisited: An Appraisal of Old World preColumbian evidence for treponemal infection. Am. J. Phys.
Anthropol., 146: 99133. doi: 10.1002/ajpa.21613
5.
Haas, CJ. "Molecular Evidence for Different Stages of

Tuberculosis in Ancient Bone Samples from
6.
Rothschild, BM. "Treponemal Disease Revisited: Skeletal

Discriminators for Yaws Bejel, and Venereal Syphilis."
Clinical Infectious Diseases (1994): n. pag. Web.
7.
Giazani, Lorenzo, and Sheila A. Lukehart. The Endemic

Treponematoses. Clinical Microbiology Reviews 27.1
(2014): 89115. PMC. Web. 11 Apr. 2015.
8.
Hungary." National Center for Biotechnology Information.

U.S. National Library of Medicine, n.d. Web. 10 Apr. 2015.
9.
Radolf, Justin D. Treponema. U.S. National Library of

Medicine, n.d. Web. 10 Apr. 2015.
4
BIOHISTORIES The Story of CC18
The Backbone
Cobb Collection Short Biohistory
The Story of CC18

Theodore Meadough1,2
Jermaine E. Robertson 1,2
1Summer
Medical and Dental Education Program Scholars,

W. Montague Cobb Research Laboratory, Howard University
3Department of English, University of California
Editors Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMCs Summer
Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a
Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone
editorial team and the name of the CC individual was redacted. All other factual information was retained.
CC18 was born in South Carolina, approximately in the

year of 1903. It can be speculated CC18s birthplace was
Rock Hill, South Carolina as both his parents were born
there. Although slavery was abolished in 1865, during
this time African Americans were faced with many
obstacles. Due to being born in the South, CC18 was not
only introduced to an atmosphere full of violence, but an
environment that was segregated. Between the end of
the nineteenth-century and early twentieth century
African Americans had a difficult time establishing their
presence in a predominantly White society. Blacks were
terrorized for attempting to access the same resources
to which Whites were privileged. Traumatizing events
such as being spat on, raped, burned, and lynched were
commonplace incidents that victimized Blacks in the
South (Washington). Violence was not the only issue for
African Americans living in the South; Jim Crow Laws,
laws that were racially discriminant and disenfranchised
African Americans, added more harsh treatment to their
cruel circumstances. In a legal sense African Americans
were separate but equal, however this was not their
reality (Dred Scott). Opportunities and privileges were
not the same for Blacks as for Whites. Jim Crow Laws
embodied White privilege as they enforced racism
through segregation of public schools, public
transportation, and public places such as restrooms,
restaurants, and drinking fountains (SandovalStrausz).Southern states were also struggling with issues
such as The Great Migration and The Great Depression.
The Great Migration was a time period where one and a
half million African Americans relocated from the south
into western and northern states in quest of equality,
along with escaping unemployment and oppression (The

Great Migration). Even though many families migrated in
hopes of a decent living, the stock market crashed in
October 1929 sparking The Great Depression (Romer). By
this time CC18 was about twenty-five years old and
experiencing the economic pressures of banks closing
down, cotton prices dropping, and a low number of job
opportunities. Due to South Carolinas economy being
depressed prior to The Great Depression, the stock
market crashing only worsened the socioeconomic
conditions of the state (The New Deal). Despite the
crash, Washington, DC suburbs continued to expand
which may have been the reason CC18 moved to the
district in 1931 (B.3.3 Modern Period). Although it is
feasible that CC18 may have relocated in desire of a
better lifestyle, he was soon faced with another
impediment. Even with forward progression, African
Americans did not benefit from the District of Columbias
Federal expansion (B.3.3 Modern Period). It was difficult
to make ends meet and even more so for Williams
because he worked as a laborer. Having to work long
hours, tirelessly for low pay could have been a daily
source of stress worsening his already jeopardized
health. CC18 was suffering from syphilis presumably in its
late stages since he would die a short time after moving
to Washington, DC. Along with extensive hours, working
conditions were severely hazardous for all blue-collar
workers during the early 1900s (Tomyn, Media). As a
laborer, CC18 was at risk of death every minute on the
job. He was regularly exposed to toxic fumes and
excessive heat while working in small spaces with
improper ventilation. Working in these conditions did not
1
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aid in his overall health at all. CC18 died at the young age
of 28, February 18th, 1932 in Gallinger Municipal
hospital due to his syphilis infection.
Syphilis is a highly contagious bacterial infection that is
primarily spread by sexual contact. Syphilis may also be
transmitted from mother to fetus during pregnancy,
labor, or breastfeeding, resulting in congenital syphilis.
Infants with congenital syphilis may have symptoms at
birth, but it is not unusual for symptoms to develop later
in life. Syphilis is caused by the spirochete bacterium
Treponema pallidum. Even the very first sign of syphilis,
designated to be a painless sore, can be easily confused
for an ingrown hair, zipper cut, or any other seemingly
innocuous bump. Syphilis infections in adults can be
divided into different stages: primary, secondary, latent,
and tertiary. The primary stage of syphilis is
characterized by one or more painless ulcers, denoted as
chancres, appearing at the site of infection. Chancres
contain millions of syphilis bacteria and are highly
contagious. On average chancres will appear three
weeks after initial contact with syphilis. The usual
locations for chancres are around the anus, mouth, or
genital area. If left untreated, the ulcers can take
anywhere between two and six weeks to heal (Syphilis).
If the infection has not been treated it will progress
into the secondary stage, which will occur six weeks to
six months after initial exposure to syphilis. The
secondary stage is known to manifest in a variety of
ways, symptoms most commonly involve the skin,
mucous membranes, and lymph nodes. The most visible
symptom is a non-itchy rash covering the whole body,
particularly the extremities, including the palms and
soles. Another perceptible symptom is white patches on
tongue or roof of the mouth. These rashes are akin to
chancre in that they carry millions of syphilis bacteria
and are highly infectious. Other, less discernible
symptoms include a flu-like illness, loss of appetite,
swollen glands, patchy hair loss, and chronic headaches.
The latent stage of syphilis is characterized by a
regression of symptoms where the infection lies dormant
without causing symptoms. If no treatment is received,
syphilis can remain inactive in the body for years without
any signs of infection. Tertiary syphilis is the most violent
form of the infection. At this stage syphilis can affect the
heart and possibly the nervous system. Symptoms
resultant of these affects includes difficulty coordinating
muscle movements, paralysis, blindness, numbness, and
dementia. In the tertiary stage of syphilis the disease can
damage internal organs, which may eventually lead to
ones death (Syphilis).
An outbreak of syphilis occurred around the turn of

twentieth century in the United States that is speculated
to have infected ten to fifteen percent of the general
population (Jabbour). Since syphilis was primarily
contracted through sexual relations the stigma
surrounding the topic dissuaded people from revealing
their possible infection. This stigma may have caused
CC18 to avoid medical care in order to avoid being
permanently exiled by his community. CC18 may also
been under more pressure to avoid such a label in order
to protect his job as a laborer. The regressive effects of
syphilis probably encouraged CC18 to go on without
seeking medical care as well. Limited access to
healthcare due to segregation in the 1900s was also a
factor that could have deterred CC18 from getting
treatment. Segregation would have also restricted CC18
from educational attainment, which in turn could have
helped him be properly informed about the illness from
which he was suffering. However, its also a possibility
that he contracted congenital syphilis from his mother
because he died of syphilis at 28 years old. Symptoms of
congenital syphilis can be latent in an infant until
adolescent years. For CC18 to have died from syphilis it
had to be in its late stages meaning it resided in his body
for many years. At the beginning of the 1900s, the
medical establishment was relatively new and at its early
stages of development as an organized profession. State
licensing and certification of physicians was only
emerging and as such there were many frauds in the
healthcare system during this time. Syphilitics often
sought the consultation of frauds or quack doctors,
who offered baths, rubs, and hot springs as therapies for
pain in order to protect their confidentiality (Jabbour).
The fragile state of the healthcare system made the
outbreak of syphilis difficult to contain because
syphilitics did not view the institution as reliable. For
example, the Tuskegee Syphilis Experiment (an
experiment performed between 1932 and 1972 on four
hundred black men in the late stages of syphilis)
heightened African Americans skepticism towards
physicians during that time. The experiment was meant
to compare how syphilis affected African Americans as
opposed to whites. African Americans were already
experiencing a lack of quality healthcare, to be told they
were being treated for bad blood without any
knowledge they had syphilis was completely unethical.
The only data collected for the Tuskegee Experiment was
from the autopsies of the men (Resnik). Events such as
the Tuskegee Experiment lead Blacks to be highly
skeptical of the healthcare they were likely to receive if
they sought out medical attention.
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One of the major issues physicians faced was simply

assessing if their patients had syphilis. Physicians were
not sure how to communicate with their patients about
such a sensitive topic without making their patients feel
they were invading their privacy. The personal
complications that the diagnosis of syphilis could
potentially cause a patient were also a burden physicians
had trouble handling. Despite efforts of legitimate
physicians like Dr. Cobb to stress the importance of
consulting professional care so a proper diagnosis could
be made patients wanted to conceal their infection. In
order to mitigate the fear of patients due to the stigma
attached to syphilis, the American Medical Association
adopted Principles of Medical Ethics in May 1903 to
replace its Code of Ethics from 1847 (Jabbour). The
new principles established explicit guidelines for patient
confidentiality.
Fritz Richard Schaudinn, a German zoologist, and Erich
Hoffmann, a dermatologist discovered the syphilis
causing bacteria, Treponema pallidum, in 1905.
Subsequently after, in 1906 August Paul von
Wassermann, a German bacteriologist, developed a
complement fixation serum antibody test for syphilis
known as the Wassermann reaction. In 1909, German
scientist Paul Ehrlich discovered arsphenamine, which
would be marketed as Salvarsan. Released in 1910,
Salvarsan was the biggest advancement in managing the
spread of syphilis until its cure was found in the year
1943 (John).
CC18 was infected with syphilis during a time when a
healthcare system was barely emerging in the United
States. The relationship medical professions had with the
state and public was at best tenuous because of the
unsure role of physicians and the ignorance of the public.
It is likely if CC18 did not have access to Salvarsan
because of his unequal access to proper healthcare due
to segregation. Cost may have also been a factor that
discouraged CC18 because of his low pay as a laborer
and many hospitals did not have provisions for the
treatment of syphilis (Jabbour). Even if CC18 had the
opportunity to receive any medical care it is very
probable he refused because of the social stigma that
coupled with syphilis. It is also likely that any hospital
that admitted him did not have the provisions for the
treatment of syphilis. A large part of the reason the
syphilis outbreak was a significant challenge for medical
practices was the stigma surrounding the disease due to
the fact it was primarily transmitted through sexual
contact. Syphilis was a disease that no one wanted to be
unfortunate enough to be infected with and have to
discuss with another.
Syphilis is now diagnosed by a blood test that is

sometimes combined with an examination of lesions on
the body. The human bodys immune system usually
responds to syphilis by releasing antibodies that can be
detected with a relatively inexpensive blood test. The
antibodies produced by the body can stay in the blood
for years after infection. The only limitation of a blood
test is it cannot measure how long a patient has been
infected with syphilis. It is highly encouraged that
women receive a blood test nowadays given the risk of
congenital syphilis (Syphilis). Discovered in 1928, and
used as a cure for syphilis in 1943, penicillin is now
widely used to treat the infection (John). A single dose of
penicillin is most effective in treating early stages of
syphilis, but it is still fairly effective in treating later
stages of the disease. However, if the disease has
progressed to the third stage when it can cause damage
to the nervous system or internal organs then the effects
will be incurable. As a substitute to penicillin for those
who might be allergic for allergy purposes, azithromycin
or doxycycline can be administered as well (Syphilis).
After receiving medication routine check ups are
advisable to ensure that the bacterial infection is
completely eradicated.
Today, if CC18 had contracted syphilis, he would have
found that seeking treatment is relatively simple. CC18
would only need to search for the nearest clinic or health
center that administers blood test and treatment for
sexually transmitted diseases. CC18 also would not have
had to deal with the pressure of being labeled an exile
because much of the social stigma surrounding sexually
transmitted infections has dissipated over the decades.
CC18 could find solace in knowing that patient
confidentiality is a much more strict policy today than it
was at the beginning of the twentieth century. Many of
the socioeconomic barriers impeding CC18 from seeking
treatment such as his wages as a laborer or segregation
are not an issue in modern day times. Treatment for
sexually transmitted diseases is widely available to all
from many sources for low cost. It is worth noting that
there are still many disparities throughout the healthcare
system in the United States today. For instance,
minorities continue to be underrepresented within the
medical workforce, despite the country becoming more
diversified. Minorities are also less likely to have access
to medical institutions for an abundance of reasons.
Through research projects similar to those conducted at
the Cobb Research Lab it is possible to eliminate these
disparities by bringing attention to them. Despite the
health disparities that exist within the United States, it is
likely that if CC18 contracted syphilis today he would
3
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have lived a much longer life instead of dying tragically at

the young age of 28, due to improper health care.
References
DRED SCOTT v. SANDFORD. Dred Scott v. Sandford. Web. 08

July 2015. <http://www.oyez.org/cases/18511900/1856/1856_0/>.

Washington, Margaret. Obstacles Faced by African
Americans. PBS. PBS. Web. 08 July 2015. <http://
www.pbs.org/wgbh/amex/1900/filmmore/reference/
interview/washing_obstaclesfaced.html>.
Wormser, Richard. The Great Migration. PBS. PBS. Web. 08
July 2015. <http://www.pbs.org/wnet/jimcrow/
stories_events_migration.html>.
Frith, John. Syphilis Its Early History and Treatment until

Penicillin and the Debate on Its Origins.
JMVH. Web. 08 July 2015. <http://jmvh.org/article/syphilis-its
-early-history-and-treatment-until-penicillin-and-the-debateon-its-origins/>.
The Great Depression and the New Deal. Choice Reviews
Online 39.01 (2001). Web. 8 July 2015.
Jabbour, Nicholas. Syphilis from 1880 to 1920: A Public Health
Nightmare and the First Challenge to Medical Ethics. Syphilis
from 1880 to 1920: A Public Health Nightmare and the First
Challenge to Medical Ethics. Corcoran Department of History.
Web. 08 July 2015. <http://www.uri.edu/artsci/com/swift/
HPR319UDD/Syphilis.html#n50>.
The Modern Period ( 1789-1999). 1999 (2002). Web. 8 July
2015.
National Institute of Environmental Health Sciences.
Research Ethics Timeline (1932-Present). Web. 08 July 2015.
<http://www.niehs.nih.gov/research/resources/bioethics/
timeline/>.
Romer, Christina D. The Great Crash and the Onset of the
Great Depression. Oxford University Press. Web. 8 July 2015.
<http%3A%2F%2Fwww.jstor.org%2Fstable%2F2937892%
3Fseq%3D1%23page_scan_tab_contents>.
Sandoval- Strauz, A. K. Travelers, Strangers, and Jim Crow:
Law, Public Accommodations, and Civil Rights in America.
American Society for Legal History, 2005. Web. 8 July 2015.
<http%3A%2F%2Fwww.jstor.org%2Fstable%2F30042844%
3Fseq%3D1%23page_scan_tab_contents>.
Syphilis Symptoms, Causes, and Diagnosis. WebMD.
WebMD. Web. 08 July 2015. <http://www.webmd.com/sexual
-conditions/guide/syphilis>.
Syphilis. Syphilis. Web. 08 July 2015. <http://
www.niaid.nih.gov/topics/syphilis/pages/default.aspx>.
Tolnay, Stewart E., and E. M. Beck. Racial Violence and Black
Migration in the American South, 1910 to 1930. American
Sociological Association. Web. 8 July 2015. <http%3A%2F%
2Fwww.jstor.org%2Fstable%2F2096147%3Fseq%3D1%
23page_scan_tab_contents>.
Tomyn, Rosanne, and Demand Media. What Were the Work
Conditions in American Factories in 1900? | The Classroom |
Synonym. The Classroom. Web. 08 July 2015. <http://
classroom.synonym.com/were-work-conditions-americanfactories-1900-23383.html>.
4
The Backbone
The Story of CC112

Turquoisia McNabb1,2
Whitley Hatton1,3
1Summer

2Department of Agricultural and Life Science, University of Florida
3Departmeny of Biology, Howard University
Editors Note
CC112, Negro, age 60, died from meningitis on

November 18, 1934 at Gallinger Municipal Hospital.
According to Sara E. Branham and Sadie A. Carlin from
the National institute of Health, the first recorded
outbreak of meningitis in the United States was in 1806.
Meningitis since then has a periodic return to epidemic2
proportions at intervals of approximately ten years. At
the National Institute of Health, meningitis showed peaks
of cases in 1918, 1929, and 1936. Since there was an
outbreak of meningitis from 1928 to 1934, we know now
that CC112 contracted this virus during the outbreak.
Looking through ancestry.com and many other websites,
we found endless records going by the name of
[Redacted]. Searching through, it was very difficult to
narrow down to just one name because there were so
many factors we had to consider. For instance, on
ancestry.com, there came up 11 different people that
had similar backgrounds to our person. One selection
was a man that died the same year, but lived in Virginia
and not D.C. Another man we looked up lived in D.C., but
died earlier than our date of death. But not one of the
sources on ancestry matched completely and none of
these sources had died from meningitis. After finding a
never ending list of [Redacted]s, we then turned our
search to the hospital and treatment of meningitis during
the 1930s. CC112 was treated at Gallinger Municipal
Hospital. This hospital resided in southeast D.C. and was
first built in 1846. This hospital was first an Asylum that
housed the citys indigent patients and a work house for
the people convicted of minor crimes. In 1922, after
placing a new building, the Asylum became more of a
hospital with a smallpox hospital, quarantine station, and
disinfectant plant.
According to Jacob Fenston, who wrote From Public
Hospital to Homeless Shelter: The long History of D.C
General, he explains that hospitals during the time it
was functional were for the poor, homeless, and
criminals. By the 1940s, the hospital was a filthy place
swarming with flies, according to a U.S. Senator. To know
who this hospital was used for, the time period our
person was living in, and what he died from, we can
make an educated assumption on CC112 and his life.
There are two types of meningitis, viral and bacterial.
Viral meningitis most often caused by enteroviruses that
live in the intestines and can be spread through food,
water, or contaminated objects. This kind of virus occurs
mostly in kids and babies. Bacterial meningitis is a very
serious illness. This is passed from one person to another
through infected saliva or mucus. Streptococcus
pneumoniae and Neisseria meningitides. This kind of
bacteria can be located in your throat without getting
sick, but can be transferred to others. Also, this kind of
meningitis occurs mostly in adults. so we can assume
that CC112 was diagnosed with bacterial meningitis since
he was older and because bacterial meningitis is more
severe than the viral infection.
Although anyone can be infected with meningitis,
there are many factors that can increase risk. Genetics,
being male, being in crowded living conditions, exposure
to insects and rodents, not having your immunizations,
and not receiving vaccinations are all factors that can
increase the chance of contracting meningitis. In all of
these factors, we can assume that since CC112 was a
1
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Negro during the early 1900s that he was of a lower

class and didnt have great access to health care. We can
also take a guess that CC112 also lived in crowded living
conditions, had a greater exposure to rodents and
insects, and was an older adult that didnt receive their
vaccinations. We can make an educated assumption that
during this time, blacks were living in a crowded
neighborhood of their own, which in the D.C. area could
be infested with insects and rodents. Since CC112 was an
older man who was diagnosed with meningitis, we can
also assume that he didnt receive his immunizations as
well. Anacostia was a city designed in the 1900s for the
working class. The only surprising thing I found, was that
most of Anacostia was for working class of whites and
not blacks. This finding made me think that maybe
CC112 was a more well off Negro that had a better
paying job, till he couldnt work anymore. So I can come
to a safe conclusion that CC112 as he got older, moved
into a more crowded area of the city, didnt receive his
immunizations due to lack of money probably from
retiring. Since he was placed in Gallinger Municipal
Hospital, makes an even better guess that he had
become poorer as he aged.
Without antibiotics and immunizations there is an
eighty percent chance mortality rate. Penicillin is used
for patients with meningitis. Since penicillin was
discovered in 1928, it was probably only available for
people who could afford it. With this knowledge, we can
assume that CC112 didnt have healthcare that could
afford him to take penicillin, or penicillin wasnt known
to help treat meningitis at this time. With all these
findings and factors, we can see how and why CC112
died. During his time, he wouldnt survive, unfortunately
should he have been alive today, he would have
probably survived.
CC112 was one of the many people in year 1934, to
catch meningitis. During this era this epidemic had over
500 different strains present in multiple communities
around the nation. On November 18, 1934 in the
Gallinger Municipal Hospital this epidemic ended
CC112s life.
The outbreak of what is now known as meningitis was
very popular in the early 19th century. CC112 most likely
went to Gallinger Municipal Hospital prior to his death
with symptoms of a stiff neck, headache, and severe
sensitivity to light. This was diagnosed with a spinal tap.
Physicians would take a long needle and stick it in the
back and draw fluid from around the spine. With this
fluid they could tell if there was inflammation in the
meninges. Symptoms for this disease varies according to
age (Healthline.com). Once diagnosed with meningitis he

was admitted into the hospital for treatment. At this
particular time there were no ground breaking vaccines
available so patients were treated with penicillin
(Chapter 28: a history of bacterial meningitis). The cause
of meningitis in this time period were identified later in
the 19th century as Streptococcus pneumoniae,
Neisseria meningitis and Haemophilus influenza (Chapter
28: a history of bacterial meningitis), but these causes
were only for bacterial meningitis which wasnt
discovered until the 20th century.
CC112 could have had one of five meningitis diseases
or another disease associated with meningitis known as
meningococcal disease. Meningitis is inflammation on
the meninges around the spinal cord and brain
(Healthline.com). It causes fever, intense headaches, stiff
neck, nausea, vomiting, drowsiness, confusion, and
sensitivity
to
light
(Healthline.com).
Unlike
meningococcal bacteria which specifically affects
adolescents aged eleven to seventeen. Meningococcal
causes an infection in the blood stream. Symptoms
include: joint pain, red or purple rash that does not turn
white when pressure is applied, and coming into close
contact with a person with the disease (Meningitis vs
Meningococcal: Difference in deadly diseases).
If CC112 would have caught this disease in the 20th
century his chances of living would have increased
greatly. Vaccinations for meningitis debuted in the early
20th century. Vaccinations against Neisseria meningitis
and Haemophilus influenzae were also created (Chapter
28: a history of bacterial meningitis). Those two diseases
were the two causes of meningitis. With new research
found on the disease doctors were able to narrow the
strands on meningitis down to: bacterial, viral, fungal,
parasitic, and noninfectious meningitis.
Bacterial meningitis is very similar to Neisseria
meningitis and Streptococcus pneumoniae (CDC). These
medical conditions require immediate medical attention.
Bacterial meningitis is usually taken care of with
antibiotics because the medication kills the bacteria.
These antibiotics include: ampicillin, claforan, rocephin,
gentamicin, penicillin G, and vancocin (Web MD). This
medications can be taken for a specific amount of time
and the disease would have been cured. If CC112 was
around during this era his life would have lasted a little
longer.
Viral meningitis is caused only by viruses like non-polio
enteroviruses, arboviruses, and herpes simplex viruses
(CDC). Compared to bacterial meningitis this is not that
severe. People with a healthy immune system can fight
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this virus on their own within 7 to 10 days (CDC). People

at risk of catching this disease are five and under (CDC).
The likeliness of CC112 having this strand is very low.
Jackson would have been one of many a survivors of

such a fatal disease.
Fungal Meningitis is caused by fungi like Cryptococcus

and Histoplasma and acquired by inhaling fungal spores
in the environment (CDC). This strand of meningitis is
rare and only caused by other fungus. People with other
diseases like diabetes, cancer, and HIV are at higher risk
of catching fungal meningitis (CDC). It also takes longer
to cure people with these diseases because they are
known for having low immune systems. The benefit of
having this strand versus any other is this strand is not
contagious and cannot be given to another person.
Fungal meningitis can be treated with high doses of
antifungal medications, usually given though IV (CDC).
References
Primary amebic meningoencephalitis (PAM), also

known as parasitic meningitis is the fourth strand it is
caused by parasites and less common in developed
countries (CDC). These parasites usually contaminate
food, water and soil. This disease is popular in places
with large bodies of warm and fresh water, the diseases
could also be contracted from pools that are not
properly maintained. Catching parasitic meningitis is very
dangerous, although there is treatment most people that
get treated still die (CDC). This disease presents
symptoms very similar to bacterial and viral meningitis
according to centers for diseases control and
prevention.
Finally, there is Non-Infectious Meningitis. This form of
meningitis is caused by cancers, systemic lupus
erythematosus, certain drugs, head injury, and brain
surgery (CDC). Its symptoms are just like the others,
sensitivity to light, confusion, vomiting, and nausea
(CDC). This form or meningitis is not contagious because
you can only get it if you have one of the causes listed
above. Since Mr. Jackson cause of death was only
meningitis I think it is safe to say he did not have
noninfectious meningitis either.
Lights, Verneda, and Elizabeth Boskey. "Meningitis."

Healthline. August 16, 2012. Accessed July 3, 2015
Ken, Tyler. "Chapter 28: A History of Bacterial Meningitis."
Pubmed.gov. 2010. Accessed July 3, 2015.
Adams, Andie. "Meningitis vs Meningococcal: Difference in
Deadly Diseases." Nbcsandiego.com. February 20, 2014.
Accessed July 2, 2015.
Bacterial Meningitis." Centers for Disease Control and
Prevention. April 1, 2014. Accessed July 3, 2015.
Thompson, Gregory. "Antibiotics for Bacterial Meningitis."
WebMD. November 14, 2014. Accessed July 3, 2015.
"Viral Meningitis." Centers for Disease Control and Prevention.
November 26, 2014. Accessed July 3, 2015.
"Fungal Meningitis." Centers for Disease Control and
"Parasitic Meningitis." Centers for Disease Control and
"Non-Infectious Meningitis." Centers for Disease Control and
Prevention. March 15, 2012. Accessed July 3, 2015.
Since 1806, meningitis has been a fatal disease and has

killed thousands of people since then. Mr. Jackson was
one of the many taken by such a fatal disease. Mr.
Jackson was at an extremely high risk of getting the
disease because he was African American, poor and
elderly living in an era when medicine was not readily
available. His chances of living a longer life would have
increased greatly if he was present in the millennium.
New medication has been invented since 1806, which
have increased the life expectancy of people with
meningitis. Discrimination in health care has also
decreased greatly so he would receive great care. Mr.
3
The Backbone
The Story of CC312

Christine Okaro1,2
Christopher Wilson1,3
1Summer

2Department of Global Health Studies, Mercer University
3Department of Psychology, Washington University
Editors Note
The death certificate of a fifty-nine year old woman

from Arlington, Virginia, was examined to discover the
relationship between her cause of death and the social,
economic and healthcare disparities. The death
certificate revealed that she died from lung abscess at
the Gallinger Hospital, an inadequate public hospital
largely serving minority populations, in Washington DC in
1943. Factors including her level of education, race and
treatment options were analyzed to interpret the
influence of ethnic and economic disparities on her
health and access to adequate care. Due to the impact of
segregation, minorities were limited regarding the type
of treatment received and often died from preventable
illnesses.
CC312 was born in 1884 and lived in Arlington, Virginia
until her death on April 11, 1943 (1920 United States
Federal Census). Though CC312 resided in post-slavery
Virginia, it is expected that she experienced racial
tensions and division in her lifetime. The effects of the
Civil War and the Reconstruction era greatly impacted
Virginians. Atrocities faced by African Americans, such as
the public whipping post, were abolished during the
Readjuster government of the early 1880s (Virginia
Historical Society).
Historical and Societal Impacts
During this Readjuster government, Virginia worked

to enfranchise Blacks by promoting voting rights. This
opportunity was short-lived. The election of Governor
Fitzhugh Lee in 1885 and the rise of the Confederacy
stifled the progress of African Americans until the
momentum of the Civil Rights Movement (Virginia

Historical Society). Although slavery was abolished in
1863 by mandate of Abraham Lincolns Emancipation
Proclamation, Virginian governance enacted laws and
regulations that greatly oppressed the civil rights of all
African Americans through rigid segregation.
Due to the economic and educational restrictions on
Black Americans living in Virginia, it is probable that
CC312 and her husband did not receive an adequate
education, which limits economic mobility. African
Americans were largely treated as second-class citizens;
this sentiment is reflected in the standard jobs available
to them. African Americans generally worked as
sharecroppers in rural areas, and menial or domestic
service jobs in urban locations of Virginia (Virginia
Historical Society). All aspects of life, including education,
career options and living conditions were inferior to
Whites.
By the 1910s and 1920s, Virginia underwent a revival
of the Klu Klux Klan and enacted the Racial Integrity Act
in 1924 passed by the Virginia General Assembly
(Sherman). This Act labeled all non-white individuals as
colored, sanctioned the one-drop rule, which labels all
individuals with any trace of African ancestry as Black,
and banned interracial marriage as a mechanism for
preserving the privilege and status of Whites in Virginia
(Sherman). CC312 likely experienced the outcome of
racial insensitivity and violence. Constant exposure to
segregation and taunting is classified as a stressor, which
can negatively affect health and contribute to the
manifestation of predispositions.
1
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CC312 lived through pivotal moments in history that

have shaped the lives of post-slavery African Americans,
which ushered in legislations towards justice for all.
Monumental moments, such as the ending of the Civil
War, and the start of the Reconstruction era, which
struggled to tackle the need for black freedom. Plessy v.
Ferguson (1896), a case which sanctioned the notion that
Blacks remaining separate, but equal from Whites was
constitutional. Along with experiencing racial
segregation, CC 312 may have later experienced the rise
of prominent Black institutions and voices.
CC312 lived approximately twenty-seven miles away

from this hospital, suggesting that this institution, based
on her economic and racial background, was her primary
source for medical care. At the time, receiving medical
care at public institutions was exclusively for poor or
minority citizens. Private physicians largely treated
affluent White individuals. Consequently, segregation led
to inadequate medical attention and little effort directed
towards improving the services rendered by public
hospitals, such as Gallinger Municipal Hospital.
The National Association for the Advancement of

Colored People (NAACP) was established in 1909. From
its founding the NAACP, the nations largest and oldest
civil rights organization, has worked to fight for social
justice for all Americans, especially minorities and
underrepresented populations (NAACP). The outbreak of
World War I in 1914 was a pivotal moment in African
American history, as events such as The Great
Depression (1929-1939), The New Deal (1933-1938), and
The Great Migration directly affected the economic
aspects of African American communities. The birth of
the NAACP and a movement towards the advancement
of Black and minority Americans likely influenced and
empowered CC312, despite the fear induced by living in
lawful segregation.
Illness and Resistance to Treatment
Analysis of Personal Life
Exploring the aspects of CC312s personal life reveals

the lifestyle and living conditions that may have led to
her death. According to the 1920 Census Record, CC312
lived in Richmond Madison Ward, Richmond
(Independent City), Virginia at the age of thirty-six.
CC312 was married and identified as the head of
households wife. Her husband was also born in Virginia
in 1877. CC312 could both read and write, which
suggests CC312 had, at the least, a basic level of
education. The parents of both CC312 and her husband
were born in Virginia. This establishes CC312 as a
generational dweller of Virginia.
Due to segregation, CC312s access to quality health
care was limited. On April 11, 1943, CC 312 died at the
Gallinger Municipal Hospital. This hospital, established in
1806, was the first public hospital in Washington, D.C.
From its inception, resources at this hospital were
inadequate. Only the poor and minorities utilized
Gallinger for treatment, which often suffered from
overcrowding, low supplies of medicine, and inefficient
laboratory and x-ray services (Fenston).
The death certificate of CC312 lists her cause of death

as abscesses of the lungs. Abscess of the lung is a
bacterial infection in the lung resulting from bacterial
growth in the mouth. This illness causes tissue to die,
and results in pus accumulating in that space (Bartlett).
The symptoms of this disease appear gradually over time
and may not be diagnosed until the disease is well
advanced. Common symptoms include coughing, fever,
shivering, and night sweats. Chest pain and shortness of
breath can also be present in some cases. In many cases,
symptoms are mistaken for a common cold, which may
have influenced the severity of her illness. CC312 died
from this disease because she either did not receive
timely, adequate medical treatment. Instead of
immediately seeking medical attention, CC312 may have
sought the aid of home remedies, until the illness
became life threatening.
Apart from the probability of CC312 neglecting the
progression of her illness, it is possible that her care at
Gallinger Hospital was subpar and ineffective -- leading
to a worsened state of health. In the early stages of
public health care, patients were not afforded advanced
medical exams, equipment and treatments. The
worsening the disease plaguing CC312 likely led to a
complicated medical case that Gallinger Hospital was not
equipped to treat. Furthermore, the severity of her
disease coupled with the second-class treatment of
minorities, especially African Americans during
segregation, directly affects the quality of medical
attention received.
Another factor contributing to CC312s lack of
treatment was the attitude of minorities and poor
individuals towards hospital-based medical treatment.
While it is true that minorities and African Americans
used public hospitals as medical resources, the
marginalization of African American lives in medicine
resulted in a culture of distrust. Due to events such as
The Tuskegee Syphilis Experiment (1932-1972), which
2
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infected African American patients with the syphilis

virus, African Americans largely lost trust in Americas
healthcare system. The fear of unwarranted medical
exploitation often outweighed the need for hospital
visits.
Early Treatment Methods
Between 1935 and 1945, the most recognized

treatment for abscess of the lung involved the use of
sulfonamides (Willis). Prior to this treatment, the disease
was managed through the draining, posturing,
conducting a bronchoscopy, or surgery. The mortality
rate of abscess to the lung before 1930 was 32-34%
(Willis). Although this treatment was widely accepted,
the introduction of sulfonamides as a form of treatment
did not significantly alter the mortality rate. However, in
the late 1940s penicillin was introduced as a method to
alleviate the effects of this disease, which lead to a lower
death rates and a 90-95% patient recovery rate.
As the benefits of penicillin were recognized, it
became the primary treatment method. It is likely that
CC 312 did not receive penicillin as a form of treatment,
which contributed to her death from an avoidable and
treatable disease. Because CC 312 died after the
discovery of penicillin method of treatment, it is unlikely
that she received penicillin. This may be one of the
reasons why she succumbed to the disease. CC 312 case
reiterates the disparities many African Americans were
faced, due to the lack of public hospitals that provided
quality medical care.
floor without offering assistance (Los Angeles Hospital to

Close). This egregious conduct led to its closure.
Similarly, reports of neglect and medical incidents lead to
the recent closing of Gallinger Hospital in 2001
(Fenston).
To withstand rising healthcare costs, The Affordable
Healthcare Act (2010) extends the coverage of medical
care and lowers the intended cost of services (U.S.
Department of Health and Human Services). Through this
health care law, disparities in the availability of health
care can be eliminated. This means more individuals are
able to obtain preventative treatment to manage
illnesses early, which avoids unnecessary deaths from
treatable diseases. Regular doctor visits, made possible
by the availability of health insurance, can lead to longer,
healthier lives for all patients, regardless of race,
financial ability, or social class.
As healthcare services have improved overtime, so has
the treatment of abscess of the lungs. At present, the
mortality rate for abscess of the lung is less than 10%
(Bartlett). This is due to new antibiotic drug discoveries.
Current treatment consists of clindamycin antibiotic
therapy for four to six weeks, followed by an x-ray to
assess the progress of treatment (Kamangar). This
advancement is acknowledged as a more effective
treatment than penicillin, the previous treatment of lung
abscess. Although laws are now enacted to ensure
equality in medical care, health disparities are still
prevalent in minority populations.
The Story of CC312

Treating CC 312 Today
Since CC312s death in 1943, the medical field has

undergone
several
changes
physically
and
technologically. As of now, patients have choices when
selecting a hospital or health care provider. Despite this,
health care disparities still exist, as the best medical
service is available to those who can afford it. Although
health insurance is meant to alleviate these disparities,
these policies equate better medical care to higher
premiums.
Generally,
poorer
and
minority
neighborhoods are still served by hospitals that provide
comparatively substandard service.
Martin Luther King, Jr. Hospital in Los Angeles
California is an example of an inner-city medical facility,
with mainly minority patients living in close proximity. In
2007, this hospitals poor patient care made headlines as
staff ignored a minority patient who lay dying on the
From the research provided, the circumstances of

CC312s life, which led to her premature death, can be
asserted. CC312, a Black woman, lived in Arlington,
Virginia during World War II and the confederacy. CC312
dismissed the early symptoms of the disease, due to the
benign signs of abscess lungs: cough and fever. As the
symptoms worsened, she weighed the inconvenience of
leaving her home and work to travel to Washington D.C.
for treatment. Due to the progression and severity of her
illness, including chest pain and shortness of breath, she
was eventually forced to travel a great distance to
twenty-seven miles to Gallinger Hospital. Closer to her
death, CC312 experienced intensified coughing
accompanied by putrid smelling mucus.
She had to part with her husband for the journey, due
to their inability to afford transportation for the two of
them. Upon arriving at Gallinger Hospital, CC312 waited
for several hours to receive services, due to the
3
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overcrowding patients and under-resourcing of staff.

After being admitted, CC312 was placed in a crowded,
under-furnished, unsanitary examination room, in which
she did not receive an adequate examination. By this
time, CC312 experienced intense pain and discomfort
while still unsure of her illness or potential treatment
methods. Because of the progression of her illness, the
lack of medical supplies at Gallinger Hospital, and the
misdiagnosing of her disease, CC312 did not receive
adequate care. This medical oversight led to her death.
If CC312 suffered from abscess lungs today, she would
be prescribed the antibiotic clindamycin (Kamangar).
This would have increased her chances of survival and
decreased her probability of death to 1/8th of the
previous treatment (Kamangar). Additionally, CC312
would have the resources to seek treatment earlier, as
Medicare or the Affordable Care Act would likely cover
her medical costs.
Coupled with an increase in the number of hospitals,
as well as affordable public transportation, CC312 would
have more opportunities to seek earlier treatment.
Educational opportunities for women and minorities
have improved over recent years, which would have
provided CC312 with economic and social advancement
resulting in employment and access to companyprovided health insurance. Due to the economic
advancements, medical innovations, and civil rights
movements The United States has become a nation
better fit to address the medical needs of individuals. If
born at this time, it is highly expected that CC312 would
live a healthier and longer life.
Sherman, Richard B. The Last Stand: The Fight for

Racial Integrity in Virginia in the 1920s. The Journal of
Southern History 54.1 (1988): 69, Web. 4 July 2015.
Therapy, Surgical Care. Medscape, 18 Dec. 2014. Web.
08 July 2015. <http://emedicine.medscape.com/
article/299425-treatment#d8>.
The Virginia Historical Society. Virginia Historical
Society, New Southerners. The Virginia Historical
Society,Web.
04
July
2015.
<http://
www.vahistorical.org/what-you-can-see/story-virginia/
explore-story-virginia/1861-1900/new-southerners>.
Willis, AT. Anaerobic Bacteria: Role in disease. Annals
of Internal Medicine Ann Intern Med 82.6 (1975): 862.
Web.
1877 Census. Richmond Madison Ward, Richmond
(Independent City), Virginia, United States Richmond
(Independent City) Virginia Male 43 1877 Head African
American Black.
1920 United States Federal Census. Official Enumeration
Date: January 1, 1920. Enumeration District: 143. Place:
Richmond Madison Ward, Richmond (Independent City),
Virginia, United States. Household ID: 59. Publication
Number: T625. Page: 3A. Line Number: 40. Microfilm
Number: 1821911. Image number: 00417.
References
Bartlett, John G. "Clinical Infectious Diseases." Oxford

Journal 40.7 (2004): 923-25. Print.
Fenston, Jacob. From Public Hospital To Homeless
Shelter: The Long History of D.C. General. WAMU 88.5.
Web. 01 July 2015.
Kamangar, Nadar. "Lung Abscess Treatment &
Management." Lung Abscess Treatment & Management:
Medical Care, Antibiotic
NAACP. National Association for the Advancement of
Colored People." NAACP. National Association for the
Advancement of Colored People. Web. 04 July 2015.
4
The Backbone
The Story of CC315

James M. Byrne III1,2
Lopriela Seabrook1,3
1Summer

2Department of Biological Sciences, University of Maryland: Baltimore
3Department of Biology, Savannah State University
Editors Note
Washington, D.C. is customarily acknowledged for

upholding past executive leaders, congressional
legislative initiations, and judicial upbringings of the
country. For centuries, however, the prestigious province
has also been the home of countless societal
movements, and renewal projects. It has also served as a
refugee for manifolds of migrants, including CC315 who
was born in the District of Columbia in 1867. Upon her
arrival, Jim Crow law manifestation and irrational
segregation became the national ideals that would come
to affect her for the rest of her life. CC315s unfortunate
placement in society would limit her chances of success,
represent her unequally under the law, dictate her
residential location, and have an influence over her
chances of survival.
CC315 resided at 210 F Street SW with her Virginian
relative, who was born in 1892. The 1940 Census
indicates that the relative was labeled as the head of the
household while CC315 was his roommate and labeled as
the roomer. Although the relationship of the two is
mistaken for kinship, they actually shared a common law
marriage. This type of marriage was established when a
man and a woman lived together for a certain amount of
time and declared themselves as being informally
married. This is a significant fact because CC315 was
originally widowed.
Listings of tracts from the 1940 U.S. Census, which are
geographical regions where population data is collected,
shows that Holmes lived in tract 60 of Washington, D.C.
Tract 60 outlines a community referred to as the
Southwest Waterfront. This area borders the south
CobbResearchLab.com/The Backbone
boundary of the Capitol mall, lies west of South Capitol

street SW, east of 4th street SW, and north of M street
SW. This area served as an affordable option of residence
for the poorest Washingtonians after the Civil War. The
waterfront had been strategically used as a commercial
wharf but was abandoned by the military around 1865
after the war concluded. In the meantime, the area
became settled by thousands of freed slaves and
European immigrants who sought after the work
opportunities along the waterfront. Around the 1900s
the government gained an interest in the waterfront and
implemented plans to utilize the area by rebuilding old
buildings and abandoned wharves, and widening streets
that led to them (Timeline). Up until the 1950s, the
area continued to attract more settlers including African
Americans who participated in the Great Migration to
escape the effects of the crop destroying boll weevil and
other economic factors in the rural South. Jim Crow laws,
segregation, and prejudice followed blacks to the north
as they became more urbanized. At least one and a half
million African Americans resided in the north by the
1940s (The Second Great Migration).
The vastly populating community eventually created
divided neighborhoods that attracted white Irish,
Scottish, and German people on the west of Fourth
Street SW, and blacks on the east. The row houses on
and around F Street, where CC315 resided, had the
cheapest rent prices that persisted well below the
average cost of forty-five dollars in the 1940s
(HCHT). Although the majority of the community was
rather poor, the scenery of the area maintained its daily
1
The Backbone
display of busy activities that included moderate traffic

and street crossing pedestrians (Abrams). The beginnings
of societal landscape shifting took place around the
1970s when the government called for an urbanizing
renewal project that would remove thousands of
businesses and lead a countless number of residents into
eviction (Timeline). This project soon modified the
population into white predominance and nonetheless
provided solutions for the concerns squalid
neighborhoods remaining near the nations capital
(Abrams). Large offices, expensive apartments, and other
new features contradicted to poorer adjacent
neighborhoods that only offered the view of tents and
shacks as homes as a result of the changes (SW
Heritage). After interstate 395 was built directly upon F
Street Northwest during the process of renewal, CC315s
home, as she knew it, had ceased.
It is important to note that CC315 lived through the
Great Depression. This historical event began with the
crash of the New York Stock Exchange in 1929 and lasted
until about 1939. During this time period, the
unemployment rate skyrocketed to around 25%
(Nelson). For blacks, the unemployment rate rose above
50% (Trotter). This means that it is very probable that
CC315 was exposed to extreme poverty; even more so
than her white counterparts. Whites called for action
stating that no black man could get a job until every
white man was employed (Trotter). Though CC315 chose
not to work later in her life, the economic times during
the Great Depression led to many black women being
employed as house maids for only $5 a week (Trotter).
Around this time, many African-Americans in this time
period were supporting Republican president Herbert
Hoover due to his views on emancipation. Under
democratic President Franklin Roosevelt, many blacks
were subject to discrimination through his introduction
of the New Deal program. Certain programs that were
part of the New Deal eliminated around 60% of AfricanAmerican government paychecks and their benefits from
social security programs (Trotter). Consequently, this led
to African-Americans fighting for their rights through
entities such as the NAACP.
Records indicate that CC315 died from burns at age 46
on August 26, 1943 at Casualty Hospital in the District of
Columbia. The Cobb Labs records incorrectly indicate
that she died at age 79. Logically, Holmes received care
from Casualty Hospital around her time of death, which
was federally funded by the government for those who
could not pay for healthcare treatment (Pohl). In order
for skin to be burned, it must be subjected to a heat
source or a chemical source that damages the skin.
There are different degrees of burns: first, second, and

third. First-degree burns indicate only the outer layer of
the skin was damaged. A second-degree burn affects the
outer layer of the skin, the epidermis, and the layer
below it, the dermis. The most severe burn, a thirddegree burn, can result in complete destruction of the
skin and even tissues below the skin such as muscle
(Burns Fact Sheet). Most burns will cause blisters,
infection, and swelling, and if they were severe enough,
they can even result in anaphylactic shock, or death.
The skin acts as a protective layer for the human body
and also allows for regulation of body heat. Therefore,
burned skin is damaged and more prone to foreign
materials entering the body and causing infection (Your
Skin). During this time burn treatment was limited and
lacked effectiveness. If 50% of a persons body was
burned it was likely that the accident would result in
death. Doctors commonly used refrigerated skin from
cadavers as a temporary dressing for burns around the
1940s (Skin Grafts). Skin grafts were first used to treat
burns in 1871, however the recipients immune system
usually ended up rejecting the foreign skin. During the
time of CC315s death, treatments for burns were rapidly
changing due to the amount of soldiers in the World War
II receiving burn wounds. Burns were treated by
irrigating the wound with saline solution or by using
Tannafax jelly, which contained some tannic acid (WW2
Burns Survivor). Tannic acid was the common
treatments for burn wounds before the war until
physicians realized it could lead to eradication of the
skin. In Holmess case, since this was a time of racial
inequality, it is likely that she did not get priority care. It
is also very likely that she did not have access to the
fairly new and lifesaving burn interventions. Some
possible home remedies for burn injury that were
probably used by those who could not afford health care
included using: white vinegar to extract heat, natural
honey for its pH balancing and antibiotic effects, a milk
bath to soothe and heal the skin, essential oils from
coconut or vitamin E to reduce scarring, and tea bags for
retrieving small amounts of tannin acid (Shea). The
condition of CC315s burns is presently unknown, which
makes it difficult to determine whether or not these
home remedies would have been beneficial for her.
However, since the burns resulted in her fate, her
condition must have been relatively severe or her burns
could have been painfully infected.
Since there is a lack of explanation about the event of
CC315s incident, one can assume that the burns she
acquired may have been the result of a house fire. While
the risks of American house fires have decreased
2
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tremendously over the past decades, studies from the

Federal Emergency Management Agency (FEMA) show
that socioeconomic factors such as poverty, undereducation, race, and income lead to an increased risk of
fire incidents. The 1997 National Fire Data Center states
that vacant and abandoned buildings serve as fire
hazards in poor neighborhoods by appealing to
individuals who are likely to ignite illegal materials. It
also recognizes the possibility of homeless people
seeking to stay warm by making fires in these places
during the winters. Furthermore, the report expresses
the notion that low income indicates poor quality of
housing with problems regarding heating systems,
inadequate electrical wiring not suitable for excessive
load, and malfunctioning plumbing issues. The report
then goes on to state that a household with a lower
income is considered less likely to invest in fire
prevention devices such as smoke detectors, which
decreased the number of deaths caused by late night
fires by 25% between 1980 and 1990. The risks caused
by overcrowded housing in poorer facilities is then
discussed to be a fire hazard due to the expected wear
and tear of appliances and larger numbers of possible
victims in need of rescue. Lastly, the factor of undereducation is linked to minorities less likely to be exposed
to public fire safety education and less likely to read
warning labels due to lower literacy rates (SFIF). The
eighth grade graduate, CC315, fits into these studies
because she more than likely received support from
Andrew Johnsons low income and resided in an
underprivileged neighborhood.
CC315 would be admitted into the Burn Center
MedStar Washington Hospital if she were a victim of
severe burns today. Similar to the Casualty Hospital that
admitted patients who could not afford treatment,
MedStar ensures to provide quality care to patients
underinsured or uninsured (About the Burn Center).
Depending on her conditions, her treatment at MedStar
could consist of retaining fluids through an IV to prevent
dehydration, pain relievers such as morphine and antianxiety medications, decompression for blood
circulation, tube feeding for nutritional purposes,
breathing assistance, skin replacement or skin
reconstruction, physical therapy for burns that may
cover bone joints, and trustworthy penicillin antibiotics
(Diseases and Conditions). Penicillin had been
discovered years before Holmess hospitalization.
However, the antibiotic was not yet made onto an
industrial scale (WW2 Burns Survivor). Therefore, if
Holmes had survived her accident, she would have faced
amputations of bacterial infected body limbs.
CC315s story remains significant because there is a

possibility that individuals currently living in settings
similar to CC315 could die from similar influences. When
taking into consideration the predicaments of those who
cannot afford healthcare or a good quality of living, the
scenario is destined to repeating itself. Modern society
must continue to search for solutions to address these
problems and provide better outcomes for people like
CC315.
References
About the Burn Center at MedStar Washington Hospital

Center. MedSeek. MedStar Health, n.d. Web. 4 Jul. 2015.
Abrams, Amanda. Southwest Waterfront: A Neighborhood
Where a Change is Gonna Come. UrbanTurf. Urban Turf LLC,
02 Dec. 2010. Web. 3 July. 2015.
Burns Fact Sheet. National Institute of General Medical
Sciences. U.S. Dept. of Health and Human Services, n.d. Web.
02 July 2015.
Diseases and Conditions: Burns. Mayoclinic. Mayo
Foundation for Medical Education and Research, n.d. Web. 4
Jul. 2015.
Historical Census of Housing Tables. U.S. Census Bureau.
Housing and Household Economic Statistics Division, 31 Oct.
2011. Web. 06 Jul. 2015.
Nelson, Cary. About the Great Depression. The Great
Depression. University of Illinois, n.d. Web. 02 July 2015.
Pohl, Robert. Lost Capitol Hill: Casualty Hospital. The Hill Is
Home. The Hill Is Home, 27 Sept. 2010. Web. 03 July 2015.
Shea, Taylor. 11 Surprising Home Remedies for Burns.
Readers Digest. Readers Digest Association Inc, n.d. Web. 8
Jul. 2015.
Skin Grafts. Brought to Life. Science Museum, n.d. Web. 02
July 2015.
3
The Backbone
The Story of CC331

Jordan Mitchell1,2
Jordan R. Howard1,3
1Summer

2Department of Biology, University of Maryland: College-Park
3Department of Biological and Physical Sciences, South Carolina State University
Editors Note
Born in the year 1915, CC331 was a colored female
races within the same room or serve the two races
native to the southern state of Georgia. The name of her
anywhere under the same license. (NPS)
mother, father, and other relatives are unknown,
These laws denied African Americans from various rights
however she did have a sister whose information was
that they deserved. It was not until 1965 until these laws
documented. Times were very rough for African
were made illegal throughout the United States.
American families because discrimination against black
In addition to dealing with a racial war of segregation
communities in Georgia was prevalent. Being that CC331
and inequality, CC331 also lived during World War II.
lived in America during this time of widespread racial
Taking place between the years 1939-1945, the effects of
imbalance, she more than likely was not born to family of
World War II were emotionally and physically damaging.
wealth. As many African Americans suffered from
During this time, over 2.5 million black men registered
countless acts of segregation and prejudice between
for the draft. Aside from casualties stemming from direct
1882-1930. Over 458 blacks were deprived of their right
combat, external situations also occurred which caused
of citizenship, and denied admission to various public
distress in peoples lives. One of the most notable
settings including restaurants, hotels, and professional
external situations was the utilization of concentration
societies.
camps by the Nazi to prosecute the Jewish people. World
During this time, Jim Crow Laws provided a strong
War II affected peoples lives in a negative way because
support system for this reoccurring racial injustice
the resulting carnage and distress it created left many
preventing African Americans from establishing and
people homeless and burdened with monumental costly
developing relationships with people not of color. For
damage. Although this might not have affected CC331
example, specifically in Georgia:
personally, there is a high possibility that one of her
It was unlawful for a white person to marry anyone
family members might have served in the war. However,
except a white person[an] officer in charge shall not
this information is unknown.
bury, or allow to be buried, any colored persons upon
Most schools in the south during this time
ground set apart or used for the burial of white persons...
period were very segregated as there were separate
[or even] all persons licensed to conduct a restaurant,
schools for both black and white students. It is also
[were only to] serve either white people exclusively or
unspecified the length of time in which CC331 lived in
colored people exclusively and shall not sell to the two
Georgia. In 1930, Georgia spent about $43 per person for
CobbResearchLab.com
49
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a white student, but only spent $10 for a black student.
segregation during the 1940s in the south served as a
From this it can be assumed that CC331 did not get as
barrier between blacks and access to healthcare. A
great of an education as her white counterparts. CC331s
possible reason why CC331 might have chosen to
education may also have been affected by her lower
relocate to Washington D.C. was probably because it was
cultural capital. Cultural capital refers to the relationship
the only location closest her with a hospital that openly
of ones socialization and cultural activities. Examples of
served people of color.
aspects that can be considered as cultural capital include
For decades, African Americans have had the worst
interest in the art of music, literature and histrionics
health care, the worst health status, and the worst
(Matthijs
CC331s
health outcome of any racial or ethnic group in the
circumstances might not have granted her access to such
U.S (Byrd). Most treatment was biased and unfair until
opportunities, it also might have had regressive impact
more black individuals became physicians and other
on the advancement of her education.
healthcare professionals. It was not until after 1965
and
Kraaykamp).
Because
Later in her life, CC331 and possibly her family moved
when black health care began to improve.
to Jacksonville, Florida. She lived on 1126 Duvall Street.
In the 1940s, there was a lack of various treatments
Unfortunately, racial discrimination in Florida was no less
and health. Equally prevalent in both males and females
common than in Georgia. Blacks dealt with white
and generally occurring in people twenty-five and
supremacy and racial dismay on a regular basis. In fact,
younger, diabetes mellitus ketoacidosis (DKA) is a form
Florida led the nation in the highest number of lynching
of metabolic acidosis that is the result of a lack of
per capita. Massive attacks on the black community
glucose in the body and can be identified as chronic or
occurred on November 2, 1920 and in Rosewood on
mild. When there is insufficient glucose in the body, the
January 1923. These attacks resulted in the burning
body begins burning fat, muscle, and liver cells, and
down of many African American homes. The exact date
using them as a means to obtain the necessary amount
and time in which CC331 relocated to Jacksonville,
of energy required for daily activity. Because of glucose
Florida is undetermined. No matter where she moved or
insufficiency, substances known as ketones produced by
lived, there is a strong possibility that CC331 faced
oxidation begin to develop within the body. The
hatred from people not of color simply because of her
presence of ketones leads to problems such as an
skin color.
increase in blood sugar, which can disable the kidneys
As CC331 progressed through life, she lived a life as a
from retaining extra sugar. Dehydration is the result of
transient worker, traveling around from place to place
ketones in the urine and can make urination
doing small jobs. Her skill level as it pertains to job
immoderate. This excessive urination may cause loss of
qualification is unknown. After once upon a time residing
vital body fluids and essential elements such as certain
in both Georgia and Florida, CC331 eventually made her
salts and potassium. Ketone buildup in the body can
way to Washington DC. Although there is no solidified
cause the body to become poisoned because of the
justification for her relocation to DC, it can be assumed
acidity it causes.
that this second known move might have been in search

of better work opportunities.
type 1 or type 2 diabetes, but is more likely to affect
Unfortunately, on June 20th, 1944 at the age of

twenty-nine,
died
of
diabetes
those who have type 1. Symptoms include low blood
mellitus
sugar, high fever, lack of insulin, confusion, lethargy, dry
ketoacidosis at Freedmens Hospital in Washington D.C.
skin, acetone breath, extreme thirst, frequent urination,
Freedmens Hospital, now known as Howard University
vomiting, abdominal pain, low blood pressure, general
Hospital was founded in 1862 by Dr. Daniel Hale
weakness, increased heart rate, difficulty of and or rapid
Williams. The enforcement of the Jim Crow laws and
breathing, increased heart rate, and loss of appetite.
CobbResearchLab.com
CC331
DKA has the potential to affect anyone with either
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The Backbone
People at risk include those who have experienced heart
treatments of disease.
attack, stroke, trauma, stress, alcohol abuse, or who
It was not until the late 1940s when insulin syringes
smoke. DKA can cause shock or even death if left
became available, which was after CC331 had died.
untreated. Although deadly, this disease can be treated,
Today, there are better treatments for diabetes and
with the proper health care. Methods of treatment are
people have better control over their sugar levels. Back
usually the introduction of sodium bicarbonate into the
then African Americans did not have healthcare or any
body, fluid replacement, or insulin administration
means of paying for treatment unless they paid for it
intravenously, which is also known as insulin therapy.
themselves. If so, it was very hard for an African
Although these treatments are beneficial, they also have
American to get medical treatment unless it was at a
side effects and potential complications such as low
hospital run by black individuals. Currently, the United
blood sugar, low potassium, both pulmonary and
States has Medicaid, which is health insurance to aid
cerebral edema, seizure and cardiorespiratory arrest.
people that are not as wealthy, such as CC331. Also,
These treatments are very beneficial because they
under the Affordable Care Act, passed on March 23,
help to prolong the lives of people with this illness, but
2010, African Americans now have better health care
prevention and self-awareness of health is better. People
coverage, quality, and financial security. Because of this
that already have diabetes are more prone to DKA.
act, there are less health care disparities and fewer
However, there are ways to help prevent individuals with
African Americans are uninsured.
type 1 or type 2 diabetes from progressing to this
Diabetes was rare among the African Americans
horrible disease. Small anatomical and physiological
population before the 1940s. During this decade, a
maintenance such as staying hydrated, monitoring blood
connection was made between diabetes and the long -
sugar levels, injections of an acting form of insulin,
term complication of kidney disease. In 1936 diabetes
consumption of sugar free fluids, and awareness of
was divided into groups based on insulin sensitivity, but
certain
Reliable
there was no clear distinction of the type until 1959.
examinations to help in the detection of DKA include
There may have been a possibility that even if CC331 had
arterial blood gas, potassium blood tests, amylase blood
access to treatment, there would not have been a
function tests, serum electrolytes, blood testing strips. In
solidified conclusion as to whether or not the disease
the case of Willie Mae, it is more likely that she suffered
stemmed from insulin dependent or non-insulin
from type 1 diabetes and it developed into to
dependent diabetes. She also did not have the chance to
ketoacidosis. Chest x-rays, an electrocardiogram, CT
receive aid from oral drugs that would have helped
scans of the brain, and urine analyses are also utilized to
lower her blood glucose levels due to the fact that these
check for the presence of this illness. Because of
drugs were not introduced until 1955.
infections
are
helpful
methods.
disadvantages, such as finances and racial inequality,
Today, there are thousands of new treatments and
CC331 probably did not have access to some of these
medical breakthroughs for diabetes, specifically for
methods of testing for the presence of this illness. In the
Diabetes Mellitus Ketoacidosis. If CC331 were still living
case of the CT brain scan, it had not been invented at the
today, she would be better off and most likely lived a
time.
healthier lifestyle. In America today, there are more
A lot has changed since CC331 has died, especially the
resources available for African Americans that they did
rights of African Americans and the abolishment of
not have access to in the past. If she had the proper
segregation. Although there is still racial prejudice in
treatment and was able to control her sugar and insulin
todays society, it is not as prevalent as it was during the
levels, she could have lived longer than twenty-nine.
1920s-1940s. African Americans have access to better
Also, CC331 might have been able to find better work
health care and there is more advancement in
other than being a transient worker. She would have
CobbResearchLab.com
51
The Backbone
The Story of CC437

Rachel Davalos1,2
Mariela A. Martnez1,3
1Summer

2College of Arts and Science, Florida Gulf Coast University
3Department of Natural Sciences, University of Puerto Rico at Cayey Campus
Editors Note
Understanding the society, era, economy, and political

status of the people during their lifetime is an essential
part of understanding someones history. The W.
Montague Cobb Research Lab is a key component in
understanding history as a result of the research being
conducted. They are advancing the development of
scientific, anthropological and biological knowledge.
They involve a combination of these disciplines to
advance their knowledge. This is achieved by obtaining a
variety of cadavers, with the main objective to study the
impact of the death of that particular person due to their
race and social status in their society in that time frame.
Research like this allows us to profoundly understand
physiological, mental, economic, cultural and
geographical details that affect a specific individual.
Ancestry.com is a website that serves as a primary
source in the recollection of data from the National
Archives and the 1920 Census of a citizen named CC437.
Due to the fact that the 1920 Census was the
fourteenth Census conducted in the USA there are some
details lacking that we would be able to find in todays
Census. They were not particularly detailed in the
information like exact address or date of birth, but
instead it focused on name, occupation, race, place, and
literacy. During this same time period there were many
changes going on in the nation, the 19th amendment
was passed and even though it didnt give the right to
vote to Southern African Americans due to their legal
status, it was a start. The Harlem Renaissance also began
in this time, it was the explosion of art, culture, and
social interest (The Harlem Renaissance). There was a
large amount of change happening with the African
American population.
CC437 was described as a Negro female that is thought
to be born around the 1890s right in at the start of The

Progressive Era of the United States. She was found to
have lived in Maryland her whole life. Both of her
parents were born in Maryland meaning that she
probably had family in the area. She seemed to be stable
in the sense that she didnt have a major move or change
in environment. When she moved, it was from areas that
were not very far from each other. From the census of
1920 there was a lot of information given to us about
CC437. In the census we found out that she was
educated because they mention she could speak English
as well as read and write. Her occupation in 1920 was as
a laundress, where she was part of the economical and
racial disadvantage, since this in that time was a
common job for African-American women. Out of all of
the African American women in the 1920s
approximately 1,500,000 were working gainful
occupations. Specifically there were around 280,000
laundresses at this time. Agricultural jobs were more
common having around 400,000 women working
gainfully and then 350,000 working servantly. Typically, if
one was not working in an agriculturally based job, one
was either a servant or laundress. Historically, it was a
poorly paid job requiring hard work and labor.
Additionally, this occupation was about 75% of the work
African American women did during this time period to
earn a living. Many sources stated that a large amount of
laundresses were employed in private homes. The
overworking of many laundress lead to The New Deal,
which helped those paid extremely poorly to have a
standard minimum wage. This also implemented a
maximum of 40 hours per weeks. These workers typically
worked for 14 to 30 cents an hour (Adna Hill 110-113).
CC437, in 1920, lived as what was called a roomer. This
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meant different people were living in the same home

with many people who were not necessarily family. She
lived at the time in Maryland on a street named Cookey
Court just 40 miles from the center of District of
Columbia. CC437 lived with three other people with the
names of Edward Alexander, Marble King, and Raymond
Proctor. They each had different lives but convened
together when it came to paying the rent for the house.
Alexander was 38 years old at the time of the census and
worked as a cement mechanic; he was the head of the
house he rented. In the census they mention he could
not read or write. King was 24 at the time, married, and
a laundress just like CC437 and was also able to read and
write. The last person, Proctor, was a 30 year old
divorced driver who was able to read and write (All 1920
United States Federal Census Results). This lifestyle is
one which can be interpreted as lack of economic
stability or in need to be close to their jobs; therefore
have to agglomerate many people in the same place in
order to survive. We imagine that she lived in this home
to be near her employer and get the best advantage.
CC437 had died at a very young age approximately
fifty- four years old. It is said to be at an early age
because life expectancy in the USA in 1951 was
approximately 71.4 years according to the website "Life
Expectancy in the USA, 1900-98." At the time of her
death she was a resident at 1876 M Street N.W. District
of Columbia, USA. She had died at the Gallinger
Municipal Hospital Psychopathic Ward on January 26th
of 1951. We propose that she had been going in and out
of the hospital since she was 28 years old since could not
find any more information about her after the 1920
census because it could be possible that they didnt take
into consideration people with mental illnesses or in a
mental ward during the census.
The cause of death of CC437 was respiration
obstruction as well as food aspiration. She died at an
early age of 54. Typically, people who experience this life
-threatening situation are experiencing a solid that is
lodged in the trachea preventing breathing or swallowing
leading to asphyxiation. Without assistance and
immediate attention this situation will result in death.
The close to complete obstruction of the airways would
cause immediate death but other smaller items could be
swallowed and stuck in your esophagus. These items
stuck in your esophagus or in other parts of the digestive
system could lead to infection if not extracted in time
causing severe pain or even death. (Warshawsky) She
was a psychiatric patient; we imagine that her mental
state was highly severe and she may not have been able
to ingest food or medications by herself. If she was
mentally capable, then it is assumed that she was

neglected care when she needed assistance.
The hospital where CC437 died at was commonly
known as Gallinger Hospital or officially known at the
time as Gallinger Municipal Hospital Psychopathic Ward.
This was located in the District of Columbia. This hospital
had later on changed its name to be District of Columbia
General Hospital in 1953. Then, after 2001, the area
where the hospital was located had changed into a
health campus with a variety of clinics. They offered
everything from women services to a detoxification
center. This hospital had been serving people for over
200 years ever since 1806. It was originally an infirmary,
later turning into an asylum. In 1922, the building where
CC437 was treated was built (Historic Medical Sites in
the Washington). From what we interpreted, due to the
time frame the hospital was open; there was segregation
between blacks and whites in the population. Due to this
fact, she may have not had the best care or attention she
needed at the time. The hospital may have had too many
patients while lacking attentive staff, causing the patients
to lack quality care. It could have been possible if there
was more staff maybe this tragedy wouldnt have
happened to CC437.
We were comparing CC437s hospital Gallinger to
another psychiatric institution that was in the same area
at that time. It could have been possible that if CC437
had been a patient of St Elizabeths Hospital she may
have had attention quicker and would have survived her
cause of death. The hospital was known for their
advanced technology since it was the first psychiatric
hospital in USA, which opened in 1855. This hospital
cared for thousands of patients in 1950s around the
same time Mahoney was hospitalized. In fact it provided
health care for mentally ill residents of the District of
Columbia, U.S. Army and U.S. Navy (Historic Medical
Sites in the Washington, DC Area).
Patients with mental illnesses were treated very
different from modern times. It was possible that CC437
had suffered electroshocks, hydrotherapy, metrazol
convulsion and insulin shocks which were very popular
methods in 1930s, the same time we believe that she
was hospitalized. Later in the 1950s, doctors used only
artificial
fever
therapy
and
electroshock.
Electroconvulsive therapy (ECT) is defined by Mayo Clinic
as a procedure in which electric currents are passed
through the brain, intentionally triggering a brief seizure.
ECT seems to cause changes in brain chemistry that can
quickly reverse symptoms of certain mental illnesses. It
often works when other treatments are unsuccessful.
Much of the stigma attached to ECT is based on early
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treatments in which high doses of electricity were

administered without anesthesia, leading to memory
loss, fractured bones and other serious side
effects. Patients described this as a horrible treatment
that put them at risk for further physical trauma.
We have concluded that if CC437 lived in modern day
society she may have had a longer life than what she had
experienced. With hospitals such as Psychiatric Institute
of Washington with services for adults, she could have
had intensive short-term care that treats disorders such
as depression, schizophrenia and bipolar disorder. In
modern day society there are many qualified psychiatrist
that she could have gone to diagnose her mental illness
and consider possible treatments. With better resources
and higher staff to patient ratio, CC437 would have hand
more consistent and effective treatment in this modern
day. In the last several decades there have been many
new changes and advancements in understanding and
treating mental illness. We now have a better
understanding of the brain as well as technology to see
the brain like MRI. In the 1950s the era of over the
counter drugs for treatment mental illnesses was just
starting and obviously the poor could not afford those
medications. Many patients during that time were sent
to hospitals for care and spent years there which are
what we suspect happened to CC437. Besides this, many
people intentionally went to these hospitals as
alternatives to incarceration or homelessness. We
believe due to situations like CC437s, healthcare
professionals have learned to prevent problems like
respiration obstruction and food aspiration by being
attentive to inhibited patients during meal times. Its
highly probable that CC437 would have received better
and more urgent care now than in her time frame. It
could be possible that she could have died due to neglect
because of her skin color. We believe her cause of death
is becoming less of an issue in modern day due to the
amount of commoners who know CPR and the Heimlich
maneuver.

Web.
02
July
2015.http://www.crimeandjustice.org/
councilinfo.cfm?pID=54>.
"Historic Medical Sites in the Washington, DC Area - District of
Columbia General Hospital." U.S National Library of Medicine.
NIH U.S. National Library of Medicine. Web. 3 July 2015.
<http://www.nlm.nih.gov/hmd/medtour/dcgeneral.html>.
"Life Expectancy in the USA, 1900-98." Life Expectancy in the
USA, 1900-98. Web. 3 July 2015.
Rosenberg, Jennifer. "The 1920s - Historical Timeline of
Events." About Education. Web. 3 July 2015.
"The Harlem Renaissance." PBS The Rise and Fall of Jim Crow.
Educational Broadcasting Corporation, 2002. Web. 3 July 2015.
<http://www.pbs.org/wnet/jimcrow/
stories_events_harlem.html>.
"The Progressive Era (1890 - 1920)." The Eleanor Roosevelt
Paper Project. N.p., n.d. Web. 29 June 2015.
Warshawsky MD, Martin E. "Foreign Body Aspiration."
Medscape : Background, Pathophysiology, Epidemiology.
Medscape, 20 Nov. 2013. Web. 3 July 2015.
References
Adna Hill, Joseph. "Women in Gainful Occupations, 1870 to

1920 Pages 110-113." Google Books. United States
Government Printing Office, 1929. Web. 3 July 2015. Web.
Anderson, Mark, and Lynda Cannova. "50 Years of Mental
Health Hope and Struggle: 1957-2007." Council on Crime and
Justice. 2005. Web. 3 July 2015. < Arnesen, E. (2007).
Encyclopedia of U.S. Labor and Working-class History. New
York: Taylor & Francis Group, LLC.
"Electroconvulsive Therapy (ECT)." - Mayo Clinic. N.p., n.d.
3
The Backbone
The Story of CC459

Jasmine Mack1,2
Ambra Palushi1,3
1Summer

2Department of Biological Sciences, Troy University
3Department of Family Science, University of Maryland: College Park
Editors Note
CC459 was an African American female born in

Washington, DC in the early 19th century (1901). CC459s
birth date and month are unknown. She resided on
Northwest Street in Washington, DC. The 19th century
was a time when African Americans had to adjust to their
newly found freedom from slavery (Maloney, Thomas).
Sadly, African Americans did not reap the full benefits of
being a citizen as whites did because of the lack of
progress made from the mid-1800s to the 20th century.
As segregation was at its peak, there was a significant
gap between people of color and whites.
African Americans were disadvantaged in areas such as
the job market, education system, and home ownership.
Facts reveal that about 50% of black men and 35%
percent of black women reported that they worked on a
farm as a laborer, however, only about 33% of white
men and 8% of white women reported to working on
farms as well (EHnet). According to the 1939 census
report, black women averaged a mean income around
$331.42 compared to the average pay of a white woman,
which was around $771.69, which was quite a notable
difference. Compared to the 1989 census report, black
women were making an average of $15,319.29, which
was a dramatic increase. However, they were still ranked
the lowest paid group of all.
Based on Integrated Public Use Microdata Series
Census 1900 and 1990, a vast number of African
Americans were involved in jobs that did not require
much skill because they were undereducated. A vast
CobbResearchLab.com
number of African American children had not even

attended school. On the other hand, the white children
had more than likely attended a school and would
continue their studies in college. The percentage of
whites attending school almost doubled those of African
Americans.
African Americans also did not have the privilege of
home ownership. Typically an average African American
family lived and worked on a farm owned by whites.
Unfortunately, only about one-fifth of African Americans
owned their own homes, which was less than half the
percentage of whites. As these facts show, African
Americans were not treated with equality among whites.
Unfortunately, CC459 developed degeneration of the
spinal cord. Spinal degeneration affects the spine, brain,
and nerves. CC459 received an autopsy on February 4,
1952, which confirmed that she suffered from this
disease. She also suffered from encephalomalacia, which
is the softening of the frontal lobe in the brain. Spinal
degeneration is the result of a lack of vitamin B12 in
ones diet. Diagnosis of vitamin B12 deficiency is typically
based on measurement of serum vitamins. A test known
as Schilling test is used in order to test for vitamin B12
deficiency. Based on research, spinal degeneration
overall lead to CC459s encephalomalacia. Symptoms of
encephalomalacia include headaches, terminal coma,
blindness, severe head spinning, or lack of movement
coordination.
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We were unable to locate CC459s information on any

census reports; however, we can assume that she lived
with someone else. The recession may have caused a
lack of resources as well. We are uncertain if CC459 had
an occupation. However, if she did work, research
suggests that maybe CC459s work life could have
contributed to her illness. According to EH.net, there was
a great need for cheap laborers for Northern employers.
More than likely, CC459 decided to join the workforce as
a laborer in order to earn an income. Although research
does not include the kind of environment CC459 may
have worked in, other facts suggests that CC459 could
have worked in an atmosphere that requires a
tremendous amount of manual labor such as lifting,
bending, and twisting. Actions such as these could have
caused her condition to worsen over time. These
working conditions may have eventually contributed to
her death.
Vitamin B12 is gained by consuming foods such as
beef, liver, and most dairy products. CC459s diet may
have lacked these items. This deficiency of vitamin B12
leads to the abnormal buildup of fatty acids primarily
around the spinal cord, but it could also affect the brain
and peripheral nerves. The buildup of fatty acids causes
the areas to become softer and the areas begin to lose
their stability. Some symptoms of this spinal
degeneration include abnormal sensations such as
tingling or burning, sleepiness/drowsiness, change in
mental state, depression, and decreased vision.
CC459 checked into Freedmans Hospital in
Washington, DC to receive medical attention.
Freedmans Hospital, which was controlled by the
federal government, became the first hospital to provide
medical care for former slaves after its founding in 1862
in Washington, DC. This hospital became a refuge for the
majority of disabled, aged, and freed African Americans.
Poor whites were also going to Freedmans Hospital to
receive medical attention. Unfortunately, Freedmans
Hospitals leadership team, in the beginning, was
involved in several malpractices and misconduct. These
acts were very common in low-income hospitals. The
malpractice cases consisted of being charged with using
the hospital service for selfish gains, along the lines of
neglect and even embezzlement. Despite these awful
circumstances, a few doctors and nurses working in this
hospital continued to help serve the poor by providing
treatment whenever possible. Soon states ruled that
hospital care should be provided to everyone. In 1990,
CobbResearchLab.com
there were about 40 black hospitals operating across the

country.
Freedmans Hospital was relocated from 13th and R
Streets in Northwest Washington, DC to Bryant and 6th
Street in 1909.
The older building still stands today and it is now
known as the Howard Universitys School of
Communications. In order to preserve the history of the
building, it has yet to be completely remodeled, with old
hospital rooms still being located in the basement. As
for the new facility, it houses 278 state-of-the-art beds,
which attracted many potential administrators. One of
those administrators was Dr. Charles Drew who is well
known for his exceptional blood plasma research. Dr.
Drew eventually gained a leadership role and he
successfully ran the hospital from 1941 until 1950. The
hospitals reputation was remarkable and it continued to
grow in size (Freedmans Hospital/Howard University
Hospital). CC459 most likely visited this hospital because
of how close it was to her home. CC459 was likely to
have passed from degeneration of the spinal cord as a
result of inadequate treatment or lack thereof. Through
research, its unclear whether CC459s death occurred
due to failure of administering treatment on the
hospital's behalf, affordability on her behalf, or
availability/existence of treatment options during this
time period. Sadly, CC459, age 51, passed away at
Freedmans Hospital in the year 1952.
Societal conditions during CC459s life are significantly
different than modern day society. Today, African
Americans are able to enjoy the luxury of having
opportunities to advance, such as through higher
education and availability of resources. According to Fast
Facts, between 2000 and 2012, the percentage of college
students who were black rose from 11.7 to 14.9 percent.
Due to education, African Americans are able to
compete in the workforce through accomplishments
such as owning businesses, teaching, working for
congress, in the healthcare field, and in a variety of other
employment sectors. According to the 2012 U.S. Census
Bureau report, a resounding 64% of African American
women worked in white collar and 50% of African
American men held white collar jobs. Today, home
ownership is available to all who can afford it regardless
of race and gender. According to the 2012 U.S. Census
Bureau report, African American home ownership has
decreased from 46% to 42.5% between 2005 and 2012.
This could have been contributed to the housing crisis,
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which caused many Americans to lose their homes due to

foreclosure.
Unfortunately, in modern day society, all Americans do
not have access to healthcare and cannot receive the
treatments offered now. According to FastStats 2012
report, the percentage of African Americans under the age
of 65 with health care was 17.8%. Sadly, these people
could be in the similar situation as CC459. Those
individuals fate could be the same as CC459s if left
untreated.
Interpreting the facts found through research, it shows
that CC459 was born in a time period where blacks were
not treated as citizens, but rather foreigners. CC459 had to
work in an unsafe environment with low pay in order to
survive. CC459s illness may have been the result of an
accident on the job that caused severe head trauma. We
can assume she continued to work in order to sustain a
standard of living, which led to negative progression of her
health problems. We presume that by the time she took
measures to see a physician her illness was rather
irreversible.
More than likely, if CC459 lived today, she would have
received treatment for her spinal degeneration and
encephalomalacia. In present day, CC459 may have
endured a better standard of living where she would be
presented with educational or employment opportunities
that do not require intensive manual labor. Today, there
are treatment options available such as physical therapy
or spinal surgery. If she were a member of society today,
under good conditions, the likelihood of her developing
this illness would be very low. Overall, CC459 would have
been able to enjoy a less stressful life by being provided
with more opportunities to advance in modern society,
therefore leading her to live a healthier lifestyle and
prevent her tragic illness.
References

Encephalomalacia: Symptoms, Causes, and Treatment.
http://www.buzzle.com/articles/ encephalomalaciasymptoms-causes-and-treatment.html
Foods Highest in B12. http://nutritiondata.self.com/foods
-000116000000000000000.html
Freedmens Hospital/Howard University Hospital. http://
www.blackpast.org/aah/freedmen-s-hospital-howarduniversity-hospital-1862
Historic Medical Areas in Washington, D.C. Area. http://
www.nlm.nih.gov/hmd/medtour/howard.html
J Craniofac Surg. 2011 Nov;22(6):2374-5. doi: 10.1097/
SCS.0b013e318231e511.
Maloney, Thomas. African Americans in the Twentieth
Century. EH.Net Encyclopedia.
Robert Whaples. January 14, 2002. URL http://eh.net/
encyclopedia/african-americans-in-the-twentieth-century
National Center for Education Statistics. http://
nces.ed.gov/fastfacts/display.asp?id=98
Spinal Degenerative Disease. http://
neurosurgery.med.miami.edu/clinical-subspecialties/thespine-institute/spinal-degenerative-disease
Subacute combined degeneration. http://
www.nlm.nih.gov/medlineplus/ency/article/000723.htm
U.S. Census 2012 American Community Survey. http://
blackdemographics.com/households/housing/
CDC/NCHS, National Health Interview Survey. 2012.

http://www.cdc.gov/nchs/data/series/sr_10/sr10_259.pdf
Census ACS 2012. http://blackdemographics.com/
economics/employment/
Corinna Underwood. Schilling Test. http://
www.healthline.com/health/schilling-test#Overview1
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RECENT ABSTRACTS Validation of Cobb Collection Biohistories
The Backbone
Recent Abstract from the Cobb Research Lab
Validation of Cobb Collection Biohistories

Davlyn Hollie1,2
1W.

2Department of History, Howard University
The Summer Medical Dental Medical Education Program, (SMDEP) scholars from the 2015 class of the
Howard University site conducted hands-on interdisciplinary bio-anthropological and biomedical research
on the 19th and 20th century human skeletal and dental remains, artifacts of the Cobb Collection (CC). For
publication in The Backbone, these scholars reconstructed and presented a case studies on the culture,
health, lives and deaths of selected individuals in the CC. The purpose of this research is to validate the nine
CC Biohistories prepared by the students of the SMDEP summer program. The cases were lightly edited , as
the Social Science research group decided to confirm all subjective information before publication. The
three History Majors in the W. Montague Cobb Research Lab (CRL) Social Science Committee were
assigned a total of three cases. This validation of this information provides an additional experience to the
SMDEP students and an opportunity for the history students to conduct primary research. Furthermore,
this provides a robust framework for the completion of biohistories for the entire Cobb Collection.
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RECENT ABSTRACTS The Cobb Research Laboratory and Increasing STEM-affiliated Students
How the Cobb Research Lab succeeds in increasing the number of STEM and STEM-affiliated Students
Sherese Taylor1,2
1W.

of Sociology and Anthropology, Howard University
2Department
While research indicates an under-representation of African Americans and women in STEM (Science,
Technology, Engineering and Mathematics), programs that mediate the problem have not been
significantly effective. However, minority-serving institutions have been leaders in increasing the number of
minority participants in STEM fields, particularly the W. Montague Cobb Research Laboratory at Howard
University. The W. Montague Cobb Research Laboratory succeeds in their recruitment efforts because of
the sociological insight provided to African American undergraduate STEM majors. The research will aim to
understand how this insight is used to effectively recruit African American undergraduate STEM majors.
Using participant data, a longitudinal study was conducted from 2014-2016 to investigate the levels of
student participation in research and learning. The data is anticipated to indicate that a combination of
purely scientific thought and sociological insight, if it aligned with their identity, increases the likelihood of
African American undergraduate students participation in STEM fields and further in graduate and
professional school.
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RECENT ABRACTS Investigation of the Cobb Collection, A Statistical Approach
Investigation of the Cobb Collection, A Statistical Approach

Nicholas Guthrie1,2
1W.

Health disparities for African Americans (AA) include differences in rates of cardiovascular diseases,
diabetes, periodontitis and life expectancy. In addition, populations living in poverty also exhibit health
issues including asthma attacks, obesity, and because a greater percent of Afro-descendant people
continue to live below the poverty line, a duality of risk factors exist for this population. The Cobb
Collection (CC) is an invaluable snapshot of AA medical history in the late 19th and early 20th centuries,
being the largest skeletal archive for AAs in the United States. Archiving numerous points of medical data
in a randomized fashion, the CC is a perfect candidate collection to compare pathology incident rates over
the last 150 years. The data points of the CC include cause of death, place of death with a corresponding
morgue number, death certificate number, age, sex, race, birthplace, maternal and paternal birthplace,
address, and duration dwelling in Washington, DC. This study aims to present the patterns of these AAs
from the Washington DC Area, including migration patterns and pathology incident rates. Once completed,
this data will be compared to patterns in the modern day to provide a historical background and make
inferences on medical progress and health disparities over the past 150 years.
1
RECENT ABSTRACTS
The Backbone
The Cobb Research Lab and SMDEP
Overview of the Interface of the Cobb Research Laboratory

and the Robert Wood Johnson Summer Medical and Dental
Education Program (SMDEP) at Howard University
Donna Grant-Mills, RDH, M.Ed., DDS1,2
1W.

2College of Dentistry, Howard University
The Summer Medical Dental Medical Education Program (SMDEP), funded by Robert Wood Johnson and
hosted by Howard University Colleges of Dentistry and Medicine provides 80 academically talented premedical and pre-dental students from under-represented groups with STEM based academic enrichment,
mentoring, clinical shadowing opportunities and cultural enrichment. The scholars conduct hands-on
interdisciplinary bio-anthropological and biomedical research on the 19th and 20th century human skeletal
and dental remains, artifacts, and publish in The Backbone, the official journal of the Cobb Research
Laboratory. Scholars are trained, paired with, and work closely with peer mentors, and senior scientists to
reconstruct and present case studies on the culture, health, lives and deaths of the individuals in the Cobb
Collection. The scholars that complete their research objectives and case studies are presented with a
certificate of meritorious research at the SMDEP Closing Ceremony. The value the collaboration is
multifaceted. First, for the majority of the 2015 cohort (82.5%), it was their first formal research
experience. Second, it connected the scholars to mentors in STEM and other disciplines thus providing
them with team based inter-professional experience which is the new gold standard for healthcare
delivery. Third, they gain more confidence in their ability to pursue future STEM based opportunities, and
fourth they gained a firm understanding of importance of approaching research with cultural sensitivity and
respect, by taking into account the socio- economics, history, racial climate, inequalities, and other factors
faced by the individuals of the Cobb Collection. As people of color, primarily African Americans, the scholars
gained a sense of ownership over and respect of their cultural legacy, and a sense of responsibility with
regard to how their ancestors are treated, studied, and documented for future generations.
1
The Backbone
RECENT ABSTRACTS
Analysis of DNA Extraction Techniques from Teeth
Comparative Analysis of DNA Extraction Techniques on DNA

yield from Ancient Teeth
Latifa Jackson, Ph.D.1,2
Christopher Cross, M.A.,2,3 Muneer Abbas1,4
1National
Human Genome Center, Howard University Hospital

3Department of Anatomy, College of Medicine, Howard University
4Department of Microbiology, College of Medicine, Howard University
2W.
While much reporting has been done to understand ancient DNA techniques for archaic human
populations, little work has been done to characterize the feasibility of extracting DNA from historical
populations of humans who lived less than 200 years ago. Here we examine three methods for DNA
extraction from skeletal remains using CC672, an individual from the W. Montague Cobb Skeletal
Collection, who died 85 years ago. Dentine-cement powder was obtained from molar teeth. Molars were
scraped free of cementum (CC), calculus (CL), and periodontal ligament (PDL). Each was isolated separately
and then the remaining CC, CL, and PDL debris was combined in a mixed sample (MX). Extraction was
conducted using Oragene (saliva based), Qiagen (blood and tissue), and phenol-chloroform. These
techniques were implemented in parallel. Extractions were then measured for DNA concentration,
confirmed for DNA quality and finally amplified to further assess DNA viability. We were able to recover
DNA from all three methods in all samples. The phenol chloroform extraction yielded the largest DNA
amounts (138.2-1865.6 ng/L), next the Qiagen yielded between (12.7-13.9 ng/L for S samples, 6.5-9.7
ng/L for CC672 samples) and Oragene yielded intermediate DNA amounts (S5:75.5 ng/L and MX:21.2 ng/
L). DNA was amplified using the FOXP3 gene with 90% success. This molecular analysis suggests that
conventional extraction methods for ancient DNA are robust to analysis of Cobb Collection samples.
Amplification of the DNA extracted shows that human DNA was present in sufficient quality. This exciting
result will be followed up with further analysis.
1
RECENT ABSTRACTS
The Backbone
Geospatial Assessment of CC Individuals
Geospatial Assessment of Residential and Work Sites for

Cobb Collection Individuals
Hasan Jackson1,2
1W.

of Geographical Studies, University of Maryland
2Department
Due to the history of segregation in the Washington area it is likely that the populations of certain
neighborhoods were mostly uniform in terms of ethnicity. There may have also been important geographic
substructure by occupation as well, resulting in significant clustering of African Americans (AAs) from the
Cobb Collection (CC) individuals in the Washington DC region. Social status, occupation, education, and
affluence may also have contributed to the selection of neighborhoods and worksites. Communities with
lower socioeconomic status likely resided and worked in non-favorable neighborhoods with close proximity
to pollutants and increased distance from major roads. The residential and work settings of 19th and 20th
century CC individuals resulted in increased levels of exposure to pollutants for some neighborhoods
compared with others. Spatial analyses are used to understand the chemical and physical exposure
dynamics of Cobb Collection individuals in the District of Columbia metropolitan area from 1920-1960 to
environmental factors that could modify the gene expression patterns in 150 individuals. Specifically, this
research looks for possible signs of community segregation related to disease status, ethnic background
and occupation. The residences and worksites of CC individuals are mapped and the demographic,
genomic, and potentially epigenomic influences stratified horizontally across the Washington DC region.
Historical maps of the District of Columbia and its surrounding areas dated to the mid-20th century will be
obtained from databases of historical maps located in the National Archives as well as gathered from other
peer reviewed sources. The CC has address-based residential and occupational information on each
individual in the target population. These data will be used to provide a single reference location for each
CC individual under study. Residences will be geocoded based upon the historical maps of the region,
providing a latitudinal and longitudinal reference for each individual. The Cartesian plane of residences will
be ingested into a spatially referenced database. This will allow spatial comparisons to be made for each
residential point, the center for each residence (centroid) will be used, and at the level of neighborhood/
ward. Previous studies of spatial clustering in urban areas have used spatial aggregation of geocoded data
points to identify area level characteristics in studies of health patterns (25-28). ArcGIS 10.2 version (ESRI,
Redlands, CA) is used to perform geocoding tasks
1
The Backbone
RECENT ABSTRACTS
Minimally Invasive Method to Extract DNA
Minimally Invasive Method to extract DNA from Dentition

using Cobb Collection Human Skeletal Remains
Alexis Payne1,2
Christopher Cross, M.S.1,3, Latifa Jackson, Ph.D.1
John Harvey, D.D.S.4, Fatimah Jackson, Ph.D.1,2
1W.

3Department of Anatomy, Howard University
4College of Dentistry, Meharry Medical College
Teeth have been used as a source of DNA for identifying fragmented and degraded human remains.
Cellular cementum is collected and analyzed for DNA sequencing. Cementum is the outside layer of the
tooth that is located on the roots. The location of teeth within the jawbone makes them a great choice due
to the protection the bone provides. Teeth selection for extraction is based on studies of the anatomical
characteristics of teeth. Additionally, it is known that cellular cementum will be greatest on teeth with the
largest root surface area, like molars, premolars and canines. The extraction process of removing
cementum, however is not as widely understood. With the use of the Cobb Collections dental remains, a
new procedure for cementum extraction that grants preservation of the entire tooth has been developed.
The Cobb Collection provides a unique source of 19th and 20th century African American biological
histories. Cementum extraction and DNA sequencing of these individuals will support further subsample
studies on raw material of human remains. The procedure also supports oral microbiome analysis to
understand dietary habits and disease exposure in studied individuals. Cementum extraction through the
roots is a minimally invasive. It can provide critical information that can advance clinical science. Our
methodology re-engineers current clinical dental practices for research purposes by curvette removal of
plaque, calculus, cementum, and remnant periodontal ligament tissue. We have successfully extracted
dental-derived DNA from all of the aforementioned layers and are currently optimizing these procedures.
This technique both protects and makes use of the precious material for current studies and future
generations.
1
The Backbone
RECENT ABSTRACTS Causes of African American Osteoarthritis in the Cobb Collection
Trends and Causes of African American Osteoarthritis and

Osteoporosis within the Cobb Collection
Sierra Williams1,2
2Department
1W.

of Health, Human Performance and Leisure Studies, Howard University
Like many other health problems, the misconception that African Americans should not be concerned
about developing osteoporosis leads to African American women being under diagnosed and treated.
Statistically, African American women have a higher bone mineral density than European American women.
Bone mineral density represents the strength of the bone and the amount of calcium within the bone.
Degeneration and wear and tear on the bones will show aging in the bones, a sign of osteoarthritis. It is a
condition expected to be seen in the collection due to the lifestyles of the individuals. Within the Cobb
Collection we will be looking for the presence of osteoarthritis and osteoporosis likely caused by disease,
poor nutrition, inadequate physical activity, excessive thinness and being post menopausal. There are
increased risks of fracture and bone strength with those suffering from osteoporosis. By observing the
skeletal remains we will be able to recognize some of these conditions that may cause osteoporosis. From
our observations we hope to validate the presence of bone disease in the African American females of the
CC, though we anticipate the prevalence to be much lower than that of their white counterparts. This study
will focus on a subset of African American and European American post-menopausal women, who from
clinical and physical clues suggest evidence of bone disease. These groups will then be analyzed for
statistical significance using ANOVA/t-test. We hope to shed light on the need for further research in the
area of bone disease in African Americans.
1
RECENT ABSTRACTS
The Backbone
Osteoarthritis within the Cobb Collection
Evidence for Arthritis and Specifically Osteoarthritis in the

Cobb Collection
Maimouna Traore1,2
1W.

Arthritis is a chronic disease characterized as the inflammation of joints caused by the degradation of the
fundamental cartilage. The symptoms associated with arthritis are severe pain, swelling and stiffness
amidst the affected joints which can impede the motility of the affected individual. Consequently, arthritis
has risen as the main cause of disability amongst Americans. Although there are a multitude of forms of the
disease, one of the most common forms is osteoarthritis. Osteoarthritis occurs predominantly on joints
that endure the pressure of weight such as the knees and hips of the human body. Naturally, the risk of
acquiring osteoarthritis increases with age as the cartilage degrades over the course of several years.
Currently, between 10%-20% of adults are suffering from a degree of osteoarthritis in North America alone.
However, age is not the only variable with which the disease correlates. Studies analyzing knee
radiographics have shown that osteoarthritis has a greater prevalence amongst African Americans, more
specifically African American women. Therefore, the Cobb Research Lab intends to investigate the African
American individuals of the skeletal collection for evidence of osteoarthritis. The determined severity of the
disease in each case can give further insight into the identity of the individuals as it suggests age, physical
health and range of motility.
1
The Backbone
RECENT ABSTRACTS
Bio-Historical Analysis of Cardiovascular Disease
Bio-Historical Analysis of Cardiovascular Disease

in the Cobb Collection
Jameshisa Alexander1,2
1W.

Cardiovascular disease, commonly known as heart disease, consists of multiple complications involving
the cardiovascular system. People with medical conditions like diabetes and obesity and live lifestyles with,
poor diet, lack of exercise and high alcohol consumption are at increased risk for cardiovascular disease.
The greatest risk factors for cardiovascular disease are high blood pressure, high cholesterol and smoking.
The incidence and prevalence of CVD is directly related to the incidence and prevalence of CVD risk factors.
There has been an increasing prevalence of obesity from 15 to 30 percent between 1960 and 2000 and in
diabetes rising from 1.8 to 5.0 percent. However, some major risk factors like high cholesterol,
hypertension and smoking have decreased. The prevalence statistics show that high cholesterol has
decreased from 34 to 17 percent, hypertension from 31 to 15 percent, and smoking from 39 to 26 percent.
Even though the prevalence of some major risk factors have increased, the prevalence of CVD has
decreased. About 610,000 deaths occur in the United States every year is caused by cardiovascular disease
(CVD), making it the leading cause of death for both men and women. Cardiovascular disease is divided into
four main categories: heart valve complications (regurgitation and stenosis), arrhythmia, heart attack and
stroke. Atherosclerosis is the building of plaque in arteries commonly leading to heart attacks or strokes.
Physicians diagnose patients with these ailments based on risk factors identified from medical history,
physical exam and a variety of specific tests. These conditions are treated with medications, institution of
medical devices such as pacemakers, implantable cardioverter defibrillator (ICD) or Left Ventricular Assist
Devices (LVAD), procedures like heart value replacements/repairs, heart transplants, and surgery. In the
Cobb Collection (CC), we have multiple cases of cardiovascular disease such as congestive heart failure,
atherosclerotic heart disease, value issues and hypertrophy. Using the data collected on the individuals in
the CC, we can compare the trends and of cardiovascular disease previously and presently. This allows us to
examine this chronic disease from a unique historical perspective.
1
The Backbone
RECENT ABSTRACTS
Trends of Hypertension and Cardiovascular Disease in the CC
Historical Trends of Hypertension and Cardiovascular

Disease within the Cobb Collection
Janet Mansaray1,2
1W.

Hypertension is a current health issue that greatly affects the African American community. It is linked to
the cause of cardiovascular conditions such as rheumatic heart disease, arteriosclerotic heart disease,
hypertensive heart disease, cerebrovascular accidents (CVA), and inflammatory heart disease (carditis). To
investigate the progression of such conditions in African Americans and their evolution of treatment, we
will analyze these clinical manifestations within the Cobb Collection. In the database, the number of cause
of deaths for each condition found is as follows: rhuemeric-2, hypertensive-11, arteriosclerotic-23, CVA-17,
inflammatory-11, general cardiovascular diease-8, and those with a condition called myocarditis-6. This is a
total of 78 individuals revealing that hypertension and its related cardiovascular conditions was a problem
for African Americans, as it today. 5 individuals out of the 78 were chosen for case studies and their
biological histories were reconstructed. This information was then compared to modern profiles of African
Americans in order to observe whether modern treatments have affected the life expectancy within people
who suffer from cardiac disease. The main purpose of this study was to provide a historical prospective on
cardiovascular conditions caused by hypertension in hopes of seeing why such conditions are still prevalent
in African Americans.
1
RECENT ABSTRACTS
The Backbone
Biohistory of Congestive Heart Failure in the CC
The Prevalence and Biohistory of Congestive Heart Failure in

the Cobb Collection
Kayla Bedeau1,2
2Department
1W.

Congestive heart failure (CHF) is a common cause of death, affecting over 5 million people in the United
States in 2013. CHF occurs when the muscle of the heart weakens, failing to provide oxygenated blood
throughout the body. In the later stages, blood will pool inside of the heart, leading to complete failure.
Among others, hypertension is a major risk factor for CHF. Commonly known as high blood pressure,
hypertension is indicated when the systolic blood pressure and diastolic blood pressure are above 140
mmHg and 90 mmHg respectively. Hypertension continues to be a major health risk, especially in the
African American (AA) community where over 40 percent of AAs are affected. Because of this prevalence,
the Cobb Collection (CC) is an invaluable source, being the largest collection of AA archeological material in
the country. We have identified 36 individuals from the CC who have died from Congestive Heart Failure in
order to analyze their medical history and lifestyles. Then, a comparison of incidents and treatments
between the 1900s and modernity will create a better understanding of the impact that hypertension has
on congestive heart failure, while also contributing to the sparse amount of scientific literature on the AA
community.
1
The Backbone
RECENT ABSTRACTS
Factors of Diabetes in the African American Community
The Correlations between African-American Life Experiences

and Type 2 Diabetes
Whitney Griffith1,2
1W.

2Department of Computer Science, Howard University
The increasing prevalence of diabetes is considered problematic, as it is the seventh leading cause of
death in the United States. The CDCs 2014 National Diabetes Statistics Report states that in the US, 29.1
million people are living with diabetes out of which 13.2% (3,841,200) are African-Americans. Interestingly,
this number is approximately 1.7 times more than the number of diabetic whites in the US. Diabetes is a
disease that involves abnormal levels of blood glucose resulting from problems in how insulin is produced
or works. There are two types of diabetes, Type 1, which is caused by the destruction of the insulinproducing cells in the pancreas and Type 2, which is a result of insulin resistance among cells. Type 2
diabetes is described as a lifestyle disease as it develops due to specific risk factors in ones life. This
research intends to show that the prevalence of Type 2 diabetes among African Americans is not due to
personal life choices but that it results from the stresses society places on African Americans such as
residential, economic, and educational segregation. The Cobb Collection offers a special resource of the
study of African Americans from the 19th and 20th century. It is highly suited for this research as it contains
African Americans who were living in a time of Jim Crow Laws. Thus, individuals in the Cobb Collection that
were diagnosed with Type 2 diabetes can be identified and their lifestyles analyzed in an attempt to
indicate the environmentally- caused emotional, physical and nutritional stressors that contributed to their
development of Type 2 Diabetes.
1
RECENT ABSTRACTS
The Backbone
Cerebrovascular Accident within the CC
Prevalence of Cerebrovascular Accident within African

Americans of the Cobb Collection
Natalia Christian1,2
1W.

of World Languages and Culture, Howard University
2Department
In the African American community, cerebral vascular accident (or stroke) is one of the leading causes of
death. Hypertension causes approximately 50% of ischemic strokes, which are caused by a development of
atherosclerosis. Studies show that African-Americans have the highest rate of hypertension in the United
States. Stress can significantly contribute to the development of hypertension through recurrent blood
pressure elevation and stimulation of the nervous system to produce large amounts of vasoconstriction
hormones that eventually lead to elevated blood pressure. Socio-economical, sociological and
psychological factors coupled with familial history in the African American community contribute to the
development of this fluctuation in blood pressure and nervous response. From the clinical materials
available on the Cobb Collection, I will identify the individuals who reportedly died from ischemic stroke. I
will use additional resources to reconstruct the biological histories of a subset of individuals with stroke and
relating ailments. By performing case studies on the affected individuals in the Cobb Collection and delving
into their personal lives, the causes of hypertension and eventual stroke will be identified and placed in
historical context. This information will provide insight into the progression of modern day environmental
circumstances and treatments that have contributed to the clinical expression of cerebrovascular accident.
1
RECENT ABSTRACTS
The Backbone
The Resurgence of Rickets and Scoliosis
Assessment on the Resurgence of Rickets and Scoliosis on

African Americans
Khristian Ifill1,2
2Department
1W.

The purpose of this study is to identify and comprehensively assess the effects of scoliosis and rickets on
the African American community. Prior studies have shown that African Americans are at greater risk of
being diagnosed with scoliosis and are more susceptible to rickets as well. This increased risk factor for
African Americans stems from the decreased levels of vitamin D able to be synthesized by people of darker
skin complexions. By using the laboratory materials in the Cobb Research Lab, I will examine and analyze
subjects reported to have passed away from rickets and scoliosis. I will also use a multitude of various
resources such as scientific evidence, medical journals and the reports made by the Cobb Research Lab to
reform the biological history of specific groups of affected people. By analyzing these diseases in detail, I
will in turn develop a better overall level of understanding of the historical causes and treatments of
scoliosis and rickets and how they matriculated over time.
1
The Backbone
Recent Abstracts Effects and Treatment of Alzheimers in African Americans
Identifying the effects and treatment of Alzheimers disease in

African Americans
Youngho Jung1,2
1W.

The first ever recorded case of Alzheimers can be credited to Dr. Alois Alzheimer, a pioneer in linking
symptoms to microscopic brain changes. He describes the haunting case of Auguste D. in 1906, a patient
who had profound memory loss, unfounded suspicions about her family, and other worsening
psychological changes. After her death 5 years later, Dr. Alois discovered that her brain underwent
dramatic shrinkage and abnormal deposits in an around the nerve cells. Early discoveries regarding the
peculiar disease were initiated using the electron microscope, for example, to allow further study of the
brain. Beta-amyloid, a novel cerebrovascular amyloid protein and the chief component of Alzehimers brain
plaques and the trigger for nerve cell damage was discovered in 1984. Since then, major strides have been
taken to deterimine the genes responsible for Alzheimers disease. In 1991, a clinical study was launched by
the federal governments. This led to the new criteria and guidelines for Alzheimers disease diagnosis, and
in turn, paved the way for the first major clinical trial for the prevention of Alzheimers disease. But as with
much progress, there are still an estimated 5.3 million Americans with Alzheimers today, and more than
half are African Americans. What is most surprising is that, it wasnt until August 11, 2015, they discovered
the disease occurred much differently among patients from the European and non-European communities.
That convinced researchers to further investigate patients treated historically. The Cobb Collection is an
excellent site. Currently, I am attempting to elucidate the clear differences on how Alzheimers affects the
African-American community, and the mistreatment in turn to the patients that lived before our lifetime.
1
The Backbone
RECENT ABSTRACTS
Reconstructing Environmental Biohistory and Health
Lead in Teeth: Reconstructing Environmental Biohistory and

Health at the New York African Burial Ground Using Laser
Ablation-Inductively Coupled Plasma-Mass Spectrometry (LAICP-MS)
Joseph L. Jones, Ph.D.1,2
1W.

of Anthropology, College of William and Mary
2Department
The study of ancestral skeletal remains continues to reveal new dimensions and important details of
African diasporic biohistory. Teeth, for example, develop at known ages (through adolescence) while
incorporating environmental chemical exposures associated with forced migration, diet and health. Even a
single tooth crown formed over several years serves as an archive of childhood and/or adolescent living
conditions; biohistories potentially formed across varied African and American settings. Here, I report on
the recent analysis of enamel-lead for 44 children, women and men excavated at the 17th- and 18thcentury New York African Burial Ground in lower Manhattan. This study is the first quantitative
investigation of human lead exposure in early America via laser ablation- inductively coupled plasma-mass
spectrometry (LA-ICP-MS). This recently-developed microprobe methodology enables the spatial mapping
of lead concentration in teeth such that age-related changes in the extent and (acute versus chronic)
nature of exposure are detectable. Among the key findings, enamel-lead concentrations ranged from 0.39
g g-1 (i.e., the instrument limit of detection or LOD) to 14.7 g g-1, suggesting negligible (background
level) exposures for some while others spent their childhoods in high-lead environments. Mean enamellead concentration for young children (5.88 g g-1) is over five times that of adults (1.11 g g-1), a
significant difference reflecting these groups mostly American versus African geographic origins,
respectively. These findings shed new light on lead exposure and poisoning persistent public and global
health concerns at the origins of African America and the nation.
1
RECENT ABSTRACTS Elemental Determination of Soil Samples
The Backbone
Profile and initial elemental determination of soil samples

collected from the New York African Burial Ground Remains
Candice Duncan, Ph.D.1,2
1W.

Human Genome Center, Howard University Hospital
2National
Soil analysis is an important tool to understand the bioanthropology of human habitation and grave
locations. Analysis of metals, phosphorus and other molecules can build a portrait of the environmental
conditions in which populations of interest existed. The New York African Burial Ground and the W.
Montague Cobb Research Laboratory each contain numerous grave soil samples that can enhance current
understandings of the daily lives of these 17th and 18th century populations. The initial determinations on
the grave soil samples includes:
1. Determination of total soil mass collected. The one bag soil sample will be weighed, soil transferred
into a sealed glass container and cloth bag weighed. The cloth bag will also be transferred into a
sealed glass container for future chemical analysis.
2. A grab sample of X grams will be collected, and set aside in a sealed glass container, for future
chemical and microbiological analysis.
3. A sieving process will be used to determine the particle size of soil composition to classify soil
material (i.e. sand, silt, etc.).
4. A pictorial classification will be created to identify and separate all soil and non-soil (i.e. hair or
bone) materials with the remaining sample.
An EPA Method 3052 will be used for the acid digestion of the soil followed by atomic absorption (AA)
spectroscopy to determine the iron, lead, copper, magnesium, zinc, calcium and silver compositions of the
grave soil. These data will permit complex analytical chemistry assessments upon which we can construct a
rich portrait of the environmental toxins to which these individuals were exposed and identify possible
gene X environment interactions at this site.
1
The Backbone
RECENT ABSTRACTS
Analysis of Grave Soil Samples at the NYABG
Analysis of Grave Soil Samples found in the New York African

Burial Ground
Keely Clinton1,2
1W.

The New York African Burial Ground is the location of the greatest number of free and enslaved African
burials in a common place during the 17th and 18th centuries. It is speculated that the burial ground was
more than likely established by Negro frontier residents initially being called the Negroes Burial Ground.
The burial ground was specifically found on a lot in lower Manhattan (Block 154) surrounded by Broadway
to the west, Duane St. to the north, Reade St. to the south and Elm St. to the east, with important
landmarks such as Crolius pottery to the northeast and Collect Pond to the east, as early maps indicate.
Location must be taken into account as it determines the composition and condition of the grave soil
samples. In this study we are able to observe the origin of each grave sample, their orientation in relation
to each other, the depth at which the grave soil was obtained (between 6ft. and 25 ft.) and whether or not
there was an individual/ partial remains/ artifacts associated with each sample. We are also able to observe
the stratigraphic analysis based on differences in color and type of the soil and archaeological records.
Most of the 49 grave samples are derived from the Middle Group of the African Burial Ground. The Middle
Group is documented as the collection of burials located throughout the excavated site except north of the
fence line during the time the burial ground was extensively used.
1
RECENT ABSTRACTS
The Backbone
Access to Research on the ABG Materials
Enhancing Public Access to Recent Research on the African

Burial Ground Materials: Grave Soil and Oral Microbiome
Analyses
1W.

The 17th and 18th century samples in the Cobb Research Laboratory are derived from the New York
African Burial Ground remains currently housed at Howard University and on loan from the National Park
Service. The NYABG is the nations earliest and largest African burial ground. These previously buried
samples reflect African/African American biological diversity from the late 17th to late 18th centuries in
New Amsterdam/New York City. While there are an estimated 15,000 burials, we have well-documented,
archived biological remnants from approximately 250 individuals. Research on these 17th and 18th century
samples hold the key to providing evidence for important processes in human evolutionary biology and
biological history. For example, the grave soil studies will reveal the biological relationship between
individuals in various grave sites, the molecular sex of juveniles, the extent to which deceased individuals
were exposed to specific environmental toxins and certain pathogens, and their ancestry genetics. The oral
microbiome studies will yield insights into the dietary patterns of individuals, their exposure to certain
infectious diseases, and their contact with ingested toxins in the form of medications and drugs. The two
research projects proposed will generate unique data on the life histories and background biology of
NYABG individuals. By using minimally invasive research techniques, the projects will enhance preservation
of the collection while providing essential knowledge which will then be disseminated to scientific
professionals, NPS interpreters, and the public. The research projects will optimize student outreach and
education and increase the numbers of underrepresented ethnic minority group members in science,
technology, education, and mathematics research. The NYABG is already a designated visitor site for the
entire freshman class each year at Howard University. Implementation of these projects and translation of
the research results to make them accessible to the general public will make the NYABG even more valued
and compelling site for visitation, reflection, and growth.
1

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The Backbone

The Official Journal of the

Winter 2015 Spring 2016

Howard University All Rights Reserved

Analysis of Potential Treatments for Sickle-Cell Anemia, or Drepanocytosis, in Adults

Genetic Behavioral Evidence for Autism in the Cobb Collection

A Review: Evolutionary Theories of the Pathogenesis of Schizophrenia

Prevalence and Anatomical Evidence of Treponemal Infection in the Cobb Collection

The Story of CC112

The Story of CC312

The Story of CC315

Winter 2015Spring 2016

The Story of CC331

The Story of CC437

The Story of CC459

Recent Abstracts from W. Montague Cobb Research

Investigation of the Cobb Collection, A Statistical Approach

Winter 2015Spring 2016

Evidence for Arthritis and Specifically Osteoarthritis in the Cobb Collection

Biohistorical Analysis od Cardiovascular Disease in the Cobb Collection

The Correlations between African-American Life Experiences and Type 2 Diabetes

Prevalence of Cerebrovascular Accident within African Americans of the Cobb Collection

Assessment on the Resurgence of Rickets and Scoliosis on African Americans

Identifying the effects and treatment of Alzheimers disease in African Americans

Winter 2015Spring 2016

GENETICS & EPIDEMIOLOGY

Chronic Kidney Disease and its Sequelae within the Cobb

Montague Cobb Research Laboratory, Howard University

FIGURE 1: RISK FACTORS FOR CKD5

the environment.3 It is key to understand both the

improve our statistical status on the matter. Socio-

those groups, AAs have, and have always

environmental, behavioral, biomedical, and predisposing

had, the highest rate of CKD incidents.

factors all work together towards particular health

African Americans and Native Americans share many

outcomes. Once all taken into consideration, real

social environmental stressors that may have aided in

progress can and will be made.

their correlation up until 1999. The quickly accelerating

progression of the disease has often be attributed to risk

As reported by the National Kidney and Urologic

however, this has not been able to explain the elevated

Diseases Information Clearinghouse (NKUDIC) and

rate of CKD progressing into ESRD among AAs and other

displayed in Figure 1, African-Americans (red circles)

groups with low socioeconomic status.8 Unfortunately,

have the highest occurrence of ESRD incidents and well

the consequences of the social environment is too often

as the highest exponential increase since the year of

over-looked as a contributing element. Through

1980. In second lead, incidents in Native Americans (blue

behavioral science studies, it has been established that

FIGURE 2: INCIDENT RATES OF ESRD BY RACE4

chain of risk factors that can contribute to other high risk

mechanisms. Social issues such as economic struggle and

drug use, poor diet and lowered physical activity. Many

discrimination and institutionalized racism.

diamonds) began to rise up until 1999 when a decrease

diseases such as CKD among groups such as African

began. Asians (yellow squares) and Caucasians (green

Americans (and Native Americans) are a function of

triangles) have shown the slightest increase in

economic deprivation. However, racial disparities in the