Vol.3, No.4, 236-243 (2013) Journal of Diabetes Mellitus
http://dx.doi.org/10.4236/jdm.2013.34036
The association of depression and perceived stress
with beta cell function between African and Haitian
Americans with and without type 2 diabetes
Fatma G. Huffman1*, Maria Vallasciani1, Joan A. Vaccaro1, Joel C. Exebio1, Gustavo G. Zarini1,
Ali Nayer2, Sahar Ajabshir1
1Department of Dietetics and Nutrition, Florida International University, Miami, USA; *Corresponding Author:
2Division of Nephrology and Hypertension, University of Miami, Miami, USA
Received 16 October 2013; revised 10 November 2013; accepted 17 November 2013
Copyright © 2013 Fatma G. Huffman et al. This is an open access article distributed under the Creative Commons Attribution Li-
cense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ABSTRACT
Background: Diabetes and diabetes-related com-
plications are major causes of morbidity and
mortality in the United States. Depressive symp-
toms and perceived stress have been identified
as possible risk factors for beta cell dysfunction
and diabetes. The purpose of this study was to
assess associations between depression symp-
toms and perceived stress with beta cell func-
tion bet ween African and Haitian Americans with
and without type 2 diabetes. Participants and
Methods: Informed consent and data were avail-
able for 462 participants (231 African Americans
and 231 Haitian Americans) for this cross-sec-
tional study. A demographic questionnaire de-
veloped by the Primary Investigator was used to
collect information regarding age, ge nder, smok-
ing, and ethnicity. Diabetes status was deter-
mined by self-report and confirmed by fasting
blood glucose. Anthropometrics (weight, and
height and waist circumference) and vital signs
(blood pressure) were taken. Blood samples
were drawn after 8 - 10 hours over-night fasting
to measure lipid panel, fasting plasma glucose
and serum insulin concentrations. The homeo-
static model assessment, version 2 (HOMA2)
computer model was used to calculate beta cell
function. Depression was assessed using the
Beck Depression Inventory-II (BDI-II) and stress
levels were assessed using the Perce ived S tress
Scale (PSS). Results: Moderate to severe de-
pressive symptoms were more likely for persons
with diabetes (p = 0.030). There were no differ-
ences in perceived stress betw een ethnicity and
diabetes status (p = 0.283). General linear mod-
els for participants with and without type 2 dia-
betes using beta cell function as the dependent
variable showed no association with depressive
symptoms and perceived stress; however, Hai-
tian Americans had significantly lower beta cell
function than African Americans both with and
without diabetes and adjusting for age, gender,
waist circumference and smoking. Further re-
search is needed to compare these risk factors
in other race/ethnic groups.
Keywords: Beta Cell Function; HOMA-IR2; Type 2
Diabetes; Haitian Americans; African Am ericans;
Depressive Symptoms; Perceived Stress
1. INTRODUCTION
Diabetes and diabetes related complications are major
causes of morbidity and mortality in the United States
affecting approximately 25.8 million people, or 8.3% of
the US population in 2010; these numbers are expected
to rise by 2050 [1]. Approximately 43% of the popula-
tion had some hyperglycemic condition and were at risk
of developing diabetes [2]. As diabetes progresses, insu-
lin sensitivity and beta cell function decline; albeit, the
mechanisms of reductions are not fully understood [3].
Stress and depression may be risk factors for diabetes.
There is evidence suggesting that beta cells have the
ability to adapt to the hormonal changes produced by
stressful events; however in the long term, psychological
stress may induce pancreatic islet cell failure [4-6].
Insulin resistance is associated with hyperactivation of
the hypothalamic-pituitary-adrenal (HPA) axis and ex-
cess plasma cortisol levels that may lead to depression
[7]. Other studies supported these findings, and added
that increased pro-inflammatory cytokines and distur-

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243 237
bances of serotonin levels increased the risk of develop-
ing diabetes [8,9]. Individuals had a 37% higher risk of
developing diabetes if they suffered from depressive
symptoms [7,8,10]. Conversely, other studies encoun-
tered no association between hyperglycemia and insulin
resistance with depression [9,11,12]. Further research is
needed to clarify if there are any associations between
markers of diabetes and depression.
The association of beta cell dysfunction with depres-
sion and perceived stress is controversial. African and
Haitian Americans were selected for this study for sev-
eral reasons. First, there is not much evidence of how
perceived stress and depressive symptoms are associated
with markers of diabetes in these populations. Second,
most studies do not distinguish ethnic differences among
Blacks. Yet, Blacks are high-risk groups for developing
diabetes and diabetes complications [13]. Several studies
have indicated that depression and perceived stress may
be more pronounced in Blacks as compared to the gen-
eral population [14]. Finally, due to the geographical
location of South Florida, we have accessed Haitian and
African Americans. Therefore, the primary aim of study
is to assess if there is any association between depression
symptoms and perceived stress with beta cell function
between African and Haitians Americans with and with-
out type 2 diabetes. The results could be important to
increase awareness of depression and perceived stress
symptoms in Blacks at risk for diabetes and diabetes-
related complications.
2. PARTICIPANTS AND METHODS
2.1. Participants
This cross-sectional study was conducted between Af-
rican and Haitian Americans with and without type 2
diabetes. The Institutional Review Board at Florida In-
ternational University approved this study and initial data
were collected 2008-2009. Written consent was obtained
from the participants upon explaining the purpose and
protocol of the study. For African Americans, recruitment
was based on response to flyers sent from random selec-
tion of generated mailing lists that were purchased from
Knowledge Base Marketing, Inc., Richardson, TX 75081.
These mailing lists included African Americans with and
without diabetes from Miami-Dade and Broward Coun-
ties, Florida. During a 1-year period, approximately 7550
letters were mailed to African Americans, with and
without type 2 diabetes. Approximately 6% (n = 477) of
the letters were returned due to unknown address. Re-
sponse rate was 4% (n = 256).
There was no mailing list available for Haitian Ameri-
cans. Haitian Americans (n = 259) were recruited from
multiple community sources including local diabetes
educators and community health practitioners in Mi-
ami-Dade and Broward Counties; Florida International
University (FIU) faculty, staff and students; several resi-
dential rental facilities; and advertisements that were
placed in local Haitian newspapers, churches, supermar-
kets and restaurants. In addition, radio advertisements on
local Creole stations were aired. When the recruitment
goal was achieved, recruitment efforts were stopped.
Participants were interviewed on the phone. The pur-
pose of the study was explained and the gender and age
of the subjects were assessed. In addition, age of diagno-
sis and treatment modality was obtained from those indi-
viduals who reported having diabetes. Eligible individu-
als’ participation was requested at the Human Nutrition
Laboratory at Florida International University. Subjects
participating in the study were asked not to smoke, con-
sume any food or beverages except water, and not en-
gage in any unusual physical activity for at least eight
hours prior to their blood collection. Laboratory results
revealed that twelve participants (African Americans = 4;
Haitians = 8) who reported not having diabetes were re-
classified as having type 2 diabetes in accordance to the
American Diabetes Association standards (ADA). These
participants were referred to their physicians.
2.2. Socio-Demographic Data
A standardized demographic questionnaire developed
by the Primary Investigator was used to collect informa-
tion regarding race/ethnicity, diabetes status, age, gender,
smoking, and education level. Race/ethnicity was self-
reported and confirmed by interview. Diabetes status was
confirmed by laboratory results (see methods). Anthro-
pometric measures were taken in the Nutrition Labora-
tory. Waist circumference was measured to the nearest 1
cm at a level midway between the lower rib margin and
the iliac crest with a non-stretchable tape all around the
body in a horizontal position. Weight measurements were
taken using a SECA clinical scale and calibrating after
each participant (SECA Corp, Columbia, MD). Height
and weight were measured with a subject standing erect
without shoes. BMI was calculated as weight (kg)/height
(m2).
2.3. Blood Collection
Twenty milliliters (mL) of venous blood was collected
from each participant after at least 8 hours of fasting by a
certified phlebotomist using standard laboratory tech-
niques. Two tubes were used to collect the blood samples:
a tube containing ethylenediamine tetra-acetic acid
(EDTA) to analyze hemoglobin A1c and a Vaccutainer
Serum Separator Tube (SST) to analyze glucose. Gly-
cated hemoglobin, reported as A1C percentages, was
measured from whole blood samples, with the Roche
Tina Quant method by Laboratory Corporation of Amer-

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243
238
ica (LabCorp, FL, US). Glucose levels were measured by
hexokinase enzymatic method after complete coagulated
blood had been centrifuged at 2500 RPM for 30 minutes
and placed into one labeled plastic tube. Serum insulin
levels were assessed by Human Insulin ELISA kit from
Millipore (St Charles, MZ, US).
2.4. Determination of Beta Cell Function
We calculated beta cell function using the homeostatic
model assessment, version 2 (HOMA2) computer mode,
which is based on the Oxford University HOMA2 calcu-
lator (www.ocdem.ox.ac.uk) [15]. It accounts for varia-
tions in peripheral and hepatic glucose resistance [16].
The new version, HOMA2 is designed to better match
human physiology; it is an update of the HOMA1 based
on modern insulin assays. The computer model, HOMA2,
can be used to calculate beta cell function from radio-
immunoassay insulin and paired fasting plasma glucose
across a range of 1 - 2200 pmol/l for insulin, and 1 - 25
mmol/l for glucose [15]. For data analysis, subjects un-
dergoing insulin treatment or have values <45 mg/dL or
>450 mg/dL for plasma glucose and insulin <2.88
μIU/mL or >57.60 μIU/mL were excluded.
2.5. Psychosocial Factors
Depressive symptoms were assessed using the Beck
Depression Inventory-II (BDI-II) [17]. This is a self-
reported, 21-item questionnaire that measures the pres-
ence and severity of depressive symptoms using a 0 to 3
self-rating scale (0 being least depressed and 3 being
most depressed). Summing scores for each question cal-
culated a final BDI-II score. Moderate to severe symp-
toms of depression was defined as BDI-II score ≥16. A
cutoff point ≥16 yielded a sensitivity of 0.73 and a speci-
ficity of 0.93 [18].
Stress levels were assessed using the Perceived Stress
Scale (PSS) [19]. This is a 10-item scale that measures
the subjects’ response to life stressors using a 4-point
scale ranging from never (1) to always (4). The 10-item
PSS has a higher psychometric quality than the 14-item
version and it has been validated [19].
2.6. Statistical Analysis
Statistical analyses were performed using The Statis-
tical Package for Social Sciences (SPSS), version 20.
Data were presented as a mean ± standard deviation for
general characteristics. A p value of <0.05 was consid-
ered significant. Prior to analyses, all continuous vari-
ables were tested for normality by the Kolmosorov-
Simirnov test. Beta cell function was natural log trans-
formed to achieve normality within diabetes status. De-
pressive symptoms, was converted into a binary variable
based on a clinical cut off [9,20]. General linear models
were used to test the relationships of depression and per-
ceived stress with beta cell function, as the outcome.
Due to significant differences in beta cell function by
diabetes status, separate models were run for each group
(with and without diabetes). The clinically important
covariates tested for the adjusted models were ethnicity,
age, gender, ethnicity, waist circumference, education,
and smoking status. A separate model for beta cell func-
tion in participants with diabetes was conducted with the
adjustment covariates to which ‘years with diabetes’ was
added. The same general linear models were run for per-
ceived stress and depressive symptoms with insulin re-
sistance as the dependent variable.
3. RESULTS
For this study, we had complete data for N = 462,234
without diabetes and 228 with diabetes (231 African
Americans and 231 Haitian Americans). The general
characteristics of the study population by ethnicity and
diabetes status are shown in Tabl e 1. Haitian Americans
with diabetes as compared to the other groups, were the
oldest (mean age 57.8 ± 10 years), had the lowest level
of education and beta cell function, as well as the highest
fasted plasma glucose, hemoglobin A1C and depression
score. There were no differences in perceived stress
among the groups. African Americans had a high rate of
ever-smoking (approximately 40%) as compared to Hai-
tian Americans (approximately 6%).
A difference of the means by ANOVA and post-hoc
analysis showed a significant difference in depression
score by ethnicity and diabetes status. Haitian Americans
with diabetes scored higher (had more signs of depres-
sion) (mean = 10.9 ± 7.77) than Haitians and African
Americans without diabetes (mean = 7.7 ± 7.85, p =
0.001); mean = 7.1 ± 7.50, respectively (p < 0.001). The
difference in depression score between Haitian and Afri-
can Americans with diabetes was not significant (p =
0.156).
The Chi-Squared test was used to assess depression
across diabetes status. Moderate to severe depressive
symptoms, an overall score of 16 or more, were more
likely for the combined group of African Americans and
Haitian Americans with diabetes, than without diabetes
(p = 0.030). This relationships held for mild-moderate
depressive symptoms or more (a score of 12 or more) (p
= 0.029). There were no differences in perceived stress
between ethnicity and diabetes status (p = 0.283). Ad-
justed general linear models with beta cell function as the
dependent variable were run separately for participants
with and without diabetes. Education was tested and not
retained. The final model was adjusting for age, gender,
waist circumference, and smoking. Depression and per-
ceived stress were not associated with beta cell function
for either model with (F7,220 = 3.14, p = −0.003) or

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243 239
Table 1. General characteristics of the study participants by ethnicity and diabetes.
Variable AA with T2D AA without T2D HA with T2D HA without T2Dp
Age (years) 54.4 ± 10.1 50.7 ± 8.5 57.8 ± 10.0 54.2 ± 11.0 <0.001
FPG (mg/dL) 147.3 ± 66.0 95.8 ± 12.9 162.6 ± 84.5 99.5 ± 16.6 <0.001
Hemoglobin A1c (%) 7.6 ± 1.9 5.9 ± 0.4 8.5 ± 2.6 5.9 ± 0.5 <0.001
Insulin (pmol/L) 16.3 ± 15.8 12.2 ± 8.9 8.9 ± 8.7 9.9 ± 5.6 <0.001
Beta cell function (HOMA2) 63.5 ± 53.9 108.5 ± 47.4 42.2 ± 46.2 93.3 ± 42.9 <0.001
Insulin resistance (HOMA2) 2.1 ± 1.5 1.6 ± 1.2 1.4 ± 1.0 1.3 ± 0.7 <0.001
Depression score* (0 - 63) 9.5 ± 9.7 7.1 ± 7.5 10.9 ± 7.8 7.7 ± 7.8 <0.001
Perceived stress (0 - 40) 20.4 ± 5.8 20.2 ± 5.7 20.1 ± 5.7 19.1 ± 6.2 0.282
Waist circumference (cm) 114.6 ± 17.5 102.1 ± 14.5 99.2 ± 11.4 96.2 ± 12.5 <0.001
Gender - - - - 0.841
Female 67 (52.3) 59 (50.0) 76 (55.1) 60 (50.4)
Male 61 (47.7) 59 (50.0) 62 (44.9) 59 (49.6)
Smoked >100 cigarettes (yes) 47 (36.7) 48 (40.7) 9 (6.5) 7 (5.9) <0.001
Education - - - - <0.001
<High school 22 (17.2) 16 (13.6) 74 (53.6) 48 (40.3)
High school 41 (32.0) 37 (31.4)) 29 (21.0) 25 (25.0)
Some college 48 (37.5) 42 (35.6) 19 (13.8) 23 (19.3)
College or more 17 (13.3) 23 (19.5) 16 (11.6) 23 (19.3)
Moderate to severe depressive symptoms (≥16) 23 (18.0) 15 (12.7) 23 (16.7) 12 (10.1) 0.268
AA: African Americans; HA: Haitian Americans; T2D: type 2 diabetes mellitus; FPG: fasting plasma glucose; HOMA2: homeostatic model assessment, version
2. Continuous variables are given as means ± SD and categorical variable are shown as number (%). *Depression score measures depressive symptoms.
without (F7,226 = 5.32, p < 0.001) diabetes. Haitian
Americans with diabetes [b = −0.431 (−0.693, −0170) p
= 0.001] and without diabetes [b = −0.151 (−0.277,
−0.024) p = 0.020] had lower beta cell function as com-
pared to African Americans. Years with diabetes, a factor
in beta cell function, was not significantly correlated
with ethnicity (Spearman’s Rho = −0.054, p = 0.428);
however, we ran a general linear model with just those
with diabetes entering years of having diabetes with the
other adjustment variables with beta cell function as the
dependent variable. The relationship with ethnicity and
beta cell function remained. Haitian Americans had poorer
beta cell function than African Americans [b= −0.391
(−0.685, −0.098), p = 0.009]. We tested insulin resistance
as the dependent variable for the same models and found
neither depressive symptoms, nor perceived stress was
indicative of insulin metabolism (data not shown).
4. DISCUSSION
In the present study, we examined the associations
between perceived stress/depressive symptoms and beta
cell function in 462 African Americans and Haitian
Americans with and without type 2 diabetes. To our
knowledge, this is one of the few studies comparing beta
cell function and psychosocial risk factors in two Black
ethnicities with and without type 2 diabetes.
We found no significant association of depression with
beta cell function, for Blacks with or without diabetes.
Our results agreed with those of Lawlor et al. [21],
which demonstrated no association between insulin re-
sistance, as measured by HOMA levels, and depressive
symptoms in a prospective study of middle aged men. In
contrast, Pearson et al. [7] concluded that depressive
disorder was significantly associated with insulin resis-
tance as measured by HOMA independent of demo-
graphics, dietary and behavioral factors. It is important to
note that the investigators measured depression disorder
as opposed to depressive symptoms as measured by an
index. There may be a bidirectional relationship between
insulin metabolism and depression. Whether diabetes
markers and its complications increase the risk of de-
pression, or depression causes insulin resistance and
consequently diabetes, is not known [9]. Moderate to

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243
240
severe depressive symptoms were positively associated
with insulin resistance in males without diabetes for both
a young cohort [9] and in older men [22].
In the present cross-sectional analysis, there was no
relationship with perceived stress and beta cell function.
It is important to note that risk factors for both stress and
depression may overlap. Perceived overall stress caused
by exposure to unfavorable environmental and lifestyle
factors was positively related to insulin resistance, obe-
sity, decreased adherence to treatment and medications,
and therefore, poor diabetes outcomes [11,23,24]. Tho-
mas et al. [10] suggested that some individuals were
more susceptible to depression due to genetic as well as
socioeconomic factors. In addition, racial discrimination
has a negative impact on psychological well-being. The
secretion of glucocorticoids during periods of stress
causes hyperglycemia and it is associated with insulin
resistance [25]. Novak et al. [26] found that men who
reported permanent stress during many years had an in-
creased risk of developing type 2 diabetes, independent
of demographic, socioeconomic, clinical, and lifestyle
factors. Conversely, perceived stress was associated with
beta cell dysfunction in several studies [27,28]; however,
stress was measured with physiological indicators as
opposed to reported perceived stress.
Stress may be more pronounced for minorities and
economically disadvantaged individuals [14,29]. Living
in a disadvantaged environment with limited access to
health care produces a stressful environment and in-
creases risk of depression and diabetes for African
Americans living in poverty [14,29]. Several unhealthy
behaviors used for coping with stress have been sug-
gested that lead to negative health outcomes among
Blacks [14]. Krishnan et al. [30] suggested that chronic
stress may lead to insulin resistance and diabetes among
Backs. In addition, perception of racism was related to
increased levels of stress and poor diabetic outcomes.
Wagner et al. [31] found that African Americans linked
racism to decreased diabetes self-management and con-
trol through negative emotions, physiological arousal,
and inadequate coping mechanisms.
Earlier studies, using HOMA1 were in agreement with
our findings for obesity and insulin metabolism [32,33].
In our study, we found a positive relationship between
waist circumference and insulin resistance and a negative
relationship between waist circumference and beta cell
function as measured by HOMA2. Chung et al. [5] re-
ported that obesity measured by body mass index was
negatively associated with beta cell function and posi-
tively associated with insulin resistance as measured by
HOMA1. Everson-Rose et al. [33] reported that associa-
tions between depressive symptoms and insulin resis-
tance were mediated through central adiposity and obe-
sity, and that the relationship was significant among Af-
rican American women. Although African American par-
ticipants had higher beta cell function that Haitian
Americans regardless of diabetes status, they also had a
higher percent of obesity, as compared to Haitian Ame-
ricans. Beta cell dysfunction may be a result of loss of
beta cell mass, which contributes to hyperglycemia of
type 2 diabetes, but is not clearly understood on a genetic
and molecular level [3]. There is evidence stating that in
order to maintain normal levels of blood glucose, African
Americans have a compensatory increase in beta cell
function; however, progressive loss of the ability to com-
pensate for a decreased in insulin sensitivity increases
the risk of type 2 diabetes [34].
The results of this study are in accordance with the lit-
erature finding higher depression in persons with diabe-
tes. Both African and Haitian Americans with diabetes
were more likely to have moderate to severe depression
than those without diabetes. Thomas et al. [10] reported
that the diagnosis of type 2 diabetes and its complica-
tions was associated with increased depression disorder
independent of education and gender in a group of
low-income adults. Several studies explained that unfa-
vorable environmental and lifestyle factors, in combina-
tion with diabetes and its complications, could lead to
depression in the general population. There are several
possible explanations as to why environmental factors,
together with diabetes, may increase the risk of depres-
sion. Depression is mainly caused by a disruption of so-
cial, psychological, behavioral, and biological factors [8].
Studies reported that poor eating habits, physical inactiv-
ity, low socioeconomic status and education level, smok-
ing, and limited access to health care services and
healthy foods were risk factors for depression [7,8,11,
29,35-37].
We found Haitian Americans with diabetes to be more
likely to have moderate to severe depressive symptoms
than Haitian or African Americans without diabetes. Hai-
tian American participants had a lower education level as
compared to African Americans and this may be a con-
tributing factor. Higher levels of depression were associ-
ated with limited economic and social resources in a co-
hort of African American women at risk for diabetes [29].
Many Black Americans live in precarious and stressful
environments, and engaged in many unhealthy behaviors
to be able to cope with stress and depression [14].
Therefore, overall stressful life events may outweigh
diabetes-related stress and depression. We found no dif-
ference in perceived stress between the Black ethnicities
or by diabetes status. Moreover, in our study of self-rated
health in this cohort, we found perceived stress was
higher for individuals who were younger, female, less
educated, and consumed higher calories, regardless of
ethnicity or diabetes status [37].
This study has several limitations. First, this was not a

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243 241
population-based study and recruitment techniques dif-
fered between African and Haitian Americans. Second
the cross-sectional nature of the study limits the estab-
lishment of causal relationships between variables. Third,
depressive symptoms and perceived stress were self-
reported, increasing subjectivity of the responses. Finally,
although we included education, we did not measure or
account for socioeconomic status, which may increase
depressive symptoms and perceived stress in African and
Haitian Americans. Despite these limitations, this study
is one of the few providing data on the Black American
population, differentiating Haitian and African Ameri-
cans.
5. CONCLUSION
In conclusion, Haitian Americans with type 2 diabetes
were more likely to have severe depressive symptoms
(BDS ≥ 16) than African and Haitian Americans without
type 2 diabetes. Despite having smaller waist circumfer-
ences, Haitian Americans had worse beta cell function
than African Americans. These results suggest that early
screening for insulin metabolism and depression may
improve medical care of Blacks at risk for diabetes.
6. ACKNOWLEDGEMENTS
This study was funded by NIH/NIDDK #1SC1DK083060-01 to cor-
responding author.
REFERENCES
[1] Center for Disease Control and Prevention (CDC) (2013)
Age-specific percentage of civilian, non-institutionalized
population with diagnosed diabetes, by age, race and sex,
United States, Modified, March.
http://www.cdc.gov/diabetes/statistics/prevalence_nationa
l.htm
[2] Cowie, C., Rust, K., Ford, E., Eberhardt, M., Bryd-Holt,
D., Li, C., et al. (2009) Full accounting of diabetes and
pre-diabetes in the U.S. population in 1988-1994 and
2005-2006. Diabetes Care, 32, 287-294.
http://www.ncbi.nlm.nih.gov/pubmed/19017771
http://dx.doi.org/10.2337/dc08-1296
[3] Kahn, S.E. (2003) The relative contributions of insulin
resistance and beta-cell dysfunction to the pathophysiol-
ogy of type 2 diabetes. Diabetologia, 46, 3-19.
http://www.ncbi.nlm.nih.gov/pubmed/12637977
[4] Beaudry, J. and Ridell, M. (2012) Effects of glucocorti-
coids and exercise on pancreatic B-cell function and dia-
betes development. Diabetes Metabolism Research and
Reviews, 28, 560-573.
http://www.yorku.ca/mriddell/documents/dmrr2310.pdf
http://dx.doi.org/10.1002/dmrr.2310
[5] Chung, J.-O., Cho, D.-H., Chung, D.-J. and Chung, M.-Y.
(2012) Associations among body mass index, insulin re-
sistance, and pancreatic B-cell function in Korean pa-
tients with new-onset type 2 diabetes. Korean Journal of
International Medicine, 27, 66-71.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3295991/
http://dx.doi.org/10.3904/kjim.2012.27.1.66
[6] Hasson, R., Adam, T., Pearson, J., Davis, J., Spruijt-Metz,
D. and Goran, M. (2013) Sociocultural and socioeco-
nomic influences on type 2 diabetes risk in overweight/
obese African American and Latino American children
and adolescents. Journal of Obesity, Article ID: 512914.
http://dx.doi.org/10.1155/2013/512914
[7] Pearson, S., Schmidt, M., Patton, G., Dwyer, T., Blizzard,
L., Otahal, P. and Venn, A. (2010) Depression and insulin
resistance. Diabetes Care, 33, 1128-1133.
http://care.diabetesjournals.org/content/33/5/1128.long
http://dx.doi.org/10.2337/dc09-1940
[8] Mezuk, B., Eaton, W., Albrecht, S. and Hill Golden, S.
(2008) Depression and type 2 diabetes over the lifespan.
Diabetes Care, 31, 2383-2390.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584200/
http://dx.doi.org/10.2337/dc08-0985
[9] Timonen, M., Salmenkaita, I., Jokelainen, J., Laakso, M.,
Harkonen, P., Koskela, P., et al. (2007) Insulin resistance
and depressive symptoms in young adult males: Findings
from Finnish military conscripts. Psychosomatic Medi-
cine, 69, 723-728.
http://www.ncbi.nlm.nih.gov/pubmed/17942838
http://dx.doi.org/10.1097/PSY.0b013e318157ad2e
[10] Thomas, J., Jones, G., Scarinci, I. and Brantley, P. (2003)
A descriptive and comparative study of the prevalence of
depressive and anxiety disorders in low-income adults
with type 2 diabetes and other chronic illnesses. Diabetes
Care, 26, 2311-2317.
http://www.ncbi.nlm.nih.gov/pubmed/12882854
http://dx.doi.org/10.2337/diacare.26.8.2311
[11] Engum, A., Mykletun, A., Midthjell, K., Holen, A. and
Dahl, A. (2005) Depression and diabetes: A large popula-
tion-based study of sociodemographic, lifestyle, and clini-
cal factors associated with depression in type 1 and type 2
diabetes. Diabetes Care, 28, 1904-1909.
http://care.diabetesjournals.org/content/28/8/1904.full
http://dx.doi.org/10.2337/diacare.28.8.1904
[12] Fisher, L., Mulan, J., Arean, P., Glasgow, R., Hessler, D.
and Masharani, U. (2010) Diabetes depression but not cli-
nical depression or depressive symptoms is associated
with glycemic control in both cross-sectional and longi-
tudinal analyses. Diabetes Care, 33, 23-28.
http://www.ncbi.nlm.nih.gov/pubmed/19837786
http://dx.doi.org/10.2337/dc09-1238
[13] American Diabetes Association (2013) Living with dia-
betes complications: African Americans and complica-
tions.
http://www.diabetes.org/living-with-diabetes/complicatio
ns/african-americans-and-complications.html
[14] Jackson, J., Knight, K. and Rafferty, J. (2010) Race and
unhealthy behaviors: Chronic stress, the HPA axis, and
physical and mental health disparities over the life course.
American Journal of Public Health, 100, 933-939.
http://www.ncbi.nlm.nih.gov/pubmed/19846689
http://dx.doi.org/10.2105/AJPH.2008.143446

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243
242
[15] Wallace, T.M., Levy, J.C. and Matthews, D.R. (2004) Use
and abuse of HOMA modeling. Diabetes Care, 27, 1487-
1495. http://www.ncbi.nlm.nih.gov/pubmed/15161807
http://dx.doi.org/10.2337/diacare.27.6.1487
[16] Rudenski, A., Matthews, D., Levy, J. and Turner, R.
(1991) Understanding insulin resistance: Both glucose re-
sistance and insulin resistance are required to model hu-
man diabetes. Metabolism, 40, 908-917.
http://www.ncbi.nlm.nih.gov/pubmed/1895955
http://dx.doi.org/10.1016/0026-0495(91)90065-5
[17] Beck, A.T., Steer, R.A. and Brown, G.K. (1996) Manual
for the Beck Depression Inventory-II. Psychological Cor-
poration, San Antonio.
http://www.nctsn.org/content/beck-depression-inventory-
second-edition-bdi-ii
[18] Lustman, P.J., Clouse, R.E., Griffith, L.S., Carney, R.M.
and Freedland, K.E. (1997) Screening for depression in
diabetes using the Beck Depression inventory. Psycho-
somatic M edicine , 59, 24-31.
http://www.ncbi.nlm.nih.gov/pubmed/9021863
[19] Cohen, S. and Williamson, G. (1988) Perceived stress in a
probability sample of the United States. The Social Psy-
chology of Health, 13, 31-67.
[20] Araya, R., Montero-Marin, J., Barroilhet, S., Fritsch, R.
and Montgomery, A. (2013) Detecting depression among
adolescents in Santiago, Chile: Sex differences. BMC
Psychiatry, 13, 1-12.
http://www.biomedcentral.com/1471-244X/13/122
[21] Lawlor, D., Ben-Shlomo, Y., Ebrahim, S., Smith, G.,
Stansfeld, S., Yarnell, J. and Gallacher, J. (2005) Insulin
resistance and depressive symptoms in middle aged men:
Findings from the Caerphilly prospective cohort study.
BMJ, 330, 705-706.
http://www.ncbi.nlm.nih.gov/pubmed/15684022
http://dx.doi.org/10.1136/bmj.38377.616921.F7
[22] Timonen, M., Laakso, M., Jokelainen, J., Rajala, U.,
Meyer-Rochow, V.B. and Keinänen-Kiukaanniemi, S.
(2005) Insulin resistance and depression: Cross sectional
study. BMJ, 330, 17-18.
http://www.bmj.com/content/330/7481/17
http://dx.doi.org/10.1136/bmj.38313.513310.F71
[23] Pyykkönen, A., Raikkonen, K., Tuomi, T., Eriksson, J., de
Groop, L. and Isomma, B. (2010) Stressful life events and
the metabolic syndrome. Diabetes Care, 33, 378-384.
http://www.ncbi.nlm.nih.gov/pubmed/19880581
http://dx.doi.org/10.2337/dc09-1027
[24] Räikkönen K., Matthews, K. and Kuller, L. (2007) De-
pressive symptoms and stressful life events predict meta-
bolic syndrome among middle-aged women. Diabetes
Care, 30, 872-877.
http://www.ncbi.nlm.nih.gov/pubmed/17392548
http://dx.doi.org/10.2337/dc06-1857
[25] Kim-Dorner, S., Simpson-Mackenzie, C., Poth, M. and
Deuster, P. (2009) Psychological and physiological corre-
lates of insulin resistance at fasting and in response to a
meal in African Americans and Whites. Ethnicity & Dis-
ease, 10, 104-110.
http://www.ncbi.nlm.nih.gov/pubmed/19537218
[26] Novak, M., Björck, L., Giang, K., Heden-Stahl, C., Wi-
helmsen, L. and Rosengren, A. (2013) Perceived stress
and incidence of type 2 diabetes: A 35-year follow-up
study of middle-aged Swedish men. Diabetic Medicine,
30, e8-e16.
http://www.ncbi.nlm.nih.gov/pubmed/23075206
[27] Kruyt, N., van Westerloo D. and DeVries, H. (2012)
Stress induced hyperglycemia in healthy bungee jumpers
without diabetes due to decreased pancreatic B-cell func-
tion and increased insulin resistance. Diabetes Technol-
ogy & Therapeutics, 14, 311-314.
http://www.ncbi.nlm.nih.gov/pubmed/22283617
http://dx.doi.org/10.1089/dia.2011.0171
[28] Shiloah, E., Witz, S., Abramovitch, Y., Cohen, O., Buchs,
A., Ramot, Y., et al. (2003) Effect of acute psychotic
stress in nondiabetic subjects on B-cell function and insu-
lin sensitivity. Diabetes Care, 26, 1462-1467.
http://care.diabetesjournals.org/content/26/5/1462.full.pdf
http://dx.doi.org/10.2337/diacare.26.5.1462
[29] De Groot, M., Auslander, W., Williams, J., Sherraden, M.
and Haire-Joshu, D. (2003) Depression and poverty among
African American women at risk for type 2 diabetes. An-
nals of Behavioral Medicine, 25, 172-181.
http://www.ncbi.nlm.nih.gov/pubmed/12763712
[30] Krishnan, S., Cozier, Y., Rosenberg, L. and Palmer, J.
(2010) Socioeconomic status and incidence of type 2
diabetes: Results from the Black women’s health study.
American Journal of Epidemiology, 171, 564-570.
http://www.ncbi.nlm.nih.gov/pubmed/20133518
http://dx.doi.org/10.1093/aje/kwp443
[31] Wagner, J., Osborn, C., Mendenhall, E., Budris, L., Belay,
S. and Tenner, H. (2011) Beliefs about racism and health
among African American women with diabetes: A quail-
tative study. Journal of the National Medical Association,
103, 224-232.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3082367/
[32] Chang, S., Kim, H., Yoon, K., Ko, S., Kwon, H., Kim, S.,
et al. (2004) Body mass index is the most important de-
termining factor for the degree of insulin resistance in
non-obese type 2 diabetic patients in Korea. Metabolism,
53, 142-146.
http://www.ncbi.nlm.nih.gov/pubmed/14767863
http://dx.doi.org/10.1016/S0026-0495(03)00314-7
[33] Everson-Rose, S., Meyer, P., Powell, L., Pandey, D., Tor-
rens, J., Kravitz, J., et al. (2004) Depressive symptoms,
insulin resistance, and risk of diabetes in women at mid-
life. Diabetes Care, 27, 2856-2862.
http://www.ncbi.nlm.nih.gov/pubmed/15562197
[34] Torrens, J., Skurnick, J., Davidow, A., Korenman, S.,
Santoro, N., Soto-Greene, M., et al. (2004) Ethnic differ-
ences in insulin sensitivity and B-cell function in pre-
menopausal or early perimenopausal women without dia-
betes. Diabetes Care, 27, 354-361.
http://care.diabetesjournals.org/content/27/2/354.full.pdf
http://dx.doi.org/10.2337/diacare.27.2.354
[35] Fisher, L., Skaff, M., Mullan, J., Arean, P., Mohr, D.,
Masharani, U., et al. (2007) Clinical depression versus
distress among patients with type 2 diabetes. Diabetes
Care, 30, 542-548.
http://www.ncbi.nlm.nih.gov/pubmed/17327318
http://dx.doi.org/10.2337/dc06-1614

F. G. Huffman et al. / Journal of Diabetes Mellitus 3 (2 013) 236-243 243
[36] Miller, S. (2011) Diabetes and psychological profile of
younger rural African American women with type 2 dia-
betes. Journal of Health Care for the Poor and Unde-
served, 22, 1239-1252.
http://www.ncbi.nlm.nih.gov/pubmed/22080706
[37] Huffman, F., Vaccaro, J., Ajabshir, S., Zarini, G., Exebio,
J. and Dixon, Z. (2013) Perceived stress and self-rated
health of Haitian and African Americans with and without
type 2 diabetes. Journal of Research in Medical Science,
18, 198-204.
http://www.ncbi.nlm.nih.gov/pubmed/23930115