Content uploaded by Ekkehart Dietz
Author content
All content in this area was uploaded by Ekkehart Dietz
Content may be subject to copyright.
Available via license: CC BY 2.0
Content may be subject to copyright.
RESEARCH ARTICLE Open Access
Diabetes mellitus type 2 in urban Ghana:
characteristics and associated factors
Ina Danquah
1,2
, George Bedu-Addo
3
, Karl-Johann Terpe
1
, Frank Micah
3
, Yaw A Amoako
3
, Yaw A Awuku
3
,
Ekkehart Dietz
4
, Markus van der Giet
5
, Joachim Spranger
6
and Frank P Mockenhaupt
1*
Abstract
Background: Sub-Saharan Africa faces a rapid spread of diabetes mellitus type 2 (DM2) but its potentially specific
characteristics are inadequately defined. In this hospital-based study in Kumasi, Ghana, we aimed at characterizing
clinical, anthropometric, socio-economic, nutritional and behavioural parameters of DM2 patients and at identifying
associated factors.
Methods: Between August 2007 and June 2008, 1466 individuals were recruited from diabetes and hypertension
clinics, outpatients, community, and hospital staff. Fasting plasma glucose (FPG), serum lipids and urinary albumin
were measured. Physical examination, anthropometry, and interviews on medical history, socio-economic status
(SES), physical activity and nutritional behaviour were performed.
Results: The majority of the 675 DM2 patients (mean FPG, 8.31 mmol/L) was female (75%) and aged 40-60 years
(mean, 55 years). DM2 was known in 97% of patients, almost all were on medication. Many had hypertension
(63%) and microalbuminuria (43%); diabetic complications occurred in 20%. Overweight (body mass index > 25 kg/
m
2
), increased body fat (> 20% (male), > 33% (female)), and central adiposity (waist-to-hip ratio > 0.90 (male), >
0.85 (female)) were frequent occurring in 53%, 56%, and 75%, respectively. Triglycerides were increased (≥1.695
mmol/L) in 31% and cholesterol (≥5.17 mmol/L) in 65%. Illiteracy (46%) was high and SES indicators generally low.
Factors independently associated with DM2 included a diabetes family history (adjusted odds ratio (aOR), 3.8; 95%
confidence interval (95%CI), 2.6-5.5), abdominal adiposity (aOR, 2.6; 95%CI, 1.8-3.9), increased triglycerides (aOR, 1.8;
95%CI, 1.1-3.0), and also several indicators of low SES.
Conclusions: In this study from urban Ghana, DM2 affects predominantly obese patients of rather low socio-
economic status and frequently is accompanied by hypertension and hyperlipidaemia. Prevention and
management need to account for a specific risk profile in this population.
Background
In sub-Saharan Africa (SSA), growth rates of diabetes
mellitus (DM) and hypertension are among the highest
worldwide. While today an overall DM prevalence of 4%
is assumed, the number of affected patients is projected
to double from 12 to 24 million within the next 20
years [1-4].
DM and other chronic diseases hit Africa in particular:
The health system does not reach a considerable portion
of the population, has a focus on emergencies and infec-
tious diseases, and is frequently limited in staff and
infrastructure. Not rarely, health workers are insuffi-
ciently trained in chronic disease management [2].
Severe complications and a reduced life expectancy for
both diabetic and hypertensive patients are among the
consequences [4-6].
In urban Ghana, type 2 DM (DM2) affects at least 6%
of adults and is associated with age and obesity. Some
23% of adults are overweight, and this has been related
to advanced age, female gender, urban environment,
high income and tertiary education [7,8]. Epidemiologi-
cal data suggest interactions between acculturation,
urbanisation, and genetic disposition to be involved in
DM2 among Ghanaians [5,9,10].
Contrasting increasing prevalence, severe complica-
tions and public health significance, studies on DM2 in
* Correspondence: frank.mockenhaupt@charite.de
1
Institute of Tropical Medicine and International Health, Charité - University
Medicine Berlin, Berlin, Germany
Full list of author information is available at the end of the article
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
© 2012 Danquah et al; licensee BioMed Centra l Ltd. This is an Open Access ar ticle distributed under the terms of the Creative
Commons Attri bution License (http://creativecommons.org /licenses/by/2.0), which permits unrestricte d use, distribution, and
reproductio n in any medium, provided the original work is properly cited.
SSA are remarkably scarce. Understanding manifestation
and associated factors, however, is essential to guide
diagnosis, management, and prevention of DM2 in this
region. Here, we examined clinical, anthropometric,
socio-economic, nutritional and behavioural parameters
among 1466 urban Ghanaian adults with and without
DM2 and hypertension, and present these data and an
explorative analysis of associated factors in this
population.
Methods
Study site and design
The study was conducted from August 2007 through
June 2008 at Komfo Anokye Teaching Hospital (KATH)
in Kumasi, Ghana. In this region, 6% and 29% of adults
are affected by DM2 and hypertension, respectively
[5,11,12]. At KATH, the diabetes and hypertension
clinics are frequented each by > 100 patients/week. The
study aimed at examining factors associated with DM2
and hypertension among hospital attendants with DM2
and/or hypertension and controls. Secondary objective
was to describe the patients’clinical and biochemical
characteristics. The study protocol was reviewed and
approved by the Ethics Committee, School of Medicine,
Kwame Nkrumah University of Science and Technology,
Kumasi, and informed written consent was obtained
from all participants.
Recruitment procedures and examinations
Following study-related information, patients attending
the diabetes center (n= 495) or the hypertension clinic
(n= 451) were recruited. Patients encouraged members
of their community to participate in the study as preli-
minary controls. After exclusion of DM2 and hyperten-
sion (see below), the latter were included into the study
as controls (n= 222). Likewise, further controls were
recruited among outpatients (n= 150) and hospital staff
(n= 148).
From 10:00 p.m. prior to the examination day, the
participants were instructed on fasting, alcohol and
tobacco abstinence, and avoiding excessive physical
activity. On the examination day, patients were physi-
cally examined and interviewed. Parameters assessed
included: age, gender, residence, ethnic group, previous
and current diseases and complaints, own and family
history of DM and hypertension, medications, smoking
behaviour, literacy, occupation, household size, wealth
indicators, characteristics of work and recreational
sports, fitness indicators as well as axillary temperature,
blood pressure (0’,5’,10’; measured after resting for ten
minutes; M8 Comfort, Omron, Japan), tuning fork test,
and peripheral pulses and ulcers.
Fasting venous blood and urine samples were col-
lected. Concentrations of fasting plasma glucose (FPG,
fluoride plasma, +4°C) and of urinary albumin were
measured photometrically (Glucose 201
+
Analyzer,
Albumin Systems; HemoCue, Sweden). Serum triglycer-
ides, total cholesterol and high-density lipoprotein
(HDL)-cholesterol were measured by colorimetric tests
(ABX Pentra400, Horiba Medical, Germany). Low-den-
sity lipoprotein (LDL) cholesterol was calculated accord-
ing to the Friedewald formula [13]. If triglycerides were
> 3.0 mmol/L, LDL-cholesterol was quantified directly.
Anthropometrical examinations and nutritional interviews
Weight was measured in kg using a person scale, and
height in cm by a statometer. Waist and hip circumfer-
ences were assessed in cm using a measuring tape (all
devices, SECA, Germany). Body mass index (BMI) and
waist-to-hip ratio (WHR) were calculated as: BMI (kg/
m
2
) = weight (kg)/[height (m)]
2
and WHR = waist (cm)/
hip (cm). Triplicates of triceps, biceps, subscapular and
suprailiac skin fold thickness were measured in mm on
the right-hand side of the body (Harpenden calliper, Baty
International, UK). Body fat (%) was calculated according
to Durnin & Womersley [14]. Also, body composition
was determined under fasting conditions by bioelectric
impedance analysis (BIA) and appropriate software (50
kHz, Nutrigard-S, NutriPlus 1.0; Data Input, Germany).
Daily energy expenditure was calculated as metabolic
equivalents (MET) × body weight × duration of activity
[15]. Trained nurses recorded weekly aliment intake
with a locally-adapted food frequency questionnaire.
Quantity and type of ingested foods of one day were
documented by participants using a 24-hours dietary
recall and handy-measured food units. Based on local
and international food composition tables [16], the indi-
vidual intake of macronutrients (total energy, protein,
fat, carbohydrates), sodium, and fibre was calculated.
Definitions
DM2 was defined as FPG ≥7 mmol/L and/or documen-
ted anti-diabetic medication [17]. Likewise, hypertension
denoted a mean BP ≥140/90 mmHg and/or documen-
ted anti-hypertensive treatment [18]. Controls were
negative for both conditions. Increased serum triglycer-
ides were defined as ≥1.695 mmol/L, increased total
cholesterol as ≥5.17 mmol/L and decreased HDL-cho-
lesterol as ≤0.9 mmol/L (male) or ≤1.0 mmol/L
(female) [17,19]. Overweight, obesity and central adipos-
itywereclassifiedasBMI≥25.0 kg/m
2
,BMI≥30.0 kg/
m
2
and WHR > 0.90 (male) or > 0.85 (female), respec-
tively [17]. Body fat percentage was increased at ≥20%
(male) or ≥33% (female) [20].
Statistical analysis
Assessed parameters were compared between controls
and patients with diabetes, and following stratification
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 2 of 8
of diabetic patients by hypertension. Between-group-
comparisons of continuous parameters were done by
Mann-Whitney-U-test and of proportions by c
2
-test.
We applied an explorative analysis, i.e., not hypoth-
esis-driven, of factors associated with DM2 and/or
hypertension. For that, all factors found to be univari-
ately associated with e.g., DM2, were entered into a
logistic regression model, aprioriincluding age and
gender, and odds ratios (ORs) and 95% confidence
intervals (95% CI) were calculated. Stepwise backward
removal of parameters loosing significant association
in multivariate analysis (P> 0.05) identified factors
associated with DM2 independently of each other.
These models were applied separately for DM2, DM2
only,DM2withhypertension,andhypertensiononly.
Further, an alternative, fully adjusted model was estab-
lished including age, gender and identified
confounders.
Results
Recruitment and study population
Of 1,536 consenting individuals, 70 were excluded from
analysis (missing FPG, 52; missing BP, 10; had eaten, 4;
conflicting disease status, 4). Table 1 displays the char-
acteristics of the remaining 1466 participants. Data stra-
tified by gender are shown in the Additional file 1:
Table S1 and Additional file 2: Table S2. The majority
of the study participants was female, aged 40-60 years,
of Akan ethnicity and lived in the Kumasi metropolitan
area. Many had no formal education, were illiterate and
unemployed. Those who worked mainly pursued light
physical work. Large families (median, 3 children; range,
0-20) and households prevailed; household assets were
limited. Tobacco and alcohol consumption were low
(ever smoked, 6%; any intake, 15%). Overweight, obesity
and abdominal adiposity, and increased body fat percen-
tage were frequent (Table 1). The diet was rich in car-
bohydrates (means ± standard deviation (SD), 140 ± 40
g/4.2 MJ/d), fat (35 ± 14 g/4.2 MJ/d), and sodium (3.4 ±
1.9 g/4.2 MJ/d), moderate in protein (46 ± 14 g/4.2 MJ/
d) and poor in fibre (17 ± 9 g/d). Physical activity was
generally low at a mean energy expenditure of 6.3 ± 3.6
MJ/d.
Characterisation of diabetic patients
The characteristics of the 675 diabetic patients (mean
age, 54.7 years; 75% female) are shown in Table 1 and
Additional file 1: Table S1. Almost all DM2 patients
(97%) were previously known; 63% additionally had
hypertension. Mean FPG was 8.3 ± 4.3 mmol/L, similar
in men (9.0 ± 5.2 mmol/L) and women (8.1 ± 3.1
mmol/L; P= 0.28). Overweight (53%), obesity (19%),
central adiposity (75%), and increased body fat (54%,
56%) were common, and each more frequent in women
than men (P < 0.01). Carbohydrates contributed 56 ±
13% to the daily energy intake, protein 19 ± 6%, and fat
33 ± 14%. Reported mean energy expenditure was 6.8 ±
3.7 MJ/d. Serum triglycerides were increased in 31% and
total cholesterol in 65%. Cholesterol concentrations
were higher in women (6.06 ± 1.69 mmol/L) than men
(5.61 ± 1.75 mmol/L; P= 0.003). Low HDL-cholesterol
characterised 21%.
Increased urinary albumin (≥20 mg/L) was measured
in 43% of DM2 patients and polyuria was reported by
31%. Almost 20% presented with a history of or clini-
cally assessed complications (peripheral ulcers, 40; dia-
betic coma, 35; stroke, 25; neuropathy, 13; nephropathy,
5; glaucoma, 5; erectile dysfunction, 5; myocardial
infarction, 2; coronary artery disease, 1; retinopathy, 1).
Further characteristics are shown in Table 1.
Most DM2 patients (97%) were on antidiabetic medi-
cation. The predominant regimes were based on metfor-
min (78%) and sulfonylureas (61%), in addition to
glitazones (24%) and insulin (22%, Additional file 3:
Table S3). Further medication included lipid lowering
drugs (3%), calcium-channel blockers (40%) and angio-
tensin-converting enzyme inhibitors (33%).
Univariate associations with DM2
Table 1 displays univariate differences between controls,
all DM2 patients, DM2 patients with and without
hypertension, and patients with hypertension only. Ana-
lysis stratified by gender is shown in Additional file 1:
Table S1.
In comparison with controls (each, P< 0.05), the 675
DM2 patients were older, had higher WHR, BMI, per-
centage body fat, BP, triglycerides, and urinary albumin
as well as reduced HDL-cholesterol. Twice as many
DM2 patients as controls reported a family history of
diabetes; a family history of hypertension was also more
frequent. More DM2 patients than controls resided in
Kumasi outskirts, and in larger households with fewer
assets, were illiterate or unemployed, and smokers.
Patients less frequently than controls pursued light work
and thus had a higher daily energy expenditure. Fat and
salt intakes were increased in DM2 patients as com-
pared to controls (means ± SD, fat, 36 ± 14 vs.33±12
g/4.2 MJ/d, P< 0.001; sodium, 3.4 ± 1.9 vs. 3.2 ± 1.8 g/
d, P< 0.001). No further significant differences were
observed.
Stratifying DM2 patients into those with and without
hypertension basically confirmed the above differences
as compared to controls (Table 1). However, hyperten-
sive DM2 patients presented with the worst lipid profile,
the greatest measures of obesity and the highest urinary
albumin. SES and activity level were lowest among DM2
patients with hypertension. Also, they had the highest
proportion of smokers and hypertension family history.
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 3 of 8
Nutritional values were similar to the non-hypertensive
DM2 group.
As for patients with hypertension only, they were
older and more obese than controls. FPG, triglycerides,
total cholesterol and urinary albumin were significantly
increased. Compared to controls, they more frequently
had a family history of hypertension, lived in Kumasi
outskirts, were illiterate and unemployed. Activity level
and nutritional behaviour, however, were similar in this
and the control group (Additional file 2: Table S2).
Multivariate associations with DM2
Factors independently associated with DM2 were identi-
fied in a logistic regression model (age and gender a
priori included) following a stepwise backward approach:
all univariately associated factors were included in the
model and non-associated variables (P> 0.05) were con-
secutively removed (Table 2). A family history of dia-
betes (aOR, 3.8) and abdominal adiposity (aOR, 2.6)
were the most strongly, independently associated factors.
Other independently associated parameters increasing
Table 1 Characteristics of 1466 urban Ghanaians with and without type 2 diabetes mellitus and/or hypertension
Characteristics Total Controls Diabetes mellitus type 2
(DM2)
DM2 without
hypertension
DM2 with
hypertension
No. 1466
a
377 675 251 424
Age (years) 50.6 ± 15.3 38.8 ± 14.8 54.7 ± 13.4* 48.6 ± 14.0* 58.3 ± 11.6*
Sex (female, %) 75.9 (1113) 76.4 (288) 74.7 (504) 71.7 (180) 76.2 (323)
Ethnic group (Akan, %) 87.2 (1277) 84.4 (318) 87.8 (592) 83.6 (209) 90.3 (383)
†
Residence (Kumasi metropolitan,
%)
73.8 (1079) 79.3 (299) 70.8 (476)
†
68.7 (171)
†
72.1 (305)
†
Clinical data
Fasting plasma glucose
(mmol/l)
6.28 ± 3.52 4.5 ± 0.7 8.28 ± 4.33* 9.0 ± 4.6* 7.92 ± 4.11*
Systolic blood pressure
(mmHg)
134.5 ± 23.2 116.0 ± 11.3 138.3 ± 23.9* 118.6 ± 12.6
†
149.8 ± 21.3*
Diastolic blood pressure
(mmHg)
84.8 ± 12.6 76.0 ± 7.5 85.1 ± 12.1* 76.5 ± 7.4 90.2 ± 11.4*
Triglycerides (mmol/l) 1.44 ± 0.74 1.15 ± 0.56 1.55 ± 0.81* 1.40 ± 0.64* 1.65 ± 0.88*
Total cholesterol (mmol/l) 6.08 ± 1.75 5.73 ± 1.61 5.95 ± 1.71 5.63 ± 1.54 6.13 ± 1.78
†
HDL-cholesterol (mmol/l) 1.35 ± 0.40 1.38 ± 0.41 1.29 ± 0.40* 1.31 ± 0.42
†
1.28 ± 0.39*
LDL-cholesterol (mmol/l) 4.05 ± 1.41 3.82 ± 1.31 3.92 ± 1.36 3.66 ± 1.24 4.07 ± 1.41
†
Urinary albumin (mg/l) 13.0 (3.3-
149.9)
9.0 (4.9-
150.1)
14.5 (3.3-150.1)* 10.5 (4.9-150.0) 17.5 (3.3-150.0)*
Anthropometric data
Waist-to-hip ratio 0.88 ± 0.08 0.83 ± 0.09 0.91 ± 0.07* 0.89 ± 0.07* 0.92 ± 0.07*
Body mass index (kg/m
2
) 25.8 ± 5.25 24.6 ± 4.9 25.9 ± 5.1* 24.8 ± 5.3 26.5 ± 4.8*
Body fat by BIA (%)
b
30.2 ± 9.9 28.8 ± 9.6 29.8 ± 10.1
†
27.9 ± 10.9 30.9 ± 9.4
†
History and activity
Diabetes family history (yes, %) 39.9 (585) 26.3 (99) 57.9 (391)* 59.0 (148)* 57.3 (243)*
Hypertension family history (yes,
%)
41.5 (608) 30.2 (114) 40.7 (275)* 31.1 (78) 46.5 (197)*
Smoking status (ever, %)
c
5.7 (84) 3.7 (14) 7.3 (49)
†
7.2 (18) 7.3 (31)
†
Type of main work (light, %) 88.7 (1250) 92.3 (335) 86.1 (558)
†
83.8 (202)
†
87.5 (356)
†
Working time (h/week) 49.3 ± 22.1 48.4 ± 18.3 49.0 ± 24.0 50.0 ± 24.4 48.1 ± 23.6
Recreational sports (yes, %) 21.2 (311) 22.5 (85) 22.2 (150) 19.5 (49) 23.8 (101)
Energy expenditure (MJ/d) 6.30 ± 3.57 5.34 ± 3.00 6.84 ± 3.70* 6.41 ± 3.54* 7.10 ± 3.78*
Socio-economic data
Literacy (illiterate, %) 35.2 (514) 21.3 (80) 45.8 (308)* 45.0 (113)
†
46.3 (195)*
Unemployed (%) 26.4 (386) 9.8 (37) 36.9 (248)* 24.7 (62)* 44.2 (186)*
No. of people per household 5 (1-100) 5 (1-70) 6 (1-100)* 6 (1-100)* 6 (1-100)*
Wealth score
d
0.58 ± 0.17 0.60 ± 0.15 0.57 ± 0.18
†
0.55 ± 0.18* 0.58 ± 0.18
Values are expressed as means ± standard deviation, median (range) or % (n). *, as compared to controls, P< 0.001;
†
, as compared to controls, P< 0.05;
a
, Data
of the remaining 414 patients with hypertension only are presented in Additional file 2: Table S2;
b
, measured by bioelectric impedance analysis;
c
, includes
current and quit smoking;
d
, proportion positive of 11 markers of wealth: electricity, pipe-borne water, radio, fan, cupboard, television, bicycle, motor-bike,
refrigerator, car/truck/tractor, cattle
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 4 of 8
the odds of DM2 were unemployment, crowded living
conditions, extended working time, illiteracy, outskirts
residence, increased triglycerides, and < 55% contribu-
tion of carbohydrates to the daily energy intake. In a
fully adjusted model, these findings were basically con-
firmed (Table 2).
Following stratification by hypertension, the risk esti-
mates as mentioned above remained basically the same
(Table 2), with a few exemptions: At concomitant
hypertension, the associations with DM2 strengthened
for increased triglycerides and low carbohydrate contri-
bution to energy intake. In contrast, these two factors
were not associated with DM2 in the absence of hyper-
tension (Table 2). Exclusive hypertension was indepen-
dently associated with a respective family history,
central adiposity, high triglycerides, and extended work-
ing time (Additional file 2: Table S2).
Discussion
DM2 is emerging literally epidemically in SSA [3]. This
hospital-based study from urban Ghana shows that
DM2 patients are predominantly middle-aged and of
low socio-economic status, and characterized by high
proportions of central adiposity, a respective family his-
tory, hypertension, albuminuria and hyperlipidaemia.
The study population - although not representative for
the community as a whole - displays many features of
urban life in Africa: life-style is mainly sedentary, socio-
economic conditions are severely restricted, overweight
is frequent, particularly among women, alcohol and
tobacco use are generally low, and recreational sports
not very popular [21-25]. In comparison with previous
studies on DM2 in urban Africa, our findings on obesity
and SES are similar. However, our diabetic patients
exhibited lower FPG and blood pressure, worse lipid
profiles, more frequently a family history of DM2, and
less use of tobacco and alcohol [10,23,26-28]. In com-
parison to African American DM2 patients, blood pres-
sure and lipid profiles were similar in the present study
but obesity, family history, and smoking and alcohol
intake less frequent [21,29]. In comparison to African
and African American DM2 patients, Caucasian DM2
patients show the worst lipid profiles, the highest rates
of tobacco and alcohol consumption, a male predomi-
nance in abdominal adiposity, and more physical activity
[21,30,31].
Rates of hypertension and albuminuria were high
among our DM2 patients, confirming previous findings
from Kumasi [32]. This suboptimal management of
patients may reflect both institutional and individual
factors including drug cost and availability, health policy
disparities, culturally inappropriate lifestyle recommen-
dations, and diluting effects of traditional medicine [33].
Still, complications occurred at only half the figure
reported elsewhere in SSA [28,34]. Diagnostic restric-
tions and a majority of medicated patients may be
involved. Typically, in African diabetic patients, late-
onset microvascular complications predominate over
macrovascular events [6,34]. In fact, reported rates of
retinopathy in African DM2 patients (25%) exceed those
in African Americans (10%) and Caucasians (9%),
whereas cardiovascular diseases are estimated at 8%,
33% and 48%, respectively [34,35].
Limitations of the study and of associated factor analy-
sis in particular need to be considered. Our DM2 defini-
tion by FPG is based on the IDF consensus valid during
Table 2 Factors associated with diabetes mellitus type 2 in multivariate analysis
Parameter aOR for diabetes (95%
CI)
aOR for diabetes without hypertension
(95% CI)
aOR for diabetes with hypertension
(95% CI)
Residence (Kumasi outskirts) 1.93 (1.27-2.93) 1.78 (1.12-2.84) 1.96 (1.16-3.31)
Triglycerides ≥1.695 mmol/
l
1.83 (1.13-2.97) - 2.46 (1.40-4.32)
Increased waist-to-hip ratio
a
2.63 (1.76-3.93) 2.92 (1.85-4.61) 2.93 (1.79-4.81)
Diabetes family history,
positive
3.79 (2.60-5.51) 3.92 (2.56-6.01) 3.72 (2.35-5.88)
Type of main work (light) 0.44 (0.25-0.78) 0.50 (0.26-0.96) 0.30 (0.15-0.59)
Working time > 40 h/week 1.76 (1.20-2.57) 1.85 (1.19-2.87) 1.84 (1.15-2.95)
Illiteracy 1.95 (1.28-2.97) 2.27 (1.43-3.62) -
Unemployment 4.23 (2.33-7.65) 2.58 (1.30-5.12) 5.71 (2.95-11.06)
Crowded living condition
b
2.78 (1.71-4.51) 2.59 (1.53-4.40) 3.58 (1.97-6.48)
Carbohydrate < 55% of
energy
1.63 (1.12-2.35) - 2.02 (1.27-3.22)
aOR, adjusted odds ratio from multivariate logistic regression. Age and gender were a priori included. All univariately associated variables were included and
stepwise backward removal of insignificantly associated factors (P> 0.05) identified independently associated parameters. R
2
for diabetes, 0.53; R
2
for diabetes
without hypertension, 0.39; R
2
for diabetes with hypertension, 0.65. All univariately associated parameters from Table 1 (partially dichotomised) were included in
a fully adjusted model. The type and degree of associations held true; each aOR changed < 44%.
a
, male, ≥0.90; female, ≥0.85;
b
,>75
th
percentile of the
number of people per household (n>8)
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 5 of 8
study conduct and follows general practice. Validated
nutritional questionnaires possibly could have improved
respective assessments. Importantly, the present study
was not matched for e.g., age and sex, and used a conve-
nience sample. Women predominated. Controls were
younger than patients and, related to that, roughly a
quarter originated from hospital staff. This basically was
due to limited project funds and reluctance of commu-
nity members to participate. Although the multivariate
analyses are adjusted for these and other differences, the
selection bias has implications for interpreting the
results: for instance, the increased odds of DM2 among
unemployed individuals are partially an artefact due to
the proportion of staff members among controls. This,
however, does not invalidate the identification of major
risk factors such as, e.g., family history or abdominal
adiposity. In analysis, we followed an exploratory
approach, i.e., lacking pre-formulated hypotheses, and
identified independently associated factors. Thus, asso-
ciations of e.g. unemployment or crowded living condi-
tions with DM2 are statistically independent which does
not mean that they are unrelated in real life. We strati-
fied analysis by the presence of hypertension to illustrate
differences in associated factors. For comprehensibility,
we abstained from (further) stratification by e.g. age
groups but adjusted for age, sex and obesity. Lastly and
as a matter of fact, association does not necessarily
mean causality, and the direction of an association is
subject to interpretation.
Notwithstanding the above mentioned limitations, sev-
eral and partly inter-related parameters reflecting low
SES strongly associated with DM2. The propagation of
DM2 among low social classes worldwide may be due to
low health care utilization, reduced uptake of prevention
messages and SES-dependent differences in risk factors
including nutrition and physical inactivity [36]. Associa-
tions of DM2 with outskirts residence and illiteracy
point to the possibility of inadequate access to health
information. Unemployment,expandedworkinghours,
hard work, and overcrowded households were all asso-
ciated with DM2 and may reflect stressful living condi-
tions. Psycho-social stressors are known to be capable of
adversely influencing the metabolic constitution [37].
Stress may lead to overeating and poor exercise. Also,
increased sympathetic activity may affect adipose and
pancreatic tissue regulation and contribute to insulin
resistance [38]. Detailed investigations into the associa-
tion of psycho-social stress and DM2 in SSA are thus
warranted.
The strong association in the present study of DM2
with a respective family history underlines the pro-
nounced predisposition in Africans towards DM2 [39].
However, replication of risk alleles established in
Caucasians not rarely has failed in African populations
[40], possibly as a result of their higher genetic diversity
[41]. Because of this, validated genetic markers of an
increased risk of DM2 in Africans are rare. Large-scale
studies accounting for environmental variation and, pos-
sibly, epigenetic priming, will thus be needed to disen-
tangle predisposition in, e.g. the Ghanaian population.
Obesity, a prominent DM2 risk factor worldwide [42]
and also in the present study, shows an outstanding pre-
valenceinSSA,particularlyinurbanwomen[22].In
many areas of SSA, obesity constitutes an obvious social
marker of affluence, and poor knowledge and miscon-
ceptions about lifestyle risk factors conflict with appro-
priate prevention and control of obesity and DM2.
Clearly, more research into the traditional cognitive
imagery as well as into DM2-related knowledge, atti-
tudes and behaviour is needed to be able to implement
socioculturally appropriate health promotion campaigns
[1,43]. Such is of particular importance considering the
specifically increased risk for adulthood obesity (and
DM2) as a result of frequent undernutrition in African
infants [44].
Serum lipid profiles are constantly associated with
DM2 [30], and so did hyperlipidaemia in the present
study, particularly when DM2 was complicated by
hypertension. Hyperlipidaemia may result from a com-
bination of low SES and comparatively high urban
food prices which, in turn, favours the intake of inex-
pensive and highly refined foods, i.e. poor in fibre and
protein, but rich in simple carbohydrates, fats and
sodium [10,44]. In fact, such corresponds to the diet
assessed for most study participants. Contrariwise,
popular meals based on peanut and fermented maize
may improve lipid profiles and underlie the observed
weak association of DM2 with total and HDL-choles-
terol [45,46].
Conclusions
In this study from urban Ghana, DM2 was predomi-
nately observed among individuals of rather low socio-
economic status contrasting with the still prevalent per-
ception of DM2 as a disease of affluence. High rates of
hypertension and albuminuria among the largely pre-
diagnosed DM2 patients point to the necessity of
improved management. The associations of DM2 with
factors related to low socio-economic status and/or psy-
cho-social stress indicate a specific pattern of DM2 risks
in this population. For immediate impact, improved
management of complications, access to early diagnosis
and treatment, and health worker training appear to be
vital. For primary prevention of DM2 in this population,
the verification of associated factors by longitudinal stu-
dies is warranted.
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 6 of 8
Additional material
Additional file 1: Table S1. Characteristics of 1466 urban Ghanaians
with and without type 2 diabetes mellitus and/or hypertension stratified
by gender.
Additional file 2: Table S2. Characteristics of 791 urban Ghanaians with
and without hypertension stratified by gender.
Additional file 3: Table S3. Antidiabetic medication use among 675
patients with diabetes mellitus type 2 in Ghana.
Acknowledgements
We thank all participants at Komfo Anokye Teaching Hospital and
acknowledge the study team of the Kumasi Diabetes and Hypertension
Study for on-site recruitment, data and sample collection as well as
laboratory analyses. We thank Katrin Sprengel (Department of Clinical
Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke,
Nuthetal, Germany) for technical assistance in serum lipid measurements.
This publication forms part of the doctoral thesis of KT. ID received a grant
from the Sonnenfeld Foundation, Germany. HemoCue, Germany, donated
photometers and test kits. Charité grant 89539150. JS was supported by a
Heisenberg-Professorship (SP716/2-1) and a clinical research group (KFO218/
1) of the DFG.
Author details
1
Institute of Tropical Medicine and International Health, Charité - University
Medicine Berlin, Berlin, Germany.
2
Department of Molecular Epidemiology,
German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal,
Germany.
3
Komfo Anokye Teaching Hospital, Kwame Nkrumah University of
Science and Technology, Kumasi, Ghana.
4
Institute of Biometry and Clinical
Epidemiology, Charité - University Medicine Berlin, Berlin, Germany.
5
Department of Medicine IV - Nephrology, Charité - University Medicine
Berlin, Berlin, Germany.
6
Department of Endocrinology, Diabetes and
Nutritional Medicine, Charité - University Medicine Berlin, Berlin, Germany.
Authors’contributions
ID, GBA, MvdG, JS and FPM conceived and designed the study. ID, GBA, KJT,
FM, YAAm, and YAAw were responsible for recruitment, interviews and
examinations of study participants. JS did the lipid analysis. ID, ED, and FPM
performed the statistical analysis. ID and FPM wrote the manuscript with
contributions of all authors. All authors read and approved the final
manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 19 August 2011 Accepted: 20 March 2012
Published: 20 March 2012
References
1. Mbanya JC, Motala AA, Sobngwi E, Assah FK, Enoru ST: Diabetes in sub-
Saharan Africa. Lancet 2010, 375:2254-2266.
2. Mbanya JC, Kengne AP, Assah F: Diabetes care in Africa. Lancet 2006,
368:1628-1629.
3. International Diabetes Federation: IDF Diabetes Atlas., 4 2009 [http://www.
diabetesatlas.org].
4. Hall V, Thomsen RW, Henriksen O, Lohse N: Diabetes in Sub Saharan
Africa 1999-2011: Epidemiology and public health implications. a
systematic review. BMC Public Health 2011, 11:564.
5. Cooper R, Rotimi C: Hypertension in blacks. Am J Hypertens 1997,
10:804-812.
6. Kengne AP, Amoah AG, Mbanya JC: Cardiovascular complications of
diabetes mellitus in sub-Saharan Africa. Circulation 2005, 112:3592-3601.
7. Amoah AG, Owusu SK, Adjei S: Diabetes in Ghana: a community based
prevalence study in Greater Accra. Diabetes Res Clin Pract 2002,
56:197-205.
8. Amoah AG: Sociodemographic variations in obesity among Ghanaian
adults. Public Health Nutr 2003, 6:751-757.
9. Saleh A, Amanatidis S, Samman S: Cross-sectional study of diet and risk
factors for metabolic diseases in a Ghanaian population in Sydney,
Australia. Asia Pac J Clin Nutr 2002, 11:210-216.
10. Banini AE, Allen JC, Allen HG, Boyd LC, Lartey A: Fatty acids, diet, and
body indices of type II diabetic American whites and blacks and
Ghanaians. Nutrition 2003, 19:722-726.
11. Cappuccio FP, Micah FB, Emmett L, Kerry SM, Antwi S, Martin-Peprah R,
Phillips RO, Plange-Rhule J, Eastwood JB: Prevalence, detection,
management, and control of hypertension in Ashanti, West Africa.
Hypertension 2004, 43:1017-1022.
12. Ghana Health Service: Ashanti Region: Annual Report. 2006 [http://www.
ghanahealthservice.org/documents/2006_Ashanti_Region_Report.pdf].
13. Friedewald WT, Levy RI, Fredrickson DS: Estimation of the concentration of
low-density lipoprotein cholesterol in plasma, without use of the
preparative ultracentrifuge. Clin Chem 1972, 18:499-502.
14. Durnin JV, Womersley J: Total body fat, calculated from body density,
and its relationship to skinfold thickness in 571 people aged 12-72
years. Proc Nutr Soc 1973, 32:45A.
15. Ainsworth BE, Haskell WL, Leon AS, Jacobs DR Jr, Montoye HJ, Sallis JF,
Paffenbarger RS Jr: Compendium of physical activities: classification of
energy costs of human physical activities. Med Sci Sports Exerc 1993,
25:71-80.
16. Food Research Institute: Composition of Foods Commonly Used in Ghana
Rome, Italy: Food and Agricultural Organization of the United Nations; 1975.
17. World Health Organization: Definition, diagnosis and classification of
diabetes mellitus and its complications. Report of a WHO consultation.
1999 [http://www.staff.ncl.ac.uk/philip.home/who_dmg.pdf].
18. World Health Organization: Guidelines for the management of
hypertension. Guidelines Subcommittee. J Hypertens 1999, 17:151-183.
19. Expert Panel on Detection, And Treatment of High Blood Cholesterol In
Adults: Executive summary of the third report of The National
Cholesterol Education Program. JAMA 2001, 285:2486-2497.
20. Gallagher D, Heymsfield SB, Heo M, Jebb SA, Murgatroyd PR, Sakomoto Y:
Healthy percentage body fat ranges: an approach for developing
guidelines based on body mass index. Am J Clin Nutr 2000, 72:694-701.
21. World Health Organization: World Health Report 2002. Chapter 4:
Quantifying Selected Major Risks to Health.[http://www.who.int/whr/
2002/en/].
22. Abubakari AR, Lauder W, Agyemang C, Jones M, Kirk A, Bhopal RS:
Prevalence and time trends in obesity among adult West African
populations: a meta-analysis. Obes Rev 2008, 9:297-311.
23. Clausen T, Rossow I, Naidoo N, Kowal P: Diverse alcohol drinking patterns
in 20 African countries. Addiction 2009, 104:1147-1154.
24. Owusu-Dabo E, Lewis S, McNeill A, Gilmore A, Britton J: Smoking uptake
and prevalence in Ghana. Tob Control 2009, 18:365-370.
25. United Nations Development Programme: Human Development Report
2009.[http://hdr.undp.org/en/statistics/].
26. Chen Y, Kittles R, Zhou J, Chen G, Adeyemo A, Panguluri RK, Chen W,
Amoah A, Opoku V, Acheampong J, Agyenim-Boateng K, Eghan BA Jr,
Nyantaki A, Oli J, Okafor G, Ofoegbu E, Osotimehin B, Abbiyesuku F,
Johnson T, Fasanmade O, Rufus T, Furbert-Harris P, Daniel HI, Berg KA,
Collins FS, Dunston GM, Rotimi CN: Calpain-10 gene polymorphisms and
type 2 diabetes in West Africans: The Africa America Diabetes Mellitus
(AADM) study. Ann Epidemiol 2005, 15:153-159.
27. Isezuo SA, Ezunu E: Demographic and clinical correlates of metabolic
syndrome in native African type-2 diabetic patients. J Natl Med Assoc
2005, 97:557-563.
28. Seyum B, Mebrahtu G, Usman A, Mufunda J, Tewolde B, Haile S, Kosia A,
Negassi E: Profile of patients with diabetes in Eritrea: results of first
phase registry analysis. Acta Diabetol 2010, 47:23-27.
29. Brancati FL, Kao WH, Folsom AR, Watson RL, Szklo M: Incident type 2
diabetes mellitus in African American and white adults: the
Atherosclerosis Risk in Communities study. JAMA 2000, 283:2253-2259.
30. Meigs JB, Wilson PW, Nathan DM, D’Agostino RB Sr, Williams K, Haffner SM:
Prevalence and characteristics of the metabolic syndrome in the San
Antonio Heart and Framingham Offspring Studies. Diabetes 2003,
52:2160-2167.
31. Abubakari AR, Lauder W, Jones MC, Kirk A, Agyemang C, Bhopal RS:
Prevalence and time trends in diabetes and physical inactivity among
adult West African populations: the epidemic has arrived. Public Health
2009, 123:602-614.
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 7 of 8
32. Eghan BA Jr, Frempong MT, Adjei-Poku M: Prevalence and predictors of
microalbuminuria in patients with diabetes mellitus: a cross-sectional
observational study in Kumasi, Ghana. Ethn Dis 2007, 17:726-730.
33. Beran D, Yudkin JS: Diabetes care in sub-Saharan Africa. Lancet 2006,
368:1689-1695.
34. Mbanya J, Sobngwi E: Diabetes microvascular and macrovascular disease
in Africa. J Cardiovasc Risk 2003, 10:97-102.
35. Young BA, Maynard C, Boyko EJ: Racial differences in diabetic
nephropathy, cardiovascular disease, and mortality in a national
population of veterans. Diabetes Care 2003, 26:2392-2399.
36. Connolly V, Unwin N, Sherriff R, Bilous R, Kelly W: Diabetes prevalence and
socioeconomic status: a population based study showing increased
prevalence of type 2 diabetes mellitus in deprived areas. J Epidemiol
Community Health 2000, 54:173-177.
37. Chida Y, Hamer M: An association of adverse psychosocial factors with
diabetes mellitus: a meta-analytic review of longitudinal cohort studies.
Diabetologia 2008, 51:2168-2178.
38. Sjörstrand M, Eriksson JW: Neuroendocrine mechanisms in insulin
resistance. Mol Cell Endocrinol 2009, 297:104-111.
39. Karter AJ, Ferrara A, Liu JY, Moffet HH, Acherson LM, Selby JV: Ethnic
disparities in diabetic complications in an insured population. JAMA
2002, 287:2519-2527.
40. Freeman H, Cox RD: Type-2 diabetes: a cocktail of genetic discovery.
Hum Mol Genet 2006, 15(Spec No 2):R202-R209.
41. Campbell MC, Tishkoff SA: African genetic diversity: implications for
human demographic history, modern human origins, and complex
disease mapping. Annu Rev Genomics Hum Genet 2008, 9:403-433.
42. Zimmet P, Alberti KG, Shaw J: Global and societal implications of the
diabetes epidemic. Nature 2001, 414:782-787.
43. Kiawi E, Edwards R, Shu J, Unwin N, Kamedjeu R, Mbanya JC: Knowledge,
attitudes, and behavior relating to diabetes and its main risk factors
among urban residents in Cameroon: a qualitative survey. Ethn Dis 2006,
16:503-509.
44. Fall C: Non-industrialised countries and affluence. Br Med Bull 2001,
60:33-50.
45. Anukam KC, Reid G: African traditional fermented foods and probiotics. J
Med Food 2009, 12:1177-1184.
46. Ghadimi NM, Kimiagar M, Abadi A, Mirzazadeh M, Harrison G: Peanut
consumption and cardiovascular risk. Public Health Nutr 2009, 22:1-6.
Pre-publication history
The pre-publication history for this paper can be accessed here:
http://www.biomedcentral.com/1471-2458/12/210/prepub
doi:10.1186/1471-2458-12-210
Cite this article as: Danquah et al.: Diabetes mellitus type 2 in urban
Ghana: characteristics and associated factors. BMC Public Health 2012
12:210.
Submit your next manuscript to BioMed Central
and take full advantage of:
• Convenient online submission
• Thorough peer review
• No space constraints or color figure charges
• Immediate publication on acceptance
• Inclusion in PubMed, CAS, Scopus and Google Scholar
• Research which is freely available for redistribution
Submit your manuscript at
www.biomedcentral.com/submit
Danquah et al.BMC Public Health 2012, 12:210
http://www.biomedcentral.com/1471-2458/12/210
Page 8 of 8