1 s2.0 S2001037021000751 Main PDF

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785
journal homepage: www.elsevier.com/locate/csbj
Review
Association of risk factors with type 2 diabetes: A systematic review

Leila Ismail a,⇑, Huned Materwala a, Juma Al Kaabi b,c
a
Intelligent Distributed Computing and Systems Research Laboratory, Department of Computer Science and Software Engineering, College of Information Technology, United
Arab Emirates University, Al Ain, Abu Dhabi, 15551, United Arab Emirates
b
College of Medicine and Health Sciences, Department of Internal Medicine, United Arab Emirates University, Al Ain, Abu Dhabi 15551, United Arab Emirates
c
Mediclinic, Al Ain, Abu Dhabi, United Arab Emirates
a r t i c l e i n f o a b s t r a c t
Article history: Diabetes is the leading cause of severe health complications and one of the top 10 causes of death world-
Received 5 November 2020 wide. To date, diabetes has no cure, and therefore, it is necessary to take precautionary measures to avoid
Received in revised form 28 February 2021 its occurrence. The main aim of this systematic review is to identify the majority of the risk factors for the
Accepted 1 March 2021
incidence/prevalence of type 2 diabetes mellitus on one hand, and to give a critical analysis of the cohort/
Available online 10 March 2021
cross-sectional studies which examine the impact of the association of risk factors on diabetes.
Consequently, we provide insights on risk factors whose interactions are major players in developing dia-
Keywords:
betes. We conclude with recommendations to allied health professionals, individuals and government
Aging
Cardiovascular disease
institutions to support better diagnosis and prognosis of the disease.
Depression Ó 2021 The Author(s). Published by Elsevier B.V. on behalf of Research Network of Computational and
Diabetes mellitus Structural Biotechnology. This is an open access article under the CC BY-NC-ND license (http://creative-
Dyslipidemia commons.org/licenses/by-nc-nd/4.0/).
Ethnicity
Family history of diabetes
Hypertension
Physical inactivity
Prevention
Risk factors
Serum uric acid
Sleep quality
Sleep quantity
Smoking
Type 2 diabetes
Obesity
1. Introduction
Diabetes Mellitus (DM) commonly referred to as diabetes, is a chronic disease that affects how the body turns food into energy [1]. It is one of the
top 10 causes of death worldwide causing 4 million deaths in 2017 [2,3]. According to a report by the International Diabetes Federation (IDF) [3], the
total number of adults (20–79 years) with diabetes in 2045 will be 629 million from 425 million in 2017 (48% increase). In 2017, diabetes caused at
least 727 billion USD in health expenditure, which is 12% of the total spending on adults [3]. According to the National Diabetes Statistics Report [4],
30.3 million (9.4% of the US population) people have diabetes, and 84.1 million (29.06% of the population) have pre-diabetes. 1 in 2 people (212
million) with diabetes was undiagnosed in 2017 according to IDF [5]. Diabetes if left untreated can cause serious medical issues, such as cardiovas-
cular disease, stroke, chronic kidney disease, foot ulcers, damage to the eyes, and prolonged kidney ailment. To date, there is no permanent cure for
diabetes and the patients have to rely on healthy lifestyle and timely medication [6].
There are three main types of diabetes: type 1, type 2, and gestational diabetes (diabetes while pregnant) [1]. Type 1 diabetes mostly occurs in
children and adolescents. 1,106,500 children were suffering from type 1 diabetes in 2017 [3]. The symptoms of type 1 diabetes include abnormal
thirst and dry mouth, frequent urination, fatigue, constant hunger, sudden weight loss, bed-wetting, and blurred vision. Type 2 diabetes is mostly
seen in adults, but it is increasing in children and adolescents due to the rising level of obesity, physical inactivity and unhealthy diet [5]. 372 million
⇑ Corresponding author.
E-mail address: [email protected] (L. Ismail).
https://doi.org/10.1016/j.csbj.2021.03.003
2001-0370/Ó 2021 The Author(s). Published by Elsevier B.V. on behalf of Research Network of Computational and Structural Biotechnology.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
L. Ismail, H. Materwala and J. Al Kaabi Computational and Structural Biotechnology Journal 19 (2021) 1759–1785
adults were at the risk of developing type 2 diabetes in 2019 [3]. In diabetes compared to an individual having uric acid level less than
2017, more than 21 million live births were affected by diabetes during 302 lmol/l. Niskanen et al. [15] also confirmed that change in uric acid
pregnancy [3]. In this paper, we focus on type 2 diabetes due to the levels is associated with a 2 times increase in the risk of incidence type
alarming numbers. 2 diabetes. Dehghan et al. [16] in their study showed that individuals
Type 2 Diabetes is thought to prevail in an individual from an inter- having uric acid level >370 lmol/l are at high risk of incidence type
action between several lifestyle, medical condition, hereditary, psy- 2 diabetes (HR 1.68, 95% CI 1.22–2.30) compared to those having uric
chosocial and demographic risk factors such as high-level serum uric acid level 6267 lmol/l. The authors concluded that lowering uric acid
acid, sleep quality/quantity, smoking, depression, cardiovascular dis- level can be a novel approach for diabetes prevention. Xu et al. [17]
ease, dyslipidemia, hypertension, aging, ethnicity, family history of dia- found that the association between high serum uric acid level and dia-
betes, physical inactivity, and obesity [6]. In this paper, we present a betes is the same in both men and women (RR 1.131, 95% CI
systematic review of the literature on the association of these risk fac- 1.084–1.179). The association (RR 1.17, 95% CI 1.09–1.25) is also exam-
tors with the incidence/prevalence of type 2 diabetes. We give insights ined by Kodama et al. [18]. Nakagawa et al. [19] showed that uric acid is
on the contribution of independent risk factors in the development of a significant and independent risk factor in predicting hyperinsuline-
type 2 diabetes along with possible solutions towards a preventive mia. The authors observed that serum uric acid level P5.5 mg/dl is
approach. associated with the development of hyperinsulinemia after 6 months
(OR 5.47, 90% CI 1.6–1.77) and 12 months (OR 3.4, 90% CI 1.1–10.4).
However, the cohort was controlled for gender and age (>60 years).
2. Methods
Consequently, it can not be concluded whether uric acid is an indepen-
dent risk factor or there is an integrated effect of uric acid, gender and
We conduct a systematic literature search using CINAHL, IEEE age.
Xplore, Embase, MEDLINE, PubMed Central, ScienceDirect, Scopus, Several studies argue that high-level uric acid is not an independent
Springer, and Web of Science databases. Our search criteria does not risk factor and it only emphasizes the association between independent
include a time bound. Its main objective is to retrieve all the studies risk factors such as age, obesity, hypertension, gender, and dyslipi-
which examine the association between individual risk factors and demia, and type 2 diabetes [20]. Chou et al. show that uric acid has a
the incidence/prevalence of type 2 diabetes. Table A1 shows the search significant association with type 2 diabetes in old and obese individuals
string used for each risk factor. The relevant studies have to meet the [21]. Another study by Meisinger et al. [22] shows that high-level uric
following inclusion criteria: 1) published in the English language, 2) acid is associated with incidence of type 2 diabetes in women only with
prospective cohort or cross-sectional study, 3) type 2 diabetes as a HR 2.5 per 1 mmol/L increase. Carnethon et al. [23] found that the risk
specified risk, 4) one of its risk factors, 5) findings in terms of Odds of incidence type 2 diabetes increases (OR 1.3, (1.2–1.4)) with every
Ratio (OR), Risk Ratio/Relative Risk (RR), or Hazard Ratio (HR), and 1.4 mg/dl increase in uric acid level. However, this is in combination
the corresponding 95% Confidence Intervals (CIs) for the association with an increase in waist/hip ratio, smoking and obesity. Chien et al.
between the risk factor and type 2 diabetes. To assess the quality of [24] stated that individuals with a uric acid level of 0.486 mmol/L
the studies, we use the National Institutes of Health (NIH) quality and having metabolic syndrome have a 3.3 times more risk of incidence
assessment tool [7]. The tool consists of 14 questions to evaluate the type 2 diabetes compared to those with a uric acid level of 0.211 mmol/
validity and bias risk of a study. We answered each question by either L and not having metabolic syndrome. Nan et al. [25] examined the
yes, no, cannot be determined, not applicable, or not reported. The tool impact of ethnicity and gender on the association between uric acid
then classifies each study as high quality (Good), moderate quality and incidence of type 2 diabetes. The authors found that the high serum
(Fair) and low quality (Poor). uric acid is an independent risk factor for type 2 diabetes in Mauritian
Indian men compared to Creole men, and there is a no-to-weak associ-
3. Results ation in women of both ethnicity. Similarly, Choi et al. [26] studied the
association between uric acid and type 2 diabetes in men having car-
Fig. 1 shows the result of our systematic approach that is used to diovascular risk profile. The authors concluded that men with cardio-
screen the relevant studies. Irrelevant studies that do not meet the vascular profile having high uric acid level are twice likely to develop
inclusion criteria mentioned in the previous section were excluded type 2 diabetes. The authors also stated that this association between
after screening titles, abstracts and full texts. At last, 106 papers are uric acid and diabetes is independent of other risk factors such as obe-
considered for this review. These papers are divided into ten categories sity, age, family history of diabetes, hypertension, and metabolic syn-
based on the risk factor under study (Fig. 1). Our review reveals that drome. Kramer et al. [27] analyzed the impact of age and impaired
there is no study that examines the association of age or physical inac- fasting glucose (IFG) on the association and found that high uric acid
tivity as an independent risk factor with type 2 diabetes. Table A2 level can independently predict incidence of type 2 diabetes (OR 1.65,
shows the quality assessment results for the studies included in this 95% CI 1.25–2.18) in older adults having IFG. Lv et al. [28] found that
paper. For smoking, cardiovascular disease and hypertension risk fac- high serum uric acid level is associated to type 2 diabetes in middle-
tors, the majority of the studies are of high quality. For serum uric acid, aged or older people (RR 1.56, 95% CI 1.39–1-76).
sleep quantity/quality, depression, dyslipidemia, ethnicity, family his- In summary, the association between high-level serum uric acid
tory of diabetes and obesity, the majority of the studies are of moderate remains obscure. It is debatable whether serum uric acid is an indepen-
quality. dent risk factor for type 2 diabetes or it only emphasizes the association
between other independent risk factors and type 2 diabetes. Some
studies reported a positive association between high serum uric acid
3.1. Serum uric acid level and incidence of type 2 diabetes [14–16,19,24], whereas others
[25,29] reported no association. On the contrary, some studies reported
Serum uric acid, a common component of urine generated by the an inverse association between uric acid and diabetes [30–32]. Further-
metabolic breakdown of purines, have been associated with insulin more, some studies argue that there is a reverse association, i.e., dia-
resistance and type 2 diabetes [8]. High serum uric acid level in an indi- betes leads to high uric acid levels [33,34].
vidual leads to: 1) nitric-oxide mediated vasoconstriction (contraction
of blood vessels) leading to impaired glucose uptake in the muscles [9],
2) increase in oxidative stress [10] and 3) increase in inflammation 3.2. Sleep quantity/quality
leading to a decrease in adiponectin [11,12]. Consequently, the blood
glucose level increases leading to dysfunctional and eventually dead The quality and quantity of sleep are affected by several cultural,
beta-cells [13]. As a result, the individual develops type 2 diabetes. social, behavioral, psychological, and environmental factors. The work-
Table 1 shows the characteristics and findings of the work in the liter- ing professionals often experience fatigue, tiredness and daytime nap-
ature studying the association between high serum uric acid level and ping due to irregular working hours and shifts. Evidence shows that the
type 2 diabetes. current average sleep of an individual, i.e., 6.8 h/night, is 1.5 h less than
Perry et al. [14] found that an individual having a uric acid level of that a century ago [45]. The cause of sleep loss is multi-factorial. For
more than 411 lmol/l is at 1.5 times more risk of developing type 2 instance 45% of adults report that they sleep fewer hours to get more
1760
Fig. 1. Flowchart of the selection of relevant studies.
work done, 43% reported that they watch television or use the Internet, The results in the literature show that the association between
and 22% reported to be suffering from insomnia. The unusual, disturbed smoking and diabetes increases with an increase in the number of
and reduced sleep is associated with glucose intolerance [46]. cigarettes smoked/day. Will et al. [63] analyzed the impact of gender
An individual suffering from sleep disorder, known as obstructive on this association and showed that the association between cigarette
sleep apnea (OSA), experiences: 1) deficiency in the amount of oxygen smoking and type 2 diabetes is more in men compared to women. Sim-
reaching the tissues by total/partial collapse of upper airways while ilar results are obtained by Jee et al. [64]. Wannamethee et al. [65]
sleeping (hypoxia) and 2) inflammation. Frequent Hypoxia triggers an revealed that an individual smoking pipe/cigar is 2.15 times more likely
increase in sympathetic activity [47]. Increased sympathetic activity to develop type 2 diabetes and an individual smoking cigarette is 1.6
and inflammation lead to insulin resistance condition [48,49] and even- times more likely compared to a non-smoker. Kowall et al. [66] showed
tually to type 2 diabetes. Table 2 shows the characteristics and findings that the risk of incidence type 2 diabetes is significantly high in active/-
of the work in the literature studying the association between sleep passive prediabetic smokers compared to active/passive smokers with-
quantity/quality and type 2 diabetes. out prediabetes.
The results in the literature show that compared to a reference sleep The incidence and prevalence of type 2 diabetes in ex-smokers is
duration of 7-8 h, an individual having either short sleep duration examined by [67–72]. and [73] respectively. Results show that ex-
(<6 h) or long sleep duration (>8 h) is at high risk of developing type smokers are associated with 17–60% increased risk of type 2 diabetes
2 diabetes. However, [50,51] concluded that there is no significant [67,68,70–72]. However, the results obtained by Simon et al. [73] and
association between sleep and incidence of type 2 diabetes. Mallon Manson et al. [69] showed no association between ex-smokers and
et al. [52] studied the impact of gender on the association between type 2 diabetes. This discrepancy in the results can be due to the
sleep and diabetes. The authors concluded that short sleep duration heterogeneous characteristics (sample size, age range, men/women
increases the risk of incidence diabetes in men, whereas, in women, ratio and ethnicity) of the cohorts used in these studies. Beziaud
long sleep duration dominates. The effect of ethnicity on the associa- et al. [74] examined gender-based prevalence of type 2 diabetes in
tion is analyzed by [53–55]. Zizi et al. [53] and Jackson et al. [54] ex-smokers and showed that women are at higher risk compared to
showed that the prevalence of type 2 diabetes is more in whites who men. Furthermore, the duration of smoking cessation also impacts
sleep less than 5 h or more than 8 -9 h compared to blacks. Beihl the association in ex-smokers [65,75–77]. An individual is at high risk
[55] showed that the association is more in Hispanics/Non-Hispanic of developing type 2 diabetes during first 5–10 years of smoking cessa-
Whites compared to that in African-American. Xu et al. examined the tion. The risk then decreases with an increase in cessation duration. The
association between day-time napping and type 2 diabetes and showed association between smoking cessation and the incidence of type 2 dia-
that an individual taking more than 1 h of day-time nap is at 1.5 times betes is more in women than men [78].
more risk to develop diabetes compared to an individual who does not In summary, both active and passive smoking are strongly associ-
take a nap during the day. In the context of sleep quality, the risk of ated with the incidence of type 2 diabetes. The association is more in
incidence type 2 diabetes is more in an individual having difficulty ini- men compared to women. Moreover, the association remains signifi-
tiating sleep (DIS), and the risk increases with increasing DIS frequency cant in ex-smokers during first the 5–10 years of smoking. After
[56–58]. Furthermore, the association is more in women having DIS 10 years of smoking cessation, the risk of incidence type 2 diabetes is
compared to men [59]. the same as that in a non-smoker. Women ex-smokers are at a higher
In summary, there is a strong association between sleep quantity/ risk of developing diabetes compared to men ex-smokers.
quality and the incidence of type 2 diabetes. The association is stronger
in women sleeping for more duration and in men with short sleep
duration. Moreover, this association is affected by ethnicity. 3.4. Depression
Depression is a mood disorder that negatively affects the way a per-

3.3. Smoking son feels, thinks and acts [130]. It can be due to a family history of
depression, early childhood trauma, brain structure, medical condi-
Smoking leads to more than 8 million deaths per year [60]. This is tions, drug use or surrounding environment. Depression is associated
from both active and passive uses, i.e, non-smokers exposed to smok- with multiple health conditions including diabetes [131]. It elevates
ers. Smokers are 30–40% more likely to develop type 2 diabetes com- the sympathetic nervous system activities and hypothalamic–pitui
pared to non-smokers [61]. When an individual smokes, the level of tary–adrenal axis activities [132]. Elevated sympathetic nervous sys-
nicotine increases in his/her body. This leads to a reduction in muscle tem activities lead to an increase in catecholamines and inflammation,
glucose intake, developing insulin resistance and leading to type 2 dia- and eventually causing insulin resistance [133]. On the other hand, ele-
betes [62]. The characteristics and findings of table:smokingtable:smok vated adrenal axis activities lead to an increase in cortisol and eventu-
ing/passive smoking and the incidence of type 2 diabetes are presented ally blood sugar level [134]. Both insulin resistance and increased blood
in Table 3. sugar levels develop type 2 diabetes. The characteristics and findings of
1761
Table 1
L. Ismail, H. Materwala and J. Al Kaabi

Characteristics and findings of the studies examining the association between high level serum uric acid and type 2 diabetes.
Work Year Study Design Sample size %M/W Age (Years) Ethnicity Follow-up Adjusted variables Findings
(%DM) duration
(Years)
[14] 1995 RS PCS 7577 (2.56%) 100/0 40–59 Britain 12.8 Age, BMI, history of heart disease, Uric acid (micro mol/l) OR
physical activity, alcohol intake, <302 1.0
smoking status, high blood pressure, P412 1.5 (0.9–2.5)
HDL cholesterol, and heart rate
[21] 1998 RS PCS 481 (17.6%) 53.02/ 46.98 P30 Chinese 3 Age, sex, BMI, WHR, history of Uric acid (micro mol/l) OR
hypertension, HDL cholesterol, fasting <420 1.0
insulin, and triglycerides >420 2.581 (1.083–6.149)
[22] 2002 MONICA [35] PCS 6166 (3.45%) 49.5/ 50.5 35–74 Germany Mean 7.6 Age and BMI Uric acid (micro mol/l) OR
Increase by 1000 2.05 (1.49–1.29)
[23] 2003 ARIC [36] PCS 8574 (9.90%) 42.6/ 57.4 45–65 Blacks and Whites (USA) 11 Age, sex, education, baseline insulin Uric acid (micro mol/l) OR
concentration, BMI and blood pressure Increase by 123.76 1.3 (1.2–1.4)
[19] 2005 RS PCS 60 75/25 39–80 USA 1 Age, sex, BMI, baseline insulin Uric acid (micro mol/l) OR
concentration, and glomerular 6486 1.0
filtration rate >486 (6 months) 5.47 (1.6–17.7)
>486 (12 months) 3.4 (1.1–10.4)
[15] 2006 FDPS [37] – 475 (21.68%) 33.68/66.32 40–65 Finland 3.2 Age, sex, and baseline fasting Uric acid (micro mol/l) OR
99–310 1.0
311–380 1.40 (0.82–2.39)
381–622 1.82 (1.07–3.10)
[24] 2008 CSCCS [38] PCS 2960 (20.37%) 51.7/48.3 35–97 Chinese Median 9 Age, sex, BMI, alcohol intake, exercise, Uric acid (micro mol/l) OR
marital status, educational level, 220 1.0
occupation and family history of 280 1.11 (0.82–1.49)
1762
diabetes 320 1.29 (0.96–11.73)

380 1.40 (1.04–1.90)
460 1.63 (1.20–2.23)
[16] 2008 Rotterdam [39] PCS 4536 (10.18%) NA P55 Netherlands 10.1 Age, sex, BMI, waist circumference, Uric acid (micro mol/l) HR
systolic and diastolic blood pressure, 6267 1.0

and HDL cholesterol 260–310 1.08 (0.78–1.49)
311–370 1.12 (0.81–1.53)
>370 1.68 (1.22–2.30)
[25] 2008 RS PCS 4259 (16.81%) 45.6/ 54.4 25–74 Indians and Creoles 5 Ethnicity, serum creatinine, alcohol Uric acid (micro mol/l) HR
consumption, family history of Men
diabetes and fasting serum insulin 363 1.0
367 1.19 (1.07–1.34)
Women
273 1.0
287 1.05 (0.95–1.16)
[26] 2008 MRFIT [40–42] PCS 11351 (10.70%) 100/0 35–57 Blacks and Whites (USA) 6 Smoking status, BMI, hypertension, Uric acid (micro mol/l) RR
physical activity, alcohol consumption, <333 1.0
total energy intake, cereal fibre, intake P464 1.88 (1.52–2.32)
of polyunsaturated, mono saturated
and saturated fat, coffee intake, high
fasting blood glucose, and low HDL
cholesterol
[27] 2009 RS PCS 556 (9.89%) 41/ 59 Mean 63.3 8.6 Brazil 13 Age, sex, BMI, diuretic use, and Uric acid (micro mol/l) OR
glomerular filtration rate
Increase by 88.4 1.65 (1.25–2.18)
RS-Random Sample, MONICA-Multinational MONItoring of trends and determinants in CArdiovascular disease, ARIC-Atherosclerosis Risk in Communities, FDPS-Finnish Diabetes Prevention Study, CSCCS-Chin Shan Community
Cardiovascular study, MRFIT-Multiple Risk Factor Intervention Trial, NHANES-National Health and Nutrition Examination Survey, QFS-Quebec Family Study, M-Men, W-Women, PCS-Prospective Cohort Study, CSS-Cross-Sectional
the work in the literature examining the association between depres-
sion and the incidence of type 2 diabetes are presented in Table 4.
The results show that depression is highly associated with the inci-
0.48 (0.35–0.66)
0.40 (0.29–0.56)
0.54 (0.36–0.80) dence of type 2 diabetes. In the context of gender, depressed men are at
higher risk of incidence type 2 diabetes, whereas depression in women
is not associated with type 2 diabetes [135]. Moreover, compared to
Caucasian, Hispanic, Japanese-American and Chinese-American,
1.0
OR
depressed African-Americans are at 2.56 times higher risk of incidence

type 2 diabetes [136]. Based on self rating depression scale (SDS) score,
Uric acid (micro mol/l)
an individual having a score of 48–80 is at higher risk of developing

diabetes compared to an individual having a score of 20–39 [137]. Sim-
ilarly, an individual having a score P11 using center for epidemiolog-
ical studies depression scale (CES-D) or a score P8 using beck
460–548
380–460
Findings
depression inventory (BDI) is at higher risk of incidence type 2 diabetes

>548
<380
[138,139].
In summary, depression is associated with type 2 diabetes. How-
ever, the association is different in men and women. Moreover, the
smoking, alcohol consumption, BMI,
study by Yu et al. [140] show that depression itself is not a risk factor
Age, sex, race, educational level,
for diabetes, rather the activities related to depression such as physical

hypertension, and serum total
inactivity, poor diet, and obesity lead to diabetes. In addition, the med-
ical drugs used to treat depression also have an association with the
incidence of type 2 diabetes. Consequently, similar to high-level serum
uric acid, depression is not an independent risk factor but it emphasizes
Adjusted variables
the impact of other independent risk factors such as gender, ethnicity,

physical inactivity, and obesity.
cholesterol
3.5. Cardiovascular disease
Increased heart rate and cardiovascular disease can elevate the

Follow-up
duration
blood pressure in the arteries. As a result, the body’s glucose uptake

(Years)
decreases leading to insulin resistance condition. Consequently, a per-

–
son suffering from heart disease is at a higher risk of developing type 2

diabetes. However, this association is still obscure. Few studies argue
that a history of cardiovascular disease leads to the incidence of type
2 diabetes [141], while others claim that type 2 diabetes increases
the risk of cardiovascular disease [142–144]. Yeung et al. [141] exam-
ined the association between family history of coronary heart disease
Ethnicity
(CHD) and type 2 diabetes (Table 5). The authors concluded that a high
family CHD score is associated to the incidence of type 2 diabetes in
USA
individuals who have a positive history of family diabetes. For the indi-
viduals having a negative family history of diabetes, this association
was non-significant. In summary, it is debatable whether cardiovascu-
lar disease is a risk factor for type 2 diabetes or not.
Age (Years)
3.6. Dyslipidemia
43–51
Dyslipidemia refers to an abnormal level of lipids, such as triglyc-

erides and cholesterol. It is characterized by high triglyceride levels,
increased low-density lipoproteins (LDL) levels and decreased high-
47.5/ 52.5
density lipoproteins (HDL) levels [145]. Elevated LDL and lowered

%M/W
HDL levels lead to beta-cell dysfunction inhibiting insulin secretion

and consequently type 2 diabetes [146,147]. Table 6 shows the charac-
teristics and findings of the work in the literature studying the associ-
Sample size
ation between dyslipidemia and type 2 diabetes.

Dietary fats, that raise the total cholesterol and LDL levels, are con-
(%DM)
14144
sidered significant in the development of type 2 diabetes [148]. Substi-

tuting saturated fatty acid with polyunsaturated fatty acid and animal
fat with vegetable fat can help lower blood cholesterol and eventually
Design
type 2 diabetes. This is because both polyunsaturated fatty acid and

CSS
vegetable fat are inversely related to the risk of incidence type 2 dia-
betes with RR 0.84 (95% CI 0.71–0.98) and RR 0.78 (95% CI 0.67–0.91)
NHANES III [43,44]
respectively for the highest quintile of intake [148]. Tajima et al.

[149] also confirmed the association between high cholesterol diet
intake (>273 mg/day) and type 2 diabetes (RR 1.25, 95% CI 1.16–
1.36) compared to low cholesterol intake (<185 mg/day).
Study
In order to reduce elevated LDL level, LDL lowering therapy and

Table 1 (continued)
drugs are suggested. However, these drugs and therapy are found
2011
Year
to be associated with a higher risk of type 2 diabetes [150]. Indi-

viduals having familial hypercholesterolemia, a genetic disorder that
Work
results in high LDL levels, are less likely to have type 2 diabetes
[30]
Study.
compared to individuals having high LDL levels due to dietary pat-

terns [151]. Zhang et al. [152] in their analysis found that the ratio
1763
Table 2

Characteristics and findings of the studies examining the association between sleep quantity/quality and type 2 diabetes.
Work Year Study Design Sample size (%DM) %M/W Age (Years) Ethnicity Follow-up Adjusted variables Findings
duration (Years)
[79] 2003 NHS [80] PCS 70026 (2.81%) 0/100 40–65 United States 10 Working hours, hypercholesterolemia, Sleep (Hours) OR
hypertension, smoking, snoring, 65 1.18 (0.96–1.44)
exercise, alcohol, depression, 6 1.10 (0.97–1.25)
postmenopausal hormone use, BMI, 7 1.02 (0.91–1.16)
and family history of diabetes 8 1.0
>9 1.29 (1.05–1.59)
[56] 2004 RS [81] PCS 2265 (1.67%) 100/0 – Japanese 8 Age, education, occupation, shift work, Sleep HR
BMI, leisure time, physical activity, DIS (low frequency) 1.0
smoking, alcohol consumption and DIS (high frequency) 2.98 (1.36–6.53)
family history of diabetes DMS (low frequency) 1.0
DMS (high frequency) 2.23 (1.08–4.61)
[57] 2004 MPP [82] PCS 6599 (4.3%) 100/0 Mean 42.6 Swedish and Caucasians 15.2 Age, lifestyle, family history of DIS OR
diabetes, social class, physical activity, No 1.0
BMI, smoking, and alcohol intake Yes 1.52 (1.05–2.20)
[59] 2005 MONICA [35] PCS 8269 (2.27%) 50.1/49.9 25–75 Germany 7.5 Age,educational level, parental history DIS OR
of diabetes, smoking, alcohol No 1.0
consumption, hypertension, physical Yes (M) 1.10 (0.59–2.03)
activity, history of angina pectoris, Yes (W) 1.42 (0.81–2.50)
BMI, and dyslipidemia DMS
No 1.0
Yes (M) 1.60 (1.05–2.45)
No (W) 1.98 (1.20–3.29)
[83] 2005 SHHS [84] CSS 1486 48.6/ 51.4 53–93 United States – Age, sex, ethnicity, waist girth, and Sleep (Hours) OR
apnea-hypopnea index 65 2.51 (1.57–4.02)
1764
6 1.66 (1.15–2.39)
7–8 1.0
P9 1.88 (1.21–2.91)
[52] 2005 RS PCS 1170 (7.52%) 47/53 45–65 Swedish 12 Age, marital status, living conditions, Sleep (Hours) RR
hypertension, obesity, smoking, 7–8 1.0

alcohol use, snoring and depression 65 (M) 2.8 (1.1–7.3)
65 (W) 1.8 (0.5–6.8)
P9 (W) 2.9 (0.6–15.0)
[50] 2005 RS PCS 1462 (8.62%) 0/100 38–60 Swedish 32 Age, subscapular skin-fold thickness, No association between sleep duration and
serum lipid values, blood pressure, diabetes.
resting heart rate, physical activity,
education and socio-economic status
[85] 2006 MMAS [86] PCS 1139 (7.90%) 100/0 40–70 Blacks and Whites (USA) 17 Age, hypertension, smoking, self rated Sleep (Hours) RR
health status, waist circumference, 65 1.71 (0.81–3.59)
education, testosterone, and cortisol 6 1.95 (1.06–3.58)
7 1.0
8 1.40 (0.78–2.54)
>8 3.03 (1.44–6.37)
[87] 2007 NHANES I [88] PCS 8992 (4.78%) 37.5/ 62.5 32–86 Whites and 10 Physical activity, depression, alcohol Sleep (Hours) OR
Non-whites (USA) consumption, ethnicity, education, 65 1.47 (1.03–2.09)
marital status, age, obesity and 6 1.08 (0.80–1.47)
hypertension 7 1.0
8 1.09 (0.83–1.43)
P9 1.52 (1.06–2.17)
[89] 2007 QFS [90] CSS 740 43.65/ 56.35 21–64 Europid race 12 Age, marital status, employment Sleep (Hours) OR
status, educational level, annual 5–6 2.09 (1.34–2.98)
income, physical activity, alcohol 7–8 1.0
intake, coffee intake, hypertension, 9–10 1.58 (1.13–2.31)
Table 2 (continued)
duration (Years)
heart disease and waist circumference
[58] 2007 HIPOP-OHP [91] PCS 6509 (3.53%) 78.4/21.6 32–86 Japanese 4.2 Age, sex, BMI, history of smoking, DIS HR
history of hypertension, history of high No 1.0
cholesterol, history of diabetes and Low frequency 1.42 (1.05–1.91)
physical activity High frequency 1.61 (1.00–2.58)
[92] 2008 FIN-D2D [93] CSS 2770 48.2/51.8 45–74 Finland 1 Age, BMI, medication for sleep, Subjects with 66 and P8 hours of sleep are
antidepressants, smoking, sleep apnea more likely rightarrow have type 2 diabetes.
probability, and physical activity
[94] 2009 QFS [90] PCS 274 42.7/ 57.3 21–64 Europid race 6 Age, smoking habits, employment Sleep (Hours) RR
status, annual household income, shift 66 2.42 (1.49–3.33)
working history, resting metabolic 7–8 1.0
rate, coffee intake, waist P9 2.31 (1.41–3.15)
circumference and physical activity
[55] 2009 IRAS [95] – 900 (16.22%) 43.3/56.7 40–69 Non-Hispanic Whites, 5 Age, sex, glucose tolerance, Sleep (Hours) OR
Hispanics, and African- hypertension, family history of 8 1.0
Americans diabetes, smoking, educational level, NHW/Hispanics
BMI, insulin sensitivity, and acute 67 2.36 (1.11–5.99)
insulin response P9 2.15 (0.50–9.30)
African-American
67 0.63 (0.14–2.90)
P9 0.39 (0.02–7.19)
[96] 2009 RS CSS 1741 42.6/ 57.4 P20 Pennsylvania - Age, race, sex, BMI, smoking, alcohol Sleep (Hours) OR
consumption, depression and sleep 65 2.95 (1.2–7.0)
disordered breathing 5–6 2.07 (0.68–6.4)
1765
P6 1.0
[97] 2009 RS – 515 33/67 40–64 Finland 7 Age, sex, BMI, study center, smoking, Sleep (Hours) HR
alcohol intake, hypertension 66.5 1.68 (0.79–3.59)
medication, leisure time physical 7–8.5 1.0
activity, and 1 year change in body 9–9.5 2.29 (1.38–3.80)
P10 2.74 (1.67–4.50)

weight
[98] 2010 NIH-AARP [99] PCS 174344 56.8/43.2 50–71 Whites and 8 Age, race, sex, educational level, Day napping (Hours) OR
non-whites (USA) marital status, smoking, coffee intake, 0 1.0
alcohol intake, calorie intake, BMI, and <1 1.23 (1.18–1.29)
physical activity P1 1.55 (1.45–1.66)
Sleep (Hours)
65 1.46 (1.31–1.63)
5–6 1.11 (1.06–1.16)
7–8 1.0
P9 1.11 (0.99–1.24)
[100] 2011 RS CSS 3470 (5.2%) 61.8/ 38.2 P25 Taiwan - BMI, WHR, family history of diabetes, Sleep (Hours) OR
family history of hypertension, <6 1.55 (1.07–2.24)
smoking, alcohol consumption and 6–8.49 1.0
coffee intake P8.5 2.83 (1.19–6.73)
[51] 2012 EPIC-Potsdam PCS 23620 (3.6%) 38.63/ 61.37 35–65 Germany 7.8 Age, sex, sleeping disorders, alcohol Sleep (Hours) HR
[101] intake, smoking, walking, cycling, <6 1.06 (0.80–1.40)
sports, employment status, education, 6-<7 0.94 (0.78–1.14)
BMI, WHR, hypertension, caffeinated 7-<8 1.0
beverages, life satisfaction, health 8-<9 0.92 (0.77–1.10)
satisfaction, and intake of P9 1.05 (0.82–1.33)
antidepressants
(continued on next page)

Table 2 (continued)
duration (Years)
[102] 2012 RS PCS 3570 78.6/ 21.4 (3.4%) 35–55 Japan 4 Age, sex, fasting plasma glucose level, Sleep (Hours) OR
education, working hours, shift work, 65 5.37 (1.38–20.91)
rate of sedentary work, occupational 5–6 1.38 (0.50–3.79)
stress, smoking, alcohol intake and 6–7 1.57 (0.64–3.83)
physical exercise 7–8 1.0
[53] 2012 NHIS [103] CSS 29818 53.5/ 46.5 18–85 Blacks and 10 Age, sex, income, hypertension, heart Sleep (Hours) OR
whites (USA) disease, depression and obesity 6–8 1.0
65 (Blacks) 1.66 (1.19–2.30)
65 (Whites) 1.87 (1.57–2.24)
P9 (Blacks) 1.68 (1.21–2.33)
P9 (Whites) 2.33 (1.98–2.73)
[104] 2013 IHHP [105] CSS 12514 49/ 51 P19 – – Age, sex, BMI, and waist circumference Sleep (Hours) OR
65 1.62 (1.33–1.99)
6 0.92 (0.75–1.13)
7–8 1.0
P9 1.10 (0.83–1.44)
[106] 2013 MC [107] PCS 47093 (1.85%) 74.4/ 25.6 Mean 34.9 USA 6 Age, sex, BMI, education and race Sleep (Hours) OR
65 2.04 (1.49–2.8)
5 1.46 (1.15–1.84)
6 1.19 (0.99–1.43)
7 1.0
8 1.17 (0.95–1.45)
P8 1.30 (0.93–1.81)
[54] 2013 NHIS [103] CSS 130943 (10.12%) 99.75/ 0.25 Mean 50.6 Blacks and 7 Age, sex, household income, poverty Sleep (Hours) OR
7 1.0
1766
whites (USA) status, education, occupation,

employment status, alcohol 66 (Blacks) 1.08 (0.95–1.23)
consumption, smoking, leisure time 66 (Whites) 1.16 (1.07–1.25)
physical activity, marital status, heart P8 (Blacks) 1.01 (0.89–1.15)
disease, hypertension, and BMI 8 (Whites) 1.17 (1.09–1.26)
[108] 2013 45 and up [109] PCS 156902 36/ 64 50–82 Australia - Age, sex, education, marital status, Sleep (Hours) HR

residential remoteness, alcohol
consumption, smoking status, health
insurance status, income, BMI, 7 1.0
physical activity and baseline health 66 1.29 (1.08–1.53)
DIS-Difficulty Initiating Sleep, DMS-Difficulty Maintaining Sleep, EPIC-European Prospective Investigation into Cancer and Nutrition, FIN D2D-Finnish type 2 Diabetes, HIPOP-OHP-High risk and Population Strategy for Occu-
pational Health Promotion, IHHP-Isfahan Healthy Heart Program, IRAS-Insulin Resistance Atherosclerosis Study, M-Men, MC-Millennium Cohort, MMAS-Massachusetts Male Aging Study, MONICA-Multinational MONItoring of
trends and determinants in CArdiovascular disease, MPP-Malmo Preventive Project, NHANES-National Health and Nutrition Examination Survey, NHIS-National Health Interview Survey, NHS-Nurse Health Study, NHW-Non
Hispanic Whites, NIH AARP-National Institutes of Health American Association of Retired Persons Diet and Health Study, QFS-Quebec Family Study, RS-Random Sample, SHHS-Sleep Heart Health Study, W-Women, PCS-Prospective
Cohort Study, CSS-Cross-Sectional Study.
Table 3

Characteristics and findings of the studies examining the association between smoking and type 2 diabetes.
Work Year Study Design Sample Size %M/W Age (Years) Ethnicity Follow-up Adjusted Variables Findings
(%DM) Duration
(Years)
[110] 1989 ZS [111] PCS 841 (6.9%) 100/0 40-59 Dutch 25 Age, subscapular skin-fold, resting Cigarettes/day HR
heart rate, cigarette use, alcohol intake 0 1.0
and energy intake 20 3.3 (1.4-7.9)
[67] 1993 NHS [80] PCS 114247 (2.04%) 0/100 30-55 USA 12 Age, BMI, family history of diabetes, Cigarettes/day RR
menopause, postmenopausal hormone 0 1.0
use, oral contraceptive use, alcohol 1-14 0.90 (0.68-1.19)
consumption, and physical activity 15-24 1.20 (0.96-1.50)
>25 1.49 (1.19-1.87)
Ex-smoker 1.17 (1.02-1.35)
[68] 1995 HPFS PCS 41810 (1.22%) 100/0 40-75 USA 62 Age, BMI, family history of diabetes, Cigarettes/day RR
alcohol consumption and physical 0 1.0
activity 1-14 1.37 (0.77-2.43)
15-24 2.38 (1.57-3.59)
>25 1.94 (1.25-3.03)
Ex-smoker 1.29 (1.05-1.57)
[112] 1997 RS PCS 2312 (1.77%) 100/0 - Japanese 8 - Cigarettes/day HR

0 1.0
1-15 1.33 (0.40-4.39)
16-25 3.59 (1.32-9.76)
>26 2.68 (0.88-8.05)
[73] 1997 SOF [113] CSS 9435 (7%) 0/100 P65 Non-black (USA) - Age, resting heart rate, BMI, education Cigarettes/day OR
level, alcohol intake, energy 0 1.0
expenditure, WHR, and 610 0.55 (0.30-0.99)
1767
postmenopausal hormone use >10 1.21 (0.87-1.71)

Ex-smoker 0.99 (0.82-1.19)
[114] 1999 OHS PCS 6250 (7.2%) 100/0 25-60 Japan 16 Age, BMI, alcohol consumption, Cigarettes/day RR
physical activity, parental history of 0 1.0
diabetes, fasting plasma glucose, total 1-20 1.40 (1.05-1.86)
cholesterol, and triglycerids 21-30 1.40 (1.02-1.93)

>30 173 (1.20-2.48)
[69] 2000 PHS [115] PCS 21068 (3.65%) 100/0 40-84 USA 12.10 Age, BMI, physical activity, history of Cigarettes/day RR
hypertension, history of high 0 1.0
cholesterol, parental history of <20 1.5 (1.0-2.2)
myocardial infarction, and alcohol P20 1.7 (1.3-2.3)
consumption Ex-smoker 1.1 (1.0-1.4)
[116] 2001 RS CSS 3718 19.2/ 80.0 12-88 Chinese - Age, BMI, alcohol consumption, and Smoking OR
family history of diabetes No 1.0
Yes 1.705 (1.106-
2.630)
[65] 2001 BRHS [117] PCS 7124 (4.07%) 100/0 40-59 UK 16.8 Age, BMI, physical activity, alcohol Smoking RR
intake, social class, heart disease and No 1.0
antihypertensive treatment Yes 1.61 (1.05-2.46)
Pipe/cigar 2.15 (1.24-3.70)
Ex-smoker (15 yrs.) 1.45 (0.95-2.21)
Ex-smoker (10 yrs.) 2.03 (1.22-3.37)
[63] 2001 CPS-I [118] PCS 709827 (3.6%) 38.8/ 61.2 P30 Whites and Blacks (USA) 13 Age, BMI, alcohol consumption, race, Cigarettes/day OR
amount of exercise, education level, 0 1.0
and intakes of fats and carbohydrates <20 (M) 1.05 (0.98-1.12)
<20 (W) 0.98 (0.93-1.03)
20-39 (M) 1.19 (1.13-1.26)
20-39 (W) 1.21 (1.14-1.29)

Table 3 (continued)
(%DM) Duration
(Years)
P40 (M) 1.45 (1.34-1.57)

P40 (W) 1.74 (1.49-2.03)
Ex-smoker (M) 1.07 (1.02-1.13)
Ex-smoker (W) 1.07 (0.99-1.15)
[119] 2001 NHS [80] PCS 84941 (3.9%) 0/100 30-55 USA 16 Age, family history of diabetes, Cigarettes/day OR
menopausal status, postmenopausal 0 1.0
hormone use, fat intake, and physical 1-14 1.14 (0.85-1.54)
activity P15 1.40 (1.14-1.71)
[120] 2002 NCDS [121] - 15396 M/W - UK 33 Maternal smoking during pregnancy, Cigarettes/week OR
sex, mother’s age at the time of giving Self
birth, age at which mother left school, 0 1.0
family social class at birth, birth <1 2.07 (0.25-17.19)
weight, own smoking at the age of 16, 1-9 1.92 (0.52-7.10)
and BMI at the age of 33 10-19 2.48 (0.52-11.97)v
20-29 1.61 (0.20-12.96)
P30 3.62 (1.42-9.24)
Mother
Non-smoker 1.0
Medium-smoker 1.01 (0.23-4.53)
Medium to heavy-smoker 3.53 (0.88-14.38)
Heavy-smoker 4.02 (1.14-14.14)
[74] 2004 RIH CSS 27777 45/ 55 20-69 France - Age, BMI, WHR, and alcohol Smoking OR
consumption No 1.0
Yes (M) 1.49 (1.13-1.96)
1768
Yes (W) 0.89 (0.54-1.39)

Ex-smoker (M) 1.31 (1.01-1.70)
Ex-smoker (W) 1.46 (0.92-2.22)
[122] 2004 NTHS [123] PCS 38805 46.9/ 53.1 P20 Norwegian 11 Age, BMI, and sex Cigarettes/day RR
0 1.0
P20

1.64 (1.12-2.39)
[70] 2005 IRAS [95] PCS 906 (25%) 43.3/ 56.7 40-69 Non-Hispanic Whites, 5 Age, sex, ethnicity, BMI, WHR, glucose Smoking OR
Hispanics, and African- tolerance status, HDL cholesterol level, No 1.0
Americans triglyceride level and hypertension Ex-smoker 1.31 (0.82-2.09)
Current-smoker 2.66 (1.49-4.77)
[77] 2006 KMIC [124] PCS 27635 100/0 35-44 Korea 8 Age, baseline fasting serum, glucose, Cigarettes/day OR
weight change, baseline BMI, family No 1.0
history of diabetes, alcohol <10 1.23 (1.86-1.77)
consumption, and physical activity 10-19 1.60 (1.28-2.00)
P20 1.75 (1.35-2.27)
Ex-smoker (P8 yrs.) 0.95 (0.72-1.25)
Ex-smoker (7-7.9 yrs.) 1.44 (0.96-2.15)
Ex-smoker (5-6.9 yrs.) 2.13 (1.51-3.00)
[71] 2009 RS PCS - M/W 40-69 Ansung and Ansan Korean 4 Age, family history of diabetes, rural or Cigarettes/day RR
urban area, waist, body fat, exercise, No 1.0
alcohol consumption, income, <20 2.06 (1.35-3.16)
education, WBC, HDL cholesterol, YP20 2.41 (1.48-3.93)
triglyceride, systolic BP, HOMA IR, and Ex-smoker 1.60 (1.07-2.39)
HOMA beta
Table 3 (continued)
(%DM) Duration
(Years)
[75] 2010 ARIC [36] PCS 10892 (11.51%) 43.3/ 56.7 45-64 Whites and 9 Race, sex, level of education, BMI, Smoking HR
Non-whites (USA) waist circumference, baseline age, No 1.0
physical activity, HDL cholesterol, Ex-smoker (9 yrs.) 1.16 (0.99-1.36)
triglycerides, and systolic BP Ex-smoker (6-9 yrs.) 1.21 (0.89-1.65)
Ex-smoker (3-6 yrs.) 1.54 (1.10-2.14)
Ex-smoker (<3 yrs.) 1.80 (1.44-2.25)
Current-smoker 1.26 (1.08-1.46)
[66] 2010 KORA S4/F4 PCS 885 50.4/ 49.6 55-74 Germany 7 Age, sex, parental diabetes, Smoking OR
[125] socioeconomic status, alcohol intake, No (passive+active) 1.0
physical activity, intake of meat and Passive 2.5 (1.1-5.6)
sausage, intake of salad and Passive+prediabetes 4.4 (1.5-13.4)
vegetables, intake of whole grain Active 2.8 (1.3-6.1)
bread, coffee consumption, waist Active+prediabetes 7.8 (2.4-25.7)
circumference, blood pressure,
hypertriglyceridemia, HDL cholesterol,
log insulin and log adiponectin
[64] 2010 KCPS [126] PCS 1236443 63.7/ 36.3 30-95 Korea 14 Age, alcohol drinking, BMI, and Cigarettes/day HR
physical exercise No 1.0
1-9 (M) 1.30 (1.25-1.32)
1-9 (W) 1.34 (1.25-1.44)
10-19 (M) 1.37 (1.34-1.41)
10-19 (W) 1.26 (1.14-1.38)
P20 (M) 1.55 (1.51-1.60)
P20 (W) 1.33 (1.15-1.53)
1769
[72] 2011 NHS [80] PCS 100526 (5.36%) 0/100 41-55 USA 24 Age, BMI, physical activity, husband’s Cigarettes/day RR
education, family history of diabetes, No 1.0
total energy intake, alcohol intake, Low passive 1.10 (0.94-1.23)
caffeine, total transa fat, toatl High passive 1.16 (1-1.35)
saturated fat, calcium, magnesium and 1-14 1.39 (1.17-1.64)
vitamin D 15-24 1.68 (1.43-2.01)

P25 1.98 (1.57-2.36)
Ex-smoker 1.28 (1.12-1.50)
[78] 2012 JPHC [127] PCS 59834 43.24/ 56.76 Mean 55-57.9 Japanese 5 and 10 Age, BMI, history of hypertension, Smoking OR
alcohol intake, family history of No 1.0
diabetes, weight change, study area, Current-smoker (M) 1.43 (1.16-1.76)
and leisure time physical activity Current-smoker (W) 1.42 (1.03-1.94)
Ex-smoker (<5 yrs.) (M) 1.68 (1.07-2.63)
Ex-smoker (<5 yrs.) (W) 2.84 (1.53-5.29)
[76] 2012 RS PCS 2070 (11.9%) 100/0 40-69 Japan 9.2 Age, blood glucose, fasting, systolic BP, Smoking HR
total cholesterol, log-transformed No 1.0
triglycerides, alcohol consumption, Ex-smoker (>9 yrs.) 2.22 (1.05-4.69)
exercise, family history of diabetes, Ex-smoker (6-9 yrs.) 0,59 (0.13-2.64)
BMI, and change in smoking status Ex-smoker (3-5 yrs.) 1.95 (0.62-6.17)
during follow-up period Ex-smoker (<3 yrs.) 1.91 (0.60-6.06)
No Current-smoker 2.78 (1.43-5.41)
[128] 2013 WHI [129] PCS 11838 0/100 50-79 USA 11 Age, ethnicity, education, BMI, waist Smoking HR
circumference, alcohol consumption, No 1.0
physical activvity, hypertension and Current-smoker (M) 1.28 (1.20-1.36)
medication for high cholesterol Ex-smoker (<3 yrs.) 1.43 (1.26-1.63)
ZS-Zutphen Study, NHS-Nurse Health Study, NHIS-National Health Interview Survey, HPFS-Health Professionals’ Follow-up Study, RS-Random Sample, SOF-Study of Osteoporotic Fractures, OHS-Osaka Health Survey, PHS-
Physicians Health Survey, BRHS-British Regional Health Study, CPS-Cancer Prevention Study, NCDS-National Child Development Study, RIH-Regional Institute for Health, NTHS-Nord Trondelag Health Survey, IRAS-Insulin
Resistance Atherosclerosis Study, ARIC-Atherosclerosis Risk in Communities, KCPS-Korean Cancer Prevention Study, JPHC-Japan Public Health Center, WHI-Women Health Initiative, KMIC-Korean Medical Insurance Corporation,
M-Men, W-Women, PCS-Prospective Cohort Study, CSS-Cross-Sectional Study.
Table 4
Characteristics and findings of the studies examining the association between depression and type 2 diabetes.
Work Year Study Design Sample size (%DM) %M/W Age Ethnicity Follow-up Adjusted variables Findings
(Years) Duration (Years)
[137] 1991 RS PCS 2380 (1.72%) 100/0 P18 Japanese 8 Age Depression (SDS HR
score)
20–39 1.0
40–47 1.07 (0.53–2.13)
48–80 2.32 (1.06–5.08)
[155] 1996 ECAPS [156] - 1715 (5.2%) 37.8/ 62.2 P18 USA 13 Age, sex, race and BMI Depression OR
No 1.0
Yes 2.23 (0.90–5.55)
[157] 2003 NHANES I [88] PCS 6190 45.7/ 54.3 25–74 Whites and Non-whites 15.6 Age, sex and race Depression RR
(USA) No 1.0
Mild 1.24 (0.91–1.70)
Major 2.52 (1.73–3.67)
[158] 2004 ARIC [36] PCS 11615 44.85/ 55.15 48–67 Whites and Non-whites 6 Age, sex, race, study site, fasting Depression HR
(USA) insulin, fasting glucose, HDL No 1.0
cholesterol, BMI, WHR, systolic BP, Low 1.12 (0.90–1.39)
physical activity, total calorie intake, Mild 1.03 (0.81–1.31)
smoking status, and education Major 1.31 (1.04–1.64)
1770
[136] 2004 SWAN [159] PCS 2662 (3.64%) 0/100 42–52 Caucasian, African- 3 Age, study site, race, education, and Depressed African-Americans are 2.56
American, Hispanic, medication use times more likely rightarrow have
Japanese-American and diabetes.
Chinese-American
[160] 2007 NTHS [123] PCS 37291 47.2/ 52.8 P29 Norwegian 10 Age, sex, education, smoking, physical Depression OR

activity, BMI, WHR, waist No 1.0
circumference, and marital status Yes 1.40 (1.16–1.69)
[138] 2007 CHS [161] PCS 4681 40.8/ 59.2 P65 USA 8 Age, race, sex, educational level, Depression OR
marital status, physical activity, (CES-D score)
smoking, alcohol consumption, BMI, <8 1.0
and reactive protein level P8 1.57 (1.07–2.29)
[139] 2014 RBHCDS - 971 43/ 57 P50 California 8 Age, sex, BMI and exercise Depression (BDI OR
score)
<11 1.0
P11 2.50 (1.29–4.87)
RS-Random Sample, SDS-Self rating Depression Scale, ECAPS-Epidemiologic Catchment Area Program Survey, NHANES-National Health and Nutrition Examination Survey, ARIC-Atherosclerosis Risk in Communities, RNH-
RegistratieNet Huisarts Praktijken, SWAN-Study of Womens’ Health Across the Nation, NTHS-Nord Trondelag Health Study, CHS-Cardiovascular Health Study, CESD-Center for Epidemiological Studies Depression Scale, RBHCDS-
Rancho Bernardo Heart and Chronic Disease Study, BDI-Beck Depression Inventory, M-Men, W-Women, PCS-Prospective Cohort Study, CSS-Cross-Sectional Study.
of non-HDL and HDL levels is an independent risk factor for inci- 3.8. Aging
dence diabetes. They show that an individual having a ratio of
3.1 is at 40% increased risk of incidence diabetes (OR 1.4, 95% CI The number of elderly people (above 60 years) is increasing world-
1.1–1.8) compared to an individual having a ratio of 1.4. Elevated wide. The 900 million global elderly population in 2015 is expected to
non-HDL and lowered HDL levels are significantly associated with rise to 2 billion by 2050 [171]. Aging increases the risk of metabolic
incidence diabetes [153]. syndrome and chronic diseases including type 2 diabetes. Aging
On the contrary to studies confirming the association between low- increases chronic inflammation in an elderly individual leading to insu-
HDL levels and the incidence of type 2 diabetes, Haase et al. [154] in lin resistance [172]. In addition, lipid metabolism disorder due to aging
their study concluded that a life-long reduction in HDL levels are not increases the accumulation of body fat leading to elevated free fatty
associated with an increased risk of type 2 diabetes. They found that acids concentration in the blood/plasma and eventually insulin resis-
the association is most likely reverse causation, i.e., type 2 diabetes tance [173]. Consequently, an aged individual is at higher risk of devel-
leads to low HDL levels. oping type 2 diabetes. However, there is not much work concluding
that aging is an independent risk factor for type 2 diabetes. Choi
et al. [174] concluded that the risk of diabetes increases with aging only
3.7. Hypertension in overweight individuals, and the risk decreases with a moderate level
of physical activity. Aging can be considered as triggering the associa-
Hypertension, also known as high blood pressure, is a medical con- tion between independent risk factors and risk of diabetes, but more
dition in which the blood pressure in the arteries is persistently ele- evidence and studies are required to examine the association between
vated. Hypertension elevates the sympathetic nervous system activity aging as an independent factor and diabetes.
leading to a decrease in the body’s glucose uptake. This causes the con-
dition of insulin resistance and eventually type 2 diabetes. Hyperten-
sion elevates sympathetic nervous system activities leading to 3.9. Ethnicity
impaired vasodilation of skeletal muscles. Consequently, muscle glu-
cose uptake decreases with the eventual development of type 2 dia- Ethnicity is associated with a range of health complications includ-
betes. Table 7 shows the characteristics and findings of the work in ing diabetes because of the heterogeneity in the demographic environ-
the literature studying the association between hypertension and type mental conditions and lifestyle. It is an independent risk factor which
2 diabetes. tends to be exacerbated by the social disadvantage and the affluent
Hayashi et al. [166] examined the association between high normal way of living. Table 8 shows the characteristics and findings of the
blood pressure (P130 and <140 mmHg/P85 and <90) and hyperten- work in the literature studying the association between ethnicity and
sion (P140 mmHg/P90 mmHg), and the incidence of type 2 diabetes type 2 diabetes. Compared to white individuals, type 2 diabetes is more
in men. The authors concluded that both high normal blood pressure prevalent in Pacific Islanders (OR 3.1, 95% CI 1.4–6.8), followed by
(RR 1.39, 95%1.14–1.69) and hypertension (RR 1.75, 95% CI 1.43– Blacks (OR 2.3, 95% CI 2.1–2.6), Native Americans (OR 2.2, 95% CI
2.16) are associated with an increased risk of type 2 diabetes. This asso- 1.6–2.9), Hispanics (OR 2.0, 95% CI 1.8–2.3), and Multiracial (OR 1.8,
ciation is dependent on obesity and hypertension medications. Hyper- 95% CI 1.5–2.9) [175]. In another study by Shai et al. [176], it was found
tension medications are considered to increase the risk of diabetes that compared to whites, Asians (RR 1.94, 95% CI 1.46–2.58), Hispanics
depending on the type of medication [167]. For instance, hypertensive (RR 1.70, 95% CI 1.28–2.26), and Blacks (RR 1.36, 95% CI 1.14–1.63) are
individuals taking thiazide diuretics and angiotensin-converting- at higher risk of incidence type 2 diabetes.
enzyme medications are at lower risk of diabetes compared to the A study by Zimmet et al. [177] showed that type 2 diabetes is 10
hypertensive individuals not taking any medication. However, those times more prevalent in rural Indians compared to rural Melanesians,
taking beta-blockers medication are at 28% higher risk of incidence and 2 times more prevalent in urban Indians compared to urban
type 2 diabetes (HR 1.28, 95% CI 1.04–1.57) [167]. The association Melanesians. They also revealed that the prevalence is 5 times more
between hypertension and the incidence of type 2 diabetes is signifi- in urban Melanesians compared to rural Melanesians. One of the reason
cant in women as well [168]. Women having hypertension are at 2 could be that the rural residents have an increased amount of physical
times increased risk of developing diabetes (HR 2.03, 95% CI 1.77– activity compared to the urban ones, leading to decreased risk of dia-
2.32) compared to women having normal blood pressure (<120/75) betes [178]. It should thus important to have a moderate amount of
[168]. The association is more in overweight and obese women. Irre- physical activity as a therapy for diabetes prevention. Compared to
spective of gender, prehypertension (HR 1.27, 95%CI 1.09–1.48) and Europeans, type 2 diabetes is 3.8 times more prevalent in Indians,
hypertension (HR 1.51, 95% CI 1.29–1.76) are associated with increased and the prevalence increases to 5 times for 40–64 years old individuals
risk of incidence type 2 diabetes [169]. In the context of ethnicity, [179]. In another comparison between Asian and non-Asian ethnicity, it
whites individuals having hypertension are at higher risk of developing is found that the prevalence of type 2 diabetes in Bangladeshis (Asians)
diabetes (HR 1.25, 95% CI 1.03–1.53), but no such association is seen in is more [180]. Furthermore, the prevalence is high in women (5.75
African American hypertensive individuals (HR 0.92, 95% CI 0.70–1.21) times) compared to that in men (2.2 times). However, ethnicity can
[170]. not be considered as an independent risk factor for this association as
In summary, hypertension is associated with the development of Bangladeshis had higher smoking rates and a lower ratio of polyunsat-
type 2 diabetes in both men and women. However, the association is urated fatty acids to saturated fatty acids. Consequently, ethnicity,
ethnicity-dependent. The selection of hypertensive medications should smoking and dyslipidemia all contributed to the risk of incidence type
be made properly as the medication impacts the strength of the associ- 2 diabetes. Simmons et al. [181] also confirmed in their study that the
ation. Furthermore, an obese individual with hypertension is at higher prevalence is more in Asians compared to Whites. However, in contrast
risk compared to a non-obese. to the results obtained by [180], Simmons et al. [181] found that the
Table 5
Characteristics and findings of the studies examining the association between cardiovascular disease and type 2 diabetes.
Work Year Study Design Sample size %M/W Age Ethnicity Follow-up Adjusted variables Findings
(%DM) (Years) duration
(Years)
[141] 2007 ARIC [36] PCS 11297 (11.52%) M/W 45–64 Blacks 9 Age, sex, race, smoking, alcohol CHD risk score HR
and consumption, educational level, <-0.5 1.0
Whites leisure index, BMI, WHR, systolic and 0.5 to 0.49 1.23 (0.98–1.54)
(USA) diastolic pressure, triglycerides, HDL, P0.5 1.43 (1.03–1.99)
glucose, hypertension, WBC count, and
fibrinogen
ARIC-Atherosclerosis Risk in Communities, CDH-Coronary Heart Disease, M-Men, W-Women, PCS-Prospective Cohort Study.
1771
Table 6
Characteristics and findings of the studies examining the association between dyslipidemia and type 2 diabetes.
Work Year Study Design Sample %M/ Age Ethnicity Follow- Adjusted Variables Findings
Size(% W (Years) up
DM) Duration
(Years)
[148] 2001 LWHS PCS 35988 0/100 55–69 USA 11 Age, total energy, WHR, BMI, physical Median cholesterol RR
[162] activity, cigarette smoking, alcohol intake (mg/day)
consumption, education, marital status, 185 1.0
residential area and hormone 201 0.87 (0.74–1.03)
replacement therapy 237 1.07 (0.91–1.25)
281 1.10 (0.94–1.28)
382 1.24 (1.07–1.43)
[154] 2015 CCHS PCS 47627 M/W P20 Danish 36 Age, sex, study, BMI, hypertension, HDL cholesterol RR
[163] and smoking, alcohol intake, physical (m mol/L)
CGPS inactivity, postmenopausal status and 2.5 1.0
[164] hormonal replacement in women, lipid 2 1.44 (1.08–1.91)
lowering therapy, and educational level 1.5 2.72 (2.09–3.54)
1 5.74 (4.43–7.43)
[152] 2018 REACTION PCS 4882 36.5/ P40 Chinese 3 Age, sex, smoking, alcohol, physical Non-HDL/HDL(m mol/L) OR
[165] (14.42%) 63.5 activity, family history of diabetes, BMI, 1.4 1.0
and systolic blood pressure 1.9 1.2 (0.9–1.5)
2.4 1.2 (0.9–1.5)
3.1 1.4 (1.1–1.8)
LWHS-Lowa Women’s Health Study, CCHS-Copenhagen City heart Study, CGPS-Copenhagen General Population Study, MA-Meta Analysis, REACTION-Risk Evaluation of
cAncers in Chinese diabeTic Individuals: a lONgitudinal study, RS-Random Sample, M-Men, W-Women, PCS-Prospective Cohort Study.
prevalence is more in men compared to women. This inconsistency relatives or one first-degree and at least two second-degree relatives
should be examined further. is significant for prevalence of type 2 diabetes. However, it can not be
In summary, ethnicity is associated with the incidence of type 2 dia- denied that the presence of a family history of diabetes can make the
betes. However, there is no definite explanation of why individuals of a association between obesity and diabetes stronger [198]. Given a
particular ethnicity are at higher risk of type 2 diabetes compared to BMIP35, an individual with a family history of diabetes is at a higher
the others. One possible explanation can be the ethnicity-dependent risk of incidence diabetes (OR 26.7, 95% CI 14.4–49.4) compared to
relation between BMI and body fat. For instance, Asians have around the one without a family history of diabetes (OR 6.1, 95% CI3.4–11.2).
3–4 kg/m2 lower BMI compared to Caucasians for a given percentage Furthermore, ethnicity is also considered an important factor in an
of body fat [182]. Another reason could be ethnicity-based insulin sen- obese individual with a family history of diabetes [199,200].
sitivity. Studies show that Asians, Blacks and Mexican Americans are An individual having a family history of diabetes can have an early
less insulin sensitive compared to non-Hispanic Whites [183,184]. onset of diabetes compared to the ones without a family history. How-
ever, it is hard to conclude that which among the maternal, paternal
and both maternal and paternal family history of diabetes is more sig-
3.10. Family history of diabetes
nificant for incidence/prevalence of type 2 diabetes as the results in the
literature are inconsistent [195,201–205].
Family history information can serve as a useful tool for prognosis/-
diagnosis and public health. Family history of diabetes reflects both
genetic as well as environmental factors and can lead to better predic-
3.11. Obesity
tion of incidence type 2 diabetes than only genetic factors and environ-
mental factors alone [192]. Table 9 shows the characteristics and
findings of the work in the literature studying the association between Obesity is a complex health condition that involves an excessive
family history of diabetes and type 2 diabetes. amount of body fat. It is defined by the BMI and further evaluated in
A study by Tsenkova et al. [193] revealed that a family history of terms of fat distribution via the waist-hip ratio. Abdominal fat in the
diabetes is strongly associated with incidence diabetes (OR 2.77, 95% body increases inflammation which decreases insulin sensitivity by
CI 2.03–3.78). Another study also shows that parental history of dia- disrupting the function of beta-cells. The insulin resistance condition
betes is an independent risk factor for diabetes (OR 1.73, 95% CI then leads to the prevalence of type 2 diabetes. Table 10 shows the
1.29–2.33) [194]. However, the association becomes weaker in men characteristics and findings of the work in the literature studying the
free of cardiovascular disease (OR 1.63, 95% CI 1.18-.2.24). Moreover, association between obesity and type 2 diabetes.
the association is much higher in 45–54 years old men (OR 1.99, 95% Ishikawa-Takata et al. [206] found that the risk of diabetes increases
CI 1.38–2.89) compared to 55–68 years old men (OR 1.33, 95% CI significantly for an individual having a BMI greater than 29 kg/m2 . The
0.70–2.52). Furthermore, the prevalence of type 2 diabetes is stronger relative risk of diabetes increases up to 38.8 (95% CI 31.9–47.2) for an
in men compared to women [195]. This indicates that parental history individual having a BMI greater than 34.9 kg/m2 [119]. Furthermore,
of diabetes in combination with other risk factors such as aging, gender study shows that the association between obesity and incidence diabetes
and cardiovascular diseases, increases the risk of incidence type 2 is gender-dependent [207]. For each 2 kg/m2 lower BMI, men are at 23%
diabetes. (15–30%) lower risk of diabetes, whereas women are at 27% (23–32%)
Rodríguez-Moran et al. [196] showed that a family history of dia- lower risk. Further, the association between obesity and diabetes is also
betes in first degree of relative (parents, offspring and siblings) is a dependent on ethnicity [207]. For each 2 kg/m2 lower BMI, Asians are at
strong and independent risk factor for the prevalence of impaired fast- 37% (26–46%) lower risk of diabetes, whereas Australians are at 25% (21–
ing glucose (prediabetes) (OR 11.7, 95% 9.5–21.2) in children and ado- 29%) lower risk.
lescents. This is in the absence of obesity. The results reveal that is it Ohnishi et al. [208] found that compared to overall obesity, central
important to consider the parental history of diabetes while screening obesity is highly associated with the risk of type 2 diabetes (RR 2.07,
for diabetes children and adolescents. This is because only obesity- 95% CI 1.03–4.16). This association is more in elderly people
based screening could lead to underestimation. Valdez et al. [197] also (P60 years) (OR 3.8, 95% CI 1.8–7.7) [209]. The association between
showed that the family history of diabetes in at least two first-degree central obesity and the incidence of type 2 diabetes is found significant
1772
Table 7
Characteristics and findings of the studies examining the association between hypertension and type 2 diabetes.
Work Year Study Design Sample size (%DM) %M/W Age Ethnicity Follow- Adjusted variables Findings
(Years) up
duration
(Years)
[166] 1999 RS PCS 7594 (7.9%) 100/0 30–65 Japanese 16 Age, BMI, alcohol consumption, smoking habits, leisure Blood pressure in mmHg RR
time physical activity, and parental history of diabetes 6130/685 1.0
130–139/85–89 1.39 (1.14–1.69)
P139/P89 1.76 (1.43–2.16)
[167] 2000 ARIC [36] PCS 12550 44.39/ 55.61 45–64 Blacks 3 and 6 Age, sex, race, BMI, WHR, educational level, smoking Hypertension medication HR
and status, alcohol consumption, physical activity, systolic and None 1.0
Whites diastolic blood pressure, fasting serum insulin ACE inhibitor 0.98 (0.72–1.34)
(USA) concentration, history of hypercholesterolemia, Beta-blocker 1.28 (1.04–1.57)
cardiovuscular diseases, pulmonary dieseases, renal Calcium-channel antagonist 1.17 (0.83–1.66)
insufficiency, and family history of diabetes Thiazide diuretic 0.91 (0.73–1.13)
[168] 2007 WHS [185] PCS 38172 (4.38%) 0/100 P45 USA 10.2 Age, ethnicity, smoking, BMI, exercise, alcohol Blood pressure in mmHg HR
consumption, history of hypercholesterolameia, 120–129/75–84 1.0
educational level, family history of diabetes, and 130–139/85–89 1.45 (1.23–1.71)
randomized treatment assignments P140/P90 2.03 (1.77–2.32)
[170] 2011 ARIC [36], PCS 10893 (9.45%) 43/57 35–54 African- Median Age, sex, BMI, fasting glucose, DL cholesterol and Blood pressure in mmHg HR
1773
CARDIA [186], and American 8.9 triglycerids 6119/6 79 1.0

FHS [187] and 120–139/80–89 1.32 (1.09–1.61)
Whites P140/P90 1.25 (1.03–1.53)
(USA)
[188] 2012 GPPS [189] PCS 7494 (12.02%) 100/0 47–55 Swedish 35 Age, BMI, cholesterol level, antihypertensive treatment, Blood pressure in mmHg HR
smoking, physical activity and occupational class 6129 1.0

130–159 1.43 (1.12–1.84)
P160 1.95 (1.55–2.46)
684 1.0
85–89 1.34 (1.12–1.62)
P90 1.08 (1.06–1.11)
[169] 2015 KGES [190] PCS 7150 (14.7%) 47.46/ 52.54 40–69 Korean 8 Age, BMI, fasting plasma glucose, total cholesterol, HDL Blood pressure in mmHg HR
cholesterol, family history of diabetes, education, alcohol 6120/680 1.0
consumption and smoking status 120–139/80–89 (M) 1.24 (1.01–1.52)
120–139/80–89 (W) 1.30 (1.03–1.64)
P140/P90 (M) 1.65 (1.34–2.05)
P140/P90 (W) 1.34 (1.05–1.70)
RS-Random Sample, ARIC-Atherosclerosis Risk in Communities, WHS, Women’s Health Study, CARDIA-Coronary Artery Risk Development in Young Adults, FHS-Framingham Heart Study, GPPS-Gothenburg Primary Prevention
Study, KGES-Korean Genome and Epidemiology Study, M-Men, W-Women, PCS-Prospective Cohort Study.
Table 8
Characteristics and findings of the studies examining the association between ethnicity and type 2 diabetes.
Work Year Study Design Sample size (%DM) %M/W Age Ethnicity Follow-up Adjusted variables Findings
(Years) duration
(Years)
[177] 1983 RS - 2638 46.81/53.19 P20 Melanesians and Indians - Age The prevalence of diabetes in rural Indian men is
7.5 times more than rural Melanesian men, and is
2.93 times more in urban Indian males compared
to urban Melanesian men. For women, the
prevalence in rural and urban Indians is 12.6 and
1.5 times more compared to rural and urban
Melanesians respectively.
[179] 1985 RS - 61130 (1.87%) M/W All age Asians and Europeans - Age The prevalence of diabetes in Asians was 3.8 times
higher than in Europeans. For the patients age
between 40–64, the prevalence was at least 5
times higher in Asians.
[180] 1988 RS - 253 65.6/ 34.4 35–69 Bangladeshi and Non-Asian - Age The prevalence of diabetes in Bangladeshi men
and women is 2.2 and 5.75 times compared to
Non-Asian men and women respectively.
[181] 1989 RS - 4020 48.4/ 51.6 20–79 Asian and White - Age The prevalence of diabetes in Asian men and
1774
women are 4 and 2 times compared to White men

(11.2% vs 2.8%) and women (8.9% vs 4.3%)
respectively.
[175] 2003 BRFSS [191] - 163584 48.6/51.4 P30 Asian, Black, Hispanic, Native - Age, sex and BMI Ethnicity OR
American, Pacific Islander, White, White 1.0

Other and Multiracial Asian 1.0 (10.7–1.4)
Black 2.3 (2.1–2.6)
Hispanic 2.0 (1.8–2.3)
Native American 2.2 (1.6–2.9)
Pacific Islander 3.1 (1.4–6.8)
Other 1.4 (1.0–1.9)
Multiracial 1.9 (1.5–2.9)
[176] 2006 NHS [80] PCS 78419 (4.90%) 0/100 30–55 White, Asian, Hispanic, and Black 20 Age, BMI, family history of diabetes, Ethnicity RR
alcohol consumption, physical White 1.0
exercise, and smoking Asian 1.94 (1.46–2.58)
Hispanic 1.70(1.28–2.26)
Black 1.36(1.14–1.63)
RS-Random Sample, BRFSS-Behavioral Risk Factor Surveillance System, NHS-Nurses’ Health Study, PCS-Prospective Cohort Study.
Table 9

Characteristics and findings of the studies examining the association between family history of diabetes and type 2 diabetes.
Work Year Study Design Sample size %M/W Age (Years) Ethnicity Follow-up duration Adjusted variables Findings
(%DM) (Years)
[204] 1981 RS - 3177 - >5 Pima Indians - Age and BMI Family History OR
No 1.0
Mother/father 2.3
both 3.9
[195] 1993 SAHS - 4914 43/ 57 Mean 42– Mexicans, Americans and Non- 9 Age and ethnicity Family History OR (Men)
44.8 Hispanics No 1.0
Mother 3.44 (2.32–5.12)
father 3.49 (2.16–5.64)
both 3.73 (1.72–8.08)
Family History OR (Women)
No 1.0
Mother 2.03 (1.47–2.81)
father 1.35 (0.83–2.19)
both 2.59 (1.41–4.77)
[200] 1993 MRFIT [40–42] - 5905 100/0 - Blacks and Whites (USA) 6 Age Family History RR (Black)
No 1.0
Mother/father 3.62 (1.55–8.47)
Family History RR (White)
No 1.0
Mother/father 1.85 (1.38–2.48)
[205] 1994 MA PCS 11334 M/W P40 Taiwan - - Family History OR

Age at onset 40–49
No 1.0
Mother 4.41 (1.71–10.13)
1775
father 2.21 (0.25–8.86)

Family History RR
Age at onset 50–59
No 1.0
Mother 1.57 (0.40–4.41)
father 2.80 (0.54–9.07)

Family History RR
Age at onset P60
No 1.0
Mother 1.22 (0.38–3.05)
father 0.56 (0.01–3.31)
[194] 1995 THHP - 7210 (12.81%) 100/0 45–68 Japanese-American 6 Age, BMI, subscapular Family History OR
skinfold, triceps ratio, No 1.0
physical activity, yes 1.73 (1.29–2.33)
glucose, triglycerids, and
systolic blood pressure
[201] 2000 RS PCS 1947 (7.34%) 100/0 Mean Norway 22.5 Age, BMI, fasting glucose, Family History OR
49.5–50.3 fitness and triglycerids No 1.0

Table 9 (continued)
Work Year Study Design Sample size %M/W Age (Years) Ethnicity Follow-up duration Adjusted variables Findings
(%DM) (Years)
Mother 2.51 (1.55–4.07)

Father 1.41 (0.657–3.05)
Both 3.96 (1.22–12.9)
[198] 2000 EPIC [101] CSS 6473 45.54/ 54.46 45–74 USA 22.5 Age and sex Family History OR
No
BMI 22.5–24.9 1.0
BMI 27.5–29.9 2.0 (1.2–3.1)
BMI 30–34.9 2.5 (1.6–4.0)
BMI P35 6.1 (3.4–11.2)
Yes
BMI 622.4 1.1 (0.2–5.1)
BMI 22.5–24.9 2.6 (1.3–5.3)
BMI 25–27.4 2.8 (1.5–5.3)
BMI 27.5–29.9 2.2(1.1–4.6)
BMI 30–34.9 6.4 (3.6–11.3)
BMI P35 26.7 (14.4–49.4)
[202] 2000 FHS [187] - 2527 M/W 26–82 African-American and White (USA) 40 Age Family History OR
No 1.0
Mother 3.4 (2.3–4.9)
Father 3.5 (2.3–5.2)
Both 6.1 (2.9–13.0)
[203] 2001 MONICA [35] CSS 12751 49.6/ 50.4 - Germany - Age and sex Family History OR
No 1.0
Mother 2.9 (2.3–3.6)
Father 2.8 (2.1–3.8)
1776
[197] 2007 NHANES [88] - 16388 49.3/ 50.7 P18 USA 6 sex, race/ethnicity, age, Family History OR
BMI, hypertension, and Average risk 1.0
household income Moderate risk 2.3
High risk 5.5
[199] 2009 NHANES [88] CSS 10899 48/ 52 Mean Blacks, Whites and Hispanics 5 Age and sex Black OR

51.3–61 Average risk, BMI624.9 1.0
High risk, BMI624.9 20.4 (6.5–64.5)
High risk, 256BMI629.9 5.2 (2.2–12.3)
High risk, BMIP30 5.0 (2.5–10.3)
Hispanic
Average risk, BMI624.9 1.0
High risk, BMI624.9 14.0 (3.4–58.0)
High risk, 256BMI629.9 5.6 (1.8–17.3)
High risk, BMIP30 8.5 (3.8–19.4)
[196] 2011 RS CSS 3723 49.1/ 50.9 7–15 Mexican 2 Age, sex, and BMI Family History OR
No 1.0
Yes 11.7 (9.5–21.2)
[193] 2016 MIDUS 1 and - 978 45/ 55 34–84 Black and White (USA) - Age, sex, and Family History OR
2 [212] socioeconomic status
No 1.0
Yes 2.77 (2.03–3.78)
RS-Random Sample, SAHS-San Antonio Heart Study, MRFIT-Multiple Risk Factor Intervention Trial, MA-Meta Analysis, THHP-The Honolulu Heart Program, EPIC-European Prospective Investigation into Cancer, FHS-Framingham
Heart Study, MONICA-Multinational MONItoring of trends and determinants in CArdiovascular disease, NHANES-National Health and Nutrition Examination Survey, PD-Prediabetes, IFG-Impaired Fasting Glucose, IGT-Impaired
Glucose Tolerance, M-Men, W-Women, PCS-Prospective Cohort Study, CSS-Cross-Sectional Study.
Table 10
Characteristics and findings of the studies examining the association between obesity and type 2 diabetes.
Work Year Study Design Sample size (%DM) %M/W Age Ethnicity Follow- Adjusted variables Findings
(Years) up
duration
(Years)
[206] 2002 - PCS 4737 100/0 45–64 Japanese 4 Age, smoking status, alcohol intake, BMI (kg/m2 ) RR
family history, and baseline value of 618.49 1.0
fasting blood glucose. 629 5.16 (1.92–13.80)
630 and <35 5.25 (1.96–14.04)
[213] 2007 BWHS [214] - 49766 (4.96%) 0/100 21–69 African- 8 Age, physical activity, family history of BMI (kg/m2 ) IRR
American diabetes, cigarette smoking, years of <23 1.0
(USA) education, and time period of data P45 23 (17–31)
collection
[119] 2001 - PCS 84941 (3.88%) 0/100 30–55 - 16 Age (in five-year categories), time BMI (kg/m2 ) RR
(eight periods), presence or absence of <23 1.0
a family history of diabetes, 23–24.9 2.67 (2.13–3.34)
menopausal status, and use or nonuse 25–29.9 7.59 (6.27–9.19)
of postmenopausal hormone therapy 30–34.9 20.1 (16.6–24.4)
P35 38.8 (31.9–47.2)
[207] 2006 27 cohorts PCS 154989 (0.20%) 54/ 46 Mean - Mean 8 Age, sex, cohort, and smoking habit 5.3 cmEach 2 kg/m2 lower BMI is associated with a
+ CSS 51 23% (15–30%) lower risk of total DM in men and
27% (23–31%) lower risk in women. In the Asian
cohort, each 2 kg/m2 lower BMI was associated
with a 37% (26–46%) lower risk and in
Australasian cohorts the same reduction in BMI
was associated with 25% (21–29%) lower risk.
1777
[208] 2006 RS - 827 (7.86%) - - Japanese 10 Age, sex, total cholesterol, systolic WC (cm) RR
pressure, smoking and overall obesity P85 (M) 2.07 (1.03–4.16)
P90 (W)
[209] 2006 TLGS PCS 4479 (3.70%) 41.34/ 58.66 >3 Tehran 3.6 Age, smoking, family history of 5.3 cmCentral obesity is defined as WC P102 cm
(mean) diabetes, HTN, TG, HDL and other in men and WC P88 cm in women. The central
anthropometric variables obese individuals P60 years old are at higher risk

of incidence type 2 diabetes (OR 3.8, 95% CI 1.8–
7.7).
[210] 2009 RS - 5071 37.80/ 62.2 P40 Chinese - Educational level, age group, smoking WC (cm) OR
and alcohol drinking <90(M) 1.0
P90(M) 2.308 (1.473–3.615)
<80(W) 1.0
P80(W) 2.875(1.987–4.160)
[211] 2001 MAHES - 835 39.16/ 60.84 60–92 Hispanics - Age, physical activity and smoking WC (cm) OR
and Non- >102(M)(H) 2.1(1.2–3.9)
Hispanics >102(M)(NH) 0.9 (0.3–3.1)
>88(W)(H) 1.6 (1.0–2.8)
>88(W)(NH) 15.1(1.9–117.6)
SWHS-Shanghai Women’s Health Study, BWHS- Black Women’s Health Study, RS-Random Sample, WC-Waist Circumference, TLGS-Tehran Lipid and Glucose Study, MAHES-Massachusetts Hispanic Elderly Study, H-Hispanics, NH-
Non Hispanics, M-Men, W-Women, PCS-Prospective Cohort Study, CSS-Cross-Sectional Study.
in both men and women. However, centrally obese women are at diabetes using standardized measurement techniques, such as A1C test
higher risk (OR 2.875, 95% CI 1.987–4.160) compared to centrally obese [217]. Hypertension is a significant risk factor for type 2 diabetes and
men (OR 2.308, 95% CI 1.473–3.615) [210]. The prevalence of type 2 this is further elevated in obese individuals. Ethnicity strongly associ-
diabetes in obese individual is ethnicity dependent [211]. Non- ates with the development of type 2 diabetes. This could be due to
Hispanics centrally obese women are at higher risk of developing type the fact that insulin sensitivity varies among individuals of different
2 diabetes (OR 15.1, 95% CI 1.9–117.6) compared to centrally obese His- ethnicity. Family history of diabetes in first degree of relatives is
panic women (OR 1.6, 95% CI 1.0–2.8). The centrally Hispanic men are strongly associated with the development of type 2 diabetes. In addi-
also at risk of developing type 2 diabetes (OR 2.1, 95% CI 1.2–3.9). No tion, family history of diabetes also signifies the association between
such association is found in centrally obese Non-Hispanic men. How- obesity and type 2 diabetes. Obesity is found to a significant risk factor
ever, all these studies examining the association between central obe- for incidence of type 2 diabetes and the association is stronger in
sity and the incidence of type 2 diabetes consider different definitions women compared to men.
of central obesity. For instance, [208] defines central obesity as waist The association between serum uric acid and type 2 diabetes
circumference (WC) P85 cm in men and P90 cm in women, whereas remains obscure. It can not be concluded that serum uric acid is an
[211] defines it as WC>102 cm in men and >88 cm in women. Conse- independent risk factor for type 2 diabetes or it only elevates the asso-
quently, it is difficult to conclude the association between central obe- ciation between other independent risk factors such as obesity, hyper-
sity and the incidence of type 2 diabetes. tension, and dyslipidemia, and type 2 diabetes. Moreover, our analysis
In summary, although obesity is a significant predictor, the associa- shows that there might be no association between serum uric acid and
tion between obesity and diabetes is a factor of gender and ethnicity. the development of type 2 diabetes, but rather there might be a reverse
Women with high BMI are at greater risk of diabetes compared to association, i.e., diabetes leads to elevated serum uric acid level. Simi-
men. Moreover, the association is stronger in Asians compared to Aus- larly, based on the evidence in the literature, aging can not be consid-
tralians. The association between central obesity is also found to be sig- ered as an independent risk factor for type 2 diabetes. Aging only
nificant for the prevalence of type 2 diabetes. This association is the emphasizes the association between obesity and type 2 diabetes.
strongest in Non-Hispanics women. However, more studies are Depression as well is not found to an independent risk factor contribut-
required to examine the association between central obesity and type ing to the development of type 2 diabetes. Rather, the activities related
2 diabetes following one standard criterion defining central obesity. to depression such as physical inactivity, poor diet, and obesity leads to
diabetes. There is no sufficient evidence to conclude the association
3.12. Physical inactivity between cardiovascular disease and type 2 diabetes. It is debatable
whether cardiovascular disease leads to the development of type 2 dia-
An individual is considered physically inactive if he/she does not get betes. Consequently, more studies are required to study the direct asso-
the recommended 30–60 min of exercise three to four times a week. ciation between these risk factors, i.e., serum uric acid, aging,
Physical inactivity decreases insulin sensitivity with progressive loss depression, and cardiovascular disease, and incidence of type 2
of beta-cells. This leads to impaired glucose tolerance and eventually diabetes.
type 2 diabetes. However, no work examines the association between Based on this study, we devise recommendations to different stake-
physical inactivity as an independent factor and the prevalence of dia- holders leading to better patient care. In particular, we provide recom-
betes. One of the reasons that physical inactivity leads to type 2 dia- mendations for allied healthcare professionals, individuals, and
betes can be that physical inactivity can cause obesity which in turn government institutions as follows:
is a significant risk factor for type 2 diabetes.
Allied healthcare professionals:The hypertensive medications
and the LDL lowering therapy and drugs should be carefully
4. Conclusion
prescribed as they are associated with increased risk of type 2
Diabetes is a global crisis that is primarily driven by rapid urbaniza- diabetes. In addition, overweight and obese adults should be
tion, changing lifestyles, and uneven dietary patterns [215,216]. It is screened for diabetes.
crucial to predict the prevalence of diabetes in an individual to reduce Individuals:A healthy lifestyle, which involves intake of
the risk of diabetes development and save lives. Diabetes is thought to polyunsaturated fatty acids and vegetable fats, regular exercise,
prevail due to several risk factors such as high-level serum uric acid, a healthy diet and proper sleep, is crucial. Individuals should
sleep quality/quantity, smoking, depression, cardiovascular disease, avoid both active and passive smoking.
dyslipidemia, hypertension, aging, ethnicity, family history of diabetes, Government:Physical activity in the nation should be promoted
physical inactivity, and obesity. Studies in the literature have examined for a healthy nation. Law policies should be implemented to
the association between each of these risk factors and the risk of devel-
restrict public smoking as passive smoking significantly
oping type 2 diabetes. In this review, we provide an analysis of the
increases the risk of type 2 diabetes. For instance, designated
studies in the literature to deduce inferences on the relationship
between the risk factors and incidence/prevalence of type 2 diabetes. smoking areas can be established to eliminate the risk of devel-
In conclusion, it can be observed that sleep quantity/quality, smok- oping passive smokers. It would be beneficial to have periodic
ing, dyslipidemia, hypertension, ethnicity, family history of diabetes, surveys that include the demographic and lifestyle features of
obesity and physical inactivity are strongly associated with the devel- the citizens and the surveys’ results can be then used to develop
opment of type 2 diabetes. Both sleep quantity and quality are found a nation-wide diabetes prevention plan, in coordination with
to be strongly associated with the development of type 2 diabetes. the allied health professionals.
The association is stronger in women sleeping for more hours and in
men sleeping for fewer hours. However, the sleeping quantity and
quality data in these studies are self-reported by the participants, and CRediT authorship contribution statement
therefore, prone to errors. More studies are required that use measure-
ment techniques for data collection to validate the association between Leila Ismail: Conceptualization, Methodology, Investigation, Writ-
sleep quantity/quality and type 2 diabetes. Smoking is also found to be ing - original draft, Writing - review & editing. Huned Materwala:
a significant risk factor for type 2 diabetes. Both active and passive Investigation, Writing - original draft. Juma Al Kaabi: Validation, Writ-
smokers are at higher risk of developing type 2 diabetes. Moreover, ing - review & editing.
the risk for developing type 2 diabetes remains high in ex-smokers
for the first 5–10 years of smoking cessation. Dyslipidemia is associated
with the development of type 2 diabetes. Increased non-HDL and
Declaration of Competing Interest
decreased HDL levels are strongly associated with type 2 diabetes.
However, in the majority of these studies, the incidence or prevalence The authors declare that they have no known competing finan-
of type 2 diabetes is self-reported. Consequently, further studies are cial interests or personal relationships that could have appeared
needed to validate this association between dyslipidemia and type 2 to influence the work reported in this paper.
1778
Acknowledgments Appendix A
This work is funded by the National Water and Energy Center of

the United Arab Emirates University (Grant No. 31R215). We thank
the anonymous reviewers for their valuable comments which
helped us improve the paper.
Table A1
Search string used to retrieve the studies on the association between risk factor and type 2 diabetes.
Risk factor Search string
Serum uric acid (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘uric acid” OR uric-acid OR hyperuricemia OR
‘‘serum uric acid” OR gout) AND (diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR
‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent diabetes”)
Sleep quantity/ (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘sleep hour” OR ‘‘sleeping hour” OR ‘‘hours of
quality sleep” OR ‘‘sleep duration” OR ‘‘sleep time” OR ‘‘sleep length” OR ‘‘sleep period” OR ‘‘sleeping time” OR ‘‘sleep span” OR nap OR napping OR ‘‘daytime
sleep” OR vsleep quality” OR ‘‘sleep disturbance” OR ‘‘sleep apnea” OR insomnia OR ‘‘sleep deprivation”) AND (diabetes OR ‘‘diabetes mellitus” OR
‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent
diabetes”)
Smoking (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (smoking OR ‘‘smoking cessation” OR cigarette
OR ‘‘cigarette smoking” OR ‘‘passive smoking” OR ‘‘secondhand tobacco smoke”) AND (diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type
II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent diabetes”)
Depression (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘depressive disorder” OR depression OR
‘‘dysthymic disorders”) AND (diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR
‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent diabetes”)
Cardiovascular (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘cardiovascular disease” OR stroke OR ‘‘heart
disease disease”) AND (diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin
dependent diabetes” OR ‘‘noninsulun dependent diabetes”)
dyslipidemia (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (cholesterol OR ‘‘cholesterol intake” OR
‘‘cholesterol consumption” OR diet* OR fat OR ‘‘density lipoprotein” OR density-lipoprotein OR dyslipidemia) AND (diabetes OR ‘‘diabetes mellitus”
OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent
diabetes”)
Hypertension (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘high blood pressure” OR ‘‘blood pressure” OR
hypertensi* OR ‘‘Hypertension-*”) AND (diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent
diabetes” OR ‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent diabetes”)
Aging (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (age OR aging OR old OR elderly) AND (diabetes
OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR
‘‘noninsulun dependent diabetes”)
Ethnicity (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (ethnicity OR race OR *rac* OR community) AND
(diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent
diabetes” OR ‘‘noninsulun dependent diabetes”)
Family history of (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘family history” OR ‘‘parental history” OR
diabetes ‘‘parental diabetes” OR ‘‘parental transmission” OR paternal OR maternal) AND (diabetes OR ‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II
diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR ‘‘noninsulun dependent diabetes”)
Physical inactivity (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘physical inactivity”) AND (diabetes OR
‘‘diabetes mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR
‘‘noninsulun dependent diabetes”)
Obesity (risk OR ‘‘risk factor” OR etiology OR association OR development OR progression OR incidence) AND (‘‘body mass index” OR BMI OR ‘‘body fat
distribution” OR ‘‘over weight” OR overweight OR obesity OR ‘‘weight change” OR ‘‘weight gain” OR ‘‘central obesity”) AND (diabetes OR ‘‘diabetes
mellitus” OR ‘‘type 2 diabetes” OR ‘‘type II diabetes” OR ‘‘non-insulin dependent diabetes” OR ‘‘non insulin dependent diabetes” OR ‘‘noninsulun
dependent diabetes”)
Table A2
Quality assessment of the included studies according to the Quality assessment tool for observational cohort and cross-sectional studies.
Work Q1 Q2 Q3 Q4 Q5 Q6 Q7 Q8 Q9 Q10 Q11 Q12 Q13 Q14 Quality
High-level serum uric acid

[14] Yes Yes Yes Yes No Yes Yes Yes Yes Yes* NR NR Yes Yes Good
[21] Yes Yes NR Yes No CD No No NR No CD NR No Yes Poor
[22] Yes Yes Yes CD No Yes Yes CD Yes Yes No NR No Yes Fair
[23] No Yes NR Yes No Yes Yes CD Yes Yes Yes NR CD Yes Fair
[19] No No NR NR No Yes CD No NR Yes NR NR NR No Poor
[15] No Yes NR Yes No Yes Yes Yes Yes Yes Yes NR NR Yes Good
[16] Yes Yes NR Yes No Yes Yes Yes NR Yes NR NR NR Yes Fair
[25] Yes Yes NR No No Yes Yes No Yes Yes Yes NR NR Yes Fair
[26] Yes Yes NR Yes No Yes Yes No Yes Yes Yes NR Yes Yes Fair
[27] Yes No NR CD No Yes Yes No Yes Yes Yes NR NR Yes Fair
[30] No Yes NR Yes No No No Yes Yes NR Yes NR NR Yes Fair
Sleep quantity/quality
[79] Yes Yes NR Yes No Yes Yes Yes No Yes Yes NR NR Yes Fair
[56] No No NR Yes No Yes Yes NA No Yes Yes NR Yes Yes Fair
[57] Yes Yes NR Yes No Yes Yes NA No No No NR NR Yes Fair
[59] Yes Yes Yes Yes No Yes Yes NA No No Yes NR NR Yes Good
[83] No Yes NR Yes No No No Yes No NR Yes NR NR Yes Fair
1779
Table A2 (continued)
[52] Yes Yes Yes Yes No Yes Yes Yes No No No NR Yes Yes Fair
[50] Yes Yes Yes Yes No Yes Yes No No Yes Yes NR No Yes Fair
[85] Yes Yes NR Yes No Yes Yes Yes No Yes NR NR No Yes Fair
[87] Yes Yes NR Yes No Yes Yes Yes No Yes No NR Yes Yes Fair
[89] Yes Yes NR Yes No No No Yes No No Yes NR NR Yes Fair
[58] Yes Yes No Yes No Yes Yes Yes No CD Yes NR NR Yes Fair
[92] Yes Yes NR Yes No No No Yes No NR Yes NR NR Yes Fair
[94] Yes Yes NR Yes No Yes Yes Yes No NR Yes NR NR Yes Fair
[55] Yes Yes No Yes No Yes Yes Yes No No Yes NR Yes Yes Fair
[96] CD Yes Yes No No No No Yes No NR Yes NR CD Yes Fair
[97] Yes No No Yes No Yes Yes Yes No NR Yes NR NR Yes Fair
[98] Yes Yes CD Yes No Yes Yes Yes No No No NR NR Yes Fair
[100] Yes Yes NR CD No No No Yes No NR Yes NR NR Yes Fair
[51] No Yes CD Yes No Yes No Yes No Yes No NR Yes Yes Fair
[102] Yes Yes NR Yes No Yes Yes Yes No NR No NR Yes Yes Fair
[53] Yes Yes Yes No No No No Yes No NR No NR NR Yes Fair
[104] Yes Yes NR CD No No No Yes No NR Yes NR NR Yes Fair
[106] Yes Yes Yes Yes No Yes Yes Yes No Yes Yes NR No Yes Good
[54] Yes Yes Yes No No No No Yes No Yes No NR NR Yes Fair
[108] Yes Yes No Yes No Yes NR No No NR No NR NR Yes Poor
Smoking
[110] No Yes NR Yes No Yes Yes No NA Yes No NR NR Yes Fair
[67] No Yes NR Yes No Yes Yes Yes NA Yes Yes Yes NR Yes Good
[68] Yes Yes NR Yes No Yes Yes Yes NA Yes Yes No Yes Yes Good
[112] No No Yes Yes No Yes Yes Yes NA Yes Yes NR Yes Yes Good
[73] CD Yes NR Yes No No No Yes NA NR No NR NR Yes Poor
[114] Yes Yes NR Yes No Yes Yes Yes NA Yes Yes NR Yes Yes Good
[69] Yes Yes NR Yes No Yes Yes Yes NA Yes No Yes NR Yes Good
[116] No Yes NR Yes No No No No NA NR Yes NR NR Yes Poor
[65] Yes Yes NR Yes No Yes Yes No NA Yes Yes NR Yes Yes Fair
[63] Yes Yes NR Yes No Yes Yes Yes NA NR CD NR NR Yes Fair
[119] No Yes No Yes No Yes Yes Yes NA Yes Yes NR Yes Yes Good
[120] No CD NR CD No Yes Yes Yes NA Yes NR NR NR Yes Fair
[74] Yes Yes Yes CD No No No No NA No Yes NR NR Yes Fair
[122] Yes Yes Yes Yes No Yes Yes No NA No Yes No No Yes Good
[70] Yes Yes No Yes No Yes Yes No NA No Yes NR NR Yes Fair
[77] Yes Yes Yes Yes No Yes Yes Yes NA Yes Yes NR CD Yes Good
[71] Yes CD Yes Yes No Yes Yes Yes NA Yes Yes NR NR Yes Good
[75] Yes Yes NR Yes No Yes Yes Yes NA Yes Yes NR NR Yes Good
[66] No Yes Yes Yes No Yes Yes No NA No Yes NR No Yes Good
[64] Yes Yes NR Yes No Yes Yes Yes NA Yes CD NR NR Yes Fair
[72] Yes No NR CD No Yes Yes Yes NA Yes Yes NR Yes Yes Good
[78] Yes Yes Yes Yes No Yes Yes No NA Yes Yes NR Yes Yes Good
[76] Yes Yes NR Yes No Yes Yes Yes NA Yes Yes NR Yes Yes Good
[128] No Yes NR Yes No Yes Yes No NA NR No NR NR Yes Fair
Depression
[137] Yes Yes Yes Yes No Yes Yes Yes Yes No Yes NR Yes Yes Good
[155] No Yes NR Yes No Yes Yes No Yes No No NR NR Yes Fair
[157] Yes Yes NR Yes No Yes Yes Yes No NR No NR NR Yes Fair
[158] Yes Yes NR Yes No Yes Yes Yes Yes NR Yes NR NR Yes Fair
[136] Yes Yes NR Yes No Yes CD No Yes Yes Yes NR CD Yes Fair
[160] Yes Yes Yes Yes No Yes Yes No Yes Yes Yes NR NR Yes Good
[138] No Yes NR Yes No Yes Yes No Yes No CD NR NR Yes Fair
[139] No Yes NR Yes No Yes Yes No Yes No Yes NR NR Yes Fair
Cardiovascular disease
Dyslipidemia
[148] Yes Yes NR Yes No Yes Yes Yes CD CD No NR No Yes Fair
[154] Yes Yes NR Yes No Yes Yes Yes NR NR NR NR Yes Yes Fair
[152] No Yes NR Yes No Yes CD Yes Yes No Yes NR Yes Yes Fair
Hypertension
[166] Yes Yes NR Yes No Yes Yes Yes Yes NR Yes NR Yes Yes Good
[167] Yes Yes NR Yes No Yes Yes Yes Yes No Yes NR NR Yes Good
[168] Yes Yes NR Yes No Yes Yes Yes No No No NR CD Yes Fair
[170] Yes Yes NR No No Yes Yes Yes Yes No Yes NR NR Yes Good
[188] Yes Yes Yes Yes No Yes Yes Yes Yes No Yes NR CD Yes Good
[169] Yes Yes Yes Yes No Yes Yes Yes Yes No Yes NR NR Yes Good
Ethnicity
[177] No Yes Yes No No No No NA NA NR Yes NR NR Yes Fair
[179] No Yes Yes No No No No NA NA NR NR NR NR Yes Poor
[180] No Yes Yes No No No No NA NA No Yes NR NR Yes Fair
[181] Yes Yes Yes CD No No No NA NA No Yes NR NR Yes Fair
[175] Yes Yes Yes Yes No No No NA NA No No NR NR Yes Poor
[176] Yes Yes NR Yes No Yes Yes NA NA Yes Yes NR NR Yes Good
Family history of diabetes
[204] No No NR CD No Yes NR No Yes NA Yes NR NR Yes Fair
[195] Yes Yes Yes Yes No No No Yes No NA Yes NR NR Yes Fair
1780
Table A2 (continued)
[200] Yes Yes NR Yes No Yes Yes Yes No NA Yes NR NR Yes Fair
[205] No Yes NR No No Yes CD Yes NR NA NR NR NR No Poor
[194] No Yes NR Yes No Yes Yes No NR NA Yes NR NR Yes Fair
[201] Yes Yes Yes Yes No Yes Yes Yes CD NA Yes NR Yes Yes Good
[198] Yes Yes NR Yes No No No No No NA Yes NR NR Yes Poor
[202] No Yes NR Yes No Yes Yes Yes Yes NA Yes NR NR Yes Good
[203] Yes Yes Yes No No No No Yes No NA No NR NR Yes Fair
[197] Yes Yes NR Yes No No No Yes No NA Yes NR NR Yes Fair
[199] Yes Yes No No No No No Yes Yes NA Yes NR NR Yes Fair
[196] Yes Yes Yes Yes No No No No Yes NA Yes NR NR Yes Fair
[193] Yes Yes Yes Yes No CD NR No No NA Yes NR NR Yes Fair
Obesity
[206] Yes Yes NR Yes No Yes Yes Yes Yes Yes Yes NR NR Yes Good
[213] Yes Yes NR Yes No Yes Yes No Yes Yes Yes NR Yes Yes Fair
[119] No Yes No Yes No Yes Yes Yes NA Yes Yes NR Yes Yes Good
[207] No No NR CD No Yes Yes Yes NR NR Yes NR NR Yes Fair
[208] No Yes NR Yes No Yes Yes No Yes NR Yes NR NR Yes Fair
[209] Yes Yes Yes Yes No Yes Yes No Yes NR Yes NR No Yes Good
[210] Yes Yes Yes Yes No CD CD No Yes NR Yes NR NR Yes Fair
[211] Yes Yes NR Yes No Yes CD No Yes NR Yes NR NR Yes Fair
Q1. Was the research question or objective in this paper clearly stated?.
Q2. Was the study population clearly specified and defined?.
Q3. Was the participation rate of eligible persons at least 50%?
Q4. Were all the subjects selected or recruited from the same or similar populations (including the same time period)? Were inclusion and exclusion criteria for being in the
study prespecified and applied uniformly to all participants?.
Q5. Was a sample size justification, power description, or variance and effect estimates provided?.
Q6. For the analyses in this paper, were the exposure(s) of interest measured prior to the outcome(s) being measured?.
Q7. Was the timeframe sufficient so that one could reasonably expect to see an association between exposure and outcome if it existed?.
Q8. For exposures that can vary in amount or level, did the study examine different levels of the exposure as related to the outcome (e.g., categories of exposure, or exposure
measured as continuous variable)?.
Q9. Were the exposure measures (independent variables) clearly defined, valid, reliable, and implemented consistently across all study participants?.
Q10. Was the exposure(s) assessed more than once over time?.
Q11. Were the outcome measures (dependent variables) clearly defined, valid, reliable, and implemented consistently across all study participants?.
Q12. Were the outcome assessors blinded to the exposure status of participants?.
Q13. Was loss to follow-up after baseline 20% or less?.
Q14. Were key potential confounding variables measured and adjusted statistically for their impact on the relationship between exposure(s) and outcome(s)?.
CD-Cannot be Determined; NA-Not Applicable; NR-Not Reported.
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Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

journal homepage: www.elsevier.com/locate/csbj

Association of risk factors with type 2 diabetes: A systematic review

Fig. 1. Flowchart of the selection of relevant studies.

Depression is a mood disorder that negatively affects the way a per-

L. Ismail, H. Materwala and J. Al Kaabi

diabetes 320 1.29 (0.96–11.73)

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

depressed African-Americans are at 2.56 times higher risk of incidence

an individual having a score of 48–80 is at higher risk of developing

depression inventory (BDI) is at higher risk of incidence type 2 diabetes

for diabetes, rather the activities related to depression such as physical

the impact of other independent risk factors such as gender, ethnicity,

3.5. Cardiovascular disease

Increased heart rate and cardiovascular disease can elevate the

blood pressure in the arteries. As a result, the body’s glucose uptake

decreases leading to insulin resistance condition. Consequently, a per-

son suffering from heart disease is at a higher risk of developing type 2

Dyslipidemia refers to an abnormal level of lipids, such as triglyc-

density lipoproteins (HDL) levels [145]. Elevated LDL and lowered

HDL levels lead to beta-cell dysfunction inhibiting insulin secretion

ation between dyslipidemia and type 2 diabetes.

sidered significant in the development of type 2 diabetes [148]. Substi-

type 2 diabetes. This is because both polyunsaturated fatty acid and

respectively for the highest quintile of intake [148]. Tajima et al.

In order to reduce elevated LDL level, LDL lowering therapy and

to be associated with a higher risk of type 2 diabetes [150]. Indi-

compared to individuals having high LDL levels due to dietary pat-

L. Ismail, H. Materwala and J. Al Kaabi

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

heart disease and waist circumference

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

(continued on next page)

whites (USA) status, education, occupation,

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

L. Ismail, H. Materwala and J. Al Kaabi

[112] 1997 RS PCS 2312 (1.77%) 100/0 - Japanese 8 - Cigarettes/day HR

postmenopausal hormone use >10 1.21 (0.87-1.71)

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

(continued on next page)

P40 (M) 1.45 (1.34-1.57)

Yes (W) 0.89 (0.54-1.39)

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

CARDIA [186], and American 8.9 triglycerids 6119/6 79 1.0

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

women are 4 and 2 times compared to White men

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

L. Ismail, H. Materwala and J. Al Kaabi

[205] 1994 MA PCS 11334 M/W P40 Taiwan - - Family History OR

father 2.21 (0.25–8.86)

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

(continued on next page)

Mother 2.51 (1.55–4.07)

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

Computational and Structural Biotechnology Journal 19 (2021) 1759–1785

This work is funded by the National Water and Energy Center of