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REVIEW ARTICLE

Obesity and type 2 diabetes mellitus: A complex association

Abdulkareem Jassem Al-Quwaidhi, Mark S. Pearce1, Julia A. Critchley2, Martin O’Flaherty3

Department of Public Health, General Directorate of Health Affairs at Al-Ahssa Region, Ministry of Health, Saudi Arabia, 1Sir James
Spence Institute of Child Health, Institute of Health and Society, Newcastle University, 2Population Health Research Centre, St. George’s
University of London, 3Division of Public Health, Institute of Psychology, Health and Society, University of Liverpool, United Kingdom

ABSTRACT

Obesity is a growing epidemic affecting all ages in both industrialized and developing countries. The most common
suggested cause of this epidemic is the increasing levels of urbanization and lifestyle changes toward sedentary life
and adopting “western” dietary patterns. The association between obesity and type 2 diabetes mellitus (T2DM)
has been reproducibly observed in cross-sectional and prospective studies across various populations, even when
using different fatness measures and diagnostic criteria for T2DM. However, there are some modifying factors that
make such an association complex and multifactorial. These modifying factors include the duration of obesity, body
fat distribution, physical activity, diet, and genetics/ethnicity. This review aims to summarize the evidence of this
association and its potential modifying factors.

Key words: Association, obesity, type 2 diabetes mellitus

INTRODUCTION region of Middle East and North Africa had the seventh
(among the 21 regions of the Global Burden of Disease
Obesity is the “accumulation of adipose tissue to excess Study) highest prevalence of obesity in men, and the
and to extent that impairs physical and psychosocial second highest in women between 1980 and 2008.[4]
health and well-being”.[1,2] According to the World Health
Organization (WHO), the world-wide obesity has more The association between obesity and type 2 diabetes
than doubled since 1980, and in 2008, there were around mellitus (T2DM) has been reproducibly observed in
1.5 billion overweight adults (aged ≥20 years). Of these, both cross-sectional[5,6] and prospective studies,[7,8] and
over 200 million men and 300 million women were obese, has been consistent across various populations even
which means that more than one in ten of the world’s adult when using different measures of fatness and T2DM
population was obese in 2008.[3] In 2010, approximately diagnostic criteria.[9] It is often stated that obesity is the
35 million overweight children were living in developing most important risk factor for T2DM, and the current
countries, compared to 8 million in industrialized epidemics of these two conditions seem to be related.
countries.[3] The estimated economic burden of obesity in
developed countries ranges between 2% and 7% of health This review aims to summarize the evidence of the
care costs, and is higher in developing countries.[2] The association between obesity and type 2 diabetes mellitus
and its potential modifying factors.

Access this article online METHODOLOGY

Quick Response Code:
Website:
www.saudijobesity.com
To achieve the objective of this review, a comprehensive
literature review was conducted using Google Scholar
and Medline database (1980-January 2014). The review
DOI: consisted of two stages. In the first stage, we used
10.4103/2347-2618.128627 several terms of titles and keywords to search for
relevant articles of different types (e.g., original research,

Address for correspondence: Dr. Abdulkareem Jassem Al-Quwaidhi, P.O. Box 35515, Al-Ahssa 31982, Saudi Arabia. E-mail: aal-qwidi@moh.gov.sa

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Al-Quwaidhi, et al.: Obesity and type 2 diabetes mellitus

reviews, systematic reviews and meta-analyses) in order BMI measures the “total” adiposity of the body and may
to form a general picture of the recent evidence on the miss many cases of “central/abdominal” obesity, in
association between obesity and T2DM and the proposed which the body fat accumulates mainly around the waist.
pathophysiological pathways of such an association. The simple clinical measure of central obesity is the waist
Examples of terms used were ‘obesity’, ‘fatness’, ‘body circumference (WC). The WHO recommends a cut-off
weight’, ‘weight’, ‘body mass index’, ‘BMI’, ‘waist of WC≥102 cm in men and ≥88 cm in women to define
circumference’, ‘diabetes’, ‘type 2 diabetes’, ‘association’, central obesity.[13] Again, Asian populations, particularly
etc. In the second stage, we used relevant search terms of people of South Asian origin seem more prone to carrying
titles and keywords for each of the five themes we used excess fat centrally than the white populations and show
to explain the complexity of association. These themes raised obesity-related risk although they may not be
include (1) duration of obesity; (2) body fat distribution; considered obese by conventional BMI criteria. Hence,
(3) physical activity; (4) diet; and (5) genetics/ethnicity. the WHO thresholds for central obesity in Asians are a
After combination of the search terms for each theme and WC≥90 cm in men and ≥80 cm in women.[13] In addition
reviewing titles and then abstracts, we included 10 articles to WC, the waist-to-hip circumference ratio (WHR)
for the first theme, 16 for the second theme, 23 for the is another measure of central obesity. A WHR>1.0 in
third theme, 19 for the fourth theme, and 7 for the fifth men and WHR>0.85 in women are used as cut-offs for
theme, respectively. We included original research papers, identifying individuals with central obesity. However,
reviews, and systematic reviews/ meta-analyses. We did WC is the preferred and more commonly used measure
not cite all articles obtained through the search strategy. of abdominal obesity compared with WHR.[13]
Instead, whenever possible, we critically appraised
articles and attempted to cite those with the most recently Pathophysiological pathways
published data in each theme, in combination with The pathophysiological link between obesity and T2DM
having good sampling sizes/ techniques, and proper relates primarily to the adipose tissue, which has been
study designs and outcome ascertainment (determined recognized as an endocrine organ that secretes hormones
by fulfilling at least 3 items from the ‘guidelines and and communicates with the central nervous system to
checklist for appraising a medical article’ published by the regulate appetite and metabolism.[14] The main proposed
BMJ).[10] To compare between different studies’ findings, pathways which link obesity and T2DM are briefly
we included studies that reported either a positive or no summarized in the following points:
association for each theme. 1. Elevated leptin levels. Leptin is a protein produced
by adipocytes. The main role of leptin is to regulate
food intake and energy expenditure by reducing food
OBESITY AND T2DM intake and increasing sympathetic nervous system
outflow, therefore inducing weight loss.[15] Recent
Obesity measurements evidence showed that leptin levels fall during weight
The WHO recommends the body mass index (BMI) as a loss and increase brain activity in areas involved in
measure of obesity.[3] BMI is a simple index of weight-for- emotional, cognitive, and sensory control of food
height and is defined as the weight in kilograms divided intake.[15] Restoration of leptin levels maintain weight
by the square of height in meters (kg/m2). Overweight in loss and reverse the changes in brain activity. Thus,
adults is defined as a BMI of ≥25 kg/m2, and obesity as leptin is a critical factor linking reduced energy
a BMI of ≥30 kg/m2.[3] BMI provides the most useful and stores to eating behavior.[15] In obese individuals,
widely accepted measure of overweight and obesity at leptin levels are elevated, but this has been found to
the clinical and population level, as it is the same for both positively correlate with insulin resistance. Leptin
sexes and for all ages, and has been widely used in most can impair the production of insulin and reduce the
studies world-wide.[3] However, BMI is prone to some effects of insulin on the liver.[14]
limitations in persons with extremes of age, very muscular 2. Elevated levels of adipocyte-derived free fatty acids.
builds (overestimates obesity), and extreme height.[1,3,11] In adipose tissues, glucose is involved in lipogenesis
In addition, in some ethnic groups, particularly Asians, through its conversion to glycerol-3-phosphate,
the above-mentioned cut-offs are not suitable to classify which is then combined with “non-esterified fatty
overweight and obesity. The mean or median BMI in acids (NEFAs)” to form triglycerides. An important
Asians has been found to be lower than that observed in role of insulin is also to prevent the breakdown of
non-Asian populations; so the BMI distribution is shifted to triglycerides (lipolysis), which liberates NEFAs.[14]
the left.[12] This trend leads to the concern that application In obese individuals, the levels of these fatty acids
of the standard WHO’s cut-offs will underestimate obesity- are raised, resulting in impairment of glucose
related risks in these populations, and therefore, new metabolism by reducing insulin-stimulated glucose
cut-offs of 23-27.5 kg/m2 for overweight and ≥27.5 kg/m2 uptake in skeletal muscle, and increasing the hepatic
for obesity have been recommended for Asians.[12] glucose output.[14]
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Al-Quwaidhi, et al.: Obesity and type 2 diabetes mellitus

3. Elevated levels of proteins secreted by adipose tissue. developed incident diabetes. Following adjustment for
In addition to leptin, adipose tissue secretes many socio-demographic variables (age, sex), family history of
other proteins that modulate glucose metabolism and diabetes, time varying WC, energy intake, PA, smoking,
insulin action. Examples of these proteins include and alcohol, each additional year of abdominal obesity
adiponectin, adipsin and resistin. Again, studies have was associated with a 4% higher risk of developing
generally suggested that circulating levels of these diabetes [hazard ratio (HR) 1.04 (95% confidence interval
proteins are elevated in individuals with T2DM.[14] [CI]: 1.02-1.07)].[7]
4. Elevated levels of adipocyte-nonspecific proteins.
There are some proteins which are secreted by In another prospective study,[20] a total of 1256 participants
adipocytes and other cells and tissues. For instance, who were free from T2DM at baseline, but were obese
cytokines, such as tumor necrosis factor-α and on at least two consecutive of the study’s twenty-four
interleukin-6 are produced by macrophages and biennial examinations, were included. T2DM status
also by adipocytes.[14] These proteins are involved was collected throughout the 48 years of follow-up of
in innate immunity and contribute to the process the study. The unadjusted HR for the risk of T2DM for
of inflammation, either directly through acting on men was 1.13 (95% CI: 1.09, 1.17) and for women was
inflammatory cells or indirectly by acting on the 1.12 (95% CI: 1.08, 1.16) per additional 2-year increase in
liver to produce acute phase proteins.[14] Cytokines the duration of obesity (BMI≥30 kg/m2). There was no
have been found to induce “suppressor of cytokine
significant difference to these HRs after adjustment for
signaling-3 (SOCS-3),” which is an intracellular
several covariates (socio-demographic variables, family
signaling molecule that impairs the signaling of
both leptin and insulin. In obesity, SOCS-3 levels history of T2DM, health behavior and PA).[20]
are elevated and thus may result in obesity-
associated resistance to the actions of both leptin Body fat distribution
and insulin.[14] There is considerable evidence suggesting that both
overall adiposity and fat distribution are independent risk
factors for T2DM in both men and women. Some studies,
MODIFYING FACTORS OF THE
such as that of Meisinger et al.,[8] have shown that there
ASSOCIATION BETWEEN OBESITY AND was an ‘additive’ effect of overall and abdominal obesity
T2DM on the prediction of the risk of T2DM. They followed a
cohort of 3055 men and 2957 women, aged 35-74 years
Not every obese individual develops diabetes and and free of T2DM at baseline, for a mean period of
therefore, obesity alone is not sufficient to cause 9.2 years. A total of 243 cases of incident T2DM occurred
T2DM.[9] The relationship between obesity and T2DM is in men and 158 in women. Multivariable-adjusted HRs
complicated by the effects of several modifying factors. across quartiles of BMI were 1.0, 1.37, 2.08, and 4.15 in
These factors include duration of obesity,[7] distribution of men and 1.0, 3.77, 4.95, and 10.58 in women; while those
body fat,[16] physical activity (PA),[17] diet,[18] and genetics/ of WC were 1.0, 1.15, 1.57, and 3.40 in men and 1.0, 3.21,
ethnicity.[19] The following subsections concisely discuss 3.98, and 10.70 in women; and those of WHR were 1.0,
these factors and their possible modifying effects. Table 1 1.14, 1.80, and 2.84 in men and 1.0, 0.82, 2.06, and 3.51 in
summarizes the primary research studies included in women. In joint analyses, the highest risk was observed
this review for each of the modifying factors. in men and women with a high BMI in combination
with a high WC and a high WHR. Therefore, the authors
Duration of obesity concluded that WC should be measured in addition to
The evidence quantifying the relationship between BMI to assess the risk of T2DM in both sexes.[8] These
obesity duration and risk of T2DM is complicated by the findings are supported by a meta-analysis[16] conducted
difficulty to measure the actual onset of obesity and to based on 32 studies from 1966 to 2004, and demonstrated
differentiate between the effects of degree and duration that the three major obesity indicators (BMI, WC, and
of obesity in case the weight is changing.[9] WHR) have similar associations with incident diabetes.
The pooled relative risks (RRs) for incident diabetes were
Examples of recent studies that reported an association 1.87 (95% CI: 1.67-2.10), 1.87 (95% CI: 1.58-2.20), and
include the study of Reis et al.,[7] who followed a cohort 1.88 (95% CI: 1.61-2.19) per standard deviation of BMI,
of 5,115 white and black adults aged 18-30 years WC, and WHR respectively.
in 1985-1986. Years spent abdominally obese were
calculated for participants without abdominal obesity Balkau et al.[5] have conducted the International Day
(WC>102 cm in men and>88 cm in women) or diabetes for the Evaluation of Abdominal obesity study, which
at baseline (n = 4,092) and was based upon repeat evaluates whether WC in addition to BMI is a useful
measurements conducted 2, 5, 7, 10, 15, 20, and 25 years clinical marker of physician-reported cardiovascular
later. After 25 years of follow-up, 392 participants disease and diabetes. It covered a total of 168,000 primary
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Al-Quwaidhi, et al.: Obesity and type 2 diabetes mellitus

care patients (aged 18-80 years) in 63 countries from 1.67 (1.64-1.71) in women. The exceptions were the
different regions of the world, including Saudi Arabia Middle East and Australia, where the ORs for diabetes
and other Middle East and North African countries. The mellitus were consistently higher for BMI than for WC
standardized odds ratios (ORs) for diabetes mellitus in both genders. In North Africa, men with diabetes
were higher for WC than for BMI in almost all regions, have equivalent ORs for WC and BMI. [5] In contrast,
with overall ORs (95% CI) of 1.59 (1.56-1.63) versus Abolfotouh et al.[21] have conducted a large home-based
1.52 (1.49-1.56) in men and 1.83 (1.79-1.87) versus survey among 1800 participants (aged ≥18 years) in

Table 1: Summary of the primary studies included in the review (for each of the modifying factors studied)
Study Year of Type Target population/ Sample Main relevant results Reference
publication country size
Duration of obesity
Reis et al. 2013 Prospective White and black 5,115 Each additional year of abdominal obesity 7
cohort adults aged was associated with a 4% HR of developing
18‑30 years; United DM; adjusted HR: 1.04 (95% CI: 1.02‑1.07)
States
Abdullah et al. 2011 Prospective Framingham Heart 1,256 HR for the risk of T2DM for men was 20
cohort Study participants in 1.13 (95% CI: 1.09‑1.17) and for women
1948‑1998; United was 1.12 (95% CI: 1.08‑1.16) per additional
States 2‑year increase in the duration of obesity
Body fat distribution
Meisinger et al. 2006 Prospective Men and women 3,055 Multivariable‑adjusted HRs of T2DM across 8
cohort aged 35‑74 years men quartiles of BMI were 1.0, 1.37, 2.08 and
from the sec- and 4.15 in men and 1.0, 3.77, 4.95 and 10.58
ond (1989‑1990) or 2,957 in women; while those of WC were 1.0,
third (1994‑1995) women 1.15, 1.57 and 3.40 in men and 1.0, 3.21,
MONICA Augsburg 3.98 and 10.70 in women; and those of
Survey; Germany WHR were 1.0, 1.14, 1.80 and 2.84 in men
and 1.0, 0.82, 2.06 and 3.51 in women
Balkau et al. 2007 Cross‑sectional Primary care patients 168,000 Standardized ORs for DM were higher for 5
(aged 18‑80 years) WC than for BMI in almost all regions, with
in 63 countries from overall ORs (95% CI) of 1.59 (1.56‑1.63)
different regions of versus 1.52 (1.49‑1.56) in men and
the world 1.83 (1.79‑1.87) versus 1.67 (1.64‑1.71) in
women. In Middle East and Australia, ORs
for DM were higher for BMI than for WC
Abolfotouh et al. 2008 Cross‑sectional Men and women 1,800 A significant association between WC 21
aged ≥18 years and the risk of DM was reported (P=0.02);
from12 primary health BMI was not significantly associated with
care centers in 4 DM (P=0.11)
governorates; Egypt
Lear et al. 2007 Cross‑sectional Healthy Aboriginal, 822 BMI significantly underestimated VAT in 6
Chinese, European, all non‑European groups. VAT was not
and South Asian significantly different between the Aborigi-
participants aged nals and the Europeans. With total body
30‑65 years; Canada fat >9.1 kg, Chinese participants had
increasingly greater amounts of VAT than
did the Europeans (P=0.008). South Asians
had less VAT with total body fat >37.4 kg
but more VAT below that amount than did
Europeans (P<0.001)
Physical activity and diet
Ross et al. 2000 Randomized Obese men (mean 52 Body weight decreased by 7.5 kg (8%) 24
controlled trial BMI 31.3±2.0 kg/m2; in both weight loss groups and did not
mean WC 110.1±5.8 change in the exercise without weight loss
cm) recruited through and control groups. Average reduction
general media from was 1.3 kg (95% CI: 0.3‑2.3 kg) greater
Kingston, Ontario; in the exercise‑induced weight loss group
Canada than in the diet‑induced weight loss
group (P=0.03). Abdominal and visceral
fat also decreased in the exercise without
weight loss group (P=0.001). Plasma
glucose and insulin values did not change
in the treatment groups compared with
controls (P=0.10 for all comparisons)
Contd....
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Table 1: Contd.....
Stookey 2001 Cross‑sectional Chinese adults aged 5,783 Energy density positively and significantly 31
20‑59 years from the associated with energy intake from all
1991 China Health macronutrients and overweight status
and Nutrition Surveys; (P<0.05)
China
Ledikwe et al. 2006 Cross‑sectional Adults aged >19 years 7,356 Men and women with a low‑energy‑dense 32
from the 1994 to 1996 diet had lower energy intakes (≈425 and
Continuing Survey 275 kcal/d less, respectively) than did those
of Food Intakes by with a high‑energy‑dense diet, even though
Individuals; United they consumed more food (≈400 and 300
States g/d more, respectively)
Messier et al. 2004 Randomized Community‑dwelling 316 The weight‑loss groups lost significantly 33
controlled trial overweight and obese (P<0.05) more body weight (for diet, 4.9%;
adults aged≥60 years for diet plus exercise, 5.7%) than did the
with a BMI≥28 kg/m2, healthy lifestyle group (1.2%)
knee pain, radio-
graphic evidence of
knee osteoarthritis,
and self‑reported
physical disability;
United States
Genetics/ethnicity
Farooqi et al. 2003 Laboratory Subjects with severe 500 5.8% of subjects had mutations in MC4R 35
experiment obesity of early on- gene. Mutation carriers had severe
set (before 10 years obesity, increased lean mass, increased
of age), Cambridge; linear growth, hyperphagia, and severe
United Kingdom hyperinsulinemia
Branson et al. 2003 Laboratory Severely obese 469 5.1% of subjects and 4% of controls had 36
experiment white subjects aged MC4R mutation. All mutation carriers
41.0±0.5 years reported binge eating, as compared with
(mean BMI 44.1±2.0 14.2% of obese subjects without mutations
kg/m2) referred to (P<0.001) and 0% of the normal‑weight
a refractory obesity subjects without mutations
clinic; Switzerland
Gibson et al. 2007 Population‑based Children aged 329 Maternal BMI and family structure 38
prospective study 6‑13 years and their (single‑parent versus two‑parent families)
mothers, recruited were the only significant predictors of child
from a pediatric BMI z‑scores
hospital endocrinology
department, Perth;
Australia
Al‑Rukban 2003 Cross‑sectional Saudi male 894 Family history (OR: 2.49; 95% 39
adolescents aged CI: 1.72‑3.61) and lack of physical activity
12‑20 years from (OR: 1.63; 95% CI: 1.01‑2.62) were
intermediate and associated with adolescent obesity
secondary schools in
Riyadh; Saudi Arabia
Jaber et al. 2003 Cross‑sectional Adult Arab Americans 626 Overall prevalence of DM was 15.5% 41
aged 20‑75 years of (95% CI: 12.2‑18.7%) in women and
age, from randomly 20.1% (15.0‑25.2%) in men (P=0.13).
selected households Subjects with DM had greater BMI and
in Dearborn, WHR than subjects with normal glucose
Michigan; United tolerance
States
Shai et al. 2006 Prospective White and black 78,419 Risk of DM is significantly higher among 42
cohort healthy women from Asians, Hispanics, and blacks than among
The Nurses’ Health whites before and after taking into account
Study; United States differences in BMI (RRs: 2.26, 1.86, 1.34
respectively)
T2DM: Type 2 diabetes mellitus, DM: Diabetes mellitus, BMI: Body mass index, RRs: Relative risks, WHR: Waist‑to‑hip circumference ratio, HR: Hazard ratio, CI: Confidence interval,
WC: Waist circumference, ORs: Odds ratios, VAT: Visceral adipose tissue

4 Egyptian governorates, and reported a significant As indicated earlier, Asian populations are generally
association between WC and the risk of diabetes more prone to abdominal obesity and low muscle mass
(P = 0.02). However, BMI was not significantly associated with increased insulin resistance compared with white
with diabetes (P = 0.11).[21] western individuals.[22,23] The risk of T2DM was found

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Al-Quwaidhi, et al.: Obesity and type 2 diabetes mellitus

to start at a lower BMI for Asians than their European self-deception.[28] The evidence is inconsistent regarding
counterparts.[22,23] the relation between intake of individual macronutrients
(fat, carbohydrate and protein) and obesity, with fat
Lear et al.[6] compared the relation between abdominal overconsumption being the most commonly suggested
adipose tissue and total body fat between persons dietary factor to have a role in the etiology. It has been
living in Canada of Aboriginal, Chinese, and South suggested that fat appears to have a weaker satiating
Asian origin with persons of European origin. They capacity than that of carbohydrates and proteins, so that
matched healthy Aboriginal, Chinese, European, and individuals readily overeat in response to high fat foods.
South Asian participants (n = 822) aged 30-65 years As fat has twice as much energy per gram as protein
by sex, ethnicity, and BMI. Total abdominal adipose or carbohydrate, this may eventually result in energy
tissue (TAT), subcutaneous abdominal adipose tissue density.[29] Nevertheless, some studies have shown a
(SAT), visceral adipose tissue (VAT), total body fat positive linear relationship between energy density
mass, lifestyle, and demographics were assessed. They and fat consumption, but a modest negative correlation
investigated the relations between BMI and total body with carbohydrate intake.[30,31] On the other hand, some
fat, TAT, SAT, and VAT and between total body fat studies have found that a dry high-carbohydrate food
and TAT, SAT, and VAT.[6] It has been found that BMI such as pretzels can have similar energy density as high-
significantly underestimated VAT in all non-European fat foods such as cheese.[32] Moreover, some researchers
groups. Throughout a range of total body fat mass, VAT now suggest that it is the “total” energy intake which
was not significantly different between the Aboriginals has a more obvious association than fat intake only.[30]
and the Europeans. With total body fat >9.1 kg, Chinese
participants had increasingly greater amounts of VAT Several intervention studies have reported that reductions
than did the Europeans (P value for interaction =0.008). in energy intake (e.g., diet) alone, or increasing energy
South Asians had less VAT with total body fat >37.4 kg expenditure (e.g., exercise) alone have a positive impact
but more VAT below that amount than did Europeans on body weight,[24] although the combination of diet
(P value for interaction < 0.001).[6] plus exercise has the greatest impact on weight loss.[33]
For example, an intervention study reported reductions
Physical activity and diet in body weight by 4.9% and 5.7% in participants
Obesity generally results from an imbalance between with 18 months of diet alone, and diet plus exercise,
energy intake (diet) and energy expenditure respectively (P < 0.05).[33]
(PA). [24] There is good evidence supporting that PA
is an important component on long-term weight Genetics and ethnicity
control.[17,25-27] PA generally affects body composition There is a continuing search for the genetic basis
and weight favorably by promoting fat loss. of predisposition to obesity. Several single gene
It has been observed by numerous studies that a mutations in rodents and humans were suggested to
minimum of 150 min/week of moderate-intensity PA cause the development of obesity.[34-36] However, these
(e.g., 30 min of brisk walking daily) is associated with are extremely rare and an increase in genetic defects
health-related benefits.[26,27] However, higher levels of is insufficient to explain the substantial increase in
PA (200-300 min/week) may be necessary to improve the prevalence of obesity over the recent decades.[37]
long-term weight loss outcomes.[26,27] Moreover, studies
have demonstrated that exercise alone can have a Some research studies suggest an association between
significant impact on body weight when maintained family history and obesity. For instance, Gibson et al.[38]
for ≥12 months, and that individuals who reduce their carried out a population-based prospective study on
level of leisure-time PA can have weight regain after a 329 children aged 6-13 years (192 healthy weight,
specific period of time. Another important observation 97 overweight and 40 obese) and their mothers (n = 265)
is that the combination of increased PA and dieting recruited from a pediatric hospital and primary schools in
appears to be more effective for long-term weight Perth, Australia. Height, weight and BMI of children and
regulation than is dieting alone.[25] mothers were among the main outcome measures in the
study. It has been found that having an overweight mother
The progress in understanding the role of diet in the increases the likelihood of a child being overweight or
etiology of obesity has been seriously confounded by obese. Maternal BMI and family structure (single-parent
the profound under-reporting, which is now widely versus two-parent families) were the only significant
recognized as a feature of obesity. Several studies have predictors of child BMI.[38] Similar findings were obtained
reported that obese individuals might under-report from a cross-sectional study in Riyadh, Saudi Arabia.[39]
their intake by an average of 30% due to many reasons, A total of 894 Saudi male adolescents (age 12-20 years)
such as forgetfulness, underestimation of portion size, were selected from intermediate and secondary schools
inadequate knowledge of food composition, or even in Riyadh. Adolescents with a BMI age-specific percentile
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Al-Quwaidhi, et al.: Obesity and type 2 diabetes mellitus

of ≥95th were considered obese. It has been found that Paciorek CJ, et al. National, regional, and global trends in
family history of obesity was associated with adolescent body-mass index since 1980: Systematic analysis of health
examination surveys and epidemiological studies with 960 country-
obesity (OR 2.49; 95% CI: 1.72-3.61).[39] years and 9.1 million participants. Lancet 2011;377:557-67.
5. Balkau B, Deanfield JE, Després JP, Bassand JP, Fox KA,
A large number of studies have revealed that some Smith SC Jr, et al. International Day for the Evaluation of
ethnic groups have an elevated risk of T2DM compared Abdominal obesity (IDEA): A study of waist circumference,
to other ethnicities.[19,40,41] In all these studies, which have cardiovascular disease, and diabetes mellitus in 168,000 primary
care patients in 63 countries. Circulation 2007;116:1942-51.
not adjusted for some confounding variables (e.g., BMI), 6. Lear SA, Humphries KH, Kohli S, Chockalingam A, Frohlich JJ,
obesity might be a modifying factor for increased levels of Birmingham CL. Visceral adipose tissue accumulation differs
the disease. However, some other studies have adjusted according to ethnic background: Results of the Multicultural
their results for BMI and still found variations by ethnicity. Community Health Assessment Trial (M-CHAT). Am J Clin
Nutr 2007;86:353-9.
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