Canadian Journal of Cardiology 28 (2012) 326 –333
Review
The Obesity Epidemic and Its Impact on Hypertension
Thang Nguyen, MD, FRCPC,a and David C.W. Lau, MD, PhD, FRCPCb
a
Division of Cardiology, Cardiac Prevention and Rehabilitation, St Michael’s Hospital, Toronto, Ontario, Canada
b
Departments of Medicine, Biochemistry and Molecular Biology, and Cardiac Sciences, Julia McFarlane Diabetes Research Centre, University
of Calgary, Calgary, Alberta, Canada
ABSTRACT
Global obesity rates have increased steadily in both developed and
emerging countries over the past several decades with little signs of
slowing down. Over 1.5 billion people worldwide are overweight or
obese and over 40 million children under the age of 5 are overweight.
Obesity is associated with increased morbidity, disability, and prema-
ture mortality from cardiovascular disease, diabetes, cancers, and
musculoskeletal disorders. The personal and societal health and eco-
nomic burden of this preventable disease pose a serious threat to our
societies. Obesity is a major risk factor for hypertension and cardio-
vascular disease. Weight loss, through health behaviour modification
and dietary sodium restriction, is the cornerstone in the treatment of
obesity-related hypertension. Pharmacotherapy and bariatric surgery
for obesity are adjunctive measures when health behaviour interven-
tions fail to achieve the body weight and health targets. Successful
management of overweight and obese persons requires a comprehen-
sive, multifaceted framework that integrates population health, public
health, and medical health models to dismantle the proximal and
Obesity has reached epidemic proportions globally and has
become a major public health concern.1 In 2008 an estimated
1.5 billion adults worldwide were overweight and 500 million
were obese. More than 40 million children under the age of 5
are overweight.2,3 Obesity rates have more than doubled since
1980, with 1 in 10 of the world’s adult population now
obese.2,3 Adiposity, or excess body fat, is associated with in-
creased morbidity, disability, and premature mortality from
cardiovascular disease (CVD), diabetes, cancers, and musculo-
skeletal disorders. Using body mass index (BMI) (calculated as
weight [kg]/height [m2]) as an anthropometric measure of ad-
iposity, each 5 units above the overweight category (BMI ⬎
25) is associated with approximately 30% higher overall mor-
tality and 40% higher for cardiovascular mortality.4 Depend-
Received for publication December 8, 2011. Accepted January 2, 2012.
Corresponding author: Dr David C.W. Lau, Departments of Medicine,
Biochemistry and Molecular Biology, and Cardiac Sciences, Julia McFarlane
Diabetes Research Centre, University of Calgary, 2998-3330 Hospital Drive
NW, Calgary, Alberta T2N 4N1, Canada. Tel.: ⫹1-403-220-2261; fax: ⫹1-
403-210-8113.
E-mail: dcwlau@ucalgary.ca
See page 331 for disclosure information.
0828-282X/$ – see front matter © 2012 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
doi:10.1016/j.cjca.2012.01.001
RÉSUMÉ
Le taux d’obésité globale a augmenté de manière régulière dans les
pays développés et les pays émergents au cours des dernières décen-
nies, tout en montrant de légers signes de ralentissement. Plus de 1,5
milliard de personnes dans le monde sont préobèses ou obèses, et
plus de 40 millions d’enfants de moins de 5 ans sont préobèses.
L’obésité est associée à une augmentation de la morbidité, de
l’incapacité et de la mortalité prématurée en raison des maladies
cardiovasculaires, du diabète, des cancers et des troubles muscu-
losquelettiques engendrés. La santé personnelle et sociale ainsi que le
fardeau économique de cette maladie évitable posent un sérieux
problème à nos sociétés. L’obésité est un facteur de risque majeur de
l’hypertension et des maladies cardiovasculaires. La perte de poids,
par la modification des comportements de santé et par la restriction
en sodium alimentaire, est la pierre angulaire dans le traitement de
l’hypertension liée à l’obésité. La pharmacothérapie et la chirurgie
bariatrique sont des moyens auxiliaires lorsque les interventions en
matière de comportement de santé ne mènent pas aux objectifs de
ing on the severity of obesity the life expectancy of overweight
and obese adults is shortened by 4 to 10 years. Globally 3
million deaths annually have been attributed to obesity.2
The excess mortality among overweight and obese (defined
as BMI ⬎ 30) people is due mainly to cardiovascular causes.
According to the World Health Organization, more than a
third of the world’s deaths can be attributed to a small number
of risk factors. Among the 5 leading risk factors are high blood
pressure (BP), tobacco use, high blood sugar, physical inactiv-
ity, overweight, and obesity.2 High BP, obesity, and physical
inactivity each accounted for 395,000, 216,000, and 191,000
preventable deaths in 2005 in the US.5 Except for tobacco use,
4 of the 5 risk factors are interrelated— both hypertension
and high blood sugar could be attributable to unhealthy
behaviours such as food overconsumption and physical in-
activity, which in turn may lead to the development of over-
weight and obesity. Indeed, obesity has eclipsed cigarette
smoking as the leading preventable cause of death and short-
ened life expectancy in the US.6
Hypertension is a common feature present in a large pro-
portion of overweight and obese people. It is correlated with
the degree of obesity and greatly exaggerates the risk of stroke,
Nguyen and Lau
Obesity and Hypertension
distal drivers of the obesogenic environment in which we live. Preven-
tion of obesity is no longer a lofty but rather necessary goal that
urgently calls for action from governments at all levels, in conjunction
with all public and private sector stakeholders, in order to combat a
serious and growing public health concern.
coronary artery, and peripheral artery diseases. The burden of
hypertension attributable to obesity is very high, and has been
estimated to be approximately 80% for men and approximately
60% for women.7 The odds ratio for hypertension is 1.7 for
overweight compared with normal weight individuals, 2.6 for
class 1 obesity (BMI 30-34.9), 3.7 for class 2 obesity (BMI
35-39.9), and 4.8 for class 3 obesity (BMI ⬎ 40).8
This review focuses on the relationship of obesity and hy-
pertension in adults and children, the mechanisms linking obe-
sity to hypertension, why weight loss is a cornerstone treatment
for obesity-related hypertension, and approaches to tackle the
global epidemic of obesity.
The Global Epidemic and Burden of Obesity
Globally the prevalence of obesity has been steadily increas-
ing over the past several decades. Data from over 9 million
adults in 199 countries have indicated that the BMI increased
by 0.4-0.5 per decade worldwide between 1980 and 2008.9
The dramatic rise in obesity rates globally is fueled by the in-
creased availability of energy-dense diets, increasingly seden-
tary physical activity behaviours and, importantly, mass urban-
ization in emerging nations. The proportion of the world’s
population living in urban areas eclipsed the 50% mark in
2008, with the urban population predicted to increase to 4.9
billion by 2030, while the rural population is expected to con-
tract by 28 million.10 Obesity is a consequence of the obeso-
genic environments that have evolved in both high and low
income countries. Urbanization is increasingly viewed as a po-
tential health hazard for vulnerable populations, namely the
urban poor from both high and low income countries.
The US leads the developed world with the highest obesity
rates, with a prevalence of 34% in adults and 17% among
children 2-19 years of age.11 Projections based on the current
obesity trends predict that there will be 65 million more obese
adults in the US by 2030.12 In Canada, the 2007-2009 cohort
from the Canadian Health Measures Survey had a 2.0 increase
in mean BMI when compared with the 1981 data.13 Twenty-
five percent of Canadian adults and 8.6% of children and
youth aged 6-17 were obese.14 The mean BMI of adult Cana-
dians is greater than 25 regardless of age or gender. Based on the
measured data, the prevalence of overweight and obesity in
2008 was an alarming 62%.14 Nineteen percent of men and
21% of women between the ages of 20 to 39 were classified as
obese, while for ages 60 to 69 years, the prevalence increased to
34% and 33% respectively.15 In adolescents aged 15 to 19
years, 25% of girls and 31% of boys were already overweight or
obese.16 If the obesity trend continues at the current rate, half
of the Canadian population over the age of 40 years will be
classified as obese within 25 years.15 Sadly, the prevalence of
327
poids corporel et de santé. La prise en charge réussie des per-
sonnes préobèses et obèses requiert un cadre multifacette, détaillé
et complet, qui intègre les modèles de santé de la population, de
santé publique et de santé médicale pour éliminer les facteurs
proximaux et distaux de l’environnement obésogène dans lequel
nous vivons. La prévention de l’obésité n’est plus un but noble, mais
plutôt un but nécessaire qui exige de manière urgente l’intervention
de tous les ordres de gouvernement, conjointement avec toutes les
parties prenantes des secteurs public et privé, pour combattre ce
sérieux et croissant problème de santé publique.
obesity is significantly higher among aboriginal peoples in both
adults and children.14
The increasing prevalence of overweight and obesity in chil-
dren and youth is particularly disturbing as childhood obesity
is predictive of adult obesity.1,17 What is even more alarming
is the observation that clustering of CVD risk factors is
already present in overweight children, leading to an in-
creased future risk of CVD in adults.18,19 When these fig-
ures are applied to a computer-simulation model of coro-
nary artery disease (CAD) to predict excess incidence and
prevalence of CAD from 2020 to 2035, the prevalence of
CAD will increase by a range of 5% to 16% by 2035, and
more than 100,000 excess cases of CAD will be directly
attributable to childhood obesity.13 Furthermore, a recent
study in a large cohort of 276,835 Danish school children
found that the CVD risks during adulthood increased linearly
with increasing BMI at each age from 7 to 13 years.19 Another
prospective study in 37,674 apparently healthy young men,
which tracked BMI from adolescence to adulthood with a
mean follow-up of 17 years, indicated that an elevated BMI at
age 17 years— one that is in the high normal range—was asso-
ciated with substantially higher risk of CAD in adulthood at
age 30 years.20 The hazard ratio for the association of adoles-
cent BMI with CAD, after multivariate analysis adjusted for
age, family history, BP, lifestyle factors, fasting glucose, and
triglyceride levels, was 6.85.20 Available evidence has led many
experts to predict that the current generation of overweight and
obese children may have a shorter life span than their par-
ents.18,21 Fortunately a recent study of 6,328 subjects with a
mean follow-up of 23 years, reported that if childhood obesity
is reduced or treated, the increased CVD risk in adulthood
could be attenuated. The CVD risks among people who were
overweight or obese as children but are no longer obese as
adults were similar to the CVD risks in those people who were
never obese.22 This study suggests that childhood obesity, if
successfully treated, does not necessarily increase the CVD risk
permanently during adulthood.
Obesity increases the risk of many chronic diseases, notably
type 2 diabetes, hypertension, heart disease, stroke, musculo-
skeletal diseases, and several forms of cancers. The acute and
chronic diseases associated with excess adiposity not only neg-
atively affect the health-related quality of life of an individual,
but also the substantially higher costs from health care and lost
productivity to the individual and the society. A systematic
review demonstrated that obesity accounts for 0.7%-2.8% of
direct health care expenditure in many developed countries but
could be as high as 7% in the US.23 Data from the US indicate
that obese people incur more frequent physician visits, higher
in- and out-patient costs, and greater prescription drug use.12
328
In Canada, the total direct health care costs attributable to
obesity have escalated from CAD$1.8 billion (2.4% of the total
health expenditures) in 1997 to CAD$4.6 billion in 2006
(4.1% of the total health care expenditures).24,25 In addition to
medical costs, the indirect costs from obesity as a result of
decreased years of working life, disability-free life, and work
absenteeism vs presenteeism are difficult to quantify but could
be quite significant. Taken together these data indicate that
obesity exacts a huge health and economic burden from both
individuals and the society.
Causal Link Between Obesity and Hypertension
Hypertension is the most common cardiovascular risk fac-
tor predisposing to CAD, stroke, and structural end organ
damage.2 The link between obesity and hypertension has been
documented in many large population and epidemiological
studies in adults and the burden of hypertension attributable to
obesity is very high in both men and women.7,8 Population-
based studies consistently demonstrate an increased risk in the
development of hypertension among overweight and obese
people. Compared with normal weight cohorts, obese individ-
uals have a 2- to 3-fold risk for developing high BP.26 The
mean systolic BP (SBP) and diastolic BP (DBP) values were
estimated to be 9 and 7 mm Hg higher in obese men and 11
and 6 mm Hg higher in obese women relative to a cohort with
normal BMI.27
The observations that overweight and obese children with
elevated BP may already have structural arterial abnormalities,
such as increased carotid intimal-medial thickness and left ven-
tricular mass, suggests a causal relationship between obesity
and hypertension.19,21 Obese adolescents have elevated 24-
hour ambulatory BP readings compared with their nonobese
cohorts, with excess values as high as ⫹19.3 mm Hg systolic
and ⫹10.1 mm Hg diastolic in 1 study.28 Not surprisingly, the
risk of developing hypertension increases with body weight. A
Canadian cohort demonstrated a 7-fold likelihood of develop-
ing hypertension in obese children.29 It is not known whether
weight loss or treatment of hypertension will completely re-
verse the structural arterial changes that have occurred in over-
weight and obese adolescents. Obesity-related hypertension is
increasingly recognized by some experts as a distinct phenotype
that requires a more vigilant approach to diagnosis, treatment,
and prevention.
The hallmark of obesity is the presence of excessive body fat,
which is the consequence of either overconsumption of food,
decreased physical activity, or both. Adipose tissue is composed
of mature adipocytes, preadipocytes, endothelial cells, and
macrophages, and is no longer merely viewed as a passive re-
pository for triacylglycerol. Mature adipocytes are active endo-
crine and paracrine cells secreting an ever-increasing number of
mediators that participate in diverse metabolic processes.30,31
The best-known adipose tissue-derived hormone is leptin,
which functions as a feedback regulator to suppress appetite
centrally in the hypothalamus.31 Circulating leptin levels are
correlated to adiposity and are elevated in obese people.31 It
turns out that many overweight and obese people develop cen-
tral leptin resistance and their appetites are not suppressed de-
spite higher plasma leptin levels. Leptin has been linked to
hypertension and this association was first reported in animal
and more recently in human studies.32-34 Several mechanisms
Canadian Journal of Cardiology
Volume 28 2012
have been proposed to explain the positive relationship. First,
leptin alters renal sodium by upregulating renal Na, K-ATPase
activity.32 Second, leptin also activates the renin-angiotensin-
aldosterone axis as well as the sympathetic nervous system,
both of which could lead to the development of hyperten-
sion.32 Third, higher leptin levels may be related to insulin
resistance which is also associated with hypertension.33,34 Fi-
nally, leptin could act in concert with other proinflammatory
cytokines to induce vascular oxidative stress and arterial hyper-
tension.34
Excess adipose tissue in overweight and obese people, espe-
cially from the visceral depot, becomes dysfunctional, and is
characterized by a preponderance of hypertrophied adipocytes
with infiltration by macrophages. These changes lead to exces-
sive release of cytokines and proinflammatory mediators from
adipose tissue, often referred to as adipokines. In addition to
leptin, interleukin-6, tumour necrosis factor-␣, plasminogen
activator inhibitor-1, and C-reactive protein are among the
proinflammatory akipokines that are upregulated in adipose
tissue and contribute to the systemic inflammatory state and
the increased vascular oxidative stress observed in obesity.30
Adiponectin, a protein abundantly produced by adipose tissue,
is an important stimulant of nitric oxide synthase activity and
confers protection against oxidative stress and insulin resis-
tance. Circulating levels of adiponectin are decreased in obesity
partly because its production is suppressed by the proinflam-
matory adipokines. Taken together, the unopposed upregula-
tion of proinflammatory adipokines and the suppression of
adiponectin wreak havoc on glucose and lipid metabolism, re-
sulting in vascular endothelial dysfunction, and the progression
of atherosclerotic changes within the vessel wall.30,31 These
metabolic abnormalities not only exaggerate the risks for CVD
but also insulin resistance and type 2 diabetes, and have led to
the development of the metabolic syndrome concept,30,35
more broadly referred to as cardiometabolic risk.36
A common feature of hypertension is the activation of the
renin-angiotensin-aldosterone axis. Animal studies suggest that
adipose tissue is a source of angiotensinogen, angiotensin-con-
verting enzyme, and renin, where its contribution to the circu-
lating levels of these components of the renin-angiotensin-al-
dosterone axis becomes an important consideration in the
presence of obesity.37 The finding of adipocyte hypertrophy,
low body weight and low BP in angiotensin knock-out mice
lends support to a more direct role of adipose tissue in the
pathogenesis of hypertension.37
It should be noted that hyperinsulinemia and insulin resis-
tance in obesity can also induce hypertension via other mech-
anisms, including chronic stimulation of sympathetic and vas-
cular tone along with antinatriuretic effects.30,37
There are other mechanisms whereby obesity could contrib-
ute to the development of hypertension. For example, sleep
apnea, a common complication of obesity, could alter the hy-
pothalamic-pituitary-adrenal axis by inducing higher cortisol
levels, as well as activating the sympathetic nervous system.
Health Behaviour Management of Obesity-
Related Hypertension in Adults
The cornerstone treatment of obesity-related hypertension
is weight loss through health behavioural changes and reduced
sodium intake in the diet. Weight loss diminishes both the
Nguyen and Lau
Obesity and Hypertension
Table 1. Expected BP response to obesity intervention
SBP/DBP (mm Hg)
Intervention Adults Adolescents
Health behaviour modifications ⫺6.6/⫺5.1 ⫺7/⫺2
Aerobic exercise only ⫺3.8/⫺2.6 No data
DASH - sodium restriction ⫺11.4/⫺5.5 No data
Orlistat ⫺2.5/⫺1.9 ⫹1.1 (NS)/⫺0.51
Adjustable gastric banding ⫹2.1/⫺1.4 (NS) ⫺12.5/⫺6.0
Roux-en-Y gastric bypass ⫺4.7/⫹10.4 (NS) Insufficient data
BP, blood pressure; DASH, Dietary Approaches to Stop Hypertension;
DBP, diastolic BP; NS, statistically nonsignificant difference from control
group; SBP, systolic BP.
augmented renin-angiotensin-aldosterone axis activity and the
activation of the sympathetic nervous system. Reduction in
body fat, especially from the visceral depot, improves insulin
resistance and also promotes natriuresis. The general principle
of weight loss is the achievement of a net negative energy bal-
ance. This can be accomplished by health behaviour modifica-
tion alone, or with adjunctive pharmacotherapy, and in some
selected cases, bariatric surgery. Adoption of a healthier lifestyle
is essential for the long-term success in achieving lower BP
values. This includes appropriate weight loss to achieve target
health goals, maintenance of weight loss, and prevention of
weight regain, regular physical activity, reduced dietary sodium
intake, moderation of alcohol consumption, smoking cessa-
tion, and stress management. The necessary health behaviour
modifications can best be delivered by an interdisciplinary
health care that includes dietary and exercise counselling, social
support, and possibly cognitive behavioural therapy.
The efficacy of health behaviour modification on BP in
overweight patients is partly dependent on the magnitude of
weight loss. A decrease of as little as 2 kg can reduce SBP by 4
mm Hg and DBP by 3 mm Hg.38 A meta-analysis of 25 ran-
domized trials concluded that a weight loss of 5.1 kg achieved
by energy restriction, increased physical activity, or both, can
lower SBP by 4.4 mm Hg and DBP by 3.6 mm Hg (see
Table 1). Each kg weight loss is associated with a reduction of
1 mm Hg in SBP of and 0.92 mm Hg in DBP.39 Weight loss
exceeding 5 kg is associated with more significant BP lowering,
up to a 6.6 mm Hg reduction in SBP and 5.1 mm Hg reduc-
tion in DBP.40 This BP lowering effect becomes more dramatic
in patients with class II (BMI 35–39.9) or class III (BMI ⬎ 40)
obesity. In this subset, reduction of 15 mm Hg SBP and 6 mm
Hg DBP was possible if a 10 kg weight loss achieved through
diet and physical activity intervention was maintained for 1
year.39
Aerobic exercise also lowers BP in both hypertensive and
normotensive subjects. A meta-analysis of 54 randomized
controlled trials concluded that aerobic exercise was associ-
ated with a reduction in both SBP and DBP, 3.8 mm Hg
and 2.6 mm Hg, respectively.41 The average intervention-
related weight loss was 0.4 kg, which was not statistically or
clinically significant. However, this points to the mecha-
nism whereby exercise lowers BP independent of weight
loss, potentially through improvements in insulin resistance
and hyperinsulinemia.
Dietary patterns also appear to exert beneficial effects on BP
lowering. The best studied is the Dietary Approaches to Stop
Hypertension (DASH) diet. Following an 8-week diet rich in
329
fruits and vegetables, and low-fat dairy products, with reduced
saturated and total fat, the SBP and DBP were reduced by 11.4
mm Hg and 5.5 mm Hg respectively in people with hyperten-
sion when compared with the control diet.42 When the DASH
diet was administered with dietary sodium restricted from 3.5
g/d to 1.2 g/d, there was a further reduction in SBP 7.1 mm Hg
in people without hypertension and 11.5 mm Hg in people
with hypertension.43 Sodium restriction is particularly relevant
and effective in overweight and obese people, as they have a
greater propensity for sodium retention as a direct consequence
of the abnormal metabolic changes described earlier.
A recent US study suggested that reducing dietary salt by 3
g/d could reduce the annual number of new cases of CAD by
60,000 to 120,000, stroke by 32,000 to 66,000, and myocar-
dial infarction by 54,000 to 99,000, in conjunction with an
annual reduction in deaths from any cause by 44,000 to
92,000.44 The authors concluded that modest reductions in
dietary salt could substantially reduce cardiovascular events,
resulting in an estimated savings of USD$10 billion to
USD$24 billion in health care costs, and should therefore be
recommended as a public health target.
Pharmacotherapy for Obesity
Pharmacotherapy for obesity is considered as an adjunct
when health behavioural changes fail to achieve the goal
targets in BP and/or other metabolic comorbidities.1 Cur-
rently, orlistat is the only drug approved as a long-term
weight loss medication. Orlistat is a gastrointestinal lipase
inhibitor that reduces dietary fat absorption and fat calorie
intake by approximately 30%.45 As expected, the common
side effects include bloating, fecal incontinence, and ab-
dominal cramps. After 4 years, orlistat can maintain a neg-
ative weight change of about 6 kg and a reduction of SBP
and DBP of 4.9 and 2.6 mm Hg respectively. However, the
additional benefit of orlistat on top of health modification
alone was minimal, only achieving an additional 1.5 mm Hg
SBP and 0.7 mm Hg DBP reduction.46 Overall, a recent
meta-analysis of 4 orlistat trials concluded a net BP benefit
of ⫺2.5 mm Hg SBP and ⫺1.9 mm Hg DBP.47
Several antiobesity drugs are currently in phase 3 clinical
trials. One that is showing promise is liraglutide, a glucagon-
like peptide-1 analogue currently approved as an antihypergly-
cemic agent in most countries, which revealed greater weight
loss (⫺5.5 to ⫺7.2 kg) compared with orlistat (⫺4.1 kg).48
Liraglutide also reduced BP modestly (⫺5.6 to ⫺6.9 mm Hg
SBP and ⫺1.2 to ⫺2.9 mm Hg DBP). Data from a large phase
III trial involving a combination of phentermine and topira-
mate demonstrated a 10 kg weight loss, along with a BP reduc-
tion of 5.6 mm Hg SBP and 3.8 mm Hg DBP at 56 weeks.49
Bariatric Surgery
At present bariatric surgery is considered for individuals
with class III obesity (BMI ⬎ 40) or class II obesity (BMI ⬎
35) with comorbid conditions such as hypertension and type 2
diabetes.1 Bariatric surgery procedures can be classified as re-
strictive, malabsorptive, or combination of both restrictive and
malabsorptive. Four types of bariatric procedures are now
available in Canada.
Firstly, adjustable gastric banding is a restrictive procedure
that involves the placement of an adjustable silicone band
330
around the upper portion of the stomach to reduce its overall
size. The absolute weight loss is about by 27 kg or 47% of
excess weight50 but its effect on hypertension has been disap-
pointing, with minimal improvement in subjects followed pro-
spectively for up to 10 years.51
Secondly, gastric bypass, or Roux-en-Y, is the gold standard
procedure, whereby the size of the stomach is reduced to create
a smaller pouch that is connected to a small segment of the
proximal jejunum. Mean absolute weight loss of gastric bypass
surgery is 43 kg and the mean excess weight loss is 62%.50
Using retrospective observational data, gastric bypass surgeries
appear to improve or resolve hypertension in the range of 30%
to 70% after 1 to 5 years.50,52-55 The Swedish Obese Subjects
(SOS) study is the largest and longest prospective trial of bari-
atric surgery to date and included a portion of gastric bypass
surgeries. At 10 years, there was a nonsignificant effect on BP in
this subgroup despite a significant weight loss.51
Thirdly, vertical sleeve gastrectomy is a relatively new re-
strictive procedure: the stomach is stapled vertically, thereby
removing about 85% of the original stomach area. It can be a
stand-alone procedure, or as a first step for the gastric bypass
surgery mentioned above. A Canadian registry of 34 patients
showed a mean weight loss of 27.4 kg and a 53% resolution of
hypertension at a mean follow-up of 10 months.56 These find-
ings are consistent with other reports on laparoscopic sleeve
gastrectomy, which demonstrated a 40%-60% rate of hyper-
tension resolution in the short-term.57,58 The above 3 bariatric
procedures are mainly performed laparoscopically; conse-
quently, peri- and postoperative complications are reduced
drastically.
Fourthly, the most technically challenging procedure is bil-
iopancreatic diversion with duodenal switch. Subtotal gastrec-
tomy is performed to create a sleeve-shaped stomach, and the
small bowel is divided into 2 limbs—the enteric limb carrying
food, and the biliopancreatic limb carrying bile and pancreatic
juice, and an ultra-short common channel after anastomosis of
the 2 limbs. This procedure results in the greatest weight loss
(64% of excess weight) along with resolution of diabetes (ap-
proximately 95%) and other comorbidities. Unfortunately, a
recent prospective comparison found no advantage of this pro-
cedure over the Roux-en-Y in the treatment of hypertension.59
Regardless of the surgical procedure a multidisciplinary weight
management team is required for assessment, selection of
proper candidates, pre- and long-term postoperative follow-up
and management.
Management of Obesity-Related Hypertension in
Overweight and Obese Adolescents
Health behaviour modification remains the cornerstone for
the treatment of overweight and obese adolescents with hyper-
tension and related metabolic comorbidities. However, no
consistent protocols are available on such interventions and few
published randomized trials report on BP lowering. With a
1-year training program of physical activity, nutrition, and be-
haviour therapy, SBP and DBP were lowered by 7 and 2 mm
Hg respectively.60 A shorter term study reported greater BP
reduction by 14 and 9 mm Hg (SBP and DBP) after only 20
weeks of lifestyle training.61
The efficacy and safety and of pharmacotherapy and surgi-
cal interventions for obesity treatment in children is limited.
Canadian Journal of Cardiology
Volume 28 2012
Two randomized controlled trials involving orlistat have been
studied in the pediatric population, with only 1 reporting BP
changes.62,63 In the 54-week trial orlistat was superior to health
behaviour modifications alone with respect to weight loss, re-
ducing BMI by a modest 0.55. No difference in SBP was
noted, while DBP was reduced by a mere 0.5 mm Hg.
For the massively obese adolescent, bariatric surgery is
sometimes considered. Laparoscopic adjustable gastric band-
ing and the Roux-en-Y procedure are the 2 procedures per-
formed to date and most of the published data consist of small
observational and not randomized studies, with follow-up in
the range of 1 to 5 years. Several studies reported improvement
in hypertension but lacked details. A prospective randomized
laparoscopic adjustable gastric banding trial in 50 adolescents
with BMI ⬎ 35 reported a mean weight loss of 34.6 kg after 2
years. This was accompanied by a reduction in SBP of 12.5 mm
Hg and DBP of 6.0 mm Hg when compared with baseline, but
was statistically nonsignificant when compared with the con-
trol group.64 Limited data exists for Roux-en-Y gastric bypass
surgery, which is reserved for adolescents with severe obesity
(BMI ⱖ 50). However, significant improvements in hyperten-
sion are reported with substantial weight loss within 1 year of
observation.65,66
Proposed Approaches to Tackle the Obesity
Epidemic and Its Impact on Hypertension
The global pandemic of obesity can only be effectively re-
versed by dismantling the principal determinants of the obeso-
genic environment. Obesity is a serious public health concern
and is a consequence of people responding normally to the
obesogenic environment where more processed, energy-dense,
affordable, and effectively marketed food are in abundant sup-
ply, in association with increasingly sedentary physical activity
behaviours promoted by the built environment and urbaniza-
tion. Undeniably the continuing trends of overconsumption of
food and decreased physical activity level over the past several
decades are the proximal causes of the unrelenting increase in
the prevalence of overweight and obesity globally. However,
the sociocultural and socioeconomic milieus within each coun-
try or local community can moderate these environmental
drivers and to some degree help reverse these proximal causes of
obesity.
Successful approaches to tackling the obesity epidemic will
require a comprehensive, multifaceted framework that inte-
grates population health, public health, and personal health
intervention strategies. Interventions aimed at reversing the
obesogenic environment will have the biggest impact. How-
ever, in order to achieve these, governments at all levels must be
persuaded to enact policies that facilitate the cooperation of
consumers, public and private sectors, nongovernmental orga-
nizations, and various industries (food, service, transportation,
and building, etc) in the promotion of higher levels of physical
activity and the consumption of healthy food choices in a man-
ner which makes these the easy choices. Policy-led interven-
tions are more likely to change the population environments
systematically and these population-wide effects are more likely
to be sustainable and longer lasting. One such example is a
country-wide sodium reduction strategy. We have compelling
evidence that high sodium intake contributes to the develop-
ment of hypertension and that reducing dietary intake by 3 g/d
Nguyen and Lau
Obesity and Hypertension
could greatly decrease new cases of heart disease and stroke, and
deaths from CVD, in a cost-effective and potentially cost-sav-
ing manner.44
The workplace and schools are where healthy behaviours
can be promoted and fostered to optimize health and reduce
the prevalence of obesity. This will require leadership and
cooperation from both the public and corporate sectors.
Incentives from governments at the municipal, provincial
and territorial, and/or federal levels could go a long way to
help in implementing the necessary changes. Healthier em-
ployees and children will benefit society by increasing pro-
ductivity and prosperity while at the same time reducing the
health care burden.
While awaiting the development of a systems approach to
tackle the obesity epidemic, health care professionals from all dis-
ciplines continue to play important roles in the prevention and
management of obesity in children adolescents and adults. Pro-
moting weight loss and weight maintenance through healthy be-
haviour modification will remain an integral component of our
clinical practice, but we need more effective and sustainable inter-
ventions as well as an efficient health care and delivery system that
facilitates and evaluates progress in reduction of body weight and
obesity.
The evidence-informed Canadian clinical practice guide-
lines on the management and prevention of obesity provided
recommendations aimed not only at primary care practitioners
but also public health and policy makers in the hope of inte-
grating population health, public health, and medical ap-
proaches to tackle the growing problem of obesity.1 Many pro-
grams and initiatives have been implemented across the
country, but much more remains to be done. Hopefully col-
laborative initiatives such as the Canadian Harmonization of
National Guidelines Endeavour (C-CHANGE) which is a
worthwhile attempt to harmonize all the Canadian clinical
practice guidelines for the prevention and treatment of
CVD, will renew our collective effort towards achieving
healthier behaviours as a direct means of curbing the obesity
epidemic and decreasing CVD.67 A global campaign, enti-
tled “Healthy weight - healthy blood pressure,” was initiated
in 2010 by the World Hypertension League, in collabora-
tion with national and international organizations, to en-
hance public awareness of obesity and hypertension.68 The
obesity epidemic is a call for action. Now, more than ever,
there is an urgent need to bring together the policy makers
and all the stakeholders to effect systems and societal
changes to abolish the obesogenic environment.
Disclosures
D.C.W.L. has received research funding, honoraria/
consulting fees from Alberta Innovates-Health Solutions,
Canadian Diabetes Association, Canadian Institutes of
Health Research, Boehringer-Ingelheim, Bristol-Myers
Squibb, Dainippon, Eli Lilly, Novo Nordisk, Pfizer, and
Sanofi; honoraria/consulting fees from Abbott, Allergan,
Amgen, Bayer, Merck, and Novartis; and peer-reviewed
funding from Alberta Innovates-Health Solutions, Canadian
Diabetes Association, and Canadian Institutes of Health Re-
search. T.G. has no conflicts of interest to disclose.
331
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