Phẫu Thuật Giảm Béo (Bariatric Surgery)

scores and the number of patients requiring the use of CPAP therapy were
recorded preoperatively and at three-month intervals. The ESS is a vali-
dated questionnaire. It asks patients their likelihood of falling asleep in
eight situations ranked from zero (would never fall asleep) to three (high
chance of dozing). An ESS score of seven or higher is considered as
abnormal with a high likelihood of a clinical diagnosis of sleep apnoea.
The mean ESS score decreased from 13.7 preoperatively to 5.3 at one
month postoperatively (p < 0.05) and maintained below the threshold
level (< 7) for the entire 12 months of follow-up. Of the 29 patients requir-
ing preoperative CPAP, only four (14 per cent) patients required CPAP at
three months postoperatively and none required CPAP at nine months.
The authors conclude that weight loss associated with RYGB significantly
improves the symptoms of sleep apnoea and is effective in discontinuation
in the clinical use of CPAP therapy. Improvement of OSA symptoms
occur as early as one month postoperatively.40 In a study by Rasheid et al.
there is evidence that weight loss following RYGB results in profound
improvement in OSA. The severity of apnoea cannot be reliably predicted
by preoperative BMI and ESS; therefore, patients with symptoms of OSA
should undergo polysomnography.41
Lankford evaluated the CPAP pressure requirements in a group of patients
undergoing rapid weight loss following RYGB. All patients experienced a
reduction in required optimal pressures. Pre-surgical optimal CPAP pressures
ranged from 7 to 18 cm H2O, with an average of 11 ± 3.0 cm H2O. The aver-
age BMI was 48 ± 7.4 kg/m2. Post-RYGB, the average BMI dropped to
32 ± 7.8 kg/m2. The post-surgical CPAP pressures ranged from 4 to 12 cm
H2O, with an average pressure of 9 ± 2.7 cm H2O. This represents an overall
reduction in CPAP pressure requirements of 18 per cent.42
Postoperative CPAP/BiPAP can be safely omitted in laparoscopic
RYGB patients with known OSA, provided they are observed in a moni-
tored setting and their pulmonary status is optimized by aggressive
incentive spirometry and early ambulation.43
Effects of AGB on OSA
Dixon et al. studied 313 consecutive patients with severe obesity who
received AGBs. The patients completed a preoperative sleep question-
naire and clinical assessment. Twelve months after AGB the same
Effects of Bariatric Surgery on Co-Morbidities
333

assessment was completed by 123 patients. There was a significant
improvement in the responses to all questions at follow-up, with habitual
snoring reduced to 14 per cent (preoperativevalue, 82 per cent), observed
sleep apnoea to two per cent (preoperative value, 33 per cent), abnormal
daytime sleepiness to four per cent (preoperative value, 39 per cent),
and poor sleep quality to two per cent (preoperative value, 39 per cent)
(p < .001 for all).44 Also patients > or = 60 years of age can experience a
significant improvement: they showed improvement one year after sur-
gery in 100 per cent of cases of OSA.45
In a recent study on Asian patients who had AGB surgery, the
authors demonstrate an improvement in sleep architecture in addi-
tion to a reduction in AHI, in association with weight loss. After the
set target weight loss of 20 kg and one year post-procedure, AHI
showed an average improvement of 50 per cent, with a cure of OSA
(AHI < 5) in many preoperatively severe cases in the repeat studies
pool (p < 0.001).46
Effects of BPD on OSA
In a consecutive series of 19 patients who have been followed-up for more
than four months after open BPD, three patients had OSA, and overnight
CPAP was able to be stopped in two patients by four months, showing the
early effect of the surgery.47
Simard et al. determined the prevalence of asthma and OSA in mor-
bidly obese patients and the effect of BPD/DS on these conditions. For the
cohort of 398 patients OSA was improved in all but one with this condi-
tion; among 29 SAS patients using CPAP before surgery, only four were
still using this treatment after two years.48
Dyslipidemia
Dyslipidemia in obesity is characterized by hypertriglyceridaemia, low
high-density lipoprotein (HDL) cholesterol, and increased prevalence of
small dense low-density lipoprotein (LDL) particles.49,50 Small, dense
LDL particles are atherogenic and associated with an increased risk of
coronary heart diseases.51,52
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Modification of diet is the first line intervention for hypercholestero-
laemia, but it has limited efficacy.53,54 The meta-analysis of Buchwald
confirmed that effective weight loss obtained by bariatric surgery in mor-
bidly obese subjects lead to an improvement of hyperlipidemia in more
than 70 per cent of patients.9 In the SOS study, bariatric surgery induced
improvement of hypertriglyceridaemia and low HDL cholesterol levels,
but not of hypercholesterolemia, in comparison with conventional
therapy.3 In 11 studies evaluated by Maggard et al. improvement or reso-
lution of dyslipidemia was seen in 60–100 per cent of surgical subjects.55
Effects of RYGB on dyslipidemia
Zlabek et al. retrospectively analysed 168 patients after RYGB and had
lipid analyses performed preoperatively and at one and two years post-
operatively. RYGB improved all lipid parameters studied and decreased
the percentage of dyslipidemic patients. Furthermore, fewer patients
were taking lipid-modifying medications postoperatively, suggesting a
substantial medication cost savings over time.56 Moreover, the improve-
ments in lipid profiles can be observed as early as three months
postoperatively.57 Those effects seem to be sustained in the long term. In
a five year follow-up study on 193 patients, the prevalence of hypercho-
lesterolemia, hypertriglyceridaemia and low HDL decreased from
41.6 per cent to 15.2 per cent, from 45.2 per cent to 4.4 per cent and from
65.8 per cent to 28.9 per cent respectively after RYGB.58 In the SOS
study, after ten years, the subjects who had undergone RYGB had greater
improvements in triglycerides (28.0 per cent versus 18.0 per cent
decrease), total cholesterol (12.6 per cent versus 5.0 per cent decrease),
and HDL levels (47.5 per cent versus 20.4 per cent increase) than those
who had AGB.3
Effects of AGB on dyslipidemia
Zambon et al. recently demonstrated that AGB produces an important
body weight reduction in morbidly obese subjects associated with an
improvement of the plasma lipoproteins, with significant reduction of
triglycerides and significant increase of HDL, reducing the small dense
Effects of Bariatric Surgery on Co-Morbidities
335

LDL fraction. These latter modifications were not related to weight
reduction nor to changes in phospholipid fatty acid composition (a marker
of habitual dietary fatty acid intake), but they were most prominently
associated with triglyceride reduction.59
In a prospective study, a total of 50 patients (17 men, 33 women) with
type 2 diabetes were studied preoperatively and again one year after AGB
surgery. There was a 43 per cent decrease in mean fasting triglyceride and
a 20 per cent decrease in the mean total cholesterol/HDL cholesterol ratio,
with an 18 per cent increase in mean HDL cholesterol levels.60
In a larger series of 709 patients, 34 per cent presented with elevated
triglyceride levels. By 12 months after surgery, only nine per cent had ele-
vated levels. Eighteen percent presented with low HDL-cholesterol levels
and by 12 months only five per cent had low levels.61
Effects of BPD on dyslipidemia
Scopinaro had remarkable results on 312 BPD obese patients with type 2
diabetes. Before BPD, the serum triglyceride and total cholesterol were
above normal values in nearly one-third and two-thirds of the patients,
respectively. A marked and highly significant reduction of the mean value
of serum triglyceride and total cholesterol concentration was seen by the
first postoperative year, with only one subject showing a serum cholesterol
value slightly above normal. The percentage of hypertriglyceridaemic
patients showed a progressive decrease, reaching one per cent at five and
ten years. In all subjects the serum total cholesterol level was in the normal
range at the second year and at all subsequent follow-up times, all subjects
being with no medication and on totally free diet. Since the simple reduc-
tion of cholesterol intestinal absorption alone cannot yield such an outcome,
a specific action of BPD on cholesterol metabolism also has to be postu-
lated. In fact, the enterohepatic bile salt circulation is partly interrupted after
BPD, with the consequent loss of bile salts causing enhancement of hepatic
bile acid synthesis at the expense of the cholesterol pool. Furthermore, a
sharp reduction of endogenous cholesterol is likely to occur, along with
other lipid absorption. The reduced availability of free cholesterol ulti-
mately stimulates the synthesis of LDL receptors, thus resulting in an
increased removal of LDL from the bloodstream. The normalization of
336
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serum total cholesterol at long term following BPD is accompanied by a rise
of HDL cholesterol.26 In addition, the reduction of gastric volume may also
play a role in the lipid malabsorption, because a reduction in the passage of
nutrients through the stomach, particularly amino acids and lipids, causes a
decrease in the secretion of gastric lipase, an enzyme that represents one of
the initial steps in lipid absorption. Another component is a reduction in the
secretion of cholecystokinin, which normally stimulates the secretion of
digestive enzymes (lipase, colipase and proteases).62 These changes are
responsible for a marked decrease in the hydrolysis of triacylglycerols to
monoacylglycerols, diacylglycerols, and fatty acids, with consequent reduc-
tion of the absorption of free fatty acids.
Garcia-Diaz et al. found a spectacular decrease of 33 per cent of total
cholesterol and 46 per cent of LDL levels in 58 patients after BPD. In
addition to the decrease of lipids, they found simultaneous reduction of
37 per cent of apolipoprotein B. The decrease in triglycerides was more
moderate, although also significant, while there were no significant
change in HDL-cholesterol.63
Type 2 Diabetes
More than 80 per cent of the diabetic type 2 patients are obese; in the USA
50 per cent of the patients diagnosed with type 2 diabetes are obese (BMI
> 30) and nine per cent morbidly obese (BMI > 40).64 Diet, exercise, oral
anti-diabetic drugs and insulin only establish glycemic control in less than
one third of patients. The UK prospective diabetes study analysed the
effect of diet, insulin and sulphonylurea on 4,075 newly diagnosed type 2
diabetes patients. HbA1c levels of less than seven per cent were attained
respectively only in nine per cent, 28 per cent and 24 per cent of the cases
after a follow-up period of nine years.65 To date, however, there is grow-
ing evidence that surgery can effectively cure type 2 diabetes. Surgical
induced diabetes resolution is not only due to weight loss but also through
certain direct mechanisms.
In the Buchwald meta-analysis complete resolution of diabetes
occurred in 76.8 per cent and resolved or improved in 86 per cent of the
patients after bariatric surgery. Complete resolution of diabetes was
demonstrated in 83.7 per cent of the patients after RYGB and in
Effects of Bariatric Surgery on Co-Morbidities
337

98.9 per cent of the patients after BPD. This effect is maintained on the
long-term and is independent of the weight loss.9 The same author con-
ducted a comprehensive review of all studies published in the English
literature containing data on weight loss and type 2 diabetes-related out-
comes for patients treated with any form of bariatric surgery. The dataset
consists of 621 studies with 888 treatment arms and 135,246 patients; 103
arms with 3,188 patients reported on the resolution of the clinical and lab-
oratory manifestations of type 2 diabetes. Nineteen studies with 43
treatment arms and 11,175 patients reported both weight loss and diabetes
resolution outcomes separately for the 4,070 diabetic patients in these
studies. The diabetic patients had an overall 78.1 per cent resolution of
their clinical manifestations of diabetes, and diabetes was improved or
resolved in 86.6 per cent. Diabetes resolution was greatest for patients
undergoing BPD/DS (95.1 per cent resolved), followed by RYGB
(80.3 per cent), gastroplasty (79.7 per cent), and then laparoscopic AGB
(56.7 per cent). The proportion of patients with diabetes resolution or
improvement was fairly constant at time points less than two years and
two years or more.66 One study suggested that insulin sensitivity improved
in proportion to weight loss with the use of predominantly restrictive pro-
cedures but was reversed completely by predominantly malabsorptive
approaches long before normalization of body weight.67
Mechanisms of diabetes control
Morbid obesity is associated with profound insulin resistance and marked
insulin hypersecretion, but the dynamics of β-cell function (i.e. β-cell glu-
cose sensitivity, rate sensitivity and potentiation) are preserved. On the
other hand, overt diabetes and impaired glucose tolerance are character-
ized by a progressive loss of β-cell glucose sensitivity, independent of
insulin resistance. It is well known that bariatric surgery leads to a large
improvement in insulin sensitivity and absolute insulin secretion
decreases significantly after bariatric surgery.68
Glucagon-like peptide-1 (GLP-1) is secreted by the L-cells that are
primarily located in the distal ileum and colon. In response to glucose and
satiety it induces insulin secretion. Since after RYGB and BPD/DS the
L-cells are stimulated earlier, GLP-1 production and consequent insulin
338
S. Van Cauwenberge and B. Dillemans

secretion could be enhanced (‘hindgut hypothesis’).69 However, studies
have questioned that GLP-1 is responsible for reversal of diabetes after
surgery. Morinigo et al. have demonstrated that GLP-1 response to a meal
is not a critical factor for the early amelioration in glucose homeostasis
after RYGB. Six weeks after surgery, the GLP-1 increase was only sig-
nificant in patients with normal glucose or impaired glucose tolerance, but
not in the diabetic patients.70 In a longitudinal study, fasting GLP-1 con-
centrations decreased and peptide YY levels increased independently of
each other in morbidly obese patients two years after dramatic weight
loss, indicating that the relationship between these gut hormones seems to
be more complicated than assumed before.71 In a three-year follow-up
study in diabetic patients, Rosa et al. have shown that reversibility of dia-
betes is dependent on the improvement of skeletal muscle insulin
sensitivity, mediated by changes in the expression of genes regulating glu-
cose and fatty acid metabolism in response to nutrient availability.72
The alternative hypothesis (‘foregut hypothesis’) states that duodenal
and proximal jejunal exclusion may prevent secretion of a putative signal
that promotes insulin resistance and type 2 diabetes. Other studies demon-
strated a decrease in plasma levels of leptin and insulin, with increased
levels of adiponectin and peptide YY3-36 after RYGB or BPD.69 The pos-
sible mechanisms for type 2 diabetes control after bariatric surgery are
summarized in Fig. 1.
Effects of RYGB on type 2 diabetes
In 2003 Schauer et al. published their report of the effect of RYGB on type
2 diabetes. They analysed 191 patients with impaired fasting glucose
and type 2 diabetes pre- and post-operative RYGB (mean follow-up of
19.7 months). Fasting plasma glucose and glycosylated haemoglobin con-
centrations returned to normal levels (83 per cent) or markedly improved
(17 per cent) in all patients. A significant reduction in use of oral anti-
diabetic agents (80 per cent) and insulin (79 per cent) followed surgical
treatment. Patients with the shortest duration (< 5 years), the mildest form
of type 2 diabetes (diet controlled), and the greatest weight loss after sur-
gery were most likely to achieve complete resolution of type 2 diabetes.74 In
the experience of Pories and Albrecht, the mortality risk from diabetes over
Effects of Bariatric Surgery on Co-Morbidities
339

a ten year follow-up after RYGB was less than that in a cohort of diabetic
patients matched for age, weight and BMI who were not operated on (1.0
per cent versus 4.5 per cent for every year of follow-up; p < .0003).75
Hickey et al. demonstrated significantly lower levels of fasting plasma
glucose, plasma insulin, and serum leptins in a group of patients maintain-
ing stable weight after RYGB compared to a group of patients matched in
weight, age, and percentage of fat who did not undergo surgery.76
Table 1 summarizes the results of some large studies regarding the
effect of RYGB on type 2 diabetes. In Fig. 2 the hypothesized mechanism
responsible for the control of type 2 diabetes after RYGB is depicted.
Effects of AGB on type 2 diabetes
The diabetes remission after AGB occurs gradually and is correlated to the
degree of weight loss. In an unblinded randomized controlled trial, 60 obese
340
S. Van Cauwenberge and B. Dillemans
Figure 1.
Proposed model for mechanisms of T2DM remission after bariatric surgery
based on available studies. Dashed lines indicate hypothetical links.73

Effects of Bariatric Surgery on Co-Morbidities
341
Figure 2.
Hypothesized mechanism responsible for the control of diabetes after
RYGB.77
Table 1.
Effect of RYGB on type 2 diabetes.
Patients with
Resolved improved
Author
N
T2DM (%)
Follow-up
unchanged
Sugerman15
1025
15
1–10 years
R = 86%
Wittgrove78
500
17
5 years
R = 98%
I = 2%
Pories79
608
27
10 years
R = 89%
I = 7%
U = 4%
Schauer74
1160
20
4 years
R = 83%
I = 17%
Diniz80
31
100
27 months
I = 100%
Rubino81
10
60
3 weeks
R = 100%
Morinigo70
34
29.4
6–12 months
I = 100%

patients (BMI > 30 and < 40) with recently diagnosed (< 2 years) type 2
diabetes were analysed. Patients either received either conventional dia-
betes therapy with a focus on weight loss by lifestyle change, or
laparoscopic AGB with conventional diabetes care. Ninety-two percent of
the patients completed the two year follow-up. Remission of type 2 dia-
betes was achieved by 22 (73 per cent) in the surgical group and four (13
per cent) in the conventional-therapy group. Remission of type 2 diabetes
was related to weight loss and lower baseline HbA1c levels.82 In a study
of 838 patients undergoing AGB, 545 patients were identified with co-
morbid illness at more than six months follow-up. After a median
follow-up of 13 months (range 6–36 months), resolution and/or improve-
ment of type 2 diabetes mellitus was 79 per cent.21 One study examined
the effect of AGB on metabolic profile of 122 diabetics. After AGB 93.1
per cent of the patients experienced an improvement in fasting glucose
levels and 75.4 per cent had an improvement in HbA1c levels at the end
of one year. All patients experienced a decrease in insulin requirements,
and 36.6 per cent were able to totally discontinue using it.83 Busetto et al.
examined the effect of AGB in older patients and one year after surgery
there was an improvement in 100 per cent of the diabetic cases.45
Korenkov evaluated the impact of AGB on obesity-associated diseases
and diabetes decreased from 10 per cent to four per cent in a group of
138 patients three to eight years postoperatively.84
Even the occurrence of type 2 diabetes can be prevented after sus-
tained and long-lasting weight loss obtained through AGB.25
Table 2 summarizes the results of some large studies regarding the
effect of AGB on type 2 diabetes.
342
S. Van Cauwenberge and B. Dillemans
Table 2.
Effect of AGB on type 2 diabetes.
Patients with
Resolved improved
Author
N
T2DM (%)
Follow-up
unchanged
Dixon60
500
11
1 year
R = 64%
I = 26%
U = 10%
Pontiroli85
143
45
3 years
R = 80%
Dixon82
55
100
2 years
R = 73%

Effects of BPD on type 2 diabetes
In a series of 312 obese patients with type 2 diabetes, fasting serum glu-
cose concentration fell to within normal values in all but two of the
patients and remained in the physiological range in all but six for a mean
follow-up of ten years.26
Palomar analysed 35 patients after BPD. Type 2 diabetes was present
in 18 per cent of the patients, 18 per cent were on hypoglycaemic therapy
and 25 per cent had impaired glucose tolerance. At 12 months after BPD,
the prevalence of diabetes decreased to zero per cent ( p < 0.01) and
impaired glucose tolerance to three per cent ( p < 0.01). Fasting glucose
levels were reduced from 117 ± 25 mg/dl at baseline to 91 ± 15 mg/dl at
one year ( p < 0.01).86
In 1998, Scopinaro et al. reported normalization of glucose levels in
100 per cent of their morbidly obese patients after BPD with no need for
medication and on a totally free diet as early as one month after operation,
when excess weight was still more than 80 per cent.87
Other Co-Morbidities
Gastro-oesophageal reflux disease
Nearly all epidemiologic studies have found an association between
increasing BMI and symptoms of gastro-oesophageal reflux disease
(GORD). GORD symptoms have been reported in 35–70 per cent of
obese patients requiring bariatric surgery.88–90
Changes in gastro-oesophageal anatomy and physiology caused by
obesity may explain the association. These include an increased preva-
lence of oesophageal motor disorders, diminished lower oesophageal
sphincter (LES) pressure, the development of a hiatal hernia, and
increased intragastric pressure. Central adiposity may be the most impor-
tant risk for the development of reflux and related complications such as
Barrett’s oesophagus and oesophageal adenocarcinoma. Weight loss,
through caloric restriction and behavioural modification, has been studied
infrequently as a means of improving reflux. Bariatric surgery and its
effects on a number of obesity-related disorders have been studied more
extensively.91 Bariatric surgery has had an impact on the frequency of
Effects of Bariatric Surgery on Co-Morbidities
343

GORD in obese patients, and GORD prevalence varies after each of the
different types of bariatric surgery.
Some studies that included patients with morbid obesity and RYGB
have reported complete improvement of symptoms in 80 per cent of the
cases and discontinuation of anti-secretory therapy in 97 per cent of the
patients.92–96 RYGB improves the reflux symptoms, oesophageal exposure to
acid, and oesophageal hypercontractility in patients with morbid obesity.97 In
addition, healing of oesophagitis and improvement in Barrett’s oesophagus
have recently been reported and some authors have proposed RYGB for
severe reflux disease after vertical banded gastroplasty (VBG).98–100
AGB has been shown to have various effects on reflux. It can act as
an antireflux procedure or it can enhance GORD.101–106 AGB also rapidly
alters oesophageal motility, with a decrease in the amplitude of contrac-
tions in the lower oesophagus as soon as nine months after surgery.105
With increasing length of follow-up, however, a growing number of long-
term complications arise, such as pouch dilatation with or without
slippage, band erosion, progressive oesophageal dilatation with
pseudoachalasia, food intolerance with gastro-oesophageal reflux and
band leaks. These complications are sometimes difficult to manage and
often lead to progressive weight regain. Reasons why some patients toler-
ate the band very well and others develop complications are essentially
unknown, although eating behaviour, which shows abnormal patterns in
the majority of morbidly obese patients, and pre-existing conditions of the
upper gastrointestinal tract like hiatus hernia, GORD and oesophageal
motility disorders have been incriminated. It would be of interest to be
able to better select morbidly obese patients for AGB and exclude from
this procedure those in whom long-term complications can be anticipated
on the basis of preoperative factors.107
Musculoskeletal problems
A causative relationship between excess weight and musculoskeletal prob-
lems has been difficult to establish for many conditions. Nevertheless,
weight loss can make a substantial difference in most musculoskeletal
symptoms, as well as help prevent heart disease and metabolic syndrome.
Some studies have looked at how major weight loss after bariatric surgery
344
S. Van Cauwenberge and B. Dillemans

affects baseline musculoskeletal symptoms. McGoey et al. reported a
prospective study of 105 patients who lost a mean of 44 kg after VBG. The
prevalence of back pain decreased from 62 per cent to 11 per cent, hip pain
from 11 per cent to two per cent, knee pain from 57 per cent to 14 per cent,
ankle pain from 34 per cent to two per cent, and foot pain from 21 per cent
to one per cent.108 Peltonen et al. looked at work-restricting musculoskele-
tal symptoms in the general population compared with those in 2,010
surgically treated obese patients ages 37–60, and those in 2,037 age-
matched and sexmatched obese patients not undergoing surgery. Obese
patients had more work restricting neck, low back, hip, knee and ankle pain,
and the prevalence increased with BMI. Patients who underwent VBG had
a significant decrease in work-restricting low back pain at all five sites.109 In
a retrospective study of 400 consecutive RYGB patients, arthritis, back or
extremity pain, and depression improved in 52–73 per cent of patients.110
Non-alcoholic steatohepatitis
The prevalence of obesity-related non-alcoholic steatohepatitis (NASH) has
increased substantially in recent years. In a study by Mattar et al. there was
a marked improvement in liver steatosis (from 88 per cent to eight per cent),
inflammation (from 23 per cent to two per cent), and fibrosis (from 31 per
cent to 13 per cent; all p < 0.001) after weight loss surgery (RYGB, AGB and
sleeve gastrectomy). Inflammation and fibrosis resolved in 37 per cent and
20 per cent of patients respectively, corresponding to improvement of
82 per cent (p < 0.001) in grade and 39 per cent (p < 0.001) in stage of liver
disease.111 Dixon et al. analysed the effect of weight loss on 36 patients with
NASH; 82 per cent had resolution of disease after AGB, nine per cent
showed improvement, and nine per cent had no change. Furthermore, nine
of ten patients who had stage three fibrosis before surgery had regression of
fibrosis at a mean follow-up of 25.6 ± 11 months.112
Pseudotumor cerebri
Pseudotumor cerebri (PTC), also known as idiopathic intracranial hyper-
tension, is a condition associated with headache, blurred vision and often
pulsatile tinnitus (an annoying auditory swishing sound synchronous with
Effects of Bariatric Surgery on Co-Morbidities
345

the heartbeat). Cranial imaging studies are normal, with the exception of
small ventricles and/or an empty sella. Cerebrospinal fluid (CSF) pres-
sures are always elevated. These patients may also have other central
nervous system and cranial nerve dysfunction, including visual distur-
bances and rarely Bell’s palsy and trigeminal neuralgia. Increased
intra-abdominal pressure associated with central obesity is the probable
etiology of PTC, a condition that should no longer be considered idio-
pathic. Bariatric surgery is the long-term procedure of choice for severely
obese patients with PTC and is shown to have a much higher rate of suc-
cess than CSF–peritoneal shunting reported in the literature, as well as
providing resolution of additional obesity co-morbidity.113
Polycystic ovary syndrome
Polycystic ovary syndrome (PCOS) was first described by Stein and
Leventhal in 1935. It is a heterogeneous disorder of unclear etiology and it
is an important cause of both menstrual irregularity and androgen excess in
women. When fully expressed, the manifestations include ovulatory dys-
function, androgen excess, polycystic ovaries and obesity. It is recognized
as one of the most common endocrine/metabolic disorders of women.114
In a study of 17 obese women with PCOS with a mean BMI of
50.7 kg/m2, bariatric surgery was associated with a mean weight loss after
12 months of 41 ± 9 kg, restoration of ovulatory cycles, and improve-
ments in insulin resistance, hyperandrogenemia and hirsutism scores.115
Eid et al. studied 24 women with PCOS who underwent elective laparo-
scopic RYGB. All women resumed normal menstrual cycles after a mean
of 3.4 ± 2.1 months postoperatively. Of the 23 women with hirsutism,
12 (52 per cent) had complete resolution at a mean follow-up of 8 ± 2.3
months; 6 (25 per cent) had moderate resolution at a mean of 21 ± 18
months; and three had minimal resolution at 34 ± 14 months. Five women
were able to conceive after surgery without the use of clomiphene.116
Quality of Life After Bariatric Surgery
The SOS study found a dramatic improvement in the quality of life at
two years among patients who had surgical treatment for obesity, particularly
346
S. Van Cauwenberge and B. Dillemans

concerning psychological performance (also see Chapter 13). There is a
strong positive correlation between the degree of improvement in quality of
life and the degree of weight loss.117 Schauer et al. reported improvement in
quality of life in 95 per cent of 275 patients who underwent laparoscopic
RYGB.89 Similar results have been reported for laparoscopic AGB.118 Several
studies have attempted to validate quality of life instruments for assessment
in bariatric surgery patients. Three instruments have been tested extensively:
the Medical Outcome Study Short Form-36 (MOS SF-36, Rand SF-36 or SF-
36), Bariatric Analysis and Reporting Outcome System (BAROS) and the
Impact of Weight on Quality of Life-Lite (IWQoL-Lite). A total of 308
RYGB patients were compared with 253 individuals who sought but did not
undergo RYGB and 272 population-based obese individuals using the
weight-related IWQoL-Lite and general MOS SF-36 health related quality of
life (HRQoL) questionnaires at baseline and two years of follow-up.
Dramatic improvements had occurred in weight-related and physical health
related quality of life for RYGB patients at two years after surgery compared
with two severely obese groups who had not undergone surgery. These
results support the effectiveness of RYGB surgery in improving patients’
HRQoL.119 Bond et al. suggest that RYGB patients who become active post-
operatively achieve weight losses and HRQoL improvements that are greater
than those experienced by patients who remain inactive and comparable to
those attained by patients who stay active.120 Psychiatrists and surgeons at the
University of Chicago compared SF-36 scores before, immediately after and
six months after RYGBP. Twenty out of 32 patients completed the follow-up
evaluation. SF-36 scores significantly improved for physical functioning,
general health, vitality and mental health.121 O’Brien and colleagues com-
pared SF-36 scores before and after AGB at one and two years with the
Australian general community. They found highly significant improvements
in QoL following AGB.61 Favretti et al. used BAROS to follow 170 patients
for at least 18 months after AGB. They were able to demonstrate improved
results after a ‘learning curve’ in their first 50 AGBs.122
Adami et al. administered the IWQoL-Lite questionnaire to 50 obese
patients prior to and at one year following BPD, to 150 post-obese sub-
jects at three years following BPD and to 50 lean controls. At one year
after the operation, the authors found a sharp improvement toward
normality in the QoL, and the cross-sectional findings suggest that this
Effects of Bariatric Surgery on Co-Morbidities
347

result was maintained in the long term. Following BPD, patients’ weight
loss and long-term maintenance are accompanied by overall beneficial
effects on their QoL.123 Moneghini and his team followed 30 patients after
BPD. The course and QoL were assessed using BAROS after a minimum
follow-up of 18 months. According to the BAROS, the outcome was clas-
sified as Excellent in 10 per cent of cases, Very Good in 63.3 per cent,
Good in 20 per cent, Fair in 6.7 per cent; no patients had Failure course.
Ninety-three percent of patients had resolution of at least one of their
major co-morbidities, and an improvement of the medical conditions was
registered in all the cases. The QoL was greatly improved in 55 per cent,
improved in 35 per cent and did not change in 10 per cent of the
patients.124
References
1. Must, A., Spadano, J., Coakley, E.H. et al. (1999). The disease burden asso-
ciated with overweight and obesity. JAMA 282(16): 1523–1529.
2. Goldstein, D.J. (1992). Beneficial health effects of modest weight loss. Int
J Obes Relat Metab Disord 16(6): 397–415.
3. Sjostrom, L., Lindroos, A.K., Peltonen, M. et al. (2004). Lifestyle, diabetes,
and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med
351(26): 2683–2693.
4. Frezza, E.E., Wei, C., Wachtel, M.S. (2009). Is surgery the next answer to
treat obesity-related hypertension? J Clin Hypertens (Greenwich) 11(5):
284–288.
5. Singer, G.M., Setaro, J.F. (2008). Secondary hypertension: obesity and the
metabolic syndrome. J Clin Hypertens (Greenwich) 10(7): 567–574.
6. Goodfriend, T.L., Calhoun, D.A. (2004). Resistant hypertension, obesity,
sleep apnoea, and aldosterone: theory and therapy. Hypertension 43(3):
518–524.
7. Phillips, B.G., Narkiewicz, K., Pesek, C.A. et al. (1999). Effects of obstruc-
tive sleep apnea on endothelin-1 and blood pressure. J Hypertens 17(1):
61–66.
8. Horvath, K., Jeitler, K., Siering, U. et al. (2008). Long-term effects of
weight-reducing interventions in hypertensive patients: systematic review
and meta-analysis. Arch Intern Med 168(6): 571–580.
348
S. Van Cauwenberge and B. Dillemans

9. Buchwald, H., Avidor, Y., Braunwald, E. et al. (2004). Bariatric surgery: a
systematic review and meta-analysis. JAMA 292(14): 1724–1737.
10. Carson, J.L., Ruddy, M.E., Duff, A.E. et al. (1994). The effect of gastric
bypass surgery on hypertension in morbidly obese patients. Arch Intern Med
154(2): 193–200.
11. Fazylov, R., Soto, E., Merola, S. (2008). Laparoscopic Roux-en-Y gastric
bypass in morbidly obese patients > or = 55 years old. Obes Surg 18(6):
656–659.
12. Fernstrom, J.D., Courcoulas, A.P., Houck, P.R. et al. (2006). Long-term
changes in blood pressure in extremely obese patients who have undergone
bariatric surgery. Arch Surg 141(3): 276–283.
13. Foley, E.F., Benotti, P.N., Borlase, B.C. et al. (1992). Impact of gastric
restrictive surgery on hypertension in the morbidly obese. Am J Surg 163(3):
294–297.
14. Reinhold, R.B. (1994). Late results of gastric bypass surgery for morbid
obesity. J Am Coll Nutr 13(4): 326–331.
15. Sugerman, H.J., Wolfe, L.G., Sica, D.A . et al. (2003). Diabetes and hyper-
tension in severe obesity and effects of gastric bypass-induced weight loss.
Ann Surg 237(6): 751–756; discussion 757–758.
16. Czupryniak, L., Strzelczyk, J., Pawlowski, M. et al. (2005). Circadian blood
pressure variation in morbidly obese hypertensive patients undergoing gas-
tric bypass surgery. Am J Hypertens 18(4 Pt 1): 446–551.
17. Hinojosa, M.W., Varela, J.E., Smith, B.R. et al. (2009). Resolution of sys-
temic hypertension after laparoscopic gastric bypass. J Gastrointest Surg
13(4): 793–797.
18. Ahmed, A.R., Rickards, G., Coniglio, D. et al. (2009). Laparoscopic Roux-
en-Y Gastric Bypass and its early effect on blood pressure. Obes Surg 19(7):
845–849.
19. Bennett, J.C., Wang, H., Schirmer, B.D. et al. (2007). Quality of life
and resolution of co-morbidities in super-obese patients remaining mor-
bidly obese after Roux-en-Y gastric bypass. Surg Obes Relat Dis 3(3):
387–391.
20. Dall’Asta, C., Vedani, P., Manunta, P. et al. (2009). Effect of weight loss
through laparoscopic gastric banding on blood pressure, plasma renin activ-
ity and aldosterone levels in morbid obesity. Nutr Metab Cardiovasc Dis
19(2): 110–114.
Effects of Bariatric Surgery on Co-Morbidities
349

21. Brancatisano, A., Wahlroos, S., Brancatisano, R. (2008). Improvement in
comorbid illness after placement of the Swedish adjustable gastric band.
Surg Obes Relat Dis 4(3 Suppl): S39–S46.
22. Weiner, R., Blanco-Engert, R., Weiner, S. et al. (2003). Outcome after
laparoscopic adjustable gastric banding — 8 years experience. Obes Surg
13(3): 427–434.
23. Mittermair, R.P., Weiss, H., Nehoda, H. et al. (2003). Laparoscopic Swedish
adjustable gastric banding: 6-year follow-up and comparison to other
laparoscopic bariatric procedures. Obes Surg 13(3): 412–417.
24. Dixon, J.B., O’Brien, P.E. (2002). Changes in comorbidities and improve-
ments in quality of life after LAP-BAND placement. Am J Surg 184(6B):
51S–54S.
25. Pontiroli, A.E., Folli, F., Paganelli, M. et al. (2005). Laparoscopic gastric
banding prevents type 2 diabetes and arterial hypertension and induces their
remission in morbid obesity: a 4-year case-controlled study. Diabetes Care
28(11): 2703–2709.
26. Scopinaro, N., Marinari, G.M., Camerini, G.B. et al. (2005). Specific effects
of biliopancreatic diversion on the major components of metabolic syn-
drome: a long-term follow-up study. Diabetes Care 28(10): 2406–2411.
27. Adami, G., Murelli, F., Carlini, F. et al. (2005). Long-term effect of bil-
iopancreatic diversion on blood pressure in hypertensive obese patients. Am
J Hypertens 18(6): 780–784.
28. Adami, G.F., Papadia, F., Carlini, F. et al. (2005). Effect of biliopancreatic
diversion on hypertension in severely obese patients. Hypertens Res 28(2):
119–123.
29. Pontiroli, A.E., Laneri, M., Veronelli, A. et al. (2009). Biliary pancreatic
diversion and laparoscopic adjustable gastric banding in morbid obesity:
their long-term effects on metabolic syndrome and cardiovascular parame-
ters. Cardiovasc Diabetol 8(1): 37.
30. Young, T., Palta, M., Dempsey, J. et al. (1993). The occurrence of sleep-
disordered breathing among middle-aged adults. N Engl J Med 328(17):
1230–1235.
31. de Sousa, A.G., Cercato, C., Mancini, M.C. et al. (2008). Obesity and
obstructive sleep apnoea–hypopnea syndrome. Obes Rev 9(4): 340–354.
32. Punjabi, N.M. (2008). The epidemiology of adult obstructive sleep apnoea.
Proc Am Thorac Soc 5(2): 136–143.
350
S. Van Cauwenberge and B. Dillemans

33. Young, T., Skatrud, J., Peppard, P.E. (2004). Risk factors for obstructive
sleep apnoea in adults. JAMA 291(16): 2013–2016.
34. Schwartz, A.R., Patil, S.P., Laffan, A.M. et al. (2008). Obesity and obstruc-
tive sleep apnoea: pathogenic mechanisms and therapeutic approaches. Proc
Am Thorac Soc 5(2): 185–192.
35. Eckert, D.J., Malhotra, A. (2008). Pathophysiology of adult obstructive
sleep apnea. Proc Am Thorac Soc 5(2): 144–153.
36. Rapoport, D.M., Sorkin, B., Garay, S.M. et al. (1982). Reversal of the
“Pickwickian syndrome” by long-term use of nocturnal nasal–airway pres-
sure. N Engl J Med 307(15): 931–933.
37. Riley, R.W., Powell, N.B., Guilleminault, C. et al. (1995). Obstructive sleep
apnoea. Trends in therapy. West J Med 162(2): 143–148.
38. Schwartz, A.R., Gold, A.R., Schubert, N. et al. (1991). Effect of weight loss
on upper airway collapsibility in obstructive sleep apnoea. Am Rev Respir
Dis 144(3 Pt 1): 494–498.
39. Smith, P.L., Gold, A.R., Meyers, D.A. et al. (1985). Weight loss in mildly to
moderately obese patients with obstructive sleep apnoea. Ann Intern Med
103(6 Pt 1): 850–855.
40. Varela, J.E., Hinojosa, M.W., Nguyen, N.T. (2007). Resolution of obstruc-
tive sleep apnoea after laparoscopic gastric bypass. Obes Surg 17(10):
1279–1282.
41. Rasheid, S., Banasiak, M., Gallagher, S.F. et al. (2003). Gastric bypass is an
effective treatment for obstructive sleep apnoea in patients with clinically
significant obesity. Obes Surg 13(1): 58–61.
42. Lankford, D.A., Proctor, C.D., Richard, R. (2005). Continuous positive air-
way pressure (CPAP) changes in bariatric surgery patients undergoing rapid
weight loss. Obes Surg 215(3): 336–341.
43. Jensen, C., Tejirian, T., Lewis, C. et al. (2008). Postoperative CPAP and
BiPAP use can be safely omitted after laparoscopic Roux-en-Y gastric
bypass. Surg Obes Relat Dis 4(4): 512–514.
44. Dixon, J.B., Schachter, L.M., O’Brien, P.E. (2001). Sleep disturbance and
obesity: changes following surgically induced weight loss. Arch Intern Med
161(1): 102–106.
45. Busetto, L., Angrisani, L., Basso, N. et al. (2008). Safety and efficacy of
laparoscopic adjustable gastric banding in the elderly. Obesity (Silver
Spring) 16(2): 334–338.
Effects of Bariatric Surgery on Co-Morbidities
351

46. Rao, A., Tey, B.H., Ramalingam, G. et al. (2009). Obstructive sleep apnoea
(OSA) patterns in bariatric surgical practice and response of OSA to weight
loss after laparoscopic adjustable gastric banding (LAGB). Ann Acad Med
Singapore 38(7): 587.
47. de Luis, D.A., Pacheco, D., Izaola, O. et al. (2005). Early clinical and sur-
gical results of biliopancreatic diversion. Obes Surg 15(6): 799–802.
48. Simard, B., Turcotte, H., Marceau, P. et al. (2004). Asthma and sleep apnoea
in patients with morbid obesity: outcome after bariatric surgery. Obes Surg
14(10): 1381–1388.
49. Manzato, E., Zambon, S., Zambon, A. et al. (1992). Lipoprotein sub-frac-
tion levels and composition in obese subjects before and after gastroplasty.
Int J Obes Relat Metab Disord 16(8): 573–578.
50. Zambon, A., Sartore, G., Passera, D. et al. (1999). Effects of hypocaloric
dietary treatment enriched in oleic acid on LDL and HDL subclass distribu-
tion in mildly obese women. J Intern Med 246(2): 191–201.
51. Carmena, R., Duriez, P., Fruchart, J.C. (2004). Atherogenic lipoprotein par-
ticles in atherosclerosis. Circulation 109(23 Suppl 1): 1112–1117.
52. Kwiterovich, P.O. Jr (2002). Clinical relevance of the biochemical, meta-
bolic, and genetic factors that influence low-density lipoprotein
heterogeneity. Am J Cardiol 90(8A): 30i–47i.
53. Hunninghake, D.B., Stein, E.A., Dujovne, C.A. et al. (1993). The efficacy
of intensive dietary therapy alone or combined with lovastatin in outpatients
with hypercholesterolemia. N Engl J Med 328(17): 1213–1219.
54. Tang, J.L., Armitage, J.M., Lancaster, T. et al. (1998). Systematic review of
dietary intervention trials to lower blood total cholesterol in free–living sub-
jects. BMJ 316(7139): 1213–1220.
55. Maggard, M.A., Shugarman, L.R., Suttorp, M. et al. (2005). Meta-analysis:
surgical treatment of obesity. Ann Intern Med 142(7): 547–559.
56. Zlabek, J.A., Grimm, M.S., Larson, C.J. et al. (2005). The effect of laparo-
scopic gastric bypass surgery on dyslipidemia in severely obese patients.
Surg Obes Relat Dis 1(6): 537–542.
57. Nguyen, N.T., Varela, E., Sabio, A. et al. (2006). Resolution of hyperlipidemia
after laparoscopic Roux-en-Y gastric bypass. J Am Coll Surg 203(1): 24–29.
58. Diniz, M.D., Passos, V.M., Barreto, S.M. et al. (2009). Different criteria for
assessment of Roux-en-Y Gastric Bypass success: does only weight matter?
Obes Surg 19(10): 1384–1392.
352
S. Van Cauwenberge and B. Dillemans

59. Zambon, S., Romanato, G., Sartore, G. et al. (2009). Bariatric surgery
improves atherogenic LDL profile by triglyceride reduction. Obes Surg
19(2): 190–195.
60. Dixon, J.B., O’Brien, P.E. (2002). Health outcomes of severely obese type
2 diabetic subjects 1 year after laparoscopic adjustable gastric banding.
Diabetes Care 25(2): 358–363.
61. O’Brien, P.E., Dixon, J.B., Brown, W. et al. (2002). The laparoscopic
adjustable gastric band (Lap-Band): a prospective study of medium-term
effects on weight, health and quality of life. Obes Surg 12(5): 652–660.
62. Bays, H.E. (2004). Current and investigational antiobesity agents and obe-
sity therapeutic treatment targets. Obes Res 12(8): 1197–1211.
63. Garcia-Diaz, J., de, D., Lozano, O., Ramos, J.C. et al. (2003). Changes in
lipid profile after biliopancreatic diversion. Obes Surg 13(5): 756–760.
64. Leibson, C.L., Williamson, D.F., Melton, L.J. III et al. (2001). Temporal
trends in BMI among adults with diabetes. Diabetes Care 24(9):
1584–1589.
65. Turner, R.C., Cull, C.A., Frighi, V. et al. (1999). Glycemic control with diet,
sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus:
progressive requirement for multiple therapies (UKPDS 49). UK
Prospective Diabetes Study (UKPDS) Group. JAMA 281(21): 2005–2012.
66. Buchwald, H., Estok, R., Fahrbach, K. et al. (2009). Weight and type 2 dia-
betes after bariatric surgery: systematic review and meta-analysis. Am J Med
122(3): 248–256 e5.
67. Muscelli, E., Mingrone, G., Camastra, S. et al. (2005). Differential effect of
weight loss on insulin resistance in surgically treated obese patients. Am J
Med 118(1): 51–57.
68. Schernthaner, G., Morton, J.M. (2008). Bariatric surgery in patients with
morbid obesity and type 2 diabetes. Diabetes Care 31(Suppl 2): S297–S302.
69. Silecchia, G., Casella, G., Rizzello, M. (2009). Surgical treatment of type 2
diabetes. Acta Chir Belg 109: 292–299.
70. Morinigo, R., Lacy, A.M., Casamitjana, R. et al. (2006). GLP-1 and changes
in glucose tolerance following gastric bypass surgery in morbidly obese
subjects. Obes Surg 16(12): 1594–1601.
71. Reinehr, T., Roth, C.L., Schernthaner, G.H. et al. (2007). Peptide YY and
glucagon-like peptide-1 in morbidly obese patients before and after surgi-
cally induced weight loss. Obes Surg 17(12): 1571–1577.
Effects of Bariatric Surgery on Co-Morbidities
353

72. Rosa, G., Mingrone, G., Manco, M. et al. (2007). Molecular mechanisms of
diabetes reversibility after bariatric surgery. Int J Obes (Lond) 31(9):
1429–1436.
73. Bose, M., Olivan, B., Teixeira, J. et al. (2009). Do incretins play a role in
the remission of type 2 diabetes after gastric bypass surgery: what are the
evidence? Obes Surg 19(2): 217–229.
74. Schauer, P.R., Burguera, B., Ikramuddin, S. et al. (2003). Effect of laparo-
scopic Roux-en-Y gastric bypass on type 2 diabetes mellitus. Ann Surg
238(4): 467–84; discussion 84–85.
75. Pories, W.J., Albrecht, R.J. (2001). Etiology of type 2 diabetes mellitus: role
of the foregut. World J Surg 25(4): 527–531.
76. Hickey, M.S., Pories, W.J., MacDonald, K.G. Jr et al. (1998). A new para-
digm for type 2 diabetes mellitus: could it be a disease of the foregut? Ann
Surg 227(5): 637–643; discussion 643–644.
77. Rubino, F., Gagner, M. (2002). Potential of surgery for curing type 2 dia-
betes mellitus. Ann Surg 236(5): 554–559.
78. Wittgrove, A.C., Clark, G.W. (2000). Laparoscopic gastric bypass, Roux-
en-Y—500 patients: technique and results, with 3–60 month follow-up.
Obes Surg 10(3): 233–239.
79. Pories, W.J., Swanson, M.S., MacDonald, K.G. et al. (1995). Who would have
thought it? An operation proves to be the most effective therapy for adult-
onset diabetes mellitus. Ann Surg 222(3): 339–350; discussion 350–352.
80. Diniz Mde, F., Diniz, M.T., Sanches, S.R. et al. (2004). Glycemic control in
diabetic patients after bariatric surgery. Obes Surg 14(8): 1051–1055.
81. Rubino, F., Gagner, M., Gentileschi, P. et al. (2004). The early effect of the
Roux-en-Y gastric bypass on hormones involved in body weight regulation
and glucose metabolism. Ann Surg 240(2): 236–242.
82. Dixon, J.B., O’Brien, P.E., Playfair, J. et al. (2008). Adjustable gastric band-
ing and conventional therapy for type 2 diabetes: a randomized controlled
trial. JAMA 299(3): 316–323.
83. Singhal, R., Kitchen, M., Bridgwater, S. et al. (2008). Metabolic outcomes
of obese diabetic patients following laparoscopic adjustable gastric banding.
Obes Surg 18(11): 1400–1405.
84. Korenkov, M., Shah, S., Sauerland, S. et al. (2007). Impact of laparoscopic
adjustable gastric banding on obesity co-morbidities in the medium- and
long-term. Obes Surg 17(5): 679–683.
354
S. Van Cauwenberge and B. Dillemans

85. Pontiroli, A.E., Pizzocri, P., Librenti, M.C. et al. (2002). Laparoscopic
adjustable gastric banding for the treatment of morbid (grade 3) obesity and
its metabolic complications: a three-year study. J Clin Endocrinol Metab
87(8): 3555–3561.
86. Palomar, R., Fernandez-Fresnedo, G., Dominguez-Diez, A. et al. (2005).
Effects of weight loss after biliopancreatic diversion on metabolism and car-
diovascular profile. Obes Surg 15(6): 794–798.
87. Scopinaro, N., Adami, G.F., Marinari, G.M. et al. (1998). Biliopancreatic
diversion. World J Surg 22(9): 936–946.
88. Fisher, B.L., Pennathur, A., Mutnick, J.L. et al. (1999). Obesity correlates
with gastro-oesophageal reflux. Dig Dis Sci 44(11): 2290–2294.
89. Schauer, P.R., Ikramuddin, S., Gourash, W. et al. (2000). Outcomes after
laparoscopic Roux-en-Y gastric bypass for morbid obesity. Ann Surg
232(4): 515–529.
90. Suter, M., Dorta, G., Giusti, V. et al. (2004). Gastro-esophageal reflux and
esophageal motility disorders in morbidly obese patients. Obes Surg 14(7):
959–966.
91. Friedenberg, F.K., Xanthopoulos, M., Foster, G.D. et al. (2008). The associ-
ation between gastro-oesophageal reflux disease and obesity. Am J
Gastroenterol 103(8): 2111–2122.
92. Clements, R.H., Gonzalez, Q.H., Foster, A. et al. (2003). Gastrointesti-
nal symptoms are more intense in morbidly obese patients and are
improved with laparoscopic Roux-en-Y gastric bypass. Obes Surg 13(4):
610–614.
93. Foster, A., Laws, H.L., Gonzalez, Q.H. et al. (2003). Gastrointestinal symp-
tomatic outcome after laparoscopic Roux-en-Y gastric bypass. J Gastrointest
Surg 7(6): 750–753.
94. Jones, K.B., Jr, Allen, T.V., Manas, K.J. et al. (1991). Roux-en-Y Gastric
Bypass: an effective anti-reflux procedure. Obes Surg 1(3): 295–298.
95. Perry, Y., Courcoulas, A.P., Fernando, H.C. et al. (2004). Laparoscopic
Roux-en-Y gastric bypass for recalcitrant gastro-oesophageal reflux dis-
ease in morbidly obese patients. JSLS 8(1): 19–23.
96. Smith, S.C., Edwards, C.B., Goodman, G.N. (1997) Symptomatic and
clinical improvement in morbidly obese patients with gastro-oesophageal
reflux disease following Roux-en-Y gastric bypass. Obes Surg 7(6):
479–484.
Effects of Bariatric Surgery on Co-Morbidities
355

97. Mejia-Rivas, M.A., Herrera-Lopez, A., Hernandez-Calleros, J. et al.
(2008). Gastro-oesophageal reflux disease in morbid obesity: the effect of
Roux-en-Y gastric bypass. Obes Surg 18(10): 1217–1224.
98. Bloomberg, R.D., Urbach, D.R. (2002). Laparoscopic Roux-en-Y gastric
bypass for severe gastro-oesophageal reflux after vertical banded gastro-
plasty. Obes Surg 12(3): 408–411.
99. Cobey, F., Oelschlager, B. (2005). Complete regression of Barrett’s esopha-
gus after Roux-en-Y gastric bypass. Obes Surg 15(5): 710–712.
100. Csendes, A., Burgos, A.M., Smok, G. et al. (2006). Effect of gastric bypass
on Barrett’s esophagus and intestinal metaplasia of the cardia in patients
with morbid obesity. J Gastrointest Surg 10(2): 259–264.
101. de Jong, J.R., van Ramshorst, B., Timmer, R. et al. (2004). The influence of
laparoscopic adjustable gastric banding on gastro-oesophageal reflux. Obes
Surg 14(3): 399–406.
102. Iovino, P., Angrisani, L., Tremolaterra, F. et al. (2002). Abnormal
esophageal acid exposure is common in morbidly obese patients and
improves after a successful Lap-band system implantation. Surg Endosc
16(11): 1631–1635.
103. Ovrebo, K.K., Hatlebakk, J.G., Viste, A. et al. (1998). Gastro-oesophageal
reflux in morbidly obese patients treated with gastric banding or vertical
banded gastroplasty. Ann Surg 228(1): 51–58.
104. Peternac, D., Hauser, R., Weber M. et al. (2001). The effects of laparoscopic
adjustable gastric banding on the proximal pouch and the esophagus. Obes
Surg 11(1): 76–86.
105. Suter, M., Dorta, G., Giusti, V. et al. (2005). Gastric banding interferes with
esophageal motility and gastro-oesophageal reflux. Arch Surg 140(7):
639–643.
106. Weiss, H., Nehoda, H., Labeck, B. et al. (2000). Treatment of morbid obe-
sity with laparoscopic adjustable gastric banding affects esophageal
motility. Am J Surg 180(6): 479–482.
107. Suter, M., Giusti, V., Calmes, J.M. et al. (2008). Preoperative upper gas-
trointestinal testing can help predicting long-term outcome after gastric
banding for morbid obesity. Obes Surg 18(5): 578–582.
108. McGoey, B.V., Deitel, M., Saplys, R.J. et al. (1990). Effect of weight loss
on musculoskeletal pain in the morbidly obese. J Bone Joint Surg Br 72(2):
322–323.
356
S. Van Cauwenberge and B. Dillemans

109. Peltonen, M., Lindroos, A.K., Torgerson, J.S. (2003). Musculoskeletal pain
in the obese: a comparison with a general population and long-term changes
after conventional and surgical obesity treatment. Pain 104(3): 549–557.
110. Peluso, L., Vanek, V.W. (2007). Efficacy of gastric bypass in the treatment
of obesity-related co-morbidities. Nutr Clin Pract 22(1): 22–28.
111. Mattar, S.G., Velcu L.M., Rabinovitz, M. et al. (2005). Surgically-induced
weight loss significantly improves nonalcoholic fatty liver disease and the
metabolic syndrome. Ann Surg 242(4): 610–617; discussion 618–620.
112. Dixon, J.B., Bhathal, P.S., Hughes, N.R. et al. (2004). Nonalcoholic fatty
liver disease: improvement in liver histological analysis with weight loss.
Hepatology 39(6): 1647–1654.
113. Sugerman, H.J., Felton, W.L. III, Sismanis, A. et al. (1999). Gastric surgery
for pseudotumor cerebri associated with severe obesity. Ann Surg 229(5):
634–640; discussion 640–642.
114. Stein, I.F., Leventhal, N.L. (1935). Amenorrhea associated with bilateral
polycystic ovaries. Am J Obstet Gynecol 29: 181–191.
115. Escobar-Morreale, H.F., Botella-Carretero, J.I., Alvarez-Blasco, F. et al.
(2005). The polycystic ovary syndrome associated with morbid obesity may
resolve after weight loss induced by bariatric surgery. J Clin Endocrinol
Metab 90(12): 6364–6369.
116. Eid, G.M., Cottam, D.R., Velcu, L.M. et al. (2005). Effective treatment of
polycystic ovarian syndrome with Roux-en-Y gastric bypass. Surg Obes
Relat Dis 1(2): 77–80.
117. Karlsson, J., Sjostrom, L., Sullivan, M. (1998). Swedish obese subjects
(SOS) –– an intervention study of obesity. Two-year follow-up of health-
related quality of life (HRQL) and eating behavior after gastric surgery for
severe obesity. Int J Obes Relat Metab Disord 22(2): 113–126.
118. Dixon, J.B., Dixon, M.E., O’Brien, P.E. (2001). Quality of life after lap-
band placement: influence of time, weight loss, and comorbidities. Obes Res
9(11): 713–721.
119. Kolotkin, R.L., Crosby, R.D., Gress, R.E. et al. (2009). Two-year changes in
health-related quality of life in gastric bypass patients compared with
severely obese controls. Surg Obes Relat Dis 5(2): 250–256.
120. Bond, D.S., Phelan, S., Wolfe, L.G. et al. (2009). Becoming physically
active after bariatric surgery is associated with improved weight loss and
health-related quality of life. Obesity (Silver Spring) 17(1): 78–83.
Effects of Bariatric Surgery on Co-Morbidities
357

121. Dymek, M.P., le Grange, D., Neven, K. et al. (2001). Quality of life and
psychosocial adjustment in patients after Roux-en-Y gastric bypass: a brief
report. Obes Surg 11(1): 32–39.
122. Favretti, F., Cadière, G.B., Segato, G. et al. (1998). Bariatric analysis and
reporting outcome system (BAROS) applied to laparoscopic gastric banding
patients. Obes Surg 8(5): 500–504.
123. Adami, G.F., Ramberti, G., Weiss, A. et al. (2005). Quality of life in obese
subjects following biliopancreatic diversion. Behav Med 31(2): 53–60.
124. Moneghini, D., Mittempergher, F., Terraroli, C. et al. (2004). Bariatric
Analysis and Reporting Outcome System (BAROS) following biliopancre-
atic diversion. Ann Ital Chir 75(4): 417–420.
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Chapter 13
Impact on Life Expectancy After
Bariatric Surgery
Luca Busetto, Elisa Calo’, Marco Mazza and Giuliano Enzi
Introduction
The use of bariatric surgery has increased exponentially in recent years.
According to the data of the American Society of Bariatric Surgeons
(ASBS), the total number of bariatric operations performed annually in
the United States, stable at around 20,000 procedures per year throughout
the 1990s, crossed the threshold of 100,000 annual procedures in the year
20031 and peaked to 121,055 in 2004.2 At a lower scale, similar trends
appeared to be present in most European countries and in Australia.3 Two
major driving forces may be hypothesized as the basis of the worldwide
explosion of bariatric surgery. The first cause of this phenomenon is prob-
ably the fact that the prevalence of morbid obesity is increasing, at a pace
that is even more accelerated than for obesity overall. According to the
National Health and Nutrition Examination Survey (NHANES)
1999–2000, 3.1 per cent of adult American men and 6.3 per cent of adult
American women suffer from morbid obesity.4 From 1986 to 2000, the
prevalence of obesity in general (BMI > 30 kg/m2) approximately doubled
in the United States, while that of morbid obesity (BMI > 40 kg/m2)
quadrupled and that of the so called ‘super-obesity’ (BMI > 50 kg/m2)
increased five-fold.5
The second force that may explain the wider clinical use of bariatric
surgery is in our opinion the increasing acceptation of this type of therapy
359

360
L. Busetto et al.
in the medical and surgical community. The reduction of the surgical
risks, associated with newer technical skills, and the recognition of the
clear clinical benefits produced by the sustained weight loss obtained by
bariatric surgery on the global health of the morbidly obese patient are the
basis of this change. In this chapter, we will briefly review the existing
evidences about the effects of bariatric surgery on the metabolic and res-
piratory co-morbidities of morbid obesity. Newer data about the impact of
bariatric surgery on health related quality of life and life expectancy will
be also reported.
Impact of Morbid Obesity on Morbidity and Mortality
A large body of epidemiologic studies evidenced that overweight and obe-
sity are associated with an increased risk of several metabolic disturbances,
respiratory problems, cancers, cardiovascular diseases and death. However,
more specific and precise data about the impact of severe obesity on health
and longevity are far more scarce, giving the undersampling of morbidly
obese people in the classic epidemiologic surveys. In the recruitment phase
of the Swedish Obese Subjects (SOS) study, the first 1,006 morbidly obese
patients included in a national obesity registry have been analysed with
respect to morbidity and compared with on-going population studies of men
and women.6 The relative risks of diabetes associated with severe obesity in
50 year-old males and females were 4.3 and 4.7 respectively. Relative risks
for hypertension were 2.1 and 4.5.6 More recent epidemiologic surveys
seem to confirm or even to enforce these figures. Of the 90,185 women
recruited for the Women’s Health Initiative Observational Study (WHIOS),
the prevalence of diabetes at baseline was 18.0 per cent in the 3,234 women
with BMI > 40 kg/m2 and 2.3 per cent in the 36,217 normal weight women
(P < 0.001).7 Seemingly, the prevalence of hypertension was 58.6 per cent
in the group with extreme obesity and 22.5 per cent in the group with nor-
mal body weight (P < 0.001).7 At baseline, prevalence of coronary heart
disease, previous myocardial infarction, congestive heart failure and cere-
brovascular accidents were all significantly higher in the morbidly obese
group.7
The much higher prevalence of metabolic and vascular disorders
observed in morbidly obese patients translated in a clear excess mortality

risk in longitudinal studies. In the WHIOS, with an average follow-up of
seven years, the age-adjusted relative risk of death in white women with
morbid obesity, as compared with normal weight white women, was 2.12
(95 per cent CI: 1.81–2.47), whereas the age-adjusted relative risk for
coronary heart disease mortality was 3.13 (95 per cent CI: 1.90–5.15).7
The association between BMI and the risk of death was recently examined
also in 527,625 men and women from the United States aged 50–71, in the
National Institutes of Health–American Association of Retired Persons
(AARP) Diet and Health Study.8 During a maximum follow-up of ten
years, the multivariate relative risk of death in people with BMI >
40 kg/m2 was 1.94 (95 per cent CI: 1.79–2.09) in women and 1.83
(95 per cent CI: 1.70–1.97) in men.8 When the confounding effect of
smoking on the relationship between BMI and mortality was taken into
account, by analysing the risk of death specifically in people who never
smoked, the effect of morbid obesity on mortality was even higher: mul-
tivariate relative risk of death in people with BMI > 40 kg/m2 was 2.52
(95 per cent CI: 2.20–2.88) in women and 2.59 (95 per cent CI: 2.30–3.06)
in men.8 Therefore, we can conclude that morbid obesity was associated
with at least a doubling of total mortality risk in both sexes. Excess rela-
tive risk may be even higher in younger patients, obviously at a lower
absolute risk of death. The impact of severe obesity on morbidity and life
expectancy is therefore clearly established. The major goal of bariatric
surgery is the reduction of such disease and death burdens.
Effects of Bariatric Surgery on Metabolic Co-Morbidities
Type 2 diabetes
Most of the clinical studies showed a benefit of bariatric surgery on dia-
betes. In a recent systematic review and meta-analysis of the outcomes of
bariatric surgery, Buchwald et al. pooled the results of 136 studies con-
ducted with different types of bariatric procedures in a total dataset of
22,094 patients.9 When defined as the ability to discontinue all diabetes-
related medications and maintain the glucose levels within the normal
range, strong evidence for improvement of type 2 diabetes was found
across all the surgery types. Within studies reporting resolution of diabetes,
Impact on Life Expectancy After Bariatric Surgery
361

1,417 (mean 76.8 per cent; 95 per cent CI: 70.7–82.9 per cent) of 1,846
patients experienced complete resolution. Within studies reporting both
resolution or improvement or only improvement of diabetes, 414 (mean
85.4 per cent; 95 per cent CI: 78.4–93.7 per cent) of 485 patients experi-
enced resolution or improvement of diabetes.9 The robustness of these
estimations may be reduced by the acknowledgment that the large major-
ity of the studies included in the review are observational, not randomized
studies without appropriate control groups, and by the fact that in most of
the studies the evaluation of outcomes is conducted shortly after surgery,
typically less than two years later. However, the results of the few pub-
lished long-term controlled trials seem to confirm this favourable picture.
The SOS study was launched in the early 1990s with the aim of
prospectively evaluating total and cause-specific ten-year mortality in a
large group of morbidly obese patients treated by several types of bariatric
procedures. A well-matched group of highly comparable morbidly obese
patients participating in a national obesity registry and not willing to
undergo surgery was used as a control group.6 Weight loss observed in the
surgical arm of the SOS study was 23.4 per cent of baseline body weight
two years after surgery and 16.3 per cent ten years after surgery. At the
same time, the control group of morbidly obese patients treated by con-
ventional medical treatment remained substantially weight stable (weight
gain of 0.1 per cent at two years and 1.6 per cent at ten years).10 In the first
two years of the SOS study, 72 per cent of 342 diabetic surgically treated
obese patients had a complete resolution of type 2 diabetes, while only
21 per cent of 248 diabetic obese controls did so. The odds ratio for being
free from type 2 diabetes two years after surgery was 8.42 (95 per cent CI:
5.68–12.5) in the surgically treated as compared with the medically
treated controls.10 In the long-term, some of the benefits observed in the
first years after surgery tend to vanish, maybe because of the slight ten-
dency to weight regain observed in the surgical group as a whole and of
the ageing of the study population. Anyway, the proportion of patients
with type 2 diabetes at baseline still normoglycaemic without pharmaco-
logic treatment ten years after surgery was higher in the surgically treated
group (36 per cent) than in the control group (13 per cent). The probabil-
ity of being free from diabetes ten years after surgery was still 3.45
(95 per cent CI: 1.64–7.28) times higher in the surgically treated group.10
362
L. Busetto et al.

The sustained weight loss observed in the surgical arm of the SOS
study was not only associated with an improvement of the diabetic state,
but also to the prevention of new cases of type 2 diabetes in those mor-
bidly obese patients free from the disease at baseline. Indeed, the
incidence of new cases of type 2 diabetes was 1 per cent in the surgically
treated patients and 8 per cent in the control group at two years (OR 0.14;
95 per cent CI: 0.08–0.24), and it was 7 per cent and 24 per cent respec-
tively at 10 years (OR 0.25; 95 per cent CI: 0.17–0.38).10 The surgical
induced weight loss seems thus to be able to prevent about 75 per cent of
new type 2 diabetes cases over a ten year follow-up.
The results of the SOS study have been recently confirmed by a
smaller prospective study evaluating the outcome of diabetes in 73 mor-
bidly obese patients treated by laparoscopic adjustable gastric banding
and in 43 eligible morbid obese patients who refused surgery for personal
reasons.11 From baseline to the end of the four-year follow-up, BMI
decreased from 45 ± 0.89 to 37.7 ± 0.71 kg/m2 in the gastric banding
group and remained steady in the non surgical group. In patients without
type 2 diabetes at baseline, the primary intervention study, 17.2 per cent
of the subjects in the control group and none of the gastric banding
patients (P = 0.0001) progressed to type 2 diabetes. In patients with type
2 diabetes at baseline, the secondary intervention study, type 2 diabetes
remitted in 4.0 per cent of the patients in the control group and in
45 per cent of the surgically treated patients (P = 0.0052).11
In the SOS study, the degree of weight loss needed to obtain an effec-
tive prevention of type 2 diabetes is not so high. By pooling the surgical
and the medical group all together, and analysing the two-year incidence
of new cases of type 2 diabetes according to the level of weight loss in the
entire study population, the SOS investigators showed that patients with
no weight loss experienced a 7–9 per cent incidence of type 2 diabetes,
patients with a weight loss of 7 per cent of the baseline body weight had
a 3 per cent incidence, and patients with a 12 per cent weight loss did not
experience any new cases.12 In a study on the short term effects of weight
loss on the cardiovascular risk factors in morbidly obese patients, we
investigated the relationship between weight loss and the recovery from
type 2 diabetes in 650 morbidly obese patients treated with laparoscopic
adjustable gastric banding. The percentage of diabetic patients showing a
Impact on Life Expectancy After Bariatric Surgery
363

normalization of glucose levels 12–18 months after surgery increased
from 44.4 per cent in the lower quartile of weight loss (0.7–11.0 per cent
of the baseline body weight) to 83.3 per cent in the 2nd quartile of weight
loss (11.1–16.8 per cent of the baseline body weight), but no further
improvements in the proportion of patients having a resolution of the dia-
betic state was observed with higher weight loss levels (Fig. 1).13
According to these data, a 10–15 per cent weight loss seems to be suffi-
cient to produce both recovery and prevention of type 2 diabetes in
morbid obesity.
The factors influencing the degree of improvement in type 2 diabetes
observed after bariatric surgery have been further recently analysed. An
Australian study of type 2 diabetic subjects after laparoscopic adjustable
gastric banding found, using strict criteria, a 64 per cent remission in type 2
diabetes one year after surgery, major improvements in blood glucose con-
trol in 26 per cent, and little change in 10 per cent.14 Remission was
predicted by greater weight loss and a shorter history of diabetes, with
improvement in insulin sensitivity best predicted by extent of weight loss
and improvement in β-cell function best predicted by a shorter duration of
the disease.15 This latter observation may be expected, given that progres-
sive deterioration of β-cell function drives the progression from glucose
intolerance to overt hyperglycaemia. If the bariatric procedure is performed
364
L. Busetto et al.
44.4
83.3
87.5
66.7
0
20
40
60
80
100
Percentage
of patients
with resolution
of type 2
diabetes
I (0.7–11.0%)
II (11.1–16.8%)
III (16.9–24.5%)
IV (24.6–-56.8%)
Figure 1.
Percentage of morbid obese patients with type 2 diabetes at baseline showing
normal glucose levels without pharmacologic 12–18 months after laparoscopic gastric
banding according to quartiles of weight loss. The percentage of baseline body weight lost
in each quartile is reported in the legend.13

before irreversible β-cell failure has occurred, then durable weight loss will
be accompanied by a high likelihood of long-term remission.
In the large systematic review and meta-analysis of the outcomes of
bariatric surgery produced by Buchwald et al., there was a difference in
diabetes outcomes according to the type of operative procedure. With
respect to diabetes resolution, there was a gradation of effect from
98.9 per cent (95 per cent CI, 96.8–100 per cent) for biliopancreatic diver-
sion or duodenal switch to 83.7 per cent (95 per cent CI,
77.3–90.1 per cent) for gastric bypass and to 47.9 per cent (95 per cent CI,
29.1–66.7 per cent) for gastric banding.9 These differences may be attrib-
uted to the corresponding differences in weight loss observed with the
three procedures, but they may also be related to the existence in some type
of operation of specific metabolic effects, independent from weight loss.
In particular, several studies showed that glycaemic control often
occurs within days after gastric by-pass, long before significant weight loss
was achieved,16–18 suggesting that the control of diabetes may be a direct
effect of the operation rather than a secondary outcome of body weight
reduction. The key differential anatomical element between gastric by-pass
and gastric banding is that in gastric by-pass the duodenum and part of the
jejunum are excluded from the transit of food. Indeed, duodenal–jejunal
exclusion without gastric restriction has been demonstrated to improve glu-
cose tolerance in non obese diabetic rats, without inducing any change in
body weight.19 Because several peptides released in this part of the bowel
are involved in glucose metabolism, changes in the so-called entero-insular
axis might explain the superiority of gastric by-pass in diabetic control.17,18
In particular, two hypotheses have been proposed to explain the effect of
duodenal–jejunal bypass on type 2 diabetes.20 The ‘hindgut hypothesis’
holds that diabetes control results from the expedited delivery of nutrients
to the distal intestine, enhancing a physiologic signal that improves glucose
metabolism. A potential candidate to be the mediator of this effect
is glucagon-like peptide 1 (GLP-1), an incretin hormone secreted by L cells
of the distal bowel in response to intestinal nutrients and a potent stimula-
tor of insulin secretion and pancreatic β-cell proliferation. Indeed, the levels
of GLP-1 were found to be elevated after gastric by-pass.20 An alternative
hypothesis is that the effect of selected bariatric procedures on glucose
metabolism depends on the exclusion of the duodenum and proximal
Impact on Life Expectancy After Bariatric Surgery
365

jejunum from the transit of nutrients, possibly preventing the secretion of
some as yet unknown molecule promoting glucose intolerance (‘foregut
hypothesis’).21 Glucose-dependent insulinotropic polypeptide (GIP) levels
are specifically increased in diabetic patients and are reduced very early
after gastric by-pass.18 GIP is synthesized and released in the duodenum and
proximal jejunum in response to glucose or fat ingestion and stimulates
insulin release and synthesis. Giving that the insulin-stimulating effect of
GIP is characteristically attenuated in type 2 diabetes, possibly as a result of
a decreased expression of the glucose-dependent insulinotropic polypeptide
receptor (GIPR), it has been speculated that in susceptible individuals,
chronic stimulation of the proximal gut with fat and carbohydrates may
induce overproduction of an unknown factor that causes impairment of
GIPR expression or GIP/GIPR interaction, leading to insufficient insulin
secretion and glucose intolerance. Accordingly, the elevated GIP levels
observed in diabetics may be a compensatory response to this phenomenon.
The duodenal–jejunal exclusion typical of gastric by-pass might resolve this
alteration, establishing normal GIP function and thus reducing circulating
GIP levels.18 Recent results from experimental animal surgery seems to sup-
port the ‘foregut hypothesis’over the ‘hindgut hypothesis’as an explanation
for the very early improvement of type 2 diabetes after gastric by-pass.21
However, the exact molecular mechanisms and the long-term sustainability
of the entero-insular hormonal changes remain to be fully elucidated.
Other metabolic mechanisms may help to explain the superiority of
biliopancreatic diversion or duodenal switch over pure restrictive proce-
dures with respect to diabetes resolution. In these types of operations the
malabsorption of fat produced by surgery is typically associated with a
highly significant reduction of the plasma triglycerides levels both in the
fasting and in the post-prandial states.22 The reduced lipid overload of the
entire body has been found to be associated with a reduced fat deposition
in the non-adipose tissue organs, skeletal muscle in particular.22
Intramyocellular fat deposition is associated with a reduced glucose
uptake and utilization by the skeletal muscle, a clear metabolic marker of
insulin-resistance. Indeed, in patients treated with bilio-pancreatic diver-
sion the improvement of insulin sensitivity after surgery was more strictly
associated with the reduction of the intramyocellular lipid content than to
the fat mass loss.22
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Hypertension
Short term studies consistently show a reduction of blood pressure levels
and the need for anti-hypertensive medications after bariatric surgery.9
Within studies reporting resolution of hypertension, 3,151 (mean
61.7 per cent; 95 per cent CI: 55.6–67.8 per cent) of 4,805 patients expe-
rienced complete resolution. Within studies reporting both resolution or
improvement or only improvement of hypertension, 1,752 (mean
78.5 per cent; 95 per cent CI: 70.8–86.1 per cent) of 2,141 patients expe-
rienced resolution or improvement of hypertension.9 The proportion of
patients whose hypertension resolved seems to be strictly graded, at least
in the short term, according to the weight loss produced by the operation,
being 43.2 per cent (95 per cent CI: 30.4–55.9 per cent) for gastric band-
ing, 67.5 per cent (95 per cent CI: 58.4–76.5 per cent) for gastric bypass,
and 83.4 per cent (95 per cent CI: 73.2–93.6 per cent) for biliopancreatic
diversion or duodenal switch.9
With respect to the control and the prevention of hypertension, the
results of long-term studies are more confusing than for diabetes. In the four
year prospective study of Pontiroli et al. evaluating the outcomes in morbidly
obese patients treated by gastric banding and in morbidly obese patients who
refused surgery, hypertension remitted in 20.5 per cent of the hypertensive
patients in the surgical group and in 2.3 per cent of the patients in the control
group (P = 0.0001).11 New cases of hypertension occurred in 25.6 per cent of
the patients with normal blood pressure levels at baseline in the control group
and in 1.4 per cent of the patients with normal blood pressure levels at base-
line in the surgical group (P = 0.0001).11 In the first two years of the SOS
study, 34 per cent of 1,204 hypertensive surgically treated obese patients had
a complete recovery from hypertension, and the same happened in
21 per cent of 880 hypertensive controls. Therefore, the odds ratio for being
free from hypertension two years after surgery was still significantly higher
in the surgically treated than in the medically treated group (OR 1.72; 95 per
cent CI: 1.40–2.12).10 However, at the ten year evaluation, only 19 per cent
of the surgically treated patients and 11 per cent of the control subjects still
had normal blood pressure levels, with a relative risk of being free from
hypertension that was only marginally higher in the surgical group (OR 1.68;
95 per cent CI: 1.09–2.58).10 On the contrary, no benefits in the prevention
Impact on Life Expectancy After Bariatric Surgery
367

of hypertension were observed for bariatric surgery in the SOS study. The
incidence of new cases of hypertension was 24 per cent in the surgically
treated patients and 29 per cent in the control group at two years (OR 0.78;
95 per cent CI: 0.60–1.01), and it was 41 per cent and 49 per cent respec-
tively at ten years (OR 0.75; 95 per cent CI: 0.52–1.08).10
The differences between the two studies and the lack of a protective
effect of surgery on new cases of hypertension observed in the SOS study
may be related to the crucial role of body weight in the disease; in the SOS
study, a significant regain of body weight was observed in the surgically
treated group,10 whereas in the study of Pontiroli et al. body weight
remained substantially stable over the four years of follow-up.11 Blood
pressure levels are probably more dependent on the energy balance of the
patient and the actual trend of his body weight (weight gain/weight
stability/weight loss) than from the absolute level of body weight or
BMI.23 In a study on the effects of gastric banding on the cardiovascular
risk factors in morbidly obese patients, we find a strict linear correlation
between the degree of weight loss and the reduction of the blood pressure
levels only in those patients actively losing weight, but not in patients who
had reached body weight stabilization, or in weight regainers.13
Maintenance of a stable body weight after surgery is therefore probably
the most critical factor in the control of hypertension in the surgically
treated morbidly obese patient.
Dyslipidemia
Hypercholesterolemia is not a specific feature of the morbidly obese
patient. In the recruitment phase of the SOS study, total cholesterol levels
was not increased in morbidly obese males and was in fact significantly
lower in the morbidly obese compared with reference women.6 By con-
sequence, it is not surprising that in the intervention phase of the SOS
study no significant differences were observed in the changes of choles-
terol levels between the surgically treated and the weight stable
medically treated groups.10 The rates of recovery to normal cholesterol
levels in patients with hypercholesterolemia at baseline were 22 per cent
in the surgical group and 17 per cent in the control group two years after
surgery (OR 1.22; 95 per cent CI: 0.98–1.51), and 21 per cent and
368
L. Busetto et al.

17 per cent respectively 10 years after surgery (OR 1.30; 95 per cent CI:
0.92–1.83).10 The incidence of new cases of hypercholesterolemia was 27
per cent in the surgically treated patients and 24 per cent in the control
group at two years (OR 1.27; 95 per cent CI: 0.95–1.69), and 30 per cent
and 27 per cent respectively at ten years (OR 1.16; 95 per cent CI:
0.69–1.95).10 In the total population analysed by Buchwald et al., meta-
analysis of the continuous measures demonstrated a significant decrease
in total cholesterol level (mean change, 33.2 mg/dl; 95 per cent CI,
23.2–43.6 mg/dl) and low-density lipoprotein cholesterol level (mean
change, 29.3 mg/dl; 95 per cent CI, 17.8–40.9 mg/dl).9 However, most of
the studies included in the meta-analysis did not have adequate control
groups, and the lack of any difference in the changes of cholesterol lev-
els between the two arms of the SOS study may suggest that any
improvement observed after surgery may be related more to the changes
in the quality of the diet than to weight loss per se. This consideration
obviously does not apply to malabsorptive procedures. A pooled mean
99.7 per cent improvement of hypercholesterolemia was reported in three
studies with biliopancreatic diversion or duodenal switch, with the
majority of patients showing very low cholesterol levels after sur-
gery.24–26 In malabsorptive procedures the reduction of cholesterol levels
was indeed the consequence of the disruption of the entero-hepatic cho-
lesterol recycling caused by the operation and it was largely independent
of weight loss.26 The use of malabsorptive procedures with or without
gastric restriction has been suggested for the treatment of severe hyperc-
holesterolemia independently of the presence of obesity.26
The long-term results of the SOS study clearly demonstrated the effi-
cacy of the weight loss induced by surgery in the treatment of the classic
obesity-associated dyslipidemia: hypertriglyceridaemia with low HDL
cholesterol levels. Recovery from hypertriglyceridaemia was observed in
62 per cent of the hypertriglyceridemic patients in the surgical group and
in 22 per cent of the control group two years after surgery (OR 5.28;
95 per cent CI: 4.29–6.49), and in 46 per cent and 24 per cent respectively
ten years after surgery (OR 2.57; 95 per cent CI: 1.85–3.57).10 Recovery
from low HDL cholesterol levels was observed in 76 per cent of the
patients in the surgical group and 39 per cent in the control group two
years after surgery (OR 5.28; 95 per cent CI: 3.85–7.23), and in
Impact on Life Expectancy After Bariatric Surgery
369

73 per cent and 53 per cent respectively ten years after surgery (OR 2.35;
95 per cent CI: 1.44–3.84).10 The sustained weight loss induced by surgery
not only normalized obesity-associated dyslipidemia in patients already
dyslipidemic at baseline, but also prevented the occurrence of new cases.
The ten-year incidence of new cases of hypertriglyceridaemia was
17 per cent in the surgically treated patients and 27 per cent in the control
group (OR 0.61; 95 per cent CI: 0.39–0.95), while the new cases of low
HDL cholesterol levels observed ten years after surgery were 3 per cent
and 6 per cent respectively (OR 0.57; 95 per cent CI: 0.29–1.15).10
The long-term benefits of surgery on hypertriglyceridaemia observed
in the SOS study were confirmed by the meta-analysis of a non-controlled
short-term series. Within studies reporting improvement of hypertriglyc-
eridaemia, 912 (mean 82.4 per cent; 95 per cent CI: 71.1–93.7 per cent) of
983 patients experienced an improvement, with a difference in outcome
according to the type of operative procedure: 100.0 per cent (95 per cent
CI, 98.1–100 per cent) for biliopancreatic diversion or duodenal switch,
91.2 per cent (95 per cent CI, 83.6–98.8 per cent) for gastric bypass, and
77.0 per cent (95 per cent CI, 54.1–99.9 per cent) for gastric banding.9 On
the contrary, the long-term benefits on HDL cholesterol levels observed in
the SOS study were only partially confirmed in short-term studies. In the
meta-analysis of Buchwald et al., there was no significant increase in HDL
cholesterol levels in the total population, while significant improvements
were seen with gastric banding (mean change 4.63 mg/dl; 95 per cent CI,
1.54–7.72 mg/dl).9 This discrepancy may be due to the particular relation-
ship between weight loss and changes of HDL cholesterol levels.
A meta-analysis of studies on blood lipids and lipoproteins designed to
examine the effects of weight reduction by dieting demonstrated an
increase of HDL cholesterol levels if patients were analysed at a stabilised,
reduced weight, but a decrease of HDL cholesterol levels if patients were
analysed when still actively losing weight.27 We studied the short term
effects of weight loss on the cardiovascular risk factors in morbidly obese
patients, in order to investigate the effects of actual energy balance on the
modifications of cardiovascular risk. Patients were divided into three
groups according to the changes of body weight observed between the time
after gastric banding in which the cardiovascular risk factors were deter-
mined, and the following clinical evaluation. We confirmed that HDL
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L. Busetto et al.

cholesterol levels significantly increased in patients with weight regain and
in patients with stabilized body weight, whereas a small decrease in HDL
cholesterol levels was observed in patients still actively losing weight (Fig.
2).13 The null effect of bariatric surgery on HDL cholesterol levels reported
by Buchwald et al.9 may be therefore partly attributed to the fact that in
most of the short-term studies included in the meta-analysis a significant
proportion of patients was probably still in a phase of active body weight
reduction.
Effects of Bariatric Surgery on Respiratory Disturbances
Pulmonary volumes and respiratory function
Evidence from several studies definitely proved that the respiratory com-
plications of morbid obesity can be improved by bariatric surgery.
Exertional dyspnoea is the most frequently reported symptom of morbid
obesity and is typically of respiratory origin. In the recruitment phase of
the SOS study, the relative risk of having dyspnoea in 50 year-old
morbidly obese males and females were 4.3 and 4.7 respectively, in
Impact on Life Expectancy After Bariatric Surgery
371
Figure 2.
Modifications of HDL cholesterol levels in morbidly obese patients treated
with laparoscopic gastric banding, according to actual energy balance 12–18 months after
surgery. The percent changes from the baseline values were reported. Patients showing a
≥2.0 kg increase of body weight in the period immediately following the redetermination
of blood lipids after surgery were classified as ‘weight gainers’, and patients with a
≥2.0 kg reduction of body weight as ‘weight losers’. Patients with in between weight
changes were classified as ‘weight stable’.13
6.5
9.7
-1.5
-10
-5
0
5
10
HDL cholesterol
changes from
baseline (%)
weight gainers
weight stable
weight losers

comparison with normal weight reference subjects.6 In a subset analysis
from the SOS study specifically devoted to the study of respiratory dis-
turbances, 87 per cent of the first 1,260 morbidly obese patients enrolled
in the intervention study complained at baseline with dyspnoea when
climbing two flights of stairs and 24 per cent when performing simple
activities of daily living such as washing or dressing. In these patients, a
sustained surgically induced weight loss was able to drastically reduce the
incidence of exertional dyspnoea, with only 19 per cent of patients still
complaining with dyspnoea when climbing stairs and 3 per cent when
washing or dressing.28
Morbidly obese patients are typically affected by a restrictive respi-
ratory impairment, with the most characteristic pulmonary function
abnormality being a reduction of the expiratory reserve volume
(ERV).29,30 Imaging studies conducted with the use of computed tomog-
raphy demonstrated that the major determinant of ERV reduction was the
amount of abdominal visceral adipose tissue, both in males and in
females.31 Small studies with determination of respiratory volumes
before and after surgery demonstrated that the reduction of dyspnoea
induced by bariatric surgery was related to increased vital capacity, FRV
and ERV.32,33
It is also noteworthy that the respiratory complications of obesity, as well
as the metabolic disorders, appeared to be positively affected, at least in the
short term, by only a moderate level of body weight reduction. Dividing 1,087
morbidly obese patients according to quartiles of weight reduction, the SOS
investigators were able to show that the larger reduction in the risk of contin-
uing to suffer from dyspnoea as compared with patients with stable weight
(+ 4.0 kg) was obtained in patients with a larger weight loss
(– 41.5 kg) (RR 0.02; 95 per cent CI 0.01–0.03). However, a significant reduc-
tion of risk was also observed in the group of patients with only a moderate
weight loss (RR 0.26; 95 per cent CI 0.18–0.33). In this group, mean weight
loss was −7.9 kg, an apparently trivial level of weight loss in patients with
severe obesity.28 If pulmonary function impairment was more dependent on
visceral fat accumulation than on the simple level of total fatness, it could be
hypothesized that the improvements of respiratory complications observed
with only a moderate body weight reduction could be ascribed to
a selective reduction of visceral fat. Indeed, in a study with total body
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L. Busetto et al.

multi-slices NMR, we demonstrated a preferential mobilization of abdominal
visceral fat with respect of total and regional subcutaneous fat in the first
phase of weight loss in a small group of six pre-menopausal women with vis-
ceral obesity treated by laparoscopic gastric banding (Fig. 3).34 In the first
eight weeks after surgery, the relative reduction of visceral adipose tissue
(19.6 ± 14.7 per cent) was significantly higher than the relative reduction of
both total adipose tissue (11.5 ± 7.9 per cent) and gluteo-femoral subcuta-
neous adipose tissue (10.7 ± 8.1 per cent).34 It is therefore possible that the
improvements of pulmonary volumes observed after a modest weight loss
should be a part of the better responsiveness of visceral than subcutaneous fat
to caloric restriction. However, this hypothesis needs to be directly proven.
Impact on Life Expectancy After Bariatric Surgery
373
0
1
2
3
4
AT REDUCTION (%/week)
TAT
AB-SAT
GF-SAT
VAT
0–8 weeks
8–24 weeks
Figure 3.
Relative reductions of total and regional adipose tissue (AT) volumes,
expressed as percentage changes from baseline levels per week of observation, in the first
eight weeks (weeks 0–8) and in the second 16 weeks (weeks 8–24) after surgery in six
morbidly obese women with visceral obesity treated by laparoscopic gastric banding.
TAT: total adipose tissue volume; AB-SAT: abdominal subcutaneous adipose tissue volume;
GF-SAT: gluteo-femoral subcutaneous adipose tissue volume; VAT: abdominal visceral adi-
pose tissue volume. Error bars represent standard deviations. Differences between total and
regional adipose tissue volumes were tested by paired Student’s t-test. Significant differences
were found only in the 0–8 weeks period, between VAT and TAT (P < 0.05) and between VAT
and GF-SAT (P < 0.05).34

Obstructive sleep apnoea syndrome
Obstructive sleep apnoea syndrome (OSAS) is particularly frequent in
morbid obesity, with an estimated prevalence of 40 per cent.35 In a subset
analysis from the SOS, the prevalence of symptoms of OSAS, as evalu-
ated by a specific questionnaire, was 23 per cent at baseline and it was
significantly reduced to 8 per cent two years after surgery.28 In a review
and meta-analysis of the outcomes of bariatric surgery, when clinical diag-
noses of sleep apnoea, sleep-disordered breathing, and pickwickian
syndrome were combined as representative of obstructive sleep apnoea,
OSAS was found to be resolved in 1,051 of 1,195 patients (mean
85.7 per cent; 95 per cent CI, 79.2–92.2 per cent).9 However, these esti-
mates may be flawed by the fact that in most studies the diagnosis of
OSAS was made clinically, and not with a more objective instrumental
registration of breathing disorders during sleeping.
Dixon et al. recently prospectively performed a polysomnographic
overnight registration both before and at least one year after surgery in
25 morbidly obese patients with severe OSAS (apnoea–hypopnoea index
[AHI] > 25 events/hour) treated by laparoscopic adjustable gastric band-
ing. Subject baseline BMI was 52.7 ± 9.5 kg/m2 and the second
polysomnographic study was performed at a BMI of 37.2 ± 7.2 kg/m2.
The authors demonstrated a significant fall in AHI from 61.6 ± 31.9 to
13.4 ± 13.0 events /hour (P < 0.001), an improved sleep architecture with
increased REM and stage III and IV sleep, and a reduced daytime sleepi-
ness. Moreover, fewer patients required nasal continuous positive airways
pressure (CPAP) after surgery than before (24 per cent versus 92 per cent;
P < 0.001).36 These new results substantially confirmed a previous meta-
analysis of 4 studies, with a total population of 92 patients, in which the
continuous objective variable of apnoeas or hypopnoea per hour was
available, that demonstrated a reduction of 33.8 events/hour (95 per cent
CI: 17.5–50.2 events/hour). 9
We recently studied a small group of 18 middle-aged men with
OSAS and severe visceral obesity (baseline BMI of 54.7 ± 9.5 kg/m2)
treated with the temporary insertion of an intragastric balloon in prepa-
ration for later laparoscopic adjustable gastric banding surgery, and we
observed a high reduction of the number of apnoeic episodes during
374
L. Busetto et al.

sleeping with a relatively modest level of weight loss and despite the fact
the patients still remained affected by severe obesity after treatment.37
A cardio-respiratory sleep study, which included assessment of air flow,
thoracic and abdominal movements, snoring, pulse rate and oximetry, was
performed at baseline and immediately after the removal of the balloon,
six months apart, at a BMI of 48.6 ± 11.2 kg/m2. The 14.5 ± 8.9 per cent
reduction from baseline body weight produced by the intragastric balloon
was associated in our study with a significant fall in AHI from 59.3 ±
18.1 to 14.0 ± 12.4 events/hour (P < 0.01). The reduction in the number
of apnoeic episodes during sleep was accompanied by improvements of
pulmonary function, standing and lying oxygen saturation, and the diur-
nal symptoms of OSAS. We also analysed the improvement in the
severity of OSAS categorically, by evaluating how many patients were
treated successfully by the intragastric balloon. We defined success
as a reduction in AHI of at least 50 per cent with a reduction of the AHI
to < 20 events/hour. According to these criteria, 10 of 17 patients
(58.8 per cent) achieved success. The mean percentage weight loss after
treatment with the intragastric balloon was higher in the responders than
in the non responders (19.7 ± 7.6 versus 6.9 ± 3.3 per cent, respectively;
P < 0.001). The lowest percentage weight loss that was associated with
success was 8.8 per cent, and the highest percentage weight loss associ-
ated with failure was 12.2 per cent.37 Therefore, in our study a moderate
10–15 per cent weight loss also appeared to be associated to a resolution
of OSAS in patients with extreme levels of obesity.
The high prevalence of OSAS among obese patients has been attributed
to a mass loading of the upper airway by adipose tissue.38 In fact, obese
patients with OSAS have been shown to have increased fat deposition adja-
cent to the upper airway39,40 and reduced pharyngeal cross-sectional area34
when compared to control subjects. We hypothesized that the higher than
expected resolution of OSAS observed in our study may be related to
changes of pharyngeal size in the first phase of weight loss, and therefore
we measured the upper airways size by acoustic pharyngometry. The main
finding of the study was that the pharyngeal cross-sectional area of the mor-
bidly obese patient subjects, which was severely reduced at baseline as
compared to a normal weight control group, increased after weight loss
(Fig. 4).37 The increase in the cross-sectional area of the pharynx was
Impact on Life Expectancy After Bariatric Surgery
375

significantly related to the level of weight loss (r 0.547; P < 0.05) and to the
reduction of waist circumference (r = 0.473; P < 0.05), sagittal abdominal
diameter (r = 0.664; P < 0.01), and neck circumference (r = 0.506; P < 0.05).
However, the reduction of sagittal abdominal diameter, the best anthropo-
metric index of visceral fat accumulation, was found to be the only variable
that was significantly related to an increase in pharyngeal cross-sectional
area in multivariate regression analysis.37 We therefore suggest that the
rapid improvements of pharyngeal patency may be another aspect of the
better responsiveness of visceral than subcutaneous fat to caloric restriction
observed in the first phase of body weight reduction.
376
L. Busetto et al.
†
*
***
*
*
***
***
††
†
*
**
**
***
ORTHOSTATIC
POSITION
CLINOSTATIC
POSITION
†
*
***
*
*
***
***
††
†
*
**
**
***
†
*
***
*
*
***
***
††
†
*
**
**
***
0
0,5
1
1,5
2
2,5
3
OPJ
PHAR
GLOT
OPJ
PHAR
GLOT
Cross-sectional area (cm2)
*
***
*
*
***
***
††
†
*
**
**
***
Figure 4.
Cross-sectional pharyngeal areas determined by acoustic reflection in 17 mor-
bidly obese patients in the upright and supine positions before intragastric balloon insertion
(black bars) and after intragastric balloon removal (light grey bars). The pharyngometric
measurements of 20 nonobese men were reported for comparison (white bars). OPJ =
oropharyngeal junction cross-sectional area; PHAR = mean pharyngeal cross-sectional area;
GLOT = glottis cross-sectional area. * = P < 0.05 (Mann–Whitney U test between obese
patients and nonobese subjects); ** = P < 0.01 (Mann–Whitney U test between obese patients
and nonobese subjects); *** = P < 0.001 (Mann–Whitney U test between obese patients and
nonobese subjects). † = P < 0.05 (Wilcoxon rank sum test between obese patients before
intragastric balloon insertion and after its removal); †† = P < 0.01 (Wilcoxon rank sum test
between obese patients before intragastric balloon insertion and after its removal).37

Impact of Bariatric Surgery on Health Related Quality of Life
As previously shown, severe obesity is associated with a wide range of
serious health complications. Consequently, it has been demonstrated that
severe obesity produces profound impairments in health-related quality of
life (HRQL). The harmful effects of obesity influence physical, psycho-
logical and social domains of HRQL and tend to be more severe at higher
BMI levels.41 Even after accounting for the pain and anxiety of surgery,
the inconveniences of dietary restrictions, and possible complications
including reoperation, quality of life improved for the majority of bariatric
surgery patients.9 The perception of wellbeing, social function, body self
image, self-confidence, ability to interact with others, and time spent in
recreational and physical activities have been also reported to increase
after successful bariatric surgery.9 It should be noted however that most of
these assumptions are derived from the results of research studies report-
ing improvements in psychosocial areas after bariatric surgery, but
suffering from important methodological limitations, principally repre-
sented by the small study samples and the short follow-up periods.42
Very recently, the SOS investigators reported on the ten-year
trends in health-related quality of life after surgical and conventional
treatment for severe obesity in the SOS intervention study.43 HRQL was
assessed before treatment and after six months, then after one, two, three,
four, six, eight and ten years in a total of 655 of 851 surgically treated and
621 of 852 conventionally treated obese men and women who completed
10 years of the study, thus allowing for a long-term sequential analysis of
the effects of bariatric surgery on quality of life. General health percep-
tions, mental well-being, mood disorders, health related dysfunctions in
social life and the impact of obesity on psychosocial functioning were
measured with the use of specific questionnaires. HRQL at baseline was
generally poorer in the severely obese than in age-matched non-obese
reference population. After surgery, changes in HRQL generally followed
phases of weight loss, weight regain and weight stability. Poor HRQL
before treatment was markedly improved after surgery and peak improve-
ments during the ten-year observation period were noted after six months
and one year, which corresponds with the maximal weight loss observed
after the operation. Thereafter, a gradual regain of weight was observed,
Impact on Life Expectancy After Bariatric Surgery
377

mainly up to six years, with about one-third of the initial weight reduction
gradually regained. During this weight regain phase, a slow but steady
decline in HRQL was noted. Finally, weight regain slowed down and body
weight stabilized between six and ten years. Accordingly, quite stable
HRQL ratings were observed in the surgical group between six and ten
years. All the HRQL domains that were examined in the study were sig-
nificantly improved in the surgical group after ten years. According to
standard criteria for interpreting treatment-related changes of HRQL, ten-
year improvements were in the small range for current health, social
interaction, overall mood, depression and anxiety, whereas the improve-
ment in psychosocial functioning was large.43 The final comment of the
authors concluded that bariatric surgery is a favourable option for the
treatment of severe obesity, resulting in substantial long-term weight loss
accompanied by improvements in health status and quality of life in a
majority of patients. Nevertheless, the authors emphasized the difficulties
that many surgical patients experienced to control and maintain weight
loss over time and the possible negative impact that these difficulties and
the associated weight regain may have on the physical and psychosocial
well being of the patients. It is possible that these difficulties may be bet-
ter coped with by the use of long-term behavioural support programmes
in the postoperative management of patients.43
Impact of Bariatric Surgery on Life Expectancy
As summarized in the first part of this review, several longitudinal stud-
ies proved that the high prevalence of metabolic and vascular disorders
observed in morbidly obese patients translates in a clear excess mortal-
ity risk. Morbid obesity was found to be associated with at least a
doubling of total mortality risk in both sexes.7,8 As reviewed above, a
large body of clinical studies has proved that bariatric surgery may
produce sustained and stable weight loss in morbidly obese patients and
that this weight loss is accompanied by a long-term reduction in both the
prevalence and the incidence of several obesity-related co-morbidities,
type 2 diabetes in particular. However, reliable scientific evidence that
these clinical benefits ultimately translate into a reduction of the excess
mortality risk of morbid obesity is still scarce. To prove that bariatric
378
L. Busetto et al.

surgery, notwithstanding the additional risks introduced by the operative
procedures and the eventual post-operative complications, is able to
cause a reduction in the excess mortality risk of the morbidly obese is
clearly a key point in the development and acceptance of surgery as a
first line therapeutic choice in severe obesity, but to comply with this
task presents important technical and logistic problems. A randomized
clinical trial prospectively comparing the mortality rate in morbidly
obese patients treated by bariatric surgery and in comparable subjects
treated by the best behavioural and pharmacologic methods should obvi-
ously provide the highest level of scientific evidence in this respect.
However, conducting a randomized clinical trial of this sort may require
a huge number of patients followed for a long time and may raise some
ethical concern given the expected benefits of bariatric surgery on body
weight, obesity-related co-morbidities and quality of life. To date, no
such trials have been conducted and it seems highly improbable that this
may happen in the future.
As previously described, the investigators of the SOS study tried to
resolve this gap by planning and conducting a large prospective study in
which the outcome of a large group of patients treated by several types of
bariatric procedures was compared with the outcome of well-matched
morbidly obese controls not choosing surgical treatment.6 The primary
aim of the study was to prospectively evaluate total and cause-specific
ten-year mortality. The SOS study produced highly valuable data about
the effect of surgery on co-morbidities and quality of life10,23,28,43 and a
very recent preliminary report from the SOS investigators declared a
24.6 per cent reduction of total ten-years mortality in the first 2,010
surgically-treated patients.44 The scientific value of this observation is
indisputable, but some concern about the applicability of the SOS results
to current bariatric surgery has been raised.45 The SOS study has a ten-
year follow-up and additional years were needed for the enrolment of
patients, so a significant proportion of the SOS patients were treated in the
1990s with procedures (vertical banded gastroplasty) and techniques
(open surgery) that are now largely abandoned.
In a recent retrospective observational study, the five-year death rate
of 1,118 morbidly obese patients surgically treated with Roux-en-Y gas-
tric bypass (RYGB) at a single Canadian academic institution was
Impact on Life Expectancy After Bariatric Surgery
379

compared with the death rate of 5,746 morbidly obese controls whose
vital status was derived from the administrative records of the provincial
health insurance database of Quebec.46 In this study, the mortality rate in
the bariatric surgery cohort, with the peri-operative mortality included in
the calculation, was found to be 0.68 per cent, compared with a total mor-
tality of 6.17 per cent in the control group. These figures translated into a
highly significant 89 per cent reduction of the relative risk of death in the
surgical group (relative risk 0.11; 95 per cent CI 0.04–0.27).46 The results
of retrospective observational studies may obviously be affected by selec-
tion biases and uncontrolled differences between the surgical and the
control cohorts. In the Canadian study in particular, the baseline BMI of
the subjects in the control cohort was not actually measured and all the
control subjects were morbidly obese patients hospitalized for acute clin-
ical problems. It could be argued that the five-year mortality rate of this
control cohort of acutely sick morbidly obese patients (6.17 per cent) may
be higher than the death rate of the general morbidly obese population,
thus inflating the difference between the bariatric surgery group and the
control group. Moreover, the peri-operative mortality rate in the Canadian
study was very low, probably reflecting the top level of expertise of the
surgical team. Much higher peri-operative mortality rates have been
reported in morbidly obese patients treated by RYGB in the community,47
raising some doubt about the applicability of the results to the current
‘real-life’ obesity surgery practice.
We recently tried to overcome the above methodological problems by
comparing the mortality rate of 821 patients with BMI > 40 kg/m2 con-
secutively treated by laparoscopic adjustable gastric banding at our
institution with the mortality rate of 821 sex, age and measured BMI-
matched morbidly obese patients observed at six Italian tertiary obesity
care centres not using bariatric surgery.48 Both our cohorts were therefore
formed by morbidly obese patients seeking treatment at highly specialized
institutions, but receiving a different type of therapy. Indeed, the seven-
year mortality rate of our control cohort (4.38 per cent) was lower than the
6.17 per cent observed by Christou et al.46 Nevertheless, we confirmed
that bariatric surgery was associated with a significant reduction in total
mortality. During a mean follow-up of 5.6 ± 1.9 years in the surgical
group and 7.2 ± 1.2 years in the reference cohort, 8 and 36 deaths were
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L. Busetto et al.

recorded respectively, for a total mortality of 0.97 per cent in the surgical
patients and 4.38 per cent in the controls. The difference in survival was
statistically significant (P = 0.0004) at the log-rank test for comparison of
Kaplan–Meier survival curves (Fig. 5), and the age, sex and BMI-adjusted
relative risk of death in the surgical cohort, as compared with the refer-
ence cohort, was 0.36 (95 per cent CI: 0.16–0.79), with a statistically
significant 60 per cent reduction in total mortality. It should be noted that
patients in our surgical group had a zero operative mortality, a figure that
is not unexpected for an operation, like laparoscopic banding, reported to
have less operative risk than gastric by-pass9 and that did not differ sub-
stantially from the low mortality rate (0.53 per cent) observed with
laparoscopic gastric banding in an Italian study including centres with
high as well low volumes of this operation.49
The results of our study seem to be confirmed by two other recent
reports. Australian investigators compared the mortality rate in 1,468
morbid obese patients treated by laparoscopic gastric banding at the
Monash University in Melbourne and in 5,960 patients with BMI
> 35 kg/m2 from the established population-based cohort of the
Melbourne Cohort Collaborative Study, recruited between 1992 and 1994
Impact on Life Expectancy After Bariatric Surgery
381
Figure 5.
Kaplan–Meier estimates of survival in 821 obese patients with BMI
> 40 kg/m2 consecutively treated with laparoscopic adjustable gastric banding (LAGB) at
the University of Padova and in 821 morbidly obese patients observed at six Italian terti-
ary obesity care centres not using bariatric surgery (no LAGB).48
90
92.5
95
97.5
100
0.5
1
2
3
4
5
years
Probability of survival
LAGB
no LAGB