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Can J Surg. Feb 2013; 56(1): 47–57.
PMCID: PMC3569476
Biological effects of bariatric surgery on obesity-related comorbidities
Sabrena F. Noria, MD, PhD and Teodor Grantcharov, MD, PhD
From the Department of Surgery, Division of General and Minimally Invasive Surgery, St. Michael’s Hospital, University of Toronto, Toronto, Ont.
Correspondence to: S.F. Noria, Ohio State University Medical Center, Department of Surgery, Division of General and Gastrointestinal Surgery, Center for Minimally Invasive Surgery, 558 Doan Hall, 410 West 10th Ave, Columbus, OH 43210, sabrena.noria/at/gmail.com
Accepted February 22, 2012.
The prevalence of obesity has increased so rapidly over the last few decades that it is now considered a global epidemic. Obesity, defined as a body mass index (BMI) of 30 or more, is associated with several comorbid conditions that decrease life expectancy and increase health care costs. Diet therapies have been reported to be ineffective in the long-term treatment of obesity, and guidelines for the surgical therapy of morbid obesity (BMI ≥ 40 or BMI ≥ 35 in the presence of substantial comorbidities) have since been established. Considering the number of bariatric surgical procedures has dramatically increased since these guidelines were established, we review the types of bariatric surgical procedures and their impact on diabetes, sleep apnea, dyslipidemia and hypertension — 4 major obesity-related comorbidities.
La prévalence de l’obésité a augmenté si rapidement au cours des quelques dernières décennies qu’on considère désormais qu’il s’agit d’une épidémie mondiale. L’obésité, définie par un indice de masse corporelle (IMC) de 30 ou plus, est associée à plusieurs comorbidités qui réduisent l’espérance de vie et font augmenter le coût des soins de santé. La diétothérapie serait inefficace pour le traitement à long terme de l’obésité et des lignes directrices concernant le traitement chirurgical de l’obésité morbide (IMC ≥ 40 ou IMC ≥ 35 en présence d’autres comorbidités importantes) ont donc été établies. Compte tenu du fait que le nombre de chirurgies bariatriques a considérablement augmenté depuis la parution de ces lignes directrices, nous passons en revue les différents types de chirurgies bariatriques et leur impact sur le diabète, l’apnée du sommeil, la dyslipidémie et l’hypertension, 4 importantes comorbidités liées à l’obésité.
Obesity is a serious public health problem associated with increased morbidity and mortality and decreased quality of life. According to the World Health Organization, in 2005 there were about 1.6 billion overweight adults (aged 15 years or older) and at least 400 million obese adults worldwide.1 The prevalence of obesity has increased so rapidly over the last few decades that it is now considered a global epidemic.
The World Health Organization defines overweight as a body mass index (BMI) of 25 or more and obesity as a BMI of 30 or more.1 Obese patients are further categorized into class I (BMI 30–34.9), class II (BMI 35–39.9) and class III (BMI 40 or more).2,3 While these subcategories are relevant when analyzing trends in prevalence, evidence suggests that the risk of chronic disease increases progressively from a BMI as low as 21.1 In addition, the risk of obesity-related comorbidities increases in individuals with a large waist circumference, even if they are categorized as healthy or overweight. Specifically, a waist circumference greater than 101.6 cm (40 inches) in men and greater than 89.9 cm (35 inches) in women predicts an increased risk of diabetes, dyslipidemia, hypertension and cardiovascular disease.
In the United States, the National Health and Nutrition Examination Surveys conducted by the Centers for Disease Control study the prevalence of obesity using directly measured heights and weights. Studies have reported that currently there are 72 million obese adults. Interestingly, while the prevalence in adults aged 20–74 years has more than doubled over the last 4 decades (13.4% in 1960–1962 v. 35.1% in 2005–2006),4 it seems to have reached a plateau in the last 3 years.57 However, when comparing the distribution of BMI in 1976–1980 with that in 2005–2006, it appears that the distribution among adults has shifted, reflecting a change in prevalence of superobesity (BMI > 50), which increased from 0.9% in 1960–1962 to 6.2% in 2005–2006.6
In Canada, statistics from 2004 demonstrated that about 23% (5.5 million people) of adults were obese compared with 14% in the late 1970s.2,8 The total direct cost of obesity in Canada has been estimated to be more than $1.8 billion, which corresponded to 2.4% of the total health care expenditures for all diseases in Canada in 1997.9 When the cost of obesity-related comorbidities was taken into account, the 3 largest contributors were hypertension ($656.6 million), type 2 diabetes mellitus (T2DM; $423.2 million) and coronary artery disease ($346.0 million).9
Studies have indicated that obesity is responsible for more than 2.8 million deaths worldwide per year10 owing to an increased prevalence of related comorbidities, including type 2 diabetes, hyperlipidemia, hypertension, obstructive sleep apnea, heart disease, stroke, asthma, back and lower extremity weight-bearing degenerative problems, several forms of cancer and depression.1012 In addition, obesity is an independent risk factor for death. A study by Fontaine and colleagues13 demonstrated that compared with an individual with a healthy weight, a 25-year-old morbidly obese man has a 22% reduction in life expectancy, representing about 12 years of life lost. A more recent study that examined 10-year mortality in more than 500 000 Americans aged 50–71 years demonstrated that in middle-aged men and women who were nonsmokers and had no pre-existing illnesses, there was a 20%–40% increase in mortality in those who were overweight and a 2- to 3-fold greater risk among those who were obese.14
As evidenced by the existence of countless weight loss programs, most adults attempt to lose weight at some point in their lives.15 However, diet therapy, with and without supports and pharmaceutical agents, is ineffective in the long-term treatment of obesity.3 In 1991, the National Institutes of Health established guidelines for surgical therapy for morbid obesity (BMI ≥ 40 or BMI ≥ 35 in the presence of substantial comorbidities),16,17 and since then the number of bariatric surgical procedures has dramatically increased. About 144 000 obese individuals received surgical treatment in 2004 compared with about 20 000 in 1999.18 The dramatic increase is most likely related to the use of minimally invasive surgical techniques, increased media coverage and increased patient satisfaction. Of the various available weight-loss strategies, bariatric surgery is the only effective long-term weight-loss therapy for obese individuals.19
The present paper reviews the types of bariatric surgical procedures and their impact on diabetes, sleep apnea, dyslipidemia and hypertension; 4 major obesity-related comorbidities.
Bariatric procedures are classified as restrictive and/or malabsorptive based on the presumed mechanism of weight loss20 (Table 1).
Table 1
Table 1
Comparison of bariatric procedures
Restrictive procedures
Restrictive procedures limit the luminal diameter of the stomach, but do not reroute food through the gastrointestinal tract by exclusion of intestinal segments. Procedures may involve some form of foreign material or “band” (i.e., laparoscopic adjustable gastric band [LAGB]) and/or surgically resize the stomach with a stapler to create a small gastric pouch (i.e., vertical-banded gastroplasty [VBG] or sleeve gastrectomy [SG]).21
The LAGB is the second most common bariatric procedure, wherein an adjustable plastic and silicone ring is placed around the proximal stomach just beneath the gas-troesophageal junction. A subcutaneous access port allows the degree of band constriction to be adjusted by the injection or withdrawal of saline. Although the risk of death and major morbidity is low, the amount of excess weight loss obtained is inferior than that achieved with the malabsorptive procedures.22,23
The laparoscopic SG is a relatively new surgical procedure for the management of obesity. The procedure involves resection of the greater curvature of the stomach by stapling it over a sizing tube 11–20 mm in diameter.24 Originally developed as part of a biliopancreatic diversion with duodenal switch (BPD+DS),25 it was subsequently used as the initial procedure of staged surgery for super-obesity.26,27 Currently, LSG is most commonly applied as a stand-alone procedure28 and is being used with increasing frequency (i.e., LSG accounted for 7.8% of primary bariatric operations in 2010).29 The effectiveness of LSG with respect to weight loss and resolution of comorbidities is less than that of Roux-en-Y gastric bypass (RYGB) but greater than that of LAGB. These results suggest that, at least in the short-term, LSG is an efficacious method of weight loss.
Primarily malabsorptive procedures with some restriction
Malabsorptive procedures are designed to reduce the area of intestinal mucosa available for nutrient absorption. The jejunoileal bypass (JIB) involves bypassing most of the small intestine by anastomosing the proximal jejunum, past the ligament of Trietz, to the terminal ileum. While excellent weight loss is achieved, the blind jejunal-ileal limb leads to nutritional complications and hepatic cirrhosis secondary to bacterial overgrowth.3032 As such, this procedure was abandoned, and the BPD was devised to improve upon the JIB.
The BPD consists of a partial gastrectomy, resulting in a 200–500 mL proximal gastric pouch and creation of a distal Roux and proximal biliary limb by division of the small bowel 250 cm proximal to the terminal ileum. The gastric pouch is then anastomosed to the end of the Roux limb, and the biliary limb is attached 50 cm proximal to the iliocecal valve, thereby creating a very short common channel.21 The procedure was later modified, creating the BPD-DS. This entails creating a gastric sleeve with a maximum reservoir of 150–200 mL. The small bowel is then divided at 2 points: 4–5 cm distal to the pylorus and 250 cm proximal to the terminal ileum. The proximal duodenal end is reconnected to the last 250 cm of small intestine, and the biliary limb is anastomosed 100 cm proximal to the terminal ileum.22,30,33 This procedure preserves the antrum, pylorus, a short segment of duodenum and vagal nerve integrity, thereby having a theoretical advantage of preserving a more physiologic digestive behaviour and diminishing the risk of dumping syndrome, ulcerogenicity and hypocalcaemia.30
Primarily restrictive procedure with some malabsorption
The RYGB is considered the “gold standard” for bariatric surgery and is the most commonly performed operation.20,30 Technically, the procedure involves creating a gastric pouch, Roux limb and biliary limb. Using surgical staplers, a small, vertically oriented gastric pouch with a volume of less than 30 cm3 is formed. The Roux and biliary limbs are created by dividing the small bowel 30–40 cm from the ligament of Trietz. Restoration of continuity occurs by connecting the distal end of the divided bowel (Roux limb) to the pouch, creating a gastrojejunostomy, and anastomosing the biliary limb about 100–150 cm distal to the gastrojejunostomy. After an RYGB, the size of the pouch restricts the volume of ingested food, and approximately 95% of the stomach, the entire duodenum and a portion of the jejunum are effectively bypassed.30
The Swedish Obesity Study is the largest, longest running prospective, nonrandomized, interventional trial that examined the effects of bariatric surgery (i.e., LAGB, VBG, RYGB) on 4047 obese patients with contemporaneously matched conventionally treated controls.34 Results demonstrated that in the surgical group there was a 23.4% decrease in weight at 2 years and a 16.1% decrease at 10 years. Conversely, there was an increase in weight in the control group at both time points (0.1% at 2 years and 1.6% at 10 years). In addition, Buchwald and colleagues19 conducted a meta-analysis on the effects of bariatric surgery on weight loss and obesity-related comorbidities. Their study demonstrated that, 2 years postoperatively, the percentage of excess weight loss was 47.5% for gastric banding, 61.6% for RYGB, 68.2% for VBG and 70.1% for BPD with or without DS (BPD±DS). The overall excess weight loss for 10 172 patients was 61.2%.
The risks of bariatric surgery were summarized in a meta-analysis that reviewed early and late mortality in 85 048 patients who underwent surgery from 478 treatment groups in 361 studies published bewteen Jan. 1, 1990, and Apr. 30, 2006.35 The results demonstrated that early mortality (i.e., ≤ 30 d) was 0.28% (95% confidence interval [CI] 0.22–0.34) in 475 treatment arms (n = 84 931); and total mortality from 30 days to 2 years was 0.35% (95% CI 0.12–0.58) in 140 treatment arms (n = 19 928).
Diabetes
The idea that bariatric surgery may “cure” diabetes has been recognized for more than 2 decades. A landmark paper by Pories and colleagues36 demonstrated that of 141 patients with diabetes or impaired glucose tolerance (IGT), all but 2 became euglycemic within 10 days after RYGB. Longer follow-up demonstrated that over 8 years, 83% of patients with preoperative T2DM and 99% of those with IGT were able to maintain normal levels of plasma glucose, HgA1C and insulin.22,37 The Swedish Obesity Study demonstrated that 2 years after surgery, 72% of patients had complete resolution of T2DM compared with 21% of control patients. Follow-up for 8 years demonstrated that the prevalence of diabetes in the surgical group remained relatively stable, whereas incidence in the control group increased from 7.8% to 24.9%.38 In an analysis of incidence,34 767 obese patients who underwent surgery were compared with 712 matched, conventionally treated controls. Results indicated that the incidence was significantly lower in the surgical group than in the control group at 2 years (0.2% v. 6.3%) and 10 years postoperatively (7% v. 24.9%).34
Meta-analysis of bariatric surgical outcomes19 demonstrated that, of studies reporting resolution of diabetes, 1417 of 1846 (76.8%) patients experienced complete resolution. Of those who reported both resolution and improvement or only improvement, 414 of 485 (85.4%) patients experienced resolution or improvement. Procedure-specific subanalysis demonstrated that the degree of diabetes resolution depended on the procedure performed. Specifically, complete resolution was observed in 98.9% of patients who underwent BPD±DS, 83.7% who underwent RYGB, 71.6% who underwent VBG and 47.9% who underwent an adjustable gastric band. However, subanalysis of studies that described both resolution and improvement did not demonstrate a similar trend, probably owing to the small sample size (n = 485).
Interestingly, the clinical resolution of diabetes via RYGB and BPD+DS, the most effective procedures, was associated with the duration and severity of the disease. Specifically, improvement of diabetes was most pronounced in patients with a milder form and shorter duration of the disease, or in patients with less central obesity as measured by waist circumference.3941 Conversely, patients whose diabetes did not resolve were usually older or had a more prolonged preoperative disease course.37,42,43
Diabetes: possible mechanism(s) of control after surgery
Rubino30 outlined 3 possible mechanisms of the effect of bariatric surgery on glucose homeostasis: the effect of weight loss, intestinal malabsorption and hormonal changes.
Weight loss, as a mechanism, may play a role in the resolution of diabetes in obese patients who undergo gastric banding.30 Indeed, Ponce and colleagues44 demonstrated that after gastric banding the rate of diabetes resolution was greater 2 years postoperatively than after the first year, and improvement correlated with the degree of weight loss. However, several studies have demonstrated a return to euglycemia and normal insulin levels within days of RYGB or BPD, changes that occur well before any significant loss in weight.37,45,46 Interestingly, restrictive techniques result in lower rates of diabetes remission than mixed procedures, suggesting that gastrointestinal tract changes after malabsorptive procedures are involved in diabetes control (48% for gastric banding v. 84% for RYGB and 98% for BPD).19 Therefore, diabetes resolution is not a result of weight loss alone.
The rationale for intestinal malabsorption as a mechanism for diabetes control is derived from the fact that both hyperglycemia and free fatty acids induce insulin resistance and β-cell dysfunction by stimulating mitochondrial production of reactive oxygen species (ROS).30,47 Therefore, in theory, by limiting the area over which nutrients are absorbed, there is less absorption of both glucose and fat, leading to a reduction in the production of ROS and improved β-cell function and insulin sensitivity. While malabsorption is clinically evident after BPD,48 it does not occur after standard RYGB,49,50 suggesting that additional factors may play a role in glucose regulation.
It has been hypothesized that rerouting food through the gastrointestinal tract leads to changes in gut hormone secretion which, in turn, may mediate the antidiabetic effect of bariatric surgery.30 Several studies have demonstrated changes in gut hormone levels after RYGB, including increased anorectic hormones that induce satiety (e.g., GLP-1, PPY) and decreased levels of orexigens like ghrelin, an appetite-stimulating hormone. Of note is the fact that GLP-1 increases the insulin response to nutrients and, in animal models, induces β-cell proliferation.51,52 Therefore, perhaps it is the postsurgical endocrine effects that mediate the antidiabetic effect of RYGB.53
Alternatively, surgical resolution of T2DM may be related to the anatomic changes associated with RYGB. To this end, Rubino30 proposed the hindgut and foregut hypotheses. The hindgut theory postulates that diabetes control is due to accelerated delivery of nutrients to the distal intestine, which boosts a “physiologic” signal (e.g., GLP-1) that improves glucose metabolism.5457 The foregut hypothesis states that excluding nutrients from the duodenum and proximal jejunum may inhibit the secretion of a signal that normally would induce insulin resistance and T2DM.58,59 Using Goto-Kakizaki rats (a nonobese Wistar substrain in which T2DM develops early in life) Rubino and colleagues60 demonstrated that a gastrojejunostomy-duodenal exclusion (GDE), a model for RYGB, improved diabetes. However, performing a simple gastrojejunostomy without the duodenal exclusion did not improve diabetes in the same animal model. In addition, glucose intolerance returned in GDE-treated animals when nutrient flow was surgically re-established through the proximal intestine despite preserving the gastrojejunostomy. Similarly, diabetes control improved in animals that originally underwent a simple gastrojejunostomy when the proximal intestine was excluded from nutrient flow, while leaving the gastrojejunostomy intact. From these studies and clinical observations, Rubino and colleagues concluded that, in individuals with diabetes, duodenal–jejunal exclusion improves glucose tolerance, characterizing T2DM as a possible duodenal–jejunal illness.
Obstructive sleep apnea: the effect of bariatric surgery
Obstructive sleep apnea (OSA) is the most prevalent subtype of sleep-disordered breathing. It consists of repetitive obstruction of the upper airway during sleep in which ineffective respiratory efforts occur.61 According to the American Academy of Sleep Medicine, OSA is present when individuals average at least 5 apneic or hypopneic events per hour. Obstructive sleep apnea is considered mild if the apnea–hypopnea index (AHI) is 5–14 events per hour, moderate if the AHI is 15–29 events per hour and severe if the AHI is 30 or more events per hour.62,63 The medical sequelae of OSA include daytime hypertension, cardiac arrhythmias, increased risk of stroke, coronary artery disease and congestive heart failure.5962 In addition, 2 population-based cohort studies confirm that untreated OSA is an independent risk factor for death.6468
An important risk factor for OSA is obesity.6972 The prevalence of OSA among obese individuals is high and correlates with increasing BMI.70,73,74 In fact, in severely obese individuals, the prevalence ranges from 55% to 100%.75,76 In addition, obese individuals often have more severe disease, as manifested by a higher AHI and lower nadir on nocturnal pulse oximetry.70,77,78 Several studies have demonstrated that weight loss, even a modest amount, can effectively manage OSA.79,80 As such, the positive effect of bariatric surgery on OSA has been repeatedly reported. Indeed, the meta-analysis by Buchwald and colleagues19 demonstrated a significant improvement in the total patient population, with resolution of OSA in 85.7% of patients.
In 2009, Greenburg and colleagues69 conducted a meta-analysis investigating the effect of bariatric surgery on OSA. The study demonstrated that bariatric surgery resulted in a mean decrease in BMI of 17.54 (from 55.28 to 37.74). This decrease was associated with a substantial improvement in the AHI. The overall effect size of the pooled, weighted data showed a reduction of 38.2 events per hour in the combined study results (from 54.7 to 15.8 events per hour), which represented a combined reduction of 71% in AHI. However, considering that the mean residual AHI was 15.78 events per hour and that an AHI of 15 or more events per hour represents moderate disease, most patients (62%) had residual disease. In fact, only 25% of patients in the 6 studies that reported individual patient data (representing 23% of all patients in the meta-analysis) were able to reach an AHI consistent with OSA resolution (< 5 events per hour). Interestingly, in logistic regression models, both younger age (odds ratio [OR] 1.08, 95% CI 1.01–1.16) and follow-up weight less than 100 kg (OR 0.18, 95% CI 0.46–0.72) independently predicted resolution of OSA.
These findings demonstrate that, while weight loss associated with bariatric surgery improved OSA, residual disease remains in most patients who, on average, are older and heavier. Symptoms of OSA may not correlate with severity (measured using polysomnographic criteria), and lack of “daytime sleepiness” does not indicate resolution of OSA.69,81,82 This is important in light of the observation that patients experiencing the benefits of surgery-induced weight loss (e.g., improved mobility, agility and physical endurance) may feel well and believe that their OSA is “cured.”81 As such, they may be reluctant to remain compliant with therapy. The clinical significance is that even moderate OSA (AHI 15–29 events per hour) can lead to cardiovascular complications of hypertension, cardiac arrhythmias, increased risk of stroke, coronary artery disease and congestive heart failure. Therefore, diagnostic sleep testing with repeat polysomnography should be pursued when a goal weight or stable weight is attained, as only follow-up polysomnography can identify patients who have achieved an AHI consistent with resolution of OSA.
Dyslipidemia: the effect of bariatric surgery
Atherogenic dyslipidemia is strongly associated with visceral obesity. It is defined as elevated triglycerides, apolipoprotein B, small low-density lipoprotein (LDL) particles, and low high-density lipoprotein (HDL) cholesterol. Dyslipidemia in association with hypertension, insulin resistance, proinflammatory/thrombotic states and visceral obesity is collectively referred to as the metabolic syndrome (MetS).75
The MetS is a cluster of risk factors for cardiovascular disease and T2DM that occur together more often than by chance alone. It is diagnosed based on the presence of any 3 of the following 5 risk factors:
  • visceral obesity/increased waist circumference, the values for which are population- and country-specific (e.g., in Canada and the United States, threshold values are ≥ 102 cm in men and ≥ 88 cm in women);
  • elevated triglycerides (> 1.7 mmol/L [> 150 mg/dL]);
  • reduced HDL cholesterol (< 1.04 mmol/L in men [< 40 mg/dL] and < 1.3 mmol/L [< 50 mg/dL] in women);
  • elevated blood pressure (systolic > 130 and/or diastolic > 85 mm Hg); and
  • elevated fasting glucose (> 5.55 mmol/L [100 mg/dL]).
Albeit debatable, of the required 3 factors, one has to include increased waist circumference.83
Alarmingly, the prevalence of MetS has been reported to be 24% in the adult population in the United States,84 the significance of which lies in the fact that it is associated with increased risk of death from coronary heart disease, cardiovascular disease or all-cause mortality. Specifically, a prospective cohort study was conducted by Malik and colleagues85 to examine the impact of MetS on coronary heart disease, cardiovascular disease and all-cause mortality. Results demonstrated that in the coronary heart disease population, those with MetS die twice as frequently (hazard ratio [HR] 2.02) and that in patients with pre-existing cardiovascular disease, those with MetS die 4 times more frequently (HR 4.19) than those without. Overall mortality was increased in patients with MetS (HR = 1.40), and in those who also had pre-existing cardiovascular disease this rate was even higher (HR 1.87). Finally, patients with even 1 or 2 MetS-related risk factors were at increased risk of death from coronary heart disease and cardiovascular disease (HR 2.10 and 1.73, respectively), although MetS predicted coronary heart disease, cardiovascular disease and total mortality more strongly than its individual components.
Several series examining the effect of bariatric surgery on dyslipidemia have reported significant improvement in lipid profiles after bariatric surgery. There are marked reductions in LDL, increased HDL and decreased triglycerides.76 In the Swedish Obesity Study,34 significant improvements were observed in triglyceride and HDL levels at 2 and 10 years in the surgical versus the control group (increased HDL: % difference 18.7%, 95% CI 20.1%–17.3% at 2 years and 13.6%, 95% CI 16.5%–10.6% at 10 years; decreased TG: % difference 29.9%, 95% CI 27.4%–32.5% at 2 years and 14.8%, 95% CI; 10.4%– 19.1% at 10 years). In the entire cohort, while total cholesterol was significantly different at 2 years (1%, 95% CI 0.1%–1.9%), there was no significant difference at 10 years. However, subgroup analysis demonstrated that in the RYGB subgroup (n = 34) total cholesterol, triglycerides and HDL were all significantly improved at 10 years (% difference 12.6%, 28% and 47.5%, respectively).
While the effect of RYGB on dyslipidemia is impressive, the Swedish Obesity Study included only 34 patients. However, its findings are supported by a retrospective study by Zlabek and colleagues,86 who examined the lipid profiles of 168 patients preoperatively and 1 and 2 years after laparoscopic RYGB. After 1 year, total cholesterol decreased by 12.5%, LDL decreased by 19.4%, HDL increased by 23.2%, triglycerides decreased by 41.2% and the percentage of dyslipidemic patients decreased from 82.3% to 28.1% (p < 0.001). In addition, 14.6% of patients were taking lipid-modifying medications postoperatively compared with 26% preoperatively (p = 0.049). After 2 years, total cholesterol decreased by 7.2%, LDL decreased by 21.7%, HDL increased by 40.3%, triglycerides decreased by 27.3% and the percentage of dyslipidemic patients decreased from 94.4% to 27.8% (p < 0.001).
In the meta-analysis by Buchwald and colleagues,19 hyperlipidemia, hypercholesterolemia and hypertrigly-ceridemia were significantly improved across all surgical procedures at 2 year follow-up. The percentage of patients whose conditions improved was typically 70% or higher, with maximum improvements in hyperlipidemia in the BPD-DS (99.1%, 95% CI 97.6%–100%) and RYGB groups (96.9%, 95% CI 93.6%–100%). In the total population, there was a significant decrease in total cholesterol (mean change 0.86 mmol/L [33.20 mg/dL], 95% CI 0.6–1.13 mmol/L [23.17–43.63 mg/dL], n = 2573), LDL (mean change 0.76 mmol/L [29.34 mg/dL], 95% CI 0.46–1.06 mmol/L [17.76–40.93 mg/dL], n = 879) and triglycerides (mean change 0.9 mmol/L [79.65 mg/dL], 95% CI 0.73–1.08 mmol/L [64.60–95.58 mg/dL], n = 2149). Although the total population did not demonstrate a significant increase in HDL, significant improvements were seen in the RYGB (mean change 0.12 mmol/L [4.63 mg/dL], 95% CI 0.04–0.2 mmol/L [1.54–7.72 mg/dL], n = 623) and VBG groups (mean change 0.13 mmol/L [5.02 mg/dL], 95% CI 0.02–0.24 mmol/L [0.77–9.27 mg/dL], n = 253). Taken together, these studies suggest that bariatric surgery not only allows for sustained weight loss, but is a viable treatment option for correcting dyslipidemia in morbidly obese individuals.
Hypertension: the effect of bariatric surgery on systolic, diastolic and pulse pressure
Obesity is a major risk factor for hypertension, and there is ample epidemiological evidence supporting the association between increased weight and increased blood pressure.8790 In addition, many studies have demonstrated that weight loss lowers blood pressure.91,92 In general, a decrease of 1% in body weight leads to a 1 mm Hg decrease in systolic blood pressure and a 2 mm Hg decrease in diastolic blood pressure.9395
As previously detailed, bariatric surgery has a dramatic effect on sustained weight loss. Therefore, by extension, bariatric surgery should decrease blood pressure. Indeed, Buchwald and colleagues19 showed a significant reduction in hypertension in the total patient population and across all surgical procedures. In particular, the percentages of patients in the total population whose hypertension resolved or improved were 61.7% and 78.5%, respectively. Interestingly, these results were obtained up to 2 years postoperatively, but were not sustained at longer time points.
The Swedish Obese Study38 examined the effect of obesity on hypertension by analyzing the 8-year incidence of hypertension in obese patients treated with bariatric surgery (VGB, GB and RYGB, n = 346), versus matched severely obese controls (n = 346). The results demonstrated that over 8 years, while there was a significant decrease in body weight in the surgical compared with the control group (120.4 [standard deviation (SD) 16.0] kg to 100.3 [SD 17.8] kg v. 114.7 [SD 17.8] kg to 115.4 [SD 19.2] kg), there was no difference in systolic blood pressure. Specifically, over the first 6 months, a period of rapid weight loss in the surgical group, systolic blood pressure decreased by 11.4 (SD 19.0) mm Hg and diastolic blood pressure decreased by 7.0 (SD 11.0) mm Hg. Over the following 6 months, when weight loss occurred at a slower rate, systolic blood pressure increased, and the reduction in diastolic blood pressure stopped. Therefore, from the first year to the eighth year, there was a gradual increase in both systolic and diastolic blood pressure. In the control group, there was a gradual increase in systolic blood pressure (5.5 [SD 19.0] mm Hg, p = 0.001) over 8 years, but a reduction in diastolic blood pressure (2.2 [SD 10.5] mm Hg, p = 0.002). Consequently there was no difference in systolic blood pressure between the surgical and control groups after 8 years. Therefore, although the 2-year incidence of hypertension was lower in the surgical arm (3.2% v. 9.9%, p = 0.032), there was no difference after 8 years (26.4% v. 25.8%, p = 0.91), suggesting that not even a maintained 16% weight loss was sufficient to achieve a reduction of the 8-year incidence of hypertension in severely obese patients. Of interest, subgroup analysis demonstrated that in patients treated with RYGB, there was a decrease in systolic and diastolic blood pressure at 10 years (4.7% and 10.4%, respectively, both p < 0.10).34
To further understand these results, the authors analyzed the change in weight to find a relationship between weight and blood pressure. Over 7 years, the surgical group regained 11.1 (SD 13.1) kg, and patients were subdivided into above median or below median groups. Subsequently, when the effect of weight regain was analyzed, the study showed that a larger relapse in body weight was associated with a larger regain in blood pressure (systolic blood pressure increased by 14.7 [SD 21] mm Hg in the above median group and 8.4 [SD 21] mm Hg in the below median group, p = 0.018; diastolic blood pressure increased by 7.3 [SD 12] and 2.9 [SD 11] mm Hg in the above median and below median groups, respectively, p = 0.004).38
These results suggest that the direction of ongoing weight change is more closely related to blood pressure than the initial body weight. However, change in weight aside, Sjöström and colleagues96 postulated that time/aging may also play a role. As such, they performed a post hoc analysis to separate the effect of aging from the effect of weight change per unit of time. Both the surgical and control groups were divided into 5 time groups based on follow-up (i.e., 3, 4, 6, 8 or 10 years of follow-up). In addition, for both groups, 5 independent variables were analyzed in relation to final blood pressure to separate the effects of weight change per year from the effect of time:
  • inclusion weight,
  • weight change (usually weight loss) during the first year (period I),
  • weight change per year between the end of the first year and the second to last observation (period II),
  • weight change per year between the second to last observation and the last observation (period III), and
  • time between the intervention and the last observation.
The results demonstrated that blood pressure at the last examination was more closely related to time (aging) and ongoing weight change than to initial body weight and initial weight loss. In addition, in the surgical group, the effect on blood pressure of 1 elapsed year was 2.5–4 times greater than the effect of 1 kg regained.
Interestingly, as noted previously,38,96 while systolic blood pressure increased in both groups, diastolic blood pressure decreased in the control group but increased in the surgical group. Therefore, given that elevated pulse pressure is associated with increased risk of coronary artery disease,9799 an analysis of bariatric surgery on pulse pressure was undertaken. In particular, given systolic blood pressure increases over a person’s lifespan and diastolic blood pressure decreases at a rate of 1–2 mm Hg per decade after 60 years of age,100,101 a rapid increase in pulse pressure is expected after the age of 60. As such, Sjöström and colleagues96 examined whether the increase in pulse pressure could be detected earlier in obese individuals and whether it could be decreased by gastric surgery. Their results demonstrated that the decrease in diastolic blood pressure was observed 10 years earlier in weight-stable severely obese controls (i.e., 49 years old at inclusion) and decreased at a rate of 3.2 mm Hg after a mean follow-up of 5.5 years (compared with 1–2 mm Hg every 10 years after 60 years of age in nonobese patients). In addition, pulse pressure increased faster in the control than the surgical group. Specifically, examining the change in blood pressure from inclusion to last observation, there was no difference in systolic blood pressure between the 2 groups (surgery: 1.4 mm Hg, 95% CI 0.4–2.4; control: 1.6 mm Hg, 95% CI 0.6–2.7), but there was a significant difference in diastolic blood pressure (surgery: −1.5 mm Hg, 95% CI −2.1 to −0.9; control: −3.2 mm Hg, 95% CI −3.8 to −2.5; p < 0.001). This resulted in a significant difference in pulse pressure (surgery: 2.9, 95% CI 2.1–3.7; control = 4.7, 95% CI 3.9–5.6; p < 0.001), suggesting that a maintained large weight reduction reduces the rate of increase in pulse pressure seen in weight-stable severely obese patients.
These results indicate that the effect of obesity and surgically induced weight loss on blood pressure is not a simple relationship. Although obesity is associated with increased risk of hypertension, many obese individuals are not hypertensive.102 Indeed, reviews of smaller surgical series have shown that normotensive or mildly hypertensive obese individuals do not achieve a significant reduction in blood pressure after gastric bypass compared with individuals with substantially elevated blood pressure.92 Therefore, while surgically induced, sustained weight loss does not seem to have a beneficial effect on blood pressure, it does lower pulse pressure which, as mentioned, is an independent predictor of coronary artery disease and cardiovascular mortality.9799
Obesity has a profound effect on blood pressure; total, LDL and HDL cholesterol; and T2DM, which are all risk factors associated with coronary heart disease. Given that coronary heart disease is a leading cause of mortality in adults in the United States103 and that bariatric surgery results in a substantial improvement in coronary heart disease risk factors, the effect of bariatric surgery on the projected risk for coronary heart disease has been evaluated by several authors.104,105 Using the Framingham risk score to estimate the postoperative reduction in 10-year risk for coronary heart disease, Vogel and colleagues104 demonstrated that the risk of coronary heart disease decreased by 39% in men and 25% in women, with an overall decrease in predicted 10-year risk for coronary heart disease from 6% (SD 5%) and 4% (SD 3%), respectively (p < 0.001). In addition, subgroup analysis demonstrated that for those without coronary heart disease, men compared favourably with the age-matched general population, with a final 10-year risk of 5% (SD 4%) versus an expected risk of 11% (SD 6%; p < 0.001). Likewise, women achieved a level below the age-adjusted expected 10-year risk in the general population, with a final risk of 3% (SD 3%) versus 6% (SD 4%; p < 0.001).
Taken together, when the individual effects of bariatric surgery on obesity-related comorbidities are integrated, it results in a profound decrease in risk for coronary heart disease and overall mortality. In addition, given the low risk of surgery itself,35 bariatric surgery has become is a powerful treatment option to help control the obesity epidemic.
Footnotes
Competing interests: None declared.
Contributors: S.F. Noria acquired the data and wrote the article. T. Grantcharov reviewed the article. Both authors participated in designing the review and approved the article’s publication.
1. Obesity and overweight Fact Sheet No. 311. Geneva (Switzerland): World Health Organization; Mar, 2011. [accessed 2012 Oct. 3]. Available: www.who.int/mediacentre/factsheets/fs311/en/print.html.
2. Kaila B, Raman M. Obesity: a review of pathogenesis and management strategies. Can J Gastroenterol. 2008;22:61–8. [PMC free article] [PubMed]
3. The practical guide Identification, evaluation, and treatment of overweight and obesity in adults NIH Publication Number 00-4084. Bethesda (MD): NHLBI Obesity Education Initiative; National Institutes of Health; National Heart, Lung, and Blood Institute; North American Association for the Study of Obesity; Oct, 2000. [accessed 2012 Oct. 3]. Available: www.nhlbi.nih.gov/guidelines/obesity/prctgd_c.pdf.
4. Ogden CL. Disparities in obesity prevalence in the United States: black women at risk. Am J Clin Nutr. 2009;89:1001–2. [PubMed]
5. Ogden CL, Carroll MD, Curtin LR, et al. Prevalence of overweight and obesity in the United States, 1999–2004. JAMA. 2006;295:1549–55. [PubMed]
6. Ogden CL, Carroll MD, McDowell MA, et al. NCHS Data Brief No. 1. Washington: US Department of Health & Human Services; 2007. [accessed 2012 Oct. 3]. Obesity among adults in the United States — no statistically significant change since 2003–2004. Available: www.cdc.gov/nchs/data/databriefs/db01.pdf.
7. Bessesen DH. Update on obesity. J Clin Endocrinol Metab. 2008;93:2027–34. [PubMed]
8. The Daily. Otatawa (ON): Statistics Canada; 2004. [accessed 2012 Oct. 3]. Canadian Community Health Survey: Obesity among children and adults. Available: www.statcan.gc.ca/daily-quotidien/050706/dq050706a-eng.htm.
9. Birmingham CL, Muller JL, Palepu A, et al. The cost of obesity in Canada. CMAJ. 1999;160:483–8. [PMC free article] [PubMed]
10. About obesity. London (UK): International Association for the Study of Obesity; 2002. [accessed 2012 Oct. 3]. Available: www.iaso.org/policy/aboutobesity/
11. Must A, Spadano J, Coakley EH, et al. The disease burden associated with overweight and obesity. JAMA. 1999;282:1523–9. [PubMed]
12. Overweight, obesity, and health risk. National Task Force on the Prevention and Treatment of Obesity. Arch Intern Med. 2000;160:898–904. [PubMed]
13. Fontaine KR, Redden DT, Wang C, et al. Years of life lost due to obesity. JAMA. 2003;289:187–93. [PubMed]
14. Adams KF, Schatzkin A, Harris TB, et al. Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old. N Engl J Med. 2006;355:763–78. [PubMed]
15. Serdula MK, Mokdad AH, Williamson DF, et al. Prevalence of attempting weight loss and strategies for controlling weight. JAMA. 1999;282:1353–8. [PubMed]
16. NIH conference. Gastrointestinal surgery for severe obesity. Consensus Development Conference Panel. Ann Intern Med. 1991;115:956–61. [PubMed]
17. Gastrointestinal surgery for severe obesity. Am J Clin Nutr; Proceedings of a National Institutes of Health Consensus Development Conference; March 25–27, 1991. Bethesda, MD; 1992. pp. 487S–619S. [PubMed]
18. Parker M, Loewen M, Sullivan T, et al. Predictors of outcome after obesity surgery in New York state from 1991 to 2003. Surg Endosc. 2007;21:1482–6. [PubMed]
19. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292:1724–37. [PubMed]
20. Steinbrook R. Surgery for severe obesity. N Engl J Med. 2004;350:1075–9. [PubMed]
21. Colquitt JL, Picot J, Loveman E, et al. Surgery for obesity. Cochrane Database Syst Rev. 2009;(2):CD003641. [PubMed]
22. Herron DM, Tong W. Role of surgery in management of type 2 diabetes mellitus. Mt Sinai J Med. 2009;76:281–93. [PubMed]
23. Parikh MS, Fielding GA, Ren CJ. US experience with 749 laparoscopic adjustable gastric bands: intermediate outcomes. Surg Endosc. 2005;19:1631–5. [PubMed]
24. Gagner M, Deitel M, Kalberer TL, et al. The Second International Consensus Summit for Sleeve Gastrectomy, March 19–21, 2009. Surg Obes Relat Dis. 2009;5:476–85. [PubMed]
25. Hess DS, Hess DW. Biliopancreatic diversion with a duodenal switch. Obes Surg. 1998;8:267–82. [PubMed]
26. Regan JP, Inabnet WB, Gagner M, et al. Early experience with two-stage laparoscopic Roux-en-Y gastric bypass as an alternative in the super-super obese patient. Obes Surg. 2003;13:861–4. [PubMed]
27. Almogy G, Crookes PF, Anthone GJ. Longitudinal gastrectomy as a treatment for the high-risk super-obese patient. Obes Surg. 2004;14:492–7. [PubMed]
28. Lee CM, Cirangle PT, Jossart GH. Vertical gastrectomy for morbid obesity in 216 patients: report of 2-year results. Surg Endosc. 2007;21:1810–6. [PubMed]
29. Hutter MM, Schirmer BD, Jones DB, et al. First Report from the American College of Surgeons Bariatric Surgery Center Network: Laparoscopic sleeve gastrectomy has morbidity and effectiveness positioned between the band and the bypass. Ann Surg. 2011;254:410–20. [PMC free article] [PubMed]
30. Rubino F. Bariatric surgery: effects on glucose homeostasis. Curr Opin Clin Nutr Metab Care. 2006;9:497–507. [PubMed]
31. McFarland RJ, Gazet JC, Pilkington TR. A 13-year review of jejunoileal bypass. Br J Surg. 1985;72:81–7. [PubMed]
32. Baddeley RM. The management of gross refractory obesity by jejunoileal bypass. Br J Surg. 1979;66:525–32. [PubMed]
33. Hess DS. Biliopancreatic diversion with duodenal switch. Surg Obes Relat Dis. 2005;1:329–33. [PubMed]
34. Sjöström L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med. 2004;351:2683–93. [PubMed]
35. Buchwald H, Estok R, Fahrbach K, et al. Trends in mortality in bariatric surgery: a systematic review and meta-analysis. Surgery. 2007;142:621–32. discussion 632–5. [PubMed]
36. Pories WJ, Caro JF, Flickinger EG, et al. The control of diabetes mellitus (NIDDM) in the morbidly obese with the Greenville Gastric Bypass. Ann Surg. 1987;206:316–23. [PubMed]
37. Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222:339–50. discussion 350–2. [PubMed]
38. Sjöström CD, Peltonen M, Wedel H, et al. Differentiated long-term effects of intentional weight loss on diabetes and hypertension. Hypertension. 2000;36:20–5. [PubMed]
39. Schauer PR, Burguera B, Ikramuddin S, et al. Effect of laparoscopic Roux-en Y gastric bypass on type 2 diabetes mellitus. Ann Surg. 2003;238:467–84. discussion 84–5. [PubMed]
40. Torquati A, Lutfi R, Abumrad N, et al. Is Roux-en-Y gastric bypass surgery the most effective treatment for type 2 diabetes mellitus in morbidly obese patients? J Gastrointest Surg. 2005;9:1112–6. discussion 1117–8. [PubMed]
41. Scopinaro N, Papadia F, Camerini G, et al. A comparison of a personal series of biliopancreatic diversion and literature data on gastric bypass help to explain the mechanisms of resolution of type 2 diabetes by the two operations. Obes Surg. 2008;18:1035–8. [PubMed]
42. Sugerman HJ, Wolfe LG, Sica DA, et al. Diabetes and hypertension in severe obesity and effects of gastric bypass-induced weight loss. Ann Surg. 2003;237:751–6. discussion 757–8. [PubMed]
43. Pories WJ, MacDonald KG, Jr, Flickinger EG, et al. Is type II diabetes mellitus (NIDDM) a surgical disease? Ann Surg. 1992;215:633–42. discussion 643. [PubMed]
44. Ponce J, Haynes B, Paynter S, et al. Effect of Lap-Band-induced weight loss on type 2 diabetes mellitus and hypertension. Obes Surg. 2004;14:1335–42. [PubMed]
45. Hickey MS, Pories WJ, MacDonald KG, Jr, et al. A new paradigm for type 2 diabetes mellitus: Could it be a disease of the foregut? Ann Surg. 1998;227:637–43. discussion 643–4. [PubMed]
46. Scopinaro N, Adami GF, Marinari GM, et al. Biliopancreatic diversion. World J Surg. 1998;22:936–46. [PubMed]
47. Evans JL, Goldfine ID, Maddux BA, et al. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev. 2002;23:599–622. [PubMed]
48. Marceau P, Hould FS, Simard S, et al. Biliopancreatic diversion with duodenal switch. World J Surg. 1998;22:947–54. [PubMed]
49. Brolin RE, LaMarca LB, Kenler HA, et al. Malabsorptive gastric bypass in patients with superobesity. J Gastrointest Surg. 2002;6:195–203. discussion 204–5. [PubMed]
50. MacLean LD, Rhode BM, Nohr CW. Long- or short-limb gastric bypass? J Gastrointest Surg. 2001;5:525–30. [PubMed]
51. Pournaras DJ, le Roux CW. Obesity, gut hormones, and bariatric surgery. World J Surg. 2009;33:1983–8. [PubMed]
52. Drucker DJ. Glucagon-like peptides: regulators of cell proliferation, differentiation, and apoptosis. Mol Endocrinol. 2003;17:161–71. [PubMed]
53. Ashrafian H, le Roux CW. Metabolic surgery and gut hormones — a review of bariatric entero-humoral modulation. Physiol Behav. 2009;97:620–31. [PubMed]
54. Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypass for obesity: mechanisms of weight loss and diabetes resolution. J Clin Endocrinol Metab. 2004;89:2608–15. [PubMed]
55. Mason EE. The mechanisms of surgical treatment of type 2 diabetes. Obes Surg. 2005;15:459–61. [PubMed]
56. Patriti A, Facchiano E, Sanna A, et al. The enteroinsular axis and the recovery from type 2 diabetes after bariatric surgery. Obes Surg. 2004;14:840–8. [PubMed]
57. Mason EE. Ileal [correction of ilial] transposition and enteroglucagon/GLP-1 in obesity (and diabetic?) surgery. Obes Surg. 1999;9:223–8. [PubMed]
58. Pories WJ, Albrecht RJ. Etiology of type II diabetes mellitus: role of the foregut. World J Surg. 2001;25:527–31. [PubMed]
59. Rubino F, Gagner M. Potential of surgery for curing type 2 diabetes mellitus. Ann Surg. 2002;236:554–9. [PubMed]
60. Rubino F, Forgione A, Cummings DE, et al. The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg. 2006;244:741–9. [PubMed]
61. Cutler MJ, Hamdan AL, Hamdan MH, et al. Sleep apnea: from the nose to the heart. J Am Board Fam Pract. 2002;15:128–41. [PubMed]
62. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep. 1999;22:667–89. [PubMed]
63. Kushida CA, Littner MR, Morgenthaler T, et al. Practice parameters for the indications for polysomnography and related procedures: an update for 2005. Sleep. 2005;28:499–521. [PubMed]
64. Silverberg DS, Oksenberg A, Iaina A. Sleep related breathing disorders are common contributing factors to the production of essential hypertension but are neglected, underdiagnosed, and undertreated. Am J Hypertens. 1997;10:1319–25. [PubMed]
65. Palomäki H. Snoring and the risk of ischemic brain infarction. Stroke. 1991;22:1021–5. [PubMed]
66. Partinen M, Guilleminault C. Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. Chest. 1990;97:27–32. [PubMed]
67. Bradley TD. Right and left ventricular functional impairment and sleep apnea. Clin Chest Med. 1992;13:459–79. [PubMed]
68. Marshall NS, Wong KK, Liu PY, et al. Sleep apnea as an independent risk factor for all-cause mortality: the Busselton Health Study. Sleep. 2008;31:1079–85. [PubMed]
69. Greenburg DL, Lettieri CJ, Eliasson AH. Effects of surgical weight loss on measures of obstructive sleep apnea: a meta-analysis. Am J Med. 2009;122:535–42. [PubMed]
70. Rajala R, Partinen M, Sane T, et al. Obstructive sleep apnoea syndrome in morbidly obese patients. J Intern Med. 1991;230:125–9. [PubMed]
71. O’Keeffe T, Patterson EJ. Evidence supporting routine polysomnography before bariatric surgery. Obes Surg. 2004;14:23–6. [PubMed]
72. Lettieri CJ, Eliasson AH, Andrada T, et al. Obstructive sleep apnea syndrome: Are we missing an at-risk population? J Clin Sleep Med. 2005;1:381–5. [PubMed]
73. Hiestand DM, Britz P, Goldman M, et al. Prevalence of symptoms and risk of sleep apnea in the US population: results from the national sleep foundation sleep in America 2005 poll. Chest. 2006;130:780–6. [PubMed]
74. Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163:19–25. [PubMed]
75. Chan DC, Barrett HP, Watts GF. Dyslipidemia in visceral obesity: mechanisms, implications, and therapy. Am J Cardiovasc Drugs. 2004;4:227–46. [PubMed]
76. Bouldin MJ, Ross LA, Sumrall CD, et al. The effect of obesity surgery on obesity comorbidity. Am J Med Sci. 2006;331:183–93. [PubMed]
77. Frey WC, Pilcher J. Obstructive sleep-related breathing disorders in patients evaluated for bariatric surgery. Obes Surg. 2003;13:676–83. [PubMed]
78. Malhotra A, White DP. Obstructive sleep apnoea. Lancet. 2002;360:237–45. [PubMed]
79. Summers CL, Stradling JR, Baddeley RM. Treatment of sleep apnoea by vertical gastroplasty. Br J Surg. 1990;77:1271–2. [PubMed]
80. Peppard PE, Young T, Palta M, et al. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. 2000;284:3015–21. [PubMed]
81. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 2008;31:1071–8. [PubMed]
82. Dixon JB, Dixon ME, Anderson ML, et al. Daytime sleepiness in the obese: not as simple as obstructive sleep apnea. Obesity (Silver Spring) 2007;15:2504–11. [PubMed]
83. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–5. [PubMed]
84. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002;287:356–9. [PubMed]
85. Malik S, Wong ND, Franklin SS, et al. Impact of the metabolic syndrome on mortality from coronary heart disease, cardiovascular disease, and all causes in United States adults. Circulation. 2004;110:1245–50. [PubMed]
86. Zlabek JA, Grimm MS, Larson CJ, et al. The effect of laparoscopic gastric bypass surgery on dyslipidemia in severely obese patients. Surg Obes Relat Dis. 2005;1:537–42. [PubMed]
87. Dyer AR, Elliott P, Shipley M. Body mass index versus height and weight in relation to blood pressure. Findings for the 10,079 persons in the INTERSALT Study. Am J Epidemiol. 1990;131:589–96. [PubMed]
88. Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988–2000. JAMA. 2003;290:199–206. [PubMed]
89. Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA. 2003;289:76–9. [PubMed]
90. Gelber RP, Gaziano JM, Manson JE, et al. A prospective study of body mass index and the risk of developing hypertension in men. Am J Hypertens. 2007;20:370–7. [PMC free article] [PubMed]
91. Neter JE, Stam BE, Kok FJ, et al. Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2003;42:878–84. [PubMed]
92. Aucott L, Poobalan A, Smith WC, et al. Effects of weight loss in overweight/obese individuals and long-term hypertension outcomes: a systematic review. Hypertension. 2005;45:1035–41. [PubMed]
93. Dornfeld LP, Maxwell MH, Waks AU, et al. Obesity and hypertension: long-term effects of weight reduction on blood pressure. Int J Obes. 1985;9:381–9. [PubMed]
94. The Hypertension Prevention Trial: three-year effects of dietary changes on blood pressure. Hypertension Prevention Trial Research Group. Arch Intern Med. 1990;150:153–62. [PubMed]
95. Reisin E, Frohlich ED. Effects of weight reduction on arterial pressure. J Chronic Dis. 1982;35:887–91. [PubMed]
96. Sjöström CD, Peltonen M, Sjostrom L. Blood pressure and pulse pressure during long-term weight loss in the obese: the Swedish Obese Subjects (SOS) Intervention Study. Obes Res. 2001;9:188–95. [PubMed]
97. Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham heart study. Circulation. 1999;100:354–60. [PubMed]
98. Benetos A, Rudnichi A, Safar M, et al. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension. 1998;32:560–4. [PubMed]
99. Lee ML, Rosner BA, Weiss ST. Relationship of blood pressure to cardiovascular death: the effects of pulse pressure in the elderly. Ann Epidemiol. 1999;9:101–7. [PubMed]
100. Lee ML, Rosner BA, Vokonas PS, et al. Longitudinal analysis of adult male blood pressure: the Normative Aging Study, 1963–1992. J Epidemiol Biostat. 1996;1:79–87.
101. Franklin SS, Gustin W, 4th, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation. 1997;96:308–15. [PubMed]
102. Alexander JK, Amad KH, Cole VW. Observations on some clinical features of extreme obesity, with particular reference to cardiorespiratory effects. Am J Med. 1962;32:512–24.
103. Anderson RN, Smith BL. Deaths: leading causes for 2002. Natl Vital Stat Rep. 2005;53:1–89. [PubMed]
104. Vogel JA, Franklin BA, Zalesin KC, et al. Reduction in predicted coronary heart disease risk after substantial weight reduction after bariatric surgery. Am J Cardiol. 2007;99:222–6. [PubMed]
105. Kligman MD, Dexter DJ, Omer S, et al. Shrinking cardiovascular risk through bariatric surgery: application of Framingham risk score in gastric bypass. Surgery. 2008;143:533–8. [PubMed]
106. Cottam D, Qureshi FG, Mattar SG, et al. Laparoscopic sleeve gastrectomy as an initial weight-loss procedure for high-risk patients with morbid obesity. Surg Endosc. 2006;20:859–63. [PubMed]
107. Akkary E, Duffy A, Bell R. Deciphering the sleeve: technique, indications, efficacy, and safety of sleeve gastrectomy. Obes Surg. 2008;18:1323–9. [PubMed]
108. Larrad-Jiménez A, Diaz-Guerra CS, de Cuadros Borrajo P, et al. Short-, mid- and long-term results of Larrad biliopancreatic diversion. Obes Surg. 2007;17:202–10. [PubMed]
109. Allen JW. Laparoscopic gastric band complications. Med Clin North Am. 2007;91:485–97. [PubMed]
110. Hocking MP, Duerson MC, O’Leary JP, et al. Jejunoileal bypass for morbid obesity. Late follow-up in 100 cases. N Engl J Med. 1983;308:995–9. [PubMed]
111. Gracia JA, Martinez M, Aguilella V, et al. Postoperative morbidity of biliopancreatic diversion depending on common limb length. Obes Surg. 2007;17:1306–11. [PubMed]
112. Lalor PF, Tucker ON, Szomstein S, et al. Complications after laparoscopic sleeve gastrectomy. Surg Obes Relat Dis. 2008;4:33–8. [PubMed]
113. Gumbs AA, Gagner M, Dakin G, et al. Sleeve gastrectomy for morbid obesity. Obes Surg. 2007;17:962–9. [PubMed]
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