Introduction
Obesity, defined as the accumulation of excessive body fat, might have serious physical and psychological health consequences and lead to premature death.1 The body mass index (BMI) - weight in kilograms divided by the height in meters squared - provides an estimate of total body fat, although it has a number of limitations.2,3 It overestimates the degree of obesity in individuals who are very muscular. It is also of limited utility in pregnancy, and in the elderly it is more useful as a measure of underweight than overweight.3 For children and adolescents (2-18 years), age and sex-specific BMI-thresholds are used to define obesity.2 Based on BMI, obesity is divided into four classes. Class 1 or mild obesity is a BMI = 30-34.9 kg/m2, class 2 or moderate obesity is a BMI = 35-39.9 kg/m2, class 3 or morbid or severe obesity is a BMI = 40-49.9 kg/m2, and class 4 or super morbid obesity is a BMI >= 50 kg/m2.2,4 In some ethnic groups, the equivalent health risks occur at a lower BMI. For example, Asians and Aboriginals are considered to be overweight at a BMI greater than 23 kg/m2.2 Whatever the case, there is no controversy about the definition of severe obesity, and the comorbidities, often serious, are easily identifiable.
Impact of obesity on health
Studies have generally reported a linear or curvilinear relationship between BMI and mortality risk in adults starting as low as 22 kg/m2.2 Even mild degrees of obesity have adverse health outcomes and are associated with diminished longevity.3,5-10 Obesity is associated with type 2 diabetes mellitus (T2DM), hypertension, cardiovascular disease, obstructive sleep apnoea, reproductive and lower urinary tract disorders, various malignancies, osteoarthritis, gastro-oesophageal reflux, liver disease and gallstones.2,4,11 The risk of developing one or more and the severity of these disorders increases almost linearly in relation to the degree of obesity.2 Psychosocial effects include impaired body image, reduced acceptance from colleagues, employment discrimination and, not mobility, as a result of severe obesity, compound of the psychosocial consequences. Moreover the very severely obese might find difficulty in accessing adequate medical care because of the limitations of wheel chairs, beds, operating theatre tables and inability to fit standard imaging equipment.12 The life expectancy of a severely obese person is reduced by an estimated 5-20 years.13,14 Obesity represents one of the major causes of preventable death.7,15,16
Prevalence and costs
Obesity is now a global epidemic with increasing prevalence in both developed and developing countries.4,17,18 In Australia, in 2005, 3.24 million adults were estimated to be obese - 1.52 million, male (15.1%) and 1.72 million, female (16.8%).2 In South Australia, during the period 1991-2006, class 3 obesity increased by over 400% (0.6-3.3%); this was by far the greatest increase in obesity prevalence in any category.19 A similar trend is being seen in the USA.20
In the USA, in 2000, direct healthcare costs attributed to obesity were in excess of $US56 billion, and while class 3 obesity accounted for 3% of overall obesity prevalence, it resulted in approximately 20% of the total expenditures.21 In Australia, the total financial cost of obesity in 2005 was estimated at $A3.767 billion, with $A1.73 billion (45%) attributable to productivity losses, $A873 million (23%) because of direct healthcare costs and $A804 million (21%) because of carer costs. The net cost of lost well-being was $A17.2 billion, bringing the total cost of obesity in Australia, in 2005 to $A21 billion.2 In Australia, in 2005, the healthcare cost of obesity-related comorbidities was calculated to be $A116.1 million, $A428.3 million, $A221.3 million and $A107.3 million attributable to T2DM, cardiovascular disease, osteoarthritis and malignancies respectively.2 The indirect healthcare cost because of obesity-related comorbidities was far greater than the direct cost to the health system with greater than $A1 billion, $A962 million, $A633 million and $A221.5 million attributable to T2DM, cardiovascular disease, osteoarthritis and malignancies respectively.2
Management of obesity
Broadly, weight loss strategies are divided into those with primarily a lifestyle management approach and those with a surgical approach, which should, but does not always, include a robust lifestyle component.4,11,18,22 Lifestyle management includes strategies, such as diet, exercise, behaviour and variably the addition of pharmacotherapy.4,18,22 Surgical treatment (i.e. bariatric surgery) is, at the current time, the only management strategy that reliably results in both substantial and sustainable loss of weight.1,11,17,18,22
Conventional management of obesity
In virtually all studies of dietary, therapy there is weight regain after a period of weight loss, and sustained weight loss is very rare.18 Low-calorie diets (3360-6300 J/day) and very-low-calorie diets (<3360 J/day) achieve weight loss by reducing energy intake below energy expenditure. Low-calorie diets can reduce bodyweight by an average of 8% over a 6-month period.22 Very-low-calorie diets result in a greater weight reduction of 15-25% after 3-6 months, but long-term results are modest with 9% weight reduction after 1 year and 5% after 4 years.23
Physical activity alone achieves only modest weight loss which is at best 2-3% of bodyweight,22,24 and it is more effective and arguably essential for the maintenance of weight loss.18,25 Combination strategies using diet, exercise and behaviour therapy have been shown to be more effective in the short term than either diet or exercise alone.22 An intensive intervention, such as the Diabetes Prevention Program, resulted in a mean weight loss of 4.1 kg in the 60% of subjects for whom follow up was available after 3.2 years.26
Current options for pharmacotherapy are limited by efficacy, compliance, cost and side-effect profiles. Weight loss pharmacotherapy is of greatest utility for the maintenance of weight loss, but only so long as drug use continues. Over a period of 4-5 years, orlistat has an acceptable side-effect profile with augmented weight loss and the prevention of T2DM resulting from lifestyle measures. The data from 5-year outcome studies using sibutramine and rimonabant are awaited.27
Bariatric surgery
In 1991, the National Institutes of Health Consensus Development Panel outlined that bariatric surgery is indicated when the BMI > 40 kg/m2 or when the BMI > 35 kg/m2 in the presence of high-risk comorbid conditions.28 Bariatric surgery might be of a restrictive or malabsorptive nature, or both.11,22 Restrictive procedures cause early satiety by creation of a small gastric pouch which leads to decreased caloric intake and prolong satiety by creation of a small outlet from the pouch.22 Examples include the laparoscopic adjustable gastric band (LAGB) and the vertical banded gastroplasty (VBG).22 Significant dietary compliance is required as the intake of high-calorie liquids or soft foods are not inhibited and will result in failure to weight lose.22 Benefits include technical simplicity with no anastomoses or bypasses of any part of the intestinal tract, and therefore nutritional deficiencies are rare.22 Disadvantages include less weight loss compared with malabsorptive procedures and more late failures because of pouch dilatation, technical problems related to the band or maladaptive eating behaviour.22 Malabsorptive procedures induce decreased absorption of nutrients by shortening the functional length of the small intestine, thereby inducing negative energy balance and subsequent weight loss.29 Examples include jejunoileal bypass which is no longer carried out because of substantial complications and bilio-pancreatic diversion (BPD) with or without duodenal switch. Benefits include significant weight loss when compared with restrictive procedures, and the weight loss is less dependent on dietary compliance; this is offset by significant metabolic and nutritional complications.11,22 The Roux-en-Y gastric bypass (RYGB) has both a restrictive and a malabsorptive component. A small gastric pouch restricts oral intake, and the small bowel reconfiguration assists weight loss by mild malabsorption.11,22
Effects of bariatric surgery on weight
On average, bariatric surgery results in a total weight loss of 20-40 kg and a 10-15 kg/m2 reduction in BMI.30,31 Exact percentages vary across the studies, but the overall pattern is consistent with the highest excess weight loss (75-80%) achieved with BPD, followed by RYGB (60-70%) and the least (44-68%) with restrictive surgical procedures (VBG or LAGB).32 The Swedish Obesity Study (SOS), in which 2010 obese subjects (BMI > 34 kg/m2 in men and BMI > 38 kg/m2 in women) who self-selected themselves into one of three surgical intervention groups (VBG, 1369 subjects; Band, 376 subjects; RYGB, 265 subjects) were compared with a lifestyle management group (2037 subjects), is the only prospective controlled surgical interventional trial. After 15 years, total weight loss was highest (32%) in the RYGB group, 25% in the VBG group and the least (20%) in the group in which a band was used, although this was not the same as the adjustable band currently in widespread use.33 Nevertheless, comparable data from a randomised trial of 100 patients showed that excess weight loss at 3 years was 58.9% versus 39% in response to the VBG and LAGB respectively.34 In two randomised clinical trials collectively enrolling 231 patients, patients assigned to the RYGB had more substantial weight loss compared with those in the VBG group: 42.43 kg versus 34.45 kg at 12 months and 39.73 kg versus 30.65 kg at 36 months.30,35,36 The BPD which results in the greatest weight loss is also accompanied by the highest complication rate and thus is neither widely used nor studied in clinical trials.17
Effects of bariatric surgery on obesity-related comorbidities
Bariatric surgery results in substantial weight loss accompanied by improved quality of life and amelioration of comorbidities in patients with morbid obesity.32 A meta-analysis of observational studies showed that bariatric surgery led to the resolution of T2DM in 76.8%, hypertension in 61.7% and obstructive sleep apnoea in 85.7% of patients.31 The improvement in glycaemic control in T2DM is dependent on the type of procedure, but the other beneficial effects on other comorbidities are procedure independent. The particularly beneficial effects on glucose metabolism occur in response to those procedures with a malabsorptive component, such as the RYGB. This is probably the result of both decreased nutrient intake and absorption, as well as increases in gut hormones, such as the incretins, glucagon-like peptide and glucose-dependent insulinotrophic polypeptide.17,37,38 Over the longer term, the benefits for glucose metabolism are also the result of improvement in insulin sensitivity and beta-cell function, related to surgically induced weight loss. Dixon et al. examined the effects of the LAGB on diabetes control in 60 obese patients with T2DM and BMI 30-40 kg/m2 who were treated in an unblinded randomised controlled trial. Half-received conventional diabetes treatment focusing on weight loss by lifestyle changes and the intervention group received LAGB in addition to their usual care. Remission of T2DM was seen in 73% of the surgical group compared with only 13% of the conventionally treated group. The surgically treated group lost 20.7% of initial weight compared with 1.7% in the conventionally treated group at 2 years of follow up.39 This effect is also seen in patients with impaired glucose tolerance with most studies reporting 99-100% prevention of progression to diabetes.40 Remission of diabetes is related to the degree of weight loss, and there was no special effect of the LAGB on glucose homeostasis; the RYGB is associated with the highest recovery rate from T2DM.18
Effects of bariatric surgery on long-term mortality
Six studies have now reported data relating to the effects of bariatric surgery on long-term mortality (Table 1). In the SOS, the mean weight loss in the surgical cohort was maximal after 1-2 years with some weight gain thereafter in all surgical groups which reached a plateau at 8-10 years. Mean total weight loss was 32%, 25% and 20% for the RYGB, VGB and Band groups respectively. In contrast mean weight of the control group increased by 0.1% and 1.6% at 2 and 10 years respectively. At 10.9 years of follow up with a follow-up rate of 99.9%, the adjusted overall mortality was reduced in the surgical group by 31.6% primarily because of a decrease in myocardial infarction, sudden death and cancer. There was no effect on the incidence of stroke, and moreover the reduction of myocardial infarction and overall mortality occurred almost exclusively in diabetic patients.33
A retrospective cohort study by Christou et al. compared 1035 patients who underwent bariatric surgery with 5746 matched controls who were identified from a population database; both cohorts were followed for a maximum of 5 years. The majority of the procedures were open RYGB (79%), 19% VBG (35% of which were subsequently converted to open RYGB because of complications) and 2% laparoscopic RYGB. There was a 67.1% mean percentage excess weight loss, 34.6% mean percentage change in BMI, and the mortality at 5 years was decreased by 89% (0.68% in the bariatric surgery cohort compared with 6.17% in the controls).1 The impact of the composition of the control group or practice patterns, particularly the use of cardiovascular preventive drugs, might have contributed to the huge difference between the two cohort studies. While this is a substantially higher reduction in mortality rate as compared with the SOS, the majority of the surgical procedures in the SOS were VBG and Bands which are both associated with lower weight loss and a more modest effect to reverse T2DM compared with the RYBG.1 This, as well as subject selection (those who are fat but metabolically fit), might account for the lesser reduction in mortality in the SOS study as compared with the Christou study which primarily used RYGB and conversion of failed VBG to RYGB.1 It seems more likely, however, that the Christou study might be an overestimate of the effects of bariatric surgery on mortality as a 27% reduction in mortality has been reported 15 years after a RYBG based on a retrospective analysis of 3328 obesity subjects aged 18-25 who were compared with 62 781 age-matched controls. There was a 33% reduction in mortality at 1-year post-surgery, and at 15 years 16.3% of controls had died as compared with 11.8% of RYBG patients.33,42
The largest study to be reported had an 18-year follow up and was similarly a retrospective cohort study, where 7925 patients undergoing RYGB in a single practice were compared with 7925 population-based controls matched for age, sex and BMI. Follow up began 1-year post-surgery. The occurrence of death was determined by follow up and searching of the National Death Registry. The gastric bypass cohort had a 40% reduction in all-cause mortality at 7.1 years of follow up. Deaths because of diabetes decreased by 92% and those because of ischaemic heart disease and cancer were reduced by 56% and 60% respectively. In contrast, deaths because of suicide, accidents and poisonings of undetermined intent were 58% higher in the surgical cohort. The reason for this is unclear, but the potential overall mortality reduction because of bariatric surgery is decreased.41,45
Two studies have reported mortality outcomes after LAGB surgery, both observational and using convenience controls. Peeters et al. compared mortality data from two Melbourne cohorts, a surgical cohort of 966 patients and an established population-based cohort of 2119 obese subjects. For both cohorts, only those between 20 and 70 years of age and a BMI greater than 35 kg/m2 were included. Mean excess weight loss in response to the LAGB was 58% at 2 years. There was a 72% mortality reduction in the surgically treated group with four deaths in the surgical cohort compared with 225 deaths in the population-based cohort. However, 23 individuals from the surgical cohort were lost to follow up, and accordingly the mortality rate might be higher. Another limitation to this study is that both cohorts were assumed to represent the same obese population. The population cohort consisted of voluntary participants with an oversampling of the Mediterranean population, while the surgical cohort consisted of individuals who had private health insurance and had attempted weight loss before surgery. Thus the results might have been biased towards a greater survival advantage in the surgical cohort.45,43 The second of the two studies compared the long-term mortality of 821 obese patients who were treated with LAGB surgery and 821 age, sex and BMI-matched controls from the Italian Study Group on Morbid Obesity. Follow up was ~6 years in the surgical cohort and ~8 years in the controls. Weight loss was stable at 40% both at 1 year and 5 years post-LAGB, and there was 62% reduction in the 5-year mortality rate in the LAGB group. The mortality rate might, however, have been higher in the LAGB group as follow up was incomplete.44
Conclusions
The evidence that bariatric surgery confers a survival benefit for patients with morbid obesity is compelling. This, together with the data relating to resolution of, or at least substantial reduction in, obesity-related disease, along with improved quality of life and productivity and reduction in healthcare costs, suggests that bariatric surgery is the management strategy of choice for extreme obesity. Whether the survival advantage is a direct result of surgically induced weight loss per se or because of the indirect effects of weight loss on improvement in particular comorbidities requires more detailed subgroup analyses, as this has implications for selection of the most suitable patients.
There is insufficient data to conclude superiority of LAGB over RYBG for mortality, and vice versa. A controlled head to head study would be required. Given the superiority for weight loss and data related to outcomes for comorbidities and complications, the RYGB remains the gold standard surgical treatment for obesity, at least for those with morbid obesity and T2DM.17,22,37
Competing interests
None.
References