To the Editor: The recent article on obesity by Proietto and Baur in the Journal1 coincided with another by Campos in New Scientist,2 in which he criticised the conventional view of the risks of obesity and the norms usually accepted. Campos quoted evidence suggesting that, in fact, the group in the overweight range (body mass index [BMI], 25–30 kg/m2) are healthier than those with a BMI below 25 kg/m2. He also noted that between 1990 and 2002, despite a further increase in the prevalence of obesity in the United States, the incidence of type 2 diabetes hardly changed, while cardiovascular death rates fell. According to Campos, similar claims about the risks of obesity have been repeated over the past 50 years and relate more to cultural and political factors than to reliable scientific evidence.

Clearly, this view is inconsistent with that articulated by Proietto and Baur. While Campos’ view obviously does not apply to the grossly obese, there is a strong suggestion that the overall evidence base is inconsistent. This may be because the assumption of a linear relationship between excess weight and illness is false. It is further likely that there is confounding of variables, with weight a proxy for lack of exercise. As Campos points out, large-scale observational studies are inevitably poorly controlled.

If this is so, then it may well be more useful for the medical profession to emphasise exercise and lifestyle rather than weight loss. It may be much easier to obtain and reinforce behavioural change in these areas, and avoid the common feeling of hopelessness (“why bother”) expressed by people who find it hard to diet and to lose weight.

To the Editor: We take issue with the recommendations on treatment of morbid obesity in the otherwise excellent article on obesity management by Proietto and Baur.1

Like most non-surgical clinicians involved in the management of obesity, they fail to differentiate between the treatment of obesity (body mass index [BMI], 30–35 kg/m2) and morbid obesity (BMI > 35 kg/m2). The literature is crystal clear — non-surgical treatments are unsuccessful in achieving and maintaining weight loss in morbid obesity.2,3 We are unaware of any branch of medicine, other than morbid obesity management, where respected clinicians routinely recommend treatments (drugs, diet and lifestyle modification) which have been proven not to be effective.

We challenge all clinicians to accept what the evidence clearly shows, that:

• the only known effective treatment for morbid obesity is surgery;2,3 and

• laparoscopic adjustable gastric banding is much safer than bypass/diversion surgery4 and just as effective; it is the treatment of choice for morbid obesity.

To the Editor: I read with interest the recent article on obesity in Australia by Proietto and Baur1 and would like to comment on the issue of proteinuria and measurement of insulin level in obese patients.

Proteinuria in obesity, commonly referred to as obesity-related glomerulopathy, is a clinical syndrome with an estimated incidence of about 2% in obese subjects.2 With a fifth of the population being obese,1 the sheer number suspected to have this condition will create an enormous management and cost burden. Furthermore, the incidence of this condition appears to have increased disproportionately to the incidence of obesity.2

The syndrome of obesity-related glomerulopathy comprises the triad of morbid obesity, marked proteinuria without oedema, and normal serum albumin concentration. It can occur in any degree of obesity but is more common in the morbidly obese group (body mass index > 40 kg/m2; Class III obesity). It often presents as proteinuria on urinary dipstick testing, with marked proteinuria seen on confirmatory testing (up to 32 g/day).2 Other features of the nephrotic syndrome do not occur, and the cholesterol level is often lower than that in patients with nephrotic syndrome. However, glomerular filtration rate is raised, and glomerulosclerosis is seen on biopsy. The pathogenesis is unknown.

Obesity-related glomerulopathy is a diagnosis of exclusion: secondary causes of proteinuria should be fully eliminated, including hypertensive renal disease and undetected type 2 diabetic renal disease. More often than not, biopsy will be required to guide management, with cost implications.

Although the condition is said to be benign, in a small proportion of patients it progresses to end-stage renal failure requiring replacement therapy, further adding to the cost of management. Fortunately, the condition is readily reversible with weight loss, which is an important emphasis in management. 3

My second comment relates to the case of the overweight adolescent described by Proietto and Baur. In this patient, measurement of insulin level is not indicated.4 There is no standardised insulin immunoassay, the sample has to be collected and processed correctly to produce a valid result, and the result would not add to or alter the management of the condition. It is doubtful if normative data exist for adolescents, but the clinical picture suggests the insulin resistance syndrome. As the primary goal would be to detect disordered glucose metabolism, appropriate testing of glucose level is all that is required.

In reply: We agree with McHenry and colleagues that, until very recently, surgery was the only effective treatment for morbid obesity. However, the development of effective pharmacotherapy that targets the underlying cause — increased hunger — may well change this situation, as evidenced by the effect of leptin treatment in leptin-deficient children.1 In the not-too-distant future, a medical alternative may be possible.

The issue of the relative merits of surgery to insert a foreign body (gastric band) or permanently alter the anatomy of the gastrointestinal tract versus lifelong pharmacotherapy will need to be considered. However, economic as well as health issues may be important, and, as McHenry and colleagues suggest, may still favour surgery as the preferred therapy.

We thank Davies for bringing to our attention Campos’ book The obesity myth, in which he claims that overweight individuals are in fact healthier than those of normal weight.2 While many of the book’s other claims can be challenged (such as the statements that the prevalence of type 2 diabetes is not rising in the United States, and that bald men have higher testosterone levels), the fact that there is no simple linear relationship between body mass index (BMI) and illness is correct. Sex, race and fat distribution can all influence the relationship. Moderately overweight women with gynoid (hip and thigh) fat are not at increased risk of illness.3 In contrast, South Asian people have an increased risk of developing diabetes at lower BMI values than people of European background. We agree with Davies that maintaining fitness through regular exercise is very important in minimising the health consequences of obesity.

Tran raises the issue of whether it is useful to measure insulin levels in children. It is not unreasonable to assume that insulin levels are raised in most obese children, but this is not always the case. The National Health and Medical Research Council clinical practice guidelines for management of overweight and obesity in children and adolescents state that: “Fasting insulin and glucose should be considered in obese children or adolescents, particularly those with a family history of type 2 diabetes, those with acanthosis nigricans and those from certain ethnic backgrounds”.4 In the presence of insulin resistance, serum glucose level remains normal because of high insulin levels. Thus, glycaemia cannot be used to monitor improvement in insulin sensitivity.