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Revised draft Clinical Practice Guidelines for the Management of Overweight and Obesity in Adults, Children and Adolescents

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Thank you for the opportunity to comment on the draft guidelines for the management of overweight and obesity in adults, adolescents and children.


As a dietitian with 30 years experience in counseling people on weight issues, I well understand the complexities of this issue. However I’m disappointed that the new guidelines offer nothing new nor constructive in our understanding, prevention nor management of overweight.


I believe that part of the problem lies with the approach that the committee has chosen to take.


The focus is purely on published studies of the efficacy of various interventions.


This is of course necessary but of at least equal importance is a discussion of the underlying causes of obesity. The committee notes that there are factors contributing to overweight and obesity, and mentions the influence of hormones such as ghrelin, leptin and insulin. However, there is a wealth of published scientific data in this area that is missing from the guidelines. Without exploring the mechanisms of hormonal control, relationships to appetite and satiety, effects of diet on hormone levels etc, we miss the opportunity to broaden intervention strategies and are left with what we know doesn’t work. Basically that is what these guidelines have done and because of that our rates of obesity are likely to continue to rise as they have been doing for the last 30 years.


The guidelines basically say that overweight people need advice and ongoing support from professionals. And that when this doesn’t work, as we know it usually doesn’t, there’s always surgery.


Even though the committee admits that ‘The causes of overweight and obesity are complex’ (p vii), the suggested dietary advice is the ancient ‘reduce energy intake to create an energy deficit of 2,500 kilojoule per day.’ We know this doesn’t work long-term and when it doesn’t, generally the individual is blamed for lacking motivation/ self-disipline or not caring about their health etc, which in my experience is untrue.


More visits and support from health professionals may be beneficial but only if they give appropriate advice. Dietitians generally follow guidelines and if the NH & MRC say reduce energy eg by reducing saturated fat, include at least 2 fruit and 5 veg etc,  then that is the advice that will continue to be given.


 However science is now clear that this advice is inadequate.


My wish is that we broaden the way that obesity is approached and understood. So rather than look at obesity simply as a condition of energy imbalance that can be corrected by less energy in and/or more out, that we look at underlying issues that may promote weight gain. Then we at least have a chance for better outcomes.


I’d like to relate a personal example here of how my understanding of obesity has changed over the last 10 years.


The trigger for change was having a daughter with quite a severe weight problem. Two of my children as youngsters ate what they liked, were normally active and stayed lean, whereas my middle child was different. From a young age she carried weight around the tummy, which didn’t disappear during growth spurts as usually happens. At 12-13 yo she gained a lot of weight quickly and went up 2 clothes’ sizes in a year. Even with 20 years experience as a dietitian I didn’t understand why she had this problem and others in the family didn’t. At 14 yo we at least had a reason when she was diagnosed with insulin resistance.


After many years of research (I have read approx. 1500 articles on the subject), I understand more about the causes of IR, its effects and management.


Insulin resistance can be understood in the context of how some of us metabolise food, particularly carbohydrates,


(My apologies if this is too basic but I don’t know who will read this).


Carbohydrate foods such as bread, potato, rice, pasta, cereals, fruit, milk, sugar etc are broken down to simple sugars, predominantly glucose. Glucose is absorbed into the blood and the subsequent rise in BGL triggers the pancreas to release insulin. Insulin aids in the transport of glucose into cells where it is either stored as glycogen or used to provide energy.


Many people are able to metabolise carbohydrate foods in this way. They are likely to release the right amount of insulin in response to a rise in BGL, glucose is quickly cleared from the blood into cells, BGLs remain in the ideal range, our person has lots of energy and doesn’t gain weight easily.


However insulin resistant people have a different metabolic response after eating carbohydrates. If their muscles are resistant to the action of insulin, glucose does not enter muscles quickly and an enhanced insulin response may be precipitated in an attempt by the body to maintain glycaemic control


High insulin levels may maintain ideal glucose levels for many years but at a cost.


In the scientific literature, there is documentation that high insulin levels are associated with high triglycerides, low HDL, fatty liver, sleep apnea, excessive hunger, weight gain, central adiposity, difficulty losing weight, tiredness, reflux/ indigestion, type 2 diabetes, gout, hypertension, anxiety, depression, loss of muscle mass, microalbuminuria, inflammation, CHD, poorer breast cancer prognosis and memory impairment. (I can provide references for all these associations if you’re interested)


To put this into real-life context, a person who has an excessive insulin response after eating carbs is likely to have hormonal responses triggered that make them excessively hungry, crave more carbs, experience mood changes associated with comfort eating and/or binge eating, tiredness/lethargy that make them less inclined to exercise and reduced satiation after meals so that they eat more without feeling full.


In addition to these effects on hunger and appetite, high insulin levels promote weight gain by increasing the conversion of glucose to fat in the liver and stimulating visceral fat receptors to take up this fat (resulting in central obesity). In addition, weight loss is made difficult by the effect of high insulin levels on lipolysis.


These are more likely to be the issues that explain the lack of success of the usual practice of focusing on energy and fat restriction, without regard to carbohydrate intake. For I.R. people, this advice sentences them to a struggle of cravings, excessive hunger, low energy and reduced satiation. More than enough reasons for the lack of success with this approach to weight loss.


Insulin resistance is already a widespread problem and its incidence is increasing.


The SPANS study published in 2004 estimated that approx. 20% of 15-16 years had high insulin levels. In addition 25% of the population is estimated to fit the criteria of metabolic syndrome, of which insulin resistance is a crucial component.


There is an abundance of evidence in the literature that a lower carbohydrate diet is beneficial in the management of insulin resistance and weight loss.


These studies have largely been omitted in the guidelines.


It could be argued that they have been omitted because they did not meet the inclusion criteria ie that intervention studies needed to be of at least one-year duration or be part of a meta-analysis or systematic review.


I’d like to make two points about this.


Firstly, there is one meta-analysis and one systematic review of lower-carbohydrate diets that I would think should qualify for inclusion but apparently did not.


 Nordmann AJ, Nordmann A, Briel M, et al (2006). "Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials". Arch. Intern. Med. 166 (3): 285–93

Conclusion: “Low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to 1 year”.


Hession, M.; Hession M, Rolland C, Kulkarni U, Wise A, Broom J (2008) "Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities". Obesity Reviews 10 (1): 36–50


Conclusion: “Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year”.



The main point, however, is not which diet approach is better in terms of weight primarily, it’s which approach better suits an individual. In my clinical experience, a lower carbohydrate intake is the diet of choice for insulin resistance because it addresses the underlying problem of carbohydrate metabolism that an IR person experiences. Insulin resistant people who reduce their carbohydrate intake report less hunger, greater satiation after eating, less anxiety, more energy and improved well-being. These positive changes then allow them to make food choices conducive to weight loss.


Hundreds of studies on lower carb intake could have been included in the review if the criteria were different. Many of these would show positive effects of lower carb intake on biochemical markers such as HDL, Tg, BGLs and liver enzymes. They would also show that BP can be reduced, kidney function improved, reflux/indigestion reduced, less hunger and cravings, improved sleep etc.


However because the criteria included long-term intervention studies only, those designed to demonstrate more immediate effects of dietary change were omitted, even though the results of which hold great importance.


I also note that potential studies were omitted on the basis of lack of a control group, even if the intervention fitted the time criteria.


A number of well-executed studies, demonstrating important results, were therefore not considered.


For example, Clifton’s study, “Long-term effects of a high-protein weight loss diet” was well executed and of adequate duration however, the committee excluded it on the basis of lack of a control group with the comment, ‘Control group does not enable intervention to be estimated’.


This study followed 2 groups randomly assigned to 2 different weight loss regimens. Important outcomes were reported but results from this study have been ignored because of the inclusion framework.


The reported results tell us clearly what the intervention achieved and as a dietitian that is the information I need.


What we need is information about how people respond to dietary approaches in terms of weight loss, biochemistry, acceptance, hunger and energy levels. A control group is actually not required as it is in a drug trial, because we want to know how individuals respond to a regimen and not how their responses differ to another group doing something different.


The problem of inclusion criteria extends further. The stringent criteria applied to single studies does not apply to those included in meta-analyses or systematic reviews.


 If the criteria for stand-alone studies is deemed important enough for some to be excluded, for consistency it should be expected that the same rules apply to the individual studies cited in pooled analyses.

However in the pooled analyses, studies are included even if they have little follow-up, some reportedly as little as 6 weeks, compared to the minimum duration of 12 months for stand-alone studies.


The draft guidelines offer nothing new. They continue the outdated message of simply eat less and exercise more, but with more visits to health professionals for support and reminders.



This approach assumes that the advice is correct and the problem is either that the public doesn’t understand it or is at fault for not following it. Hence more visits to keep on track.

I would like the committee to consider that the guidelines are inadequate to effect real change in obesity rates, health professionals are being incorrectly trained in the advice they give and the public is suffering as a result. And that rather than continue the propping up of outdated beliefs, the committee considers a complete overhaul.


Thanks for your time.


© 2012 JE



Page reviewed: 6 September, 2012