The link between diet, exercise and obesity is the topic of an editorial in British Journal of Sports Medicine, in which the authors argue that excess sugar and carbohydrate are the drivers behind the increase in obesity.
Prof. Iain Broom, Director, Centre for Obesity Research and Epidemiology, Robert Gordon University, Aberdeen, said:
“In general this editorial is similar to that of Richard Smith in the Christmas edition of the BMJ. I would tend to agree that high CHO diets tend to exacerbate insulin resistance syndrome and are really not appropriate in dealing with the metabolic problems associated with this syndrome, despite the fact they are classified by Public Health as the healthy approach to weight management. Low CHO diets are associated with much greater improvement in insulin sensitivity than low fat approaches in individuals with metabolic syndrome and this has been well documented since the 1970s.
“There are one or two misconceptions in this editorial, especially related to the satiety aspects of macroniutrients. Fat has the least satiety effect, followed by CHO and then protein and not as the authors suggest.
“Their statement that increased exercise does not contribute to weight loss is well taken – it does not. What exercise (increased activity) does, in association with appropriate dietary intervention, is to promote weight loss maintenance once weight has been lost, but it is a poor contributory factor to promoting weight loss. What is good about this editorial is that it once again focuses attention on what Richard Smith described as a global experiment in changes in food policy which has gone disastrously wrong. Public Health, unfortunately, has little experience in dealing with the obesity/diabetes epidemic worldwide and is using the wrong food.”
Ms Catherine Collins, Spokesperson for The British Dietetic Association, said:
“Anyone who’s spent time at the gym on a treadmill will have realised just how much effort is needed to burn off the calories in an average bar of chocolate. But this personal opinion piece, which extolls the purported benefits of a high-fat low-carb diet, doesn’t given sufficient recognition to the extensive research of the metabolic and physical benefits to health of even moderate intensity exercise.
“As a Registered Dietitian, seeing incomplete evidence being cited so frequently is a worrying trend in medical publications. When it comes to information on diet, exercise and health the public deserve robust, well-evidenced recommendations, which this paper fails to deliver.
“The poor interpretation of evidence cited to support the article should also be addressed. The authors state that ‘up to 40% of those with normal BMI will harbour metabolic abnormalities…’ citing a reference that did not generate this point (i).
“In my opinion there are a mere two valid points made in this opinion piece. First, that the UK Academy of Medical Royal Colleges statement on the benefits of exercise – in terms of heart health and metabolic risk – is proven. In addition to burning up a modest calorie load, exercise also improves mood, so reducing your urge to achieve the same feeling with a calorie-laden bar of chocolate. Second, sports centres should prioritise sugar-free beverages at point of sale to recreational sportsmen and women, who if overweight don’t need isotonic and other sugary drinks to rehydrate. Water will do.”
(i) Reference 3 in the paper http://www.ncbi.nlm.nih.gov/pubmed/23356701 refers to this paper http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3715098/#b18 co-authored by Lustig. It is used to cite a 40% incidence of metabolic syndrome. However, the Lustig paper makes no such claim. The 40% incidence arises from their citing reference 18 (PMID: 219202630) of their paper. Reference 18 is the excellent paper from Voulgari and colleagues http://www.sciencedirect.com/science/article/pii/S0735109711025010. Voulgari’s work (table 2) demonstrates a statistically significant reduction in heart failure risk with any level of exercise intensity. Whether exercise protects against heart failure, or that lack of ability to participate of exercise is a symptom of heart failure risk, is not qualified.
Prof. Nick Finer, Honorary Professor, National Centre for Cardiovascular Prevention and Outcomes, UCL Institute of Cardiovascular Science, UCL, said:
“This polemical article gives punchy messages on the relationships between sugar(s), physical activity, obesity and ill health. While many of the messages are valid and important in places the authors overstate their case. They set up many Aunt Sallies that they then proceed to knock down. Disappointingly they do not reference two recent important reports from the UK. The National Institute for Health and Care Excellence (NICE) report (Maintaining a Healthy Weight and preventing excess weight gain among children and adults. NICE NG7 published in March 2015. https://www.nice.org.uk/guidance/ng7) and the draft report on carbohydrates and health from the Scientific Advisory Committee on Nutrition (SACN: https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/339771/Draft_SACN_Carbohydrates_and_Health_report_consultation.pdf) from June 2014 systematically reviewed this area of huge public health importance.
“The authors correctly highlight that a ‘normal’ body mass index (presumably they mean between 18.5 and 25 kg/m2) may not be healthy, but then rather confusingly conflate a number of themes into the statement that ‘…members of the public are drowned by an unhelpful message about maintaining a ‘healthy weight’ through calorie counting, and many still wrongly believe that obesity is entirely due to lack of exercise.’ Actually public health messages more commonly talk about a healthy diet and the benefits of remaining physically active. The NICE NG7 guideline recommends that people ‘establish and maintain a combination of increased physical activity and healthier dietary habits to achieve and maintain energy balance’. There is no mention of calorie counting or obesity being entirely due to inadequate exercise.
“In their simplification of the evidence they frequently confound evidence of association with causation. Many would not accept the statement that ‘an 11-fold increase in the prevalence of type 2 diabetes, in comparison to an identical 150 calories obtained from fat or protein’ is evidence of sugar causing diabetes. In fact the SACN report specifically states that there is no evidence for sugars or sucrose intake in general and type 2 diabetes (based upon limited evidence, 6.21; 6.27) but does recognize that in the case of sugar-sweetened beverages specifically, there is moderate evidence for a biologically important association with higher diabetes incidence (6.35). The impact on weight of children exposed to sugar-sweetened beverages, while not specifically mentioned, is perhaps more strongly evidenced.
“The article is on much firmer ground in highlighting and debunking the carefully contrived marketing-speak that promulgates the need for ‘sports drinks’, carbohydrate loading and insidiously suggests that, often small, bouts of exercise can legitimise consumption of sugar-laden beverages without caloric penalty. This article is a timely stab back at industry-created myths relating to exercise, sugars and obesity that seek to drive up the unnecessary consumption of their unneeded products.”
Prof. Susan Jebb, Professor of Diet and Population Health, University of Oxford, said:
“It is true that the magnitude of weight loss following exercise-only interventions is less than that achieved in diet-only interventions as we showed in a systematic review and meta-analysis last year (Johns, Hartmann-Boyce, Jebb and Aveyard. J Acad Nutr Diet. 2014 Oct;114(10):1557-68). But in this editorial, the authors fail to note that weight loss programmes which combine diet and physical activity are the most successful route to weight loss in both the short (3-6 months) and medium term (12 months). Moreover, to constrain the intention behind efforts to treat obesity to achieving weight loss alone neglects the true purpose of intervention – to improve health. Given that obesity, an unhealthy diet and physical inactivity are all risk factors for chronic disease, it makes good sense to seek to change both diet and activity behaviours to lose weight and improve health.
“To achieve this will need a raft of changes at all levels: practical support for individuals to change their behaviour, changes in local environments to both support better food choices and greater physical activity; and some national policy action too. None of these interventions alone will solve the problem, indeed they are very likely to be synergistic. Rather than trade one off against the other – sugar vs fat, diet vs activity, individual vs population we need to take action across the full range. This was the system-wide approach advocated by the Foresight report “Tackling Obesities: Future Choices” in 2007 and which still provides a framework for comprehensive action now.”
Prof. Naveed Sattar, Professor of Metabolic Medicine, University of Glasgow, said:
“Whilst this article is provocative and includes many points of merit, with which many of us agree, there are some useful clarifications. There is certainly more evidence to support excess calorie intake as more relevant to the obesity epidemic than under activity. This statement makes sense if one considers how quickly you can eat 200 calories in the form of a calorie-dense snack (e.g. chocolate bar, crisps etc.) as opposed to burning off 200 calories. Thus the main point of the article that one cannot outrun a bad diet is true for the vast majority of the population. However, we must remember that physical activity, whatever its form, is important in preventing weight gain and helps the heart and thus both a good diet and good activity levels are important for healthy weight and general health.
“Whilst excess sugar often contributes to excess calorie intake for many individuals, fat excess is also important and many individuals are obese due to too much of both dietary sugar and fat. Likewise, there is no convincing evidence from recent high quality intervention trials for an important effect of specific diet types on risk for obesity – what matters more than anything else is overall calorie content. This also makes sense unless we wish to reinvent the laws of physics. But once again, the main sentiment about cutting average sugar or fat intakes and the power of advertising are well made in this article, as in many others. Whether a new government really has the appetite to tackle such issues via legislation targeting at foods and drinks industries or taxation measures remains to be seen.
“Irrespective of the above, in clinical practice we can help our patients who are overweight and obese and who wish to lose weight by giving them one to two realistic targets (e.g. replace sugary drinks with diet drinks or better water, or replace sugary rich cereal with fibre rich cereal, or else replace crisp snacks with piece of fruit etc.) to aim to cut their calorie intake. Most will need additional changes (so more targets subsequently) but as long as changes are embedded and achievable (and palates retrained), we will have made some helpful suggestions and our patients will be thankful.”
‘It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet’ by A Malhotra et al. published in the British Journal of Sports Medicine on Wednesday 22 April 2015.
Declared interests
Ms Catherine Collins: “I have been paid to present a talk on my personal interpretation of dietary guidelines on sugar to a group of dietitians, by a company that manufactures a fruit juice.”
Prof. Susan Jebb is employed by the University of Oxford and receives no personal funding from the food industry. Susan is the independent Chair of the Public Health Responsibility Deal Food Network and was a science advisor to the Foresight obesity report. From 2007-10 she was the principal investigator for a research study funded by the food industry to investigate the potential for a functional beverage to help weight loss. The results of this work have been published: http://www.ncbi.nlm.nih.gov/pubmed/23920353.