Gary Taubes (2018) Science Media Centre
An opinion piece in the BMJ by Gary Taubes discusses the health effects of sugar.
Prof. Tom Sanders, Professor emeritus of Nutrition and Dietetics, King’s College London, said:
“There are major flaws in the argument made by this American journalist that sugar is the cause of the current obesity epidemic as well as being an important factor in heart disease. Many people in the USA consume a diet consisting of large amounts of processed meat and carbohydrates; and while I agree there is a worrying global trend to copy this dietary pattern, especially in large metropolitan areas where there is an abundance of high energy food unsuited to a sedentary population, it is wrong just to focus on sugar!
“In the UK, sugar intake in the UK has changed little in the last fifty years. Yudkin, who was my Professor, estimated in 1970 that per capita intake was 50kg/year. This level of consumption has not increased in the UK, yet death from heart disease has fallen by more than 60% percent. Moreover, the current obesity epidemic took off in the 1980s and diabetes has increased in concert with this.
“If sugar had a specific role in causing obesity as the article purports then you would expect vegetarians and vegans to be obese and be more prone to diabetes because their intakes of sugar are high being derived mainly from fruit and vegetables. In fact, research shows that vegetarians and vegans are less likely to be obese and less likely to get diabetes.
“It is also important to differentiate the effects of added sugar in the form of soft drinks from that present in solid food. The evidence relating to sugar intake and risk of obesity is almost entirely associated with sugar sweetened beverages.
“Animal studies also show that incorporating sugar into solid diets does not cause obesity but if sugar is provided in a liquid form such as condensed milk it promotes overconsumption and obesity. This is probably a hedonic effect, rather than a biochemical effect of the fructose component of sugar on metabolism, that encourages overconsumption.
“Finally, the article unfairly derides the consensus view that overconsumption of food energy and reduced physical inactivity is the cause of obesity. Obesity in truth is an inability to cope with an ad libitum intake of food.”
Dr Katarina Kos, obesity researcher and consultant in diabetes and weight management at the University of Exeter Medical School, said:
“What I believe Taubes is trying to say is that sugar is not just a potential excess calorie, but intrinsically harmful. Evidence for this is poor. It is difficult to prove this without head to head trials comparing sugar intake with isocaloric intake of other nutrients, especially high fat intake in humans with comparable energy needs. However, there are systematic reviews comparing intake of different sugars and carbohydrates with high and low glycaemic intake – though typically short term and inconclusive.
“Emerging evidence suggests however that high sugar intake, e.g. high intake of sugar sweetened beverages, can be seen as a marker of other unhealthy lifestyles and dietary patterns (including smoking etc.)1. Thus the concept of discussing the harm of sugar and not considering overall energy excess and obesity is unrealistic and complex in a real-world situation.
“In light of the effect of sugar on appetite and consumption of other calories it may trigger, it is right to urge care with sugar intake, yet how much is good or bad for us will equally depend on the ‘emptiness of this calories’, e.g. if it will/ will not be used up for energy in the correct proportional need of the exercise workout, as in consuming glucose gel when running a marathon. We also easily forget that most of our favourite sugars and sweets also contain fats, so the picture is complex. Chocolate, ice cream and cakes have not just sugar but also a high fat content and we sometimes like to add a bit of cream. In other words, if we have more sugar we also have more overall calories, and a more unhealthy lifestyle which manifests in excess calories, leading to obesity. There is little disagreement that obesity and increasing BMI is exponentially increasing the risk of diabetes.”
1 Khan et al 2016 Eur J Nutr
Saffron Whitehead, Emeritus Professor of Endocrinology at St George’s University of London and member of the Society for Endocrinology, said:
“This piece by Taubes is an hypothesis that sugar, rather than total calorie intake, may partly be the cause of the obesity epidemic, although there is no clear experimental evidence of this yet. However, Taubes does identify fructose as the potential ‘bad sugar’. It is present in high fructose corn syrup, which is added to most sweetened commercial products, including food and sweet drinks. Unlike glucose, fructose is broken down only in the liver, where it can be converted to fats which can subsequently be deposited as fat in our central fat reserves.
“Knowing that two cans of sweetened drinks and a chocolate bar would provide about a fifth of our average calorie intake per day, and that there is no good evidence concluding that the cause of obesity is simply sugar, it may be that we should just count calories for the time being.”
Dr Victor Zammit, Professor of Metabolic Biochemistry at the University of Warwick, said:
“The article restates the need to pay more attention to the effects of fructose on lipogenic genes. It is not ‘new’, but well worth repeating. I felt it could have gone further by also highlighting that glucose arising from sucrose would also contribute to insulin secretion and fat storage, and that fructose raises uric acid, which is important in the metabolic syndrome. So it is a valid article. If anything, it didn’t go far enough in highlighting the problems associated with sucrose.
“Both ‘halves’ of the sucrose molecule (fructose and glucose) will contribute calories which, taken to excess, will contribute to obesity.
“The glucose ‘half’ will also increase insulin secretion when the sucrose molecule is hydrolysed in the gut before absorption. Insulin favours deposition of glucose in tissues, which can give rise to fats there.
“Although the fructose moiety does not raise insulin it has two additional effects.
“It activates the expression of the genes of enzymes involved in the conversion of carbohydrate into lipid in the liver. Consequently the liver increases the secretion of VLDL particles which contain triglycerides and cholesterol, and are the precursors of LDL which contains the ‘bad cholesterol’ associated with heart disease.
“Fructose also increases the formation of uric acid. Elevated uric acid concentrations in the blood (hyperuricemia) is an integral part of the ‘Metabolic Syndrome’ and increases inflammation of blood vessel lining, which can predispose to cardiovascular problems. Precipitation of uric acid in joints is the cause of gout.”
Prof. Nick Finer, Honorary Clinical Professor at the National Centre for Cardiovascular Prevention and Outcomes at UCL, said:
“Taubes’ essay highlights the growing syndemic of obesity and diabetes that threatens to swamp healthcare systems. He resurrects and repeats his long-held beliefs (as published in several best-selling books) that dietary sugar may be the cause of both. He is critical of the evidence that has driven national dietary guidelines that focus on reducing fat intake, but admits that the evidence for a specific role of sugar (or its metabolite fructose) causing diabetes independently of any effect on overweight and obesity is missing.
“There is compelling evidence that sugar consumption (with sedentary lifestyle) and obesity are linked, but not in a linear way – so any benefits from reducing sugar intake might be more or less effective according to what the starting point is in terms of sugar consumption1. Designing studies to test the effects of a single food on disease are remarkably difficult. To show that changing sugar intake would change the incidence of diseases such as diabetes and non-alcoholic liver disease independent of any effect on body weight is probably not possible, and would require many years of follow-up. We may however see evidence from an unwanted natural experiment: in 2017 the EU withdrew the restrictions on high fructose corn syrups (isoglucose) and it is likely that their consumption will markedly increase (at the expense of sucrose intakes).
“At the end of the day we have ample evidence that preventing weight gain, or losing weight if you are overweight or obese, have dramatic benefits in preventing or reversing diabetes; and reducing the calories provided by sugary snacks and drinks is an important part of the strategy to achieve these goals. Taubes’ conclusion that we should strengthen recommendations against sugar consumption – regardless of the lack of evidence that sugar has harmful effects independent of its calories – seems to smack of opinion-based rather than evidence-based public health.”
1 Public Health Nutr. 2014 Mar;17(3):587-96. doi: 10.1017/S1368980013000141. Epub 2013 Feb 18. Sugar consumption and global prevalence of obesity and hypertension: an ecological analysis. Siervo M, Montagnese C, Mathers JC, Soroka KR, Stephan BC, Wells JC.
Prof. Naveed Sattar, Professor of Metabolic Medicine at the University of Glasgow, said:
“The overall evidence that sugar exerts a meaningful risk for diabetes beyond its supply of calories is simply not supported by existing evidence, including from randomised trials. For example, there is no evidence that the Atkins diet (high protein/fat but low carbohydrate) has an extra benefit to reduce diabetes risk than more conventional diets.
“Whilst these diets don’t test low sugar per se, they suggest a general reduction in carbohydrate (a significant proportion of this reduction will be in refined sugars) does not yield a clear extra benefit on blood sugar levels compared to other forms of diet. Moreover, multiple other trials of obesity surgery and lifestyle with low calories in general suggest that the degree of weight loss is the key to diabetes improvements. These latter trial findings, in turn, fit with a wealth of population studies linking BMI to diabetes risk as well to genetic studies of weight raising genes. Other evidence (including some from our own groups) suggests that the main dietary culprit for excess weight in society remains excess fat intake, not necessarily excess sugars, whilst trial evidence suggests all forms of diets work to lessen weight.
“Of course, we should all aim for low sugar for many other reasons, not least to protect dental health, but the overall message for the public is that it is their weight which is the largest and most modifiable risk factor for their diabetes and that therefore however they intentionally lose and sustain weight loss is the most important factor to reduce their individual diabetes risks.”
* ‘What if sugar is worse than just empty calories? An essay by Gary Taubes’ by Gary Taubes will be published in The BMJ on Thursday 4 January 2018.