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Sugar and cardio-metabolic health

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Professor Luc Tappy is a senior researcher at the Institute of physiology at the University of Lausanne School of Medicine, Switzerland. His present research focuses on environmental factors involved in the pathogenesis of obesity, including several studies evaluating the role of dietary sugars in obesity and insulin resistance. He spoke at an ILSI event in Sydney late in 2015 all about sugar and health.


The Editor of Sweet bites caught up with Professor Tappy recently to ask some pertinent questions about sugar and health.

Is there anything specific to sugar to suggest it uniquely contributes to weight gain?

The specific weight gain potential of sugar is suspected for several reasons:

  1. Fructose constitutes 50% of the molecule of sucrose (the other 50% is glucose), and is more readily converted into fat in the liver than glucose;
  2. Fructose consumption, mainly from beverages, has increased markedly over the past century and epidemiological studies show an association between sugar consumption from beverages and weight gain.
  3. Unlike glucose or starch, fructose does not stimulate food intake suppressing hormones such as leptin or GLP1, and hence may encourage overfeeding.

Relative to glucose or refined starch, does fructose contribute uniquely to metabolic disease in the amounts usually consumed? If so: how?

This is difficult to answer with certainty. Any excess energy can cause adverse effects, and this is true for fructose as for starch or fat. Fructose is mainly metabolized in the liver, where it is more readily converted into fat than glucose. One concern is that fructose may not be as satiating as glucose or starch; another one is that the control of energy intake may be less accurate with beverages than with solid foods. There is growing concern that the effects of weight gain from refined cereals with a high glycemic index (GI) may be just as adverse as weight gain from fructose, or sugars generally.

Do elevated serum triglycerides increase heart disease risk?

Fasting and postprandial fructose induced hypertriglyceridemia may contribute to cardiovascular disease in the long term. In most people, however, fructose induces only a small rise in triglycerides and whether this had adverse effects over the long term is not known. In contrast, in people with insulin resistance and the metabolic syndrome, fructose may further raise plasma triglycerides and increase cardiovascular risk.

How would you rate the evidence for a relationship between added sugars intake and cardiovascular disease?

The role of sugars - mainly sugar sweetened beverages in overweight people - is highly plausible. There is, however, little evidence that sugar, independently of excess body weight, would cause high blood pressure, or increase cardiometabolic risk by itself.

How do you view the current Australian & New Zealand average population sugars intake in the context of cardiovascular disease risk?

The consumption of total sugars in Australia and NZ is around 20%, of which it is estimated just over half (10%) is added sugars. This is a little lower than Europe and USA where added sugars represent around 15-20% total energy. Decreasing sugar intake to 10% would certainly have beneficial effects IF IT WERE ASSOCIATED WITH an increase in the intake of wholegrains, fibre and lower glycemic index starches.

How do the effects of added sugars differ from those that occur naturally in fruit and milk?

Sugars in fruits and vegetables are chemically identical to added sugars but intake of fruits and vegetables is unlikely to provide as much energy from sugars in short periods of time as sugary drinks and fruit juices. The effect of natural sugars in milk (lactose) is not a concern outside patients with lactose intolerance or galactosemia (a rare inherited metabolic disorder).

Physical activity, weight control and a healthy balanced diet have well established benefits in terms of cardiometabolic disease risk. Should more emphasis be placed on dietary sugars intake within this?

I would rather say that sugars are unlikely to have adverse effects in physically active subjects.

What would you suggest are key areas of focus for new research?

There are many. For example: how can we use low-calorie sweeteners in an effective and efficient way? What are the effects of refined vs unrefined cereals on metabolic health? I suspect replacing sugars with refined cereals may fall short of exerting beneficial effects.

NEXT: Trending sweeteners  

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