Is the fruit sugar fructose good or bad for you?
Obesity, the forerunner of so many health problems, is now a global epidemic. Considering only US data, prevalence has increased by 40% in the last 30 years so that now two in three adults are overweight or obese. Average daily calorie intake has increased by 450kcal/d in this period. The biggest contributors to this increase have been flour and cereal products, followed by added fats and sugars. These have gone up by 40, 49 and 10% respectively in the last 40 years. Particular nutritional concern has centred on processed and refined products in the grain-based foods (eg cakes, biscuits, muffins, pies and pastries, and white rice) that are calorie-dense where valuable nutrients may have been lost or destroyed and/or with addition of unhealthy ingredients, in the added fats where saturated and trans fats are over-consumed rather than the unsaturated types, and in the added sugars category, especially sugarsweetened beverages (SSBs) such as colas, fruit drinks, teas, milk, yoghurt and sports drinks. These can represent 20-40% of all carbohydrates in the diet and teenagers may consume 50% more than adults when expressed as a fraction of their daily energy intakes. SSBs have nutritional negatives from many perspectives. They are empty calories; in liquid forms they’re absorbed very rapidly, causing glucose and insulin spiking, they don’t have the same satiation properties as solid foods so there’s increased risk of over-consumption, when consumed in excess there’s also an increased risk of important micronutrient dilution, and because they’re more usually consumed at irregular intervals throughout the day without teeth cleansing, the resulting continual sugar exposure is disastrous for dental caries. The American Heart Association has recommended that adult males and females should not consume more than 150 and 100kcal/d resp from all added sugars, intakes that are exceeded by most adults.
Glucose and fructose are the most common simple sugars (monosaccharides) in Western diets, with other less common ones being mannose and galactose. Table sugar (sucrose) is a 1:1 disaccharide of fructose and glucose that is very rapidly split in two in the body. There’s also a range of higher order saccharide molecules (oligosaccharides) made from 3-8 sugar units, and larger ones (polysaccharides) of varied structure and sizes up to thousands of units – in the case of starches and glycogen, consisting entirely of glucose units. Glucose is essential in the body, and if there’s an inadequate carbohydrate dietary intake it can be synthesised from various stored compounds such as glycogen. Pure glucose is very rapidly absorbed causing postprandial hyperglycemia and a large spike in insulin, which if repeated habitually can lead to insulin resistance, diabetes and other metabolic abnormalities tied to chronic diseases.
Apart from spermatazoa, fructose is not an essential energy source in the body. It is roughly 50% sweeter than sugar while glucose is 30% less, and it has bi-directional effects, beneficial at normal doses but when very high, adverse outcomes such as increased triglycerides and uric acid, and fatty liver disease. At reasonable doses, it’s almost all converted to glucose, lactose and glycogen in the liver. At much higher intakes without a comparable co-ingestion of glucose, it’s poorly absorbed and can lead to gut disturbances. It doesn’t cause a rapid spike in insulin like glucose, a benefit for diabetics. Usually SSB sweetening is achieved by adding table sugar to various foods but also in the US by high fructose corn syrup which is cheaper. Although called ‘high fructose’, it contains approximately the same proportion of fructose to glucose (55:45 respectively) as sugar. The seriousness of health problems due to calorie over-consumption, initially in the developed world but now globally, has driven a vast amount of research to improve our understanding. These efforts have led to much controversy regarding the underlying risk factors and what should be done to address them. Fructose has been heavily caught up in the SSB part of the story in the last 10 years, with some calling it ‘poison’, ‘a threat to global health’, ‘pure, white and deadly’ or ‘alcohol without the buzz’. Does it deserve these inflammatory labels or has it been falsely accused by association?
Metabolic and nutritional studies have been conducted in laboratory and animal experiments in attempts to disentangle the role of different sugars, usually at high doses of individual compounds to facilitate study of mechanisms and effects. From this work we know that high dose fructose can cause a multitude of unwanted biochemical and physiological effects. Caveats are that in human diets fructose is never eaten in isolation and always occurs with other sugars in foods, so studies with isolated fructose are unrealistic. Plus controlled laboratory and animal studies can’t be reliably used to predict effects in free-living humans, and also for relevance, we need to focus on doses that are commonly consumed, namely a mean of 133 and 103g/d added sugars for males and females resp according to a 2011-12 study. One third of the population consumes >10% of total energy from added sugars, whereas 12.5% exceed the 25% maximum recommended by the Institute of Medicine. The WHO recommends an even lower intake of added sugars set at 10% energy. On average, 133g of sugars containing roughly 66g of fructose would provide 524kcal of energy and for a normal weight/activity adult male consuming 2700kcal/d, this would be 19% of total energy coming from added sugars. Many of the experimental and animal studies on fructose have used doses up to 70% of energy! At these excessive levels it’s unwise to extrapolate back to normal levels as biochemical and physiological processes could be grossly distorted. Randomised clinical trials using realistic doses in real foods are the best way to establish the significance of effects, and as the following study focussing on obesity by European researchers concluded (Nutrition Research Reviews (2014), 27, 119–130), reasonable intakes are no more damaging than glucose. Supporting the case for fructose being falsely accused as a villain in this story, we know that fresh fruits which are the best food sources of natural fructose, are a valuable component of healthy diets.
A causal role of fructose intake in the aetiology of the global obesity epidemic has been proposed in recent years. This proposition, however, rests on controversial interpretations of two distinct lines of research. On one hand, in mechanistic intervention studies, detrimental metabolic effects have been observed after excessive isolated fructose intakes in animals and human subjects. On the other hand, food disappearance data indicate that fructose consumption from added sugars has increased over the past decades and paralleled the increase in obesity. Both lines of research are presently insufficient to demonstrate a causal role of fructose in metabolic diseases, however. Most mechanistic intervention studies were performed on subjects fed large amounts of pure fructose, while fructose is ordinarily ingested together with glucose. The use of food disappearance data does not accurately reflect food consumption, and hence cannot be used as evidence of a causal link between fructose intake and obesity. Based on a thorough review of the literature, we demonstrate that fructose, as commonly consumed in mixed carbohydrate sources, does not exert specific metabolic effects that can account for an increase in body weight. Consequently, public health recommendations and policies aiming at reducing fructose consumption only, without additional diet and lifestyle targets, would be disputable and impractical. Although the available evidence indicates that the consumption of sugar-sweetened beverages is associated with body-weight gain, and it may be that fructose is among the main constituents of these beverages, energy overconsumption is much more important to consider in terms of the obesity epidemic.
The fructose question has been a fiercely controversial one for some years but the scientific community is steadily progressing to a reasonable consensus. However as could be expected until the various facets of the research have been placed in context and then promulgated in public health recommendations, there is still confusion in media reports and public understanding. You might wonder whether all these research findings from elsewhere apply to our lifestyles in WA? Well, yes, they probably do as we’re all heading down the same track. This was illustrated, for example, in a 2013 study on the importance of SSBs on weight gain and other metabolic disturbances in 1433 14 to 17-year-old teenagers in the Western Australian Pregnancy Cohort Study. Consumption of SSBs was high, eg when they were divided into SSB intake tertiles, the highest level of 14-year-olds consumed an average of 651g/d. The authors conservatively concluded that increased SSB intake may be an important predictor of cardio-metabolic risk in young people, independent of weight status. At an overview level, numerous societies and organizations including the American Heart Association, the American Academy of Pediatrics, and the US 2010 Dietary Guidelines technical review committee have called for reductions in SSB intake to help prevent obesity and improve overall health.
As mentioned in the introductory comments, high carbohydrate and added sugar intakes are not the only worrying component of unhealthy diets. Excessive fat and protein, and insufficient fibre and micronutrients also cause their own problems. An unbalanced physiology ensues, especially when combined with a lack of physical activity, leading to increased risk of future health problems.