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Latest findings on fructose and your health

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Fructose: friend or foe?

During the past decades some researchers have blamed the large increase in fructose consumption in most Western countries for raised triglyceride levels, linked to cardiovascular disease; non-alcoholic fatty liver disease, regarded as a precursor to obesity and type 2 diabetes; obesity and all its attendant diseases; raised uric acid levels and gout; and metabolic syndrome.

Read: Part 1 - Why fructose is regarded as a baddy and the effect if has on us

Recent findings on fructose and its effect on our health

Recently, however, Dr Sievenpiper and his team at the St. Michael’s Hospital in Toronto, Canada, have conducted a series of meta-analyses of publications dealing with these different, supposedly harmful effects attributed to fructose, and have come up with the following findings:

·    Fructose does not have any impact on triglyceride levels, and on its own fructose does not cause cardiovascular disease. However, if consumption of fructose leads to an excessive intake of energy, it will increase triglyceride levels and may contribute to heart disease (Wang et al, 2014)

·    Fructose does not cause non-alcoholic fatty liver disease and its consequences such as obesity and type 2 diabetes, but if consuming fructose leads to an excessive intake of energy, then like any other carbohydrate overconsumption this can lead to non-alcoholic fatty liver disease (Chiu et al, 2014)

·    There is no reason to replace fructose with other types of sugar such as glucose in commercially prepared foods and drinks. However, overconsumption of fructose, leading to excessive energy intake needs to be avoided to prevent all the above mentioned diseases and conditions (Sievenpiper et al, 2014).

Dr Sievenpiper and his co-workers have therefore shifted the emphasis from fructose to overconsumption of any sugars, no matter what type (sucrose, glucose, fructose, etc.), as well as refined carbohydrates (sugars or starches) when it comes to trying to pinpoint which foods or factors are to blame for the many ills that plague modern society.

Read:  Too much fructose could raise BP

Not the end of the story

At this stage most people are thoroughly confused – is fructose to blame for obesity and many of the other diseases we suffer from or not? Alas, the fructose controversy is not yet over, despite the efforts of the researchers in Toronto.

Read: IBS is linked to fat and sucrose

In January 2013, Kathleen Page and her co-authors published a paper in the Journal of the American Medical Association, which mapped the effects of fructose and glucose on parts of the brain. The brain magnetic resonance imaging showed that glucose, but not fructose, reduced the flow of blood to those areas of the brain which regulate appetite.

Glucose intake produced more satiety hormones and made the experimental subjects feel fuller than fructose consumption.

Page and her team (2013), suggest that eating fructose may make people eat more because their hunger is not adequately satisfied by fructose, thereby increasing their energy intake (as postulated by Dr Sievenpiper’s group). Fructose may, therefore, still be a culprit.

Read: How hormones are linked to weight gain

Until more detailed biochemical studies are conducted to precisely define how fructose influences the human body’s reactions and metabolism, it may well be prudent to have some fructose in the form of fruit – where the sugar is embedded in a food matrix and accompanied by healthful nutrients such as vitamins, minerals, dietary fibre and phytonutrients, but not to overdo our intake of fructose, used as a sweetener in drinks or diet foods.

Dr Sievenpiper’s suggestion that we should not over-consume energy, no matter what form it takes, is of course the basis of good health and a slender figure.

Read more:

Fat forms faster with fructose

Fructose linked to obesity:  study

Is fructose making people fat?

References:
(Chiu S et al, 2014. Eu J Clin Nutr,68(4):416-23; Page KA et al. 2013. JAMA, 309(1):63-70; Sievenpiper JL et al. 2014. Curr Opin Lipidol, 25(1): 8-19; Wang D et al. 2014. Atherosclerosis, 232(1):125-33.)




 
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