Animal studies show that high intakes of fructose cause metabolic dysfunction. In particular, even after a short period of feeding fructose (a few weeks), animals develop insulin resistance and blood sugar irregularities (here, here and here). High intakes of fructose can cause metabolic dysfunction because fructose, like alcohol, can only be metabolised by the liver. When intakes of fructose are high and fibre levels are low, the fructose is rapidly absorbed and delivered to the liver. This process overloads the liver with energy, and shifts the metabolism of the hepatic tissues towards fatty acid synthesis through the de novo lipogenesis pathway. These fatty acids then accumulate in hepatic and skeletal muscle tissue where they lead to insulin resistance. Overaccumulation of fatty acids in the liver also leads to abdominal adiposity which causes an influx of macrophages and an immune reaction that leads to systemic inflammation and this in turn triggers the development of other diseases such as cardiovascular disease as the inflammation spreads to artery walls.
The over accumulation of fat in the liver from fructose may also lead to changes to the normal levels of lipoproteins. That high intakes of fructose can cause changes to plasma lipoprotein in humans has been reported in the nutritional literature in a number of clinical feeding trials. A recent meta-analysis1 examined 24 of these feeding trials and pooled the data from 474 subjects to ascertain if fructose could cause changes to plasma lipoprotein levels. The results of the analysis showed that there was indeed an effect of fructose on plasma lipoprotein levels, and this was doses related. Exchanging 100 grams of other carbohydrates for fructose in the diet daily caused an increase in total cholesterol of 13.0 mg/dL and an increase in low density lipoprotein (LDL) cholesterol of 11.6 mg/dL. Below 100 grams, no effects were seen for fructose on the plasma lipoprotein levels. Therefore fructose does cause detrimental changes to lipoproteins in humans, and this may be a byproduct of the overproduction and accumulation of fatty acids in the liver.
The 100 g dose required to elicit the detrimental changes in this study are interesting for a number of reasons. This 100 grams dose is roughly the same amount of fructose as found in three regular size cans of soft drink, which suggests that these intakes are easily achievable by someone eating a typical Western diet. Also the 100 grams levels probably represents a delineation between those that get fructose from fruit and those that get it from processed foods such as soft drinks. While 100 grams of fructose is fairly easily achievable consuming soft drinks, obtaining this level through consumption of fruit would be much harder. This supports the contention that it is not fructose per se that is damaging, but high intakes of fructose. Removing the fibre from fruit and creating fruit juice make it much easier to consume large quantities of fructose, and studies suggest that fruit juice can be just as damaging as processed soft drinks with added sugar. Whole fruit on the other hand is hard to overconsume because of the presence of fibre and its high water content.
Dr Robert Barrington’s Nutritional Recommendation: Evidence suggests that at high intakes, fructose is a metabolic poison just like alcohol. Fruit contains fructose, but in fruit the fructose is accompanied by fibre which slows its absorption, and this prevents the fructose overloading the liver with energy. In addition, fruit generally contains much lower concentrations of fructose than soft drinks and so large amounts of fruit must be eaten to cause metabolic damage. Therefore sources of refined and processed crystalline fructose, as found in sugar sweetened soft drinks, as well as concentrated forms of ‘natural fructose’ such as found in fruit juice should be avoided.
RdB
