Fructose is known to alter long chain fatty acid metabolism in mammals. In particular, fructose increase the production of triglycerides in the liver through the de novo lipogenesis pathway and also through a stimulation of the desaturation of stearic acid (C18:0) to oleic acid (C18:1 (n-9)). Copper deficiency in animals causes changes in cardiac hypertrophy and pathological changes to the heart that can lead to sudden death. Rats fed sucrose as a source of carbohydrates in the presence of a copper deficiency have accelerated pathology and an increase in mortality in comparison to rats fed starch as the source of carbohydrates. It has been speculated that the accelerated pathology caused by copper deficiency in the presence of sucrose could be due to changes in the long-chain fatty acid content of phospholipids which changes membrane structure and in turn affects cell function. Alternatively the sucrose may alter the absorption of copper this exacerbating an already low copper status.
The detrimental effects of sucrose during a copper deficient state is thought to be due to the fructose moiety of the sucrose molecule. For example, in one study1, researchers fed a rats a copper deficient or copper sufficient diet with either sucrose, fructose or starch as the main carbohydrate source for a seven week duration. The copper deficient diets caused rats to experience a drop in ceruloplasmin levels, a decrease in hepatic copper and ATP levels, as well as increases in plasma cholesterol and triglyceride levels. In addition, the copper deficient rats fed sucrose or fructose developed a severe anaemia due to significant reductions in hematocrit levels compared to those fed starch. The fasting blood glucose levels, triglyceride and cholesterol levels were also higher in the copper deficient rats fed fructose and sucrose. Death in the rats occurred through rupturing of the heart muscle tissue, and this was more apparent is the rats fed carbohydrates containing a fructose molecule.
In this experiment the mortality in the sucrose and fructose fed copper deficient rats was over 3 times that of the copper deficient rats fed starch. These results suggest that fructose is able to worsen the symptoms of a copper deficiency. This was inferable from the fact that the results from the fructose and sucrose fed rats were essentially the same. Interestingly when the same authors fed copper deficient rats glucose, no deaths occurred. As sucrose is a molecule that contains both glucose and fructose it is likely that it is the fructose component that is the cause of the detrimental changes. The reason as to why fructose can worsen the symptoms of an already present copper deficiency is not known. However, It has been speculated that fructose can inhibit the transport of copper across the gut mucosa and therefore decrease its absorption thus exacerbating a copper deficiency. Alternatively, the changes to lipid metabolism seen with fructose ingestion may aggravate the already problematic metabolism of copper.
Dr Robert Barrington’s Comments: Fructose causes a number of metabolic problems when ingested in its refined crystalline state. These changes in metabolic regulation have been shown to have detrimental health outcomes. As well as altering the metabolism of lipids, fructose may also cause changes to the metabolism of copper. This is problematic because the fructose intake in the typical Western diet is too high, and the intakes of trace minerals like copper is too low. The long term effects of sucrose and fructose ingestion in combination with poor mineral status seen in humans consuming the typical Western diet is not yet known. However, evidence from animals studies suggests that fructose may negatively influence the hepatic metabolism and that this may in turn lead to pathological changes to cardiac health through alterations in both lipid and copper metabolism.
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