Increasingly it is being shown that refined crystalline fructose is a metabolic poison. Experiments on rats show that fructose can induce insulin resistance and detrimental changes to lipoprotein metabolism within a few weeks. Humans studies confirm that high intakes of refined crystalline fructose are a primary driver of insulin resistance, and lead to serious metabolic deterioration in the function of the liver. The human intake of refined fructose, in the forms of soft drinks and other foods, mirrors closely the increase in the rates of obesity, metabolic syndrome and type 2 diabetes. This is supported by data showing that introduction of sucrose to humans consuming traditional diets causes an increase in the rates of Western lifestyle diseases in only a few years. Refined fructose is damaging because it is rapidly absorbed and passed to the liver, where it increases flux through the de novo lipogenesis pathway. The resultant fatty acids accumulate in liver and skeletal muscle and interfere with the insulin receptor function.
The result of the increased flux through the de novo lipogenesis pathway can be seen as an increase in the plasma levels of triglycerides. As fatty acid synthesis proceeds, the fatty acids are synthesised into triglycerides and packaged into the very low density lipoprotein (VLDL) particle. These VLDL particles then exit the liver and accumulate in plasma, and this increase can be detected biochemically. Because the low density lipoprotein (LDL) particle is formed from the VLDL particle through the action of lipoprotein lipase and the transfer of triglycerides to tissues (which lowers the density somewhat), levels of LDL lipoproteins also increase as a result of fructose feeding. These detrimental changes to lipoproteins have for a long time been blamed on dietary saturated fat intake, but it is becoming clear that raised levels of fasting triglycerides, induced by fructose, are not the same as the transient and harmless increase in postabsorptive triglycerides seen after consumption of a high saturated fat meal.
So the result of fructose consumption is an increase in the plasma levels of triglycerides, and this is a symptom of metabolic dysfunction in the liver. These metabolic changes are interesting biochemically, because it is known that fish oils are able to lower levels of plasma triglycerides significantly. The long chain fatty acids in fish oils may therefore be protective of the metabolic changes induced by refine fructose, and this may explain their ability to protect from the Western lifestyle diseases. In a recent study1 the protective effect of fish oil supplements on fructose-induced metabolic changes were tested in rhesus monkeys. Rhesus monkeys were fed a high refined fructose diet (75 grams per day) that caused detrimental metabolic changes that are similar to those seen in the metabolic syndrome including insulin resistance and hypertriglyceridemia. However, supplementation of the high fructose diet with 4 grams per day of fish oils containing 16 % eicosapentaenoic acid (EPA, C20:5 (n-3)) and 11 % docosahexaenoic acid (DHA, C22:6 (n-3)) prevented these fructose-induced metabolic changes.
The fish oils were also able to prevent elevations to leptin levels induced by the high fructose feeding. The addition of fish oil to the diets of the monkeys also prevented rises to the circulating levels of apolipoprotein C3 and E, components of the very low density lipoprotein particle. The monkeys fed fructose had reductions in levels of adropin, a newly discovered peptide which regulates energy metabolism through the control of insulin release. However, the feeding of fish oils attenuated this decline. The long chain fatty acids in fish oils are able to lower plasma triglyceride levels because they appear to decrease intracellular triglyceride synthesis rates and also increase extracellular triglyceride clearance rates. This may occur because they can decrease hepatic inflammation, which in turn decreases the activity of hormone sensitive lipase, and this reduces the amount of fatty acids available for hepatic triglyceride production. At the same time fish oils increase extracellular lipolysis, facilitating triglyceride breakdown and oxidation.
Dr Robert Barrington’s Nutritional Recommendation: It is interesting to note that no difference was observed in the body weight, lean mass, fat mass or fasting glucose metabolism of the two groups of monkeys. This suggests that the damage caused by fructose to the metabolism of energy is not easily detectable without detailed biochemical assessment of particular metabolic markers. This supports the contention that many individuals develop insulin resistance over long periods of time but are apparently symptomless during this period. It is only after many years of poor quality nutrition that the insulin resistant state starts to produce disease in the individual. However, often by this time it is too late to reverse much of the damage caused by the metabolic changes. Avoiding refined fructose is paramount in the prevention of insulin resistance and its associated Western lifestyle diseases. As fructose is a component of sugar, this strategy necessitates the removal of all sources of sucrose from the diet, with the exception of that found naturally in fruits, vegetables and honey.
RdB
