Fructose in the Diet Leads to Fatty Liver & Promotes Metabolic Disease
The
amount of fructose in the typical American diet has increased dramatically in
the past 20 years. This is due primarily to the increased use of high fructose
corn syrup (HFCS) as a sweetener is processed foods and drinks, especially soft
drinks. The use of HFCS as a sweetener stems from the fact that the US grows significantly
more corn than sugar beets or cane sugar and it is relatively easy and inexpensive
to chemically convert some of the glucose in corn starch (starch being a
polymer of glucose) to fructose. Consumption of soft drinks (high in HFCS) is
associated with an increased risk for obesity in adolescents and for development
of type 2 diabetes in young and middle-aged women. Excess fruit juice (also
rich in fructose) is also associated with the development of obesity in
children. One cannot, however, assume that the culprit is exclusively HFCS. In
the typical Western-style diet there is an overall excess of caloric intake
that contribute to obesity, diabetes, heart disease, and numerous other
ailments. However, this is not to say that fructose is an “innocent” molecule.
Indeed, consumption of fructose has been shown to be highly correlated with the
development of diabetes, fatty liver diseases, obesity and the metabolic syndrome.
Consumption of soft drinks (high in HFCS) is associated with an increased risk
for obesity in adolescents and for type 2 diabetes in young and middle-aged
women. Excess fruit juice (also rich in fructose) is also associated with the
development of obesity in children. These effects are related to the mechanism
of fructose metabolism versus that of glucose and also to the effects of
fructose metabolism in the brain on appetite and feeding behaviors.
For the
details go to the Fructose Metabolism page of my website.
New data recently e-published in the American
Journal of Clinical Nutrition demonstrates that dietary fructose, even under
conditions of normal caloric intake, leads to hepatic damage and endotoxemia
contributing to the development of hepatic steatosis (fatty liver) and
non-alcoholic fatty liver disease (NAFLD). This is significant because hepatic
steatosis is highly correlated with diabetes and cardiovascular disease.
This research is significant to human
health for a number of reasons, the most important being that the data was
acquired with the use of primates and not mice which are the more commonly used
mammalian model. The other significant fact is that the damaging effects of
fructose were observed even when the animals were fed a normal caloric diet.
The experiments performed in this
published study demonstrated that high dietary fructose consumption rapidly
induces liver fatty infiltration, inflammation, and damage. Significantly,
these hepatic changes were shown to occur in a short time period and under
conditions when the caloric intake was controlled and there were no changes in the
gut microbiome, overall levels of adiposity, or development of signs of the metabolic
syndrome.
The take-home from these studies is that
even if one carefully watches the total calories consumed in order to maintain
a normal body mass index (i.e. low total adiposity), if too many of the
calories are delivered in the form of fructose, either as HFCS or sucrose (a
disaccharide of glucose and fructose) metabolic disruption and disease can
result.
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