Part 1: Could Fructose And Uric Acid Be Driving Diabetes?

Published on November 15, 2012 by Dr. Paul Hrkal

Diabetes has now become an international health problem of epidemic proportions. According to the Canadian Diabetes Association there are currently 9 million Canadians living with diabetes or pre-diabetes. This number is expected to continue to grow at an accelerated pace. The center for disease control predicts that if the rate of growth continues 1 out of 3 people born today will have type 2 diabetes. These statistics have set off alarm bells at all levels of the government and health care system and they have begun dumping resources and funding into diabetes education, research and treatments.

Fortunately, we have a good idea what factors initiate and cause the progression of diabetes. Most savvy medical professionals, research scientists and knowledgeable people know that dietary and lifestyle factors such as regular physical activity and a diet low in refined, processed foods and high in fibre, low fat protein, fruits and vegetables prevents the onset of type 2 diabetes. Yet despite this knowledge, the number of people being diagnosed with diabetes is continuing to increase.

Researchers have tried to identify the key factors that are responsible for driving diabetes. There is little argument that a diet high in refined sugar has a central role. Looking back at the history of diabetes, it was non-existent before the advent of large-scale sugar farming. It was first observed in the wealthy upper class since they consumed more sugar (which was expensive at the time) (Johnson et al).

Figure One here shows the relationship between sugar consumption 

and the increase of diabetes over the last 100 years. Gross et al studied foods with highest impact on weight gain, obesity and the development of diabetes in people over the past 50 years. They found that high fructose corn syrup (HFCS) was the most strongly related food. HFCS is a very common ingredient added to many processed foods. It is favored as a sweetener since it is sweeter than glucose and is produced from corn, which is a major crop harvested in North America. Unfortunately there is mounting evidence that HFCS (fructose specifically) plays a key role is the initiation, development and progression of diabetes. Fructose has further peaked my interest since some researchers are now strongly linking a high intake of fructose with increased uric acid levels and the progression of type 2 diabetes (Johnson et al). The rest of this article will examine this connection and highlight possible natural interventions to address this possible mechanism.

Fructose is a sugar that commonly found naturally in fruits but it most often is added as a sweetener in processed foods in the form of sucrose (50% glucose 50% fructose) or HFCS (55% fructose 45% glucose). Compare to glucose, fructose has unique features in its metabolism that contribute to conditions such as insulin resistance, diabetes and metabolic syndrome. The following is a discussion of key features of fructose, which account for its harmful effects (adapted from Johnson et al).

1)      The rate-limiting enzyme in fructose metabolism is fructokinase. Unlike hexokinase, (used by glucose), fructokinase is very poorly regulated so once fructose is ingested, it rapidly is metabolized which uses up large amounts of ATP, (the energy currency of the body) stealing it from vital cell functions (especially in the liver).

2)      The depletion of ATP leads to lower levels in the vascular endothelium which can lead to transient ischemia (lack of oxygen) which causes a cascade of inflammatory signals, oxidative stress and dysfunction. This can promote decreases function and increases damage which leads to conditions such as hypertension.

3)      Fructose is highly lipogenic, which means it strongly stimulates fat production. A number of studies have shown it increases triglyceride synthesis and fatty deposition in liver. This may have been advantageous for our ancestors since they could rapidly store energy in the form of fat but in our current culture of excess calories this function has a negative effect.

4)      Unlike glucose, fructose does not stimulate insulin release. This may seem beneficial to diabetics but long-term effects are detrimental due many other effects discussed in this article (hypertension, elevated triglycerides etc.).

5)      A high intake of fructose has been found to cause abdominal weight gain. Since fructose does not stimulate insulin secretion, there no resulting ghrelin inhibition and leptin release. Leptin is the hormone that tells the brain that we are full. Low levels of leptin lead to no appetite suppression, which causes people to eat more and contributes to obesity.

6)      Sucrose (and fructose) has been identified as a very additive substance. New research has shown it may be as addicting as common recreational drugs.

7)      One of the most interesting aspects of fructose is its ability to stimulate uric acid production. Uric acid levels increase rapidly after ingestion. This can cause a number of additional negative effects. Uric acid can inhibit endothelial nitric oxide formation, which is linked to hypertension. Some evidence also indicates that it can directly cause insulin resistance via oxidative stress and inflammation in fat cells.

It is clear that a diet high

in fructose can predispose a person to multiple disease processes. Figure Two here summarizes the effects of fructose and the connection with type 2 diabetes.

For more on this topic please visit Part 2 of this blog post series here!

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