SUGAR RISKS                                                                                                      Edited: April 2010/ Updated August 2010

It is well known that our biochemistry uses carbohydrates as energy source.
What is less known is that our biochemistry also uses carbohydrates to build complex molecules.
The production of complex molecules containing carbohydrates is a precise enzymatic process. When enzymes attach carbohydrates to another molecule, they attach the carbohydrate on a specific molecule and at a specific site of the molecule only. 

In contrast, carbohydrates can also haphazardly attach to any of several sites along any available molecule. The random attachment of a carbohydrate to other molecules is termed Glycation or Glycosylation. It happens most with the most abundant carbohydrates—glucose and fructose. Glycation is as detrimental for any molecules as its oxidation by free radicals.

Figure 1: Oxidation and glycation cause the same damage.

Glycation triggers a cascade of chemical reactions that culminate in the formation, and eventual accumulation, of irreversible cross-links. Sugar “sticks” and molecules linked by random carbohydrate links lose their mobility, and their functions. Glycated molecules are out of business.

Glycation occurs all the time, and at a low rate. Glycation occurs much more in hyperglycemia.

Glycation may happen to any molecule. If glycation happens to a molecule with a high turnover rate, the damage is temporary. However, the damaged molecule is not repaired, it is destroyed and a new one may replace it. On the contrary, the damage by the glycation of a molecule with a low turnover rate lasts longer and becomes permanent for molecules that are not replaced. Glycation of molecules with a slow turnover is a factor of senescence—the aging of cells, tissue and organs at a faster pace than expected for the age of the person.


Glycated molecules attract scavenger white blood cells. This initiates an inflammatory process to eliminate the damaged and useless molecules. The glycation explains why people with hyperglycemia have more problems with chronic inflammation processes.

Damage to Red Blood Cells

Red blood cells exposed to hyperglycemia have their hemoglobin (L) altered by glycation (Hb A1c). Hb A1c is an irreversible stable product. Hb A1c is formed at rates that increase with increasing plasma glucose and fructose levels. The function of hemoglobin in red blood cells is to carry oxygen. Glycated hemoglobin carries less oxygen or no oxygen at all. Glycated hemoglobin is wasted hemoglobin. The tissue and organs of people with high levels of glycated hemoglobin lack oxygen. Glycated hemoglobine (Hb A1c) can be tested by a laboratory examination. The Hb Ac1 level is considered a reliable evaluation of what the average blood sugar level was over the past 3 months. A Hb A1c positive test is not a specific test for diagnosing diabetes. Hb A1c tests positive in people with high levels of glucose or fructose in circulation, people with diabetes included.

Damage to White Blood Cells

Several experiments demonstrate the delirious effect of hyperglycemia on the number and the function of circulating white blood cells. Hyperglycemia disrupts the communications of white blood cells, reducing their functions. We have seen that glycation—induced by hyperglycemia, triggers inflammation by attracting scavengers cells. Hyperglycemia contributes further to inflammation by stimulating the production of pro-inflammatory prostaglandins (L), critical in the progressive development of heart disease, diabetes and obesity.

Damage by Fructose

Until recently it was believed that dietary fructose—as opposed to the glucose from starch and from sugar, may produce a lesser rise in plasma glucose. Based on the prevalent opinion that fructose was less detrimental, diabetics were encouraged to use fructose.
This lesser effect of fructose on the blood sugar level is confirmed by more recent investigations that have, however, demonstrated that in healthy volunteers, as well as in people with diabetes, fructose has a higher chemical affinity for proteins than the glucose molecule. Consequently, the random attachment of fructose to other molecules causes more damage than the random attachment of glucose.

Aside from this fructose can not be used for energy unless is is changed into glucose, which is a three step enzymatic reaction that takes time. Meanwhile fructose is easily changed into fat and stored as such in the liver.

Time is the Essence

Medical textbooks and diabetic associations publish lists of complications of diabetes.
The prevalent opinion has always been that these complications occur in diabetics only, and one should have to become a diabetic before any of theses complications can arise.

Nothing is more misleading:

The complications of diabetes result from hyperglycemia. However, hyperglycemia occurs well before someone is “labeled” a diabetic.

The damage caused by hyperglycemia occurs each time the level of blood sugar surges after a starch and glucose rich meal. It occurs in young infants as well.

The National Diabetes Education Program (NDEP) cites 7 risk factors for diabetes: Overweight, Genetics, Race, Pregnancy diabetes, High blood pressure, High cholesterol and Inactivity.

However, the NDEP does not mention hyperglycemia as a factor of diabetes, and is silent about a link between a starch and sugar rich diet and hyperglycemia.


It appears that hyperglycemia is still considered a consequence of diabetes rather than a cause of it.