Carbohydrates and aging and age related diseases
Human Aging, Position Paper
Longevity of adults has changed little
Free radicals part of aging process
FAD AGING CURES EXPOSED, by leading scientists
genes that slow aging
Genes and aging
Insulin's effect upon the SKN-1 gene and aging
Telemores, sexual size dimorphism and gender gap in life expectancy
SKIN AGING: causes & treatments
Carbohydrates and aging and age related diseases
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Why Women Live Longer than Men

The sugar link to aging (from Wikipedia.org).  How the reaction with sugars (fructose, glucose and galactose produce products implicated in various age related diseases.  The best source of energy comes from starches, which are long chains of glucose. 

Fructose (or levulose) is a simple sugar (monosaccharide) found in many foods and one of the three most important blood sugars along with glucose and galactose. Honey; tree fruits; berries; melons; and some root vegetables, such as beets, sweet potatoes, parsnips and onions, contain fructose, usually in combination with sucrose and glucose. Fructose is also derived from the digestion of sucrose, a disaccharide consisting of glucose and fructose that is broken down by enzymes during digestion. Fructose is the sweetest naturally occurring sugar, estimated to be twice as sweet as sucrose.

Fructose is often recommended for, and consumed by, people with diabetes mellitus or hypoglycemia, because it has a very low Glycemic Index (GI 23) relative to cane sugar (sucrose).  However, this benefit is tempered by concern that fructose may have an adverse effect on plasma lipid and uric acid levels, and the resulting higher blood levels of fructose can be damaging to proteins (see below). The low GI is due to the unique and lengthy metabolic pathway of fructose, which involves phosphorylation and a multi-step enzymatic process in the liver. See health effects and glycation for further information.

Fructose depends on glucose to carry it into the blood stream via GLUT-5 and then GLUT-2 [1]. Absorption of fructose without glucose present is very poor, and excess fructose is carried into the lower intestine where it provides nutrients for the existing flora, which produce gas. It may also cause water retention in the intestine. These effects may lead to bloating, excessive flatulence, loose stools, and even diarrhea depending on the amounts eaten and other factors.

Fructose has been hypothesized to cause obesity [2], elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. Unlike animal experiments, some human experiments have failed to show a correlation between  fructose consumption and obesity. Short term tests, lack of dietary control, and lack of a non-fructose consuming control group are all confounding factors in human experiments. However, there are now a number of reports showing correlation of fructose consumption to obesity, especially central obesity which is generally regarded as the most dangerous type. (Wylie-Rosett, 2004)(Havel, 2005)(Bray, 2004) (Dennison, 1997)

Fructose also chelates minerals in the blood. This effect is especially important with micronutrients such as copper, chromium and zinc. Since these solutes are normally present in small quantities, chelation of small numbers of ions may lead to deficiency diseases, immune system impairment and even insulin resistance, a component of type II diabetes (Higdon).

Fructose is a reducing sugar, as are all monosaccharides. The spontaneous addition of single sugar molecules to proteins, known as glycation, is a significant cause of damage in diabetics. Fructose appears to be as dangerous as glucose in this regard and so does not seem to be the answer for diabetes (McPherson et al, 1988) This may be an important contribution to senescence and many age-related chronic diseases (Levi & Werman 1998).

Fructose is used as a substitute for sucrose (common sugar) because it is less expensive and has little effect on measured blood glucose levels. Often Fructose is consumed as high fructose corn syrup which is corn syrup (glucose) which has been enzymatically treated, by the enzyme glucose isomerase, to convert a portion of the glucose into fructose thus making it sweeter. This is done to such a degree to yield corn syrup with an equivalent sweetness as sucrose by weight. While most carbohydrates have around the same amount of calories, fructose is sweeter, so manufacturers may use less fructose to get the same sweetness. The free fructose present in fruits, their juice, and honey is responsible for the greater sweetness of these natural sugar sources.


Glycation is the result of a sugar molecule, such as fructose or glucose, bonding to a protein or lipid molecule without the controlling action of an enzyme. All blood sugars are reducing molecules. Glycation may occur either inside (endogenous) or outside (exogenous) the body. Enzyme-controlled addition of sugars to protein or lipid molecules is termed glycosylation; this process is less haphazard than glycation. Much of early laboratory research work on fructose glycations used inaccurate assay techniques that drastically understated the importance of fructose in glycation formation (Ahmed & Furth 1992).


Exogenous, which literally means 'outside the body' may also be referred to as "dietary" or "pre-formed." Exogenous glycations and Advanced Glycation Endproducts (AGEs) are typically formed when sugars are cooked with proteins or fats. Temperatures over 120C (~248F) greatly accelerate the reactions, but lower temperatures with longer cooking times also promote their formation.

These compounds are absorbed by the body during digestion with about 30% efficiency. Browning reactions (usually Maillard type reactions) are evidence of pre-formed glycations. Indeed, sugar is often added to products such as French fries and baked goods to enhance browning. Glycation may also contribute to the formation of acrylamide (Stadler et al 2002), a potential carcinogen, during cooking. Until recently, it was thought that exogenous glycations and AGEs were negligible contributors to inflammation and disease states, but recent work has shown that they are important (Vlassara, 2005). Although most of the research work has been done with reference to diabetes, these results are most likely important for all people as exogenous AGEs are implicated in the initiation of retinal dysfunction, cardiovascular diseases, type II diabetes, and many other age related chronic diseases.

Food manufacturers have added AGEs to foods, especially in the last 50 years, as flavor enhancers and colorants to improve appearance (Peppa et. al. 2003). Foods with significant browning, caramelization, or with directly added preformed AGEs can be exceptionally high in these proinflammatory and disease initiating compounds. A very partial listing of foods with very high exogenous AGEs includes: donuts, barbecued meats, cake, and dark colored soda pop (Koschinsky, et. al. 1997).


Endogenous glycations occur mainly in the bloodstream to a small proportion of the absorbed simple sugars: glucose, fructose and galactose. The balance of the sugar molecules is used for metabolic processes. It appears that fructose and galactose have approximately ten times the glycation activity of glucose, the primary body fuel (McPherson et al 1988). Glycation is the first step in the evolution of these molecules through a complex series of very slow reactions in the body known as Amadori reactions, Schiff base reactions, and Maillard reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as: type II diabetes mellitus (beta cell damage), cardiovascular diseases (the endothelium, fibrinogen and collagen are damaged), Alzheimer's disease (amyloid proteins are side products of the reactions progressing to AGEs), cancer (acrylamide and other side products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination) and blindness (mostly due to microvascular damage in the retina). This range of diseases is the result of the very basic level at which glycations interfere with molecular and cellular functioning throughout the body and the release of highly-oxidizing side products such as hydrogen peroxide.

Glycated substances are eliminated from the body slowly, since the renal clearance factor is only about 30%. This implies that the half-life of a glycation within the body is about double the average cell life. Red blood cells are the shortest-lived cells in the body (120 days), so, the half life is about 240 days. This fact is used in monitoring blood sugar control in diabetes by monitoring the glycated hemoglobin level. As a consequence, long-lived cells (such as nerves, brain cells) and long-lasting proteins (such as DNA, eye crystalline, and collagen) may accumulate substantial damage over time. Metabolically-active cells such as the glomeruli in the kidneys, retina cells in the eyes, and beta cells (insulin-producing) in the pancreas are also at high risk of damage. The epithelial cells of the blood vessels are damaged directly by glycations, which are implicated in atherosclerosis, for example. Atherosclerotic plaque tends to accumulate at areas of high blood flow (such as the entrance to the coronary arteries) due to the increased presentation of sugar molecules, glycations and glycation end-products at these points. Damage by glycation results in stiffening of the collagen in the blood vessel walls, leading to high blood pressure. Glycations also cause weakening of the collagen in the blood vessel walls, which may lead to micro- or macro-aneurisms; this may cause strokes if in the brain.





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