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Sugars, an overview


Background information on sugars and starches




The dietary sugars are linked to aging (fructose, glucose and galactose) because in the cell their reactive products of metabolism damage the mitochondria and because of glycation.  Glycation occurs when a monosaccharide latches on to a protein and adversely affects their functions.  Because of this saturated fats, and monounsaturated fats unsaturated fats are the best sources of energy.  The various health issues with the other sources of energy are explained in the following links on carbohydrates, transfats and polyunsaturated fats.    

Carbohydrates are polyhdroxy aldehydes, poyhydroxy ketones, or compounds that can be hydrolyzed to them.  A carbohydrate that cannot be hydrolyzed to a simpler compound is called a monosaccharide; hydrolyzed to two mono-hydrides is called a disaccharide, and polysaccharide for many monosaccharide molecules.

Glucose (blood sugar) also known as D-glucose, dextrose.  The open chain form is unstable and spontaneously tautomerized to the cyclic form.  One reason might be that glucose has a lower tendency, relative to other hexose sugars, to react non-specifically with the amino groups of proteins. This reaction (glycation) reduces or destroys the function of many enzymes. The low rate of glycation is due to glucose's preference for the less reactive cyclic isomer. Nevertheless, many of the long-term complications of diabetes (e.g., blindness, renal failure, and peripheral neuropathy) are probably due to the glycation of proteins or lipids.[3] In contrast, enzyme-regulated addition of glucose to proteins by glycosylation is often essential to their function.  Glucose is the human body's key source of energy, through aerobic respiration, providing approximately 3.75 kilocalories (16 kilojoules) of food energy per gram.[4]  Starch, cellulose, and glycogen ("animal starch") are common glucose polymers (polysaccharides).  Most dietary carbohydrates contain glucose, either as their only building block, as in starch and glycogen, or together with another monosaccharide, as in sucrose and lactose.

Sucrose (common name “table sugar”) is glucose and fructose glycemic index of 80 (honey 75)  humans and other mammals, sucrose is broken down into its constituent monosaccharides, glucose and fructose, by sucrase or isomaltase glycoside hydrolases, which are located in the membrane of the microvilli lining the duodenum.[9][10]

Starch or amylum is a carbohydrate consisting of a large number of glucose units joined by glycosidic bonds. This polysaccharide is produced by most green plants as an energy store. It is the most common carbohydrate in human diets and is contained in large amounts in such staple foods as potatoeswheatmaize (corn), rice, and cassava.

Glycogen is a multi-branched polysaccharide that serves as a form of energy storage in animals[2] and fungi.  It is stored primarily in the cells of the liver and the muscles, and functions as the secondary long-term energy storage (with the primary energy stores being fats held in adipose tissue).  Muscle cells lack the enzyme glucose-6-phosphatase, which is required to pass glucose into the blood, Glycogen is the analogue of starch, a glucose polymer in plants, and is sometimes referred to as animal starch. 

Galactose is a monosaccharide. When combined with glucose (monosaccharide), through a dehydration reaction, the result is the disaccharide lactose.  Galactose metabolism, which converts galactose into glucose,  Galactose is found in dairy products, sugar beets, and other gums and mucilages. It is also synthesized by the body, where it forms part of glycolipids and glycoproteins in several tissues.  Galactan can be converted to galactose by hydrolysis.

Malt is germinated cereal grains that have been dried in a process known as "malting". The grains are made to germinate by soaking in water, and are then halted from germinating further by drying with hot air.[1][2][3][4] Malting grains develop the enzymes required to modify the grain's starches into sugars, including the monosaccharide glucose, the disaccharide maltose, the trisaccharide maltotriose, and higher sugars called maltodextrines. It also develops other enzymes, such as proteases, which break down the proteins in the grain into forms that can be used by yeast. Malt also contains small amounts of other sugars, such as sucrose and fructose, which are not products of starch modification but were already in the grain.  Barley is the most commonly malted grain, in part because of its high diastatic power or enzyme content, though wheatryeoats and rice are also used.

maltobiose or malt sugar, is a disaccharide formed from two units of glucose.   Maltose is the disaccharide produced when amylase breaks down starch. It is found in germinating seeds such as barley as they break down their starch stores to use for food. It is also produced when glucose is caramelized.[4]  Maltose is a component of malt,

Fructose or levulose (from 2004 article with updates from 2012) is a simple sugar (monosaccharide) found in many foods and one of the three most important blood sugars along with glucose and galactose,  all of which are directly absorbed . 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.  All three dietary monosaccharides are transported into the liver by the GLUT2 transport. 

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) [rated at 100].  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.[1]

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).  [Article misses it role in non-alcoholic fatty liver disease, which causes first insulin resistance in the liver which develops into insulin resistance in the adipose and muscle tissues, and eventual it can progress to type-2 diabetes.  This pathway is dependent upon a high carb and high sugar diet.  Glucose raises insulin which cases fat storage, and this leads to a fatty liver, since fructose is only metabolized in the liver where it is converted into fat.  Population studies fail to adequately uncover this role of fructose because the high intake of sugar, such as from sodas and fruit drinks, often is temporary, and could happen decades early.  A large percentage of the obese population reduce their sugar consumption as part of their attempt at weight control.]

Compared to sucrose

Studies that have compared high-fructose corn syrup (an ingredient in nearly all soft drinks sold in the US) to sucrose (common table sugar) find that most measured short term physiological effects are equivalent.[dubiousdiscuss]; however, studies that compare the long term effects between sucrose and fructose have yet to be conducted. For instance, Melanson et al. (2006), studied the short term effects of HFCS and sucrose-sweetened drinks on blood glucose, insulin, leptin, and ghrelin levels. They found no significant differences in any of these parameters.[54] This is not surprising since sucrose is a disaccharide that digests to 50% fructose and 50% glucose, whereas the high-fructose corn syrup most commonly used on soft drinks is 55% fructose and 45% glucose. The difference between the two lies in the fact that HFCS contains little sucrose, the fructose and glucose being independent moieties. Even so, Melanson et al. found that "Longer-term studies on connections between HFCS, potential mechanisms, and body weight have not been conducted". 


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 often recommended for diabetics because it does not trigger the production of insulin by pancreatic β cells,

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).

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). Compared with consumption of high glucose beverages, drinking high fructose beverages with meals results in lower circulating insulin and leptin levels, and higher ghrelin levels after the meal.[62] Since leptin and insulin decrease appetite and ghrelin increases appetite, some researchers suspect that eating large amounts of fructose increases the likelihood of weight gain.[63]  Probably more important to advanced life is the low tendency of glucose, by comparison to other hexose sugars, to non-specifically react with the amino groups of proteins. This reaction (glycation) reduces or destroys the function of many enzymes.  The low rate of glycation is due to glucose's preference for the less reactive cyclic isomer. Nevertheless, many of the long-term complications of diabetes (e.g., blindness, kidney failure, and peripheral neuropathy) are probably due to the glycation of proteins or lipids. Glycosylation is another important type of reaction undergone by glucose.

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.

Exogenous glycations and Advanced Glycation End products (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. Exogenous iterally means 'outside the body' and refers to as "dietary" or "pre-formed."

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 pro-inflammatory 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 end products (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 glyc ation 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.

[1] It is tobacco science to recommend fructose for diabetics, especially those with type-2 diabetes (adult onset).  The path to their conditions starts with a fairly consistent consumption of more than 40 grams of fructose dialing along with a high carb diet, and no prolonged periods of fasting.  Fructose is metabolized only in the liver, where most of it is converted into fat.  This fat gradually accumulates in the liver resulting in a fatty liver, called Non-Alcoholic Fatty Liver Disease (NAFLD), which depending on lifestyle often results in insulin resistance.  Insulin resistance is the prerequisite condition for progression into type-2 diabetes.  Thus to recommend fructose and a high carb diet is to promote the progression of type-2 diabetes.    

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