Carbohydrate

Carbohydrate molecules made up of mono-, di- tri- andpoly-saccharides

multi-hydroxylated 5- (ribose) and6-carbon (glucose, fructose, galactose ...)cyclic molecules.

Some monosaccharides

Some Disaccharides

Mammals store glucose as glycogen (humans store approximately 350g in muscle; 90 g in liver)

Plants store glucose as starch, build cellulose for structure

Tissue Stores ~g Days Days Minutes Starvation Walking Marathon

Running

Adipose TG 9,000 34 10.8 4,018

Liver Glycogen 90 0.15 0.05 18

Muscle Glycogen 350 0.6 0.2 71

Blood Glucose 20 0.03 0.01 4

Body “Stores” of Energy

Carbohydrates primary NRG source for C&PNS

NRG for moderate/stressful activities

ribose/deoxyribose (RNA/DNA/ATP…)

muccopolysaccharides (mucus/synovial)

glycoproteins (cell membranes)

D-galactosamine (collagen/cartilage)

DRI 130 g/day45% to 65% of total calories (4 kcal/g)

IOM recommend 1 hour of moderately stressful exercise every day

NRG for moderately stressful exercise is 50 – 80% carbohydrate . . .

6 – 7 mph ~ 600 – 800 kcals @ 50% ~ 300 – 400 kcals ~ 75 – 100 g additional CHO

Therefore, a logical minimum DRI would be more than the IOM recommendation

~ 200g/day would be a reasonable estimate

- Mastication in mouth Bolus w/ saliva/mucus Salivary α-amylase

- Pancreatic enzymes pancreatic α-amylase

- Brush bordersaccharidases:

maltase sucrase lactase

Monosaccharides are absorbed via sodium co-transporters

Carbohydrates are “transported to the liver” through the portal vein and are picked up by the liver (and the rest of the body’s cells for those that the liver doesn’t get) for processing . . .

Liver stores glucose as glycogen (so does the kidney) & releases glucose to the venous circulation and it istransported to the rest of the body through the arterial circulation . . . . . . . . . .

Regulation of glucose levels in the blood is very important

Normal Fasting (Serum) ~ 70 – 100 mg/dl Elevated = Diabetes Low = Hypoglycemia

Insulin from pancreas stimulates uptake of glucose into muscle cells and fat cells by activating the GLUT4 transporters. After eating a meal, glucose levels increase in the blood and trigger an insulin response. Within a1 to 2 hours, glucose levels decline back to normal. With insulin resistance, or diabetes, glucose levels remain elevated for prolonged periods of time and the enhanced levels of glucose in the blood greatly increase risk for a variety of chronic diseases.

When serum levels of glucose decrease too much, then the pancreas releases glucagon to stimulate the liver and kidney to break down glycogen to glucose and release glucose into the blood (glycogenolysis). And the liver will automatically enhance synthesis of glucose from amino acids. Adrenals will release cortisol if levels stay too low for prolonged periods of time to enhance breakdown of protein in muscles to release amino acids so the liver can pick up the amino acids and make them into glucose (gluconeogenesis). This “breakdown” however, only occurs in non-exercising muscles. Because there always is a ready supply of amino acids in liver (even without “breakdown” of muscle protein), rates of gluconeogenesis range from 3 to 4 grams glucose produced/hour. Unfortunately, this rate is less than the amount of glucose necessary for optimal brain function and as a result, we have a minimum requirement for carbohydrates (source of the nutrient: glucose) in our diet.

Glycemic Index and Glycemic Load:

Glycemic Index: A relative measure of how rapidly the digested carbohydrate appears in the blood as glucose relative to the same amount of pure glucose over time. A 50 g amount of glucose would have a GI of 100 while a 50g amount of other carbohydrate sources would be expressed relative to the glucose GI.

GI is 70 or more is highGI of 56 to 69 is mediumGI of 55 or less is low.

Glycemic Index and Glycemic Load:

Glycemic Load: A measure of total amount of glucose appearing in the blood over time based on the total amount of digestible carbohydrate in the food.

GL = GI / 100 x g

GL of 20 or more is highGL of 11 to 19 is mediumGL of 10 or less is low

Because some high GI foods may contain relatively little total carbohydrate (or visa versa), calculating a glycemic load based on both GI and total CHO can make sense:

Wonder enriched white bread: GI = 73, GL = 10 . . . Betty Crocker chocolate cake: GI = 38, GL = 20 . . .

GL / GI per serving of some common foods(adapted from: http://www.mendosa.com/glists.htm)

Low GI Medium GI High GI - 55 56 - 69 70 – 100

Grapes 8 / 46 Pineapple 7 / 59 Watermelon 4 / 72Low Apples 8 / 42 Cantaloupe 4 / 65 Popcorn 8 / 72GL Peanuts 1 / 14 Beets 5 / 64 Wheat bread 8 / 710 - 10 Corn 9 / 54 Sugar 7 / 68 White bread 10 / 70

Baked beans 7 / 48 Rye bread 8 / 58 Waffles 10 / 76Honey 10 / 55

Bananas 12 / 52 Life cereal 16 / 66 Cake donuts 17 / 76Medium Navy beans 12 / 38 Potatoes 12 / 57 Cheerios 15 / 74GL Sourdough bread 15 / 54 Wild rice 18 / 57 Shredded wheat 15 / 7511 - 19 Parboiled rice 17 / 47 Sweet potatoes 17 / 61 Gatorade 12 / 78

Apple juice 12 / 40 Coca Cola 16 / 63 Bran flakes 13 / 74

High Linguine 23 / 52 Couscous 23 / 65 Baked potatoes 26 / 85GL Macaroni 23 / 47 White rice 23 / 64 Cornflakes 21 / 9020+ Spaghetti 20 / 42 Power bar 24 / 56 Dried dates 42 / 103

Note that “complex carbohydrates” form the basis of both high glycemic and low glycemic foods; indicating that the simplified concept that “complex carbohydrates” are better than “simple carbohydrates” doesn’t make a lot of sense. Another “note”: when eaten in combinations, then the GI/GL is completely different than the tabled values indicating that actually applying the GI/GL information to a mixed-diet is very difficult…

The concern with glucose relates only to sustained high levels in the blood. Both glucose (and fructose) can exist in a closed-ring structure (as shown on the second slide) and also as an open-chain structure. In the open-chain configuration, the aldehyde of glucose and the ketone of the fructose can form a reversible Schiff base with any free amino group of any phospholipid, protein, and even on DNA; ultimately leading to the formation of Advanced Glycation End-products (AGEs). Once formed, the AGEs can activate inflammatory processes in the local tissues in which they are formed and the inflammatory process lead to additional tissue dysfunction and various disease such as retinopathies, peripheral vascular disease, atherosclerosis, and stroke.

(~3-6 h to equilibrium) (> weeks to form)Glucose ↔ Schiff base → Amadori Products → various dicarbonyls → AGEs

Fructose ↔ Schiff base → Heyn’s Products → various dicarbonyls → AGEs

Removal of glucose from the blood is largely dependent on insulin while removal of fructose is not; as a result glucose levels in the blood are typically 500 times greater than those of fructose; indicating that glucose is the molecule we need to be concerned with in regard to chronic disease and that fructose is a relatively minor player.

Because the freely reversible Schiff bases need to be present for several weeks (or more) to rearrange into stable Amadori / Heyn’s products; only chronically elevated levels of glucose can lead to elevated risk for disease. With a rate of reversion that reaches equilibrium in approximately 3 to 6 hours, additional Schiff bases formed because of elevated glucose (or fructose) levels following a meal will essentially be back down to normal levels following a customary overnight fast. Because it takes weeks of elevated glucose to lead to additional AGE formation even a weekend of gluttony should not have a great effect as long as normal eating behaviors are followed in subsequent days. Thus, those individuals with normal insulin function have nothing to worry about when it comes to carbohydrate consumption.

Only those with insulin resistance (pre-diabetes) or diabetes need to be concerned and to try and avoid high glycemic loads throughout the day to minimize the additional risks of prolonged periods of elevated glucose (additional issues on the cause of insulin resistance & diabetes are discussed in the PPt on CAD and Cancer).

Because of the enhanced formation of AGEs in those with insulin resistance (pre-diabetes) or diabetes, they also have a greater risk for chronic diseases than those with normal insulin responses; essentially as shown below in relation to clinical “norms”…

The Schiff’s bases are freely-reversible and will equilibrate with glucose levels in approximately 3 to 6 hours. Their conversion into AGE’s requires a sustained elevation in glucose levels over several weeks.

With the traditional timing of eating meals based essentially on work schedules - a timing that includes an overnight fast; “normal” risks for chronic disease are produced (top graph).

Sustained elevation in glucose levels because of insulin-resistance (middle graph) or diabetes (bottom graph) will produce an elevated risk for chronic diseases.

Because it only takes approximately 3 to 6 hours for Schiff’s-base levels to equilibrate with the glucose-levels (regulated to be 70 – 100 mg/dl) it is highly doubtful that even with an early breakfast and late dinner eating pattern (with multiple snacks) there will be an elevated risk for AGE formation (to produce an insulin-resistant pattern and therefore increase risk for chronic diseases); as long as insulin responses are normal.

This means that only with insulin resistance and with diabetes should there be any issues with carbohydrate consumption.