Linoleic Acid (Omega-6) |
Linolenic Acid (Omega-3) |
Soybean | Flaxseed |
Safflower | Soybean |
Sunflower | Rapeseed (canola) |
Corn | Pumpkin |
Wheat germ | Walnut |
Sesame | |
_______________
*These foods are listed under their primary lipid components
ESSENTIAL FATTY ACID METABOLISM
OMEGA-6 |
|
OMEGA-3 |
Most Vegetable Oils | |
Flaxseed or Canola Oils |
|
can be converted to |
|
Linoleic acid (LA) |
———––in plants, but–––——— |
Alpha-linolenic acid (LNA) |
|
not in humans | |
Gamma-linolenic acid (GLA) |
COLD WATER FISH——— |
Eicosapentaenoic acid (EPA) |
|
such as salmon or mackerel | |
|
in the diet will introduce | |
Dihomogamma-linolenic |
EPA and DHA directly—— |
Decosahexaenoic acid (DHA) |
acid (DGLA) |
into the body | |
| | |
Arachidonic acid (AA) | | Prostaglandin E3 series (PGE3) |
| | |
Prostaglandin E1 series (PGE1) | | |
| | |
Prostaglandin E2 series (PGE2), | | | |
Thromboxane | | | |
in and out of cells. Another phospholipid, sphingomyelin, consists of glycerol, fatty acid, phosphate, choline, and an amino alcohol called sphingosine and is part of the tissues covering brain and nerve cells, as are the cerebrosides, phospholipids that contain galactose, fatty acid, and sphingosine.
Sterols/Cholesterol
Sterols, the third primary lipid, include cholesterol, phytosterols (plant sterols), and some of the steroid hormones. Cholesterol, the best known of the sterols, is the precursor of the bile acids and the sex hormones. Manufactured in the body, primarily in the liver, although all tissues of the body except the brain can make it, cholesterol is present in almost all cells and is particularly high in the liver, brain and nervous tissue, and the blood. Cholesterol, like lecithin, is also available in foods, such as egg yolk, meats, and other animal fats, including milk products. It is not readily available in most vegetable foods.
Cholesterol has been implicated in occlusive cardiovascular disease, causing plaque and obstruction of the arteries. The cholesterol in foods, however, is not really the villain. It is the oxidized cholesterol in the blood that causes the trouble, and the level of this is more a function of total dietary fat intake and genetically determined aspects of cholesterol metabolism, than of the amount of cholesterol in our food. In particular, a transport mechanism of cholesterol called the low-density lipoprotein (LDL) is likely the villain in our society’s rampant disease—atherosclerosis. This LDL is contrasted to the so-called “good” cholesterol-carrying high-density lipoprotein (HDL). The ratio of these two (LDL:HDL) is the blood test currently favored to evaluate our risk of cardiovascular disease.
Lipoproteins, the fat-protein combination molecules circulating in our blood and tissues, can move around the body only if they are surrounded by protein, because fats are not soluble in water (the basic makeup of blood and lymph). The fatty acids in these large lipoprotein molecules are positioned at the inside, as far away from the water as possible. The higher the protein portion in these molecules, the higher their density.
There are several important lipoproteins.
Chylomicrons are made in the intestines to transport digested fats (mainly triglycerides) into the circulation to be carried to the liver and other organs.
VLDLs (very-low-density lipoproteins) are made in the intestines and the liver to carry fats throughout the body. Though VLDLs carry mostly triglycerides, they carry a small component, maybe 5–15 percent, of the cholesterol to the tissues of the body.
LDLs (low-density lipoproteins) are made by the liver (and possibly by transformation of VLDLs in the blood) and are the primary molecular complexes that carry cholesterol in the blood to the organs and cells. LDL contains the highest percentage of cholesterol in most people.
HDLs (high-density lipoproteins) are large, dense protein-fat molecules that circulate in the blood, picking up already used or unused cholesterol and cholesterol esters and taking them back to the liver as part of a recycling process. Where in the body HDL is made is not certain (probably in the liver), but it may be the most protective form of lipoprotein in preventing buildup of cholesterol. People with higher HDL levels have less risk of cardiovascular disease because their cholesterol is cleared more readily from the blood. It also appears that HDL may be able to collect cholesterol from artery plaque, thus reversing the atherosclerotic process that leads to heart attacks. HDL will deliver cholesterol to the VLDL, converting them to LDL, which have more density; the liver then removes the LDLs from the blood and converts their cholesterol into bile acids, which are then eliminated.
Estrogen helps raise HDL levels, and women have less cardiovascular risk than men, possibly because of this hormone. Smoking, obesity, and a sedentary lifestyle cause a low level of HDLs, whereas low dietary fat and cholesterol intake, aerobic exercise, and keeping weight near the ideal level are factors that help raise the HDL level and diminish cardiovascular risk.
Digestion and Metabolism
Because of their viscosity and insolubility in water, fats and oil require our bodies to take special care to digest and transport them to the cells and organs. The chewing process is the first act of digestion to help separate the fats. In the stomach, gastric lipase has a very minimal effect in beginning the breakdown of fats; other enzymes and hydrochloric acid do more to digest protein and carbohydrates and free the lipids from the food. Fats and oils are less dense than water; unless they are emulsified they rise and pool at the top of the gastric contents and so are acted upon last, thus taking the longest to digest and in some ways slowing the digestion. Fatty meals seem to satisfy us longer as they cause the stomach to empty more slowly.
When the fats move into the small intestine, their main place of digestion, bile is secreted from the gallbladder (bile is made by the liver and concentrated in the gallbladder). Bile first emulsifies the fats, that is, breaks down the fat globules into smaller groups of molecules so the other enzymes can actually work on the individual triglycerides to release the fatty acids. Pancreatic lipase is the main enzyme that splits the triglycerides into diglycerides and monoglycerides, which are ultimately hydrolyzed into their components, fatty acids and glycerol.
When the digestive system is working well, most (up to 95 percent) dietary fats are absorbed into the body. (Some are excreted through the colon.) Many of the fatty acids need now be altered in order to be absorbed and transported to the liver, the principal site of fat metabolism. The short-chained fatty acids, up to 12 carbons in length, are more hydrophilic, or attracted to water, and can be absorbed directly through the cell membranes of the small intestine villi (small protrusions into the intestinal lumen lined by epithelial cells and filled with capillaries; they increase the absorption surface of the small intestine). Within the villi, these short-chained fatty acids are picked up in the capillaries and transported through the bloodstream to the liver.