Mary M. Fynn, Ph.D, RD, L.D.N



January 2016

Lipids are a group of compounds that are insoluble in water.  From a dietary standpoint, “fat” refers to solid lipid and “oils” to liquid lipid.

The simplest form of lipid is the fatty acid, which is a chain of carbons surrounded by hydrogen.  One end contains a carboxyl group and is called the “alpha end”.  The other end contains a methyl group and is the “omega end”.  Fatty acids are of varying chain length and are named using the number of carbons in the chain.  The carbons form bonds with each other in the chain and hydrogens can fill the other bonds.  If all the carbon bonds are filled by hydrogen, the fatty acid is called “saturated”.  If two adjoining carbons are missing hydrogens, a double bond forms between the carbons and the fatty acid is called “unsaturated” with one bond being a monounsaturated fatty acid and two or more bond are polyunsaturated fatty acids.

The polyunsaturated fats are essential fatty acids (EFA), meaning humans can not make them.  We require approximately 5% of our energy from essential fatty acids.  The EFA families are named by the location of the first double bone counting from the methyl/ omega end.  There are two main families: the omega 3 and the omega 6 families.

The omega 3 family:  linolenic acid is the starting compound and has 18 carbons.  The 20 carbon member is eicosapentenoic acid (EPA) and the 22 carbon is docosahexaneoic acid (DHA).  Humans are very inefficient at elongating and desaturating linolenic acid to receive the 20 and 22 carbon fatty acids.  This means that we can not readily make the EPA or DHA.  Linolenic acid is found in canola oil, walnuts, and purslane.  The 20 and 22 carbon omega 3 fatty acids are found in fatty fish.

The omega 6 family:  linoleic acid is the starting carbon and has 18 carbons.  The 20 carbon member is arachidonic acid; humans can readily elongate and desaturate linoleic acid to synthesize arachidonic.  Linoleic acid is found mainly in vegetable seed oils (corn, soybean, safflower); the main dietary source of arachidonic is beef.

The omega 3 and omega 6 fatty acids of 20 carbons or longer are used to synthesize eicosanoids which are hormone-like compounds; they are called “hormone-like” as they can work like hormones but they work where they are made (and hormones travel by the blood from where they are made to where they work).  The omega 3 family makes eicosanoids that are anti-inflammatory, anti-aggregation, and vasodilators.  The omega 6 family makes eicosanoids that are proinflammatory, proaggregatory, and vasoconstrictive.  The 20 carbon members of the families compete at the starting enzyme so the predominant fatty acid will determine what set of eiconsanoids are made.   The health benefits from the omega fatty acids are related to the blood ratio of the two fatty acid families.  The typical American diet is high in omega- 6 due to the use of vegetables oils and their products (margarine, mayonnaise, commercial salad dressings).   Some years ago, health professionals in the US started to address this by suggesting patients consume fish oil pills.  Your writer does not support this practice as all polyunsaturated fats will increase oxidation, which will contribute to a list of diseases.  I suggest that people minimize their intake of vegetable oils; this would decrease the omega-6 fatty acid in the body and would allow any longer chain omega 3 fatty acids present to work without excessive hindrance.

Triglyceride is a lipid that has a glycerol backbone with three fatty acids attached to it.  Triglyceride is the lipid that supplies energy both in food and in us (triglyceride is what is stored in the adipose tissue).  The 3 fatty acids are a mixture of fatty acids with some saturated, some unsaturated.  The fatty acids that predominate give the naming to a food as being a source of saturated fat, monounsaturated fat, or polyunsaturated.  However, no food is purely 1 type of fatty acid.  Interestingly, although beef is labeled a source of saturated fat, it contains mainly monounsaturated fat.

Trans fats are produced primarily in an industrial process.  They are made by adding hydrogen to polyunsaturated fats (liquid vegetable oils).  The process is called “hydrogenation”.  This solidifies the oil, which is how margarine and vegetable shortenings are made.  hydrogenation also makes the oil less likely to oxidize (become rancid).  This increases the shelf-life of food.  Foods with a long-shelf life, like commercial baked goods, are high in trans fatty acids.

The health concern with trans fatty acids is that in the body they can replace cis or the natural fatty acids in phospholipids and other places where one would fine triglycerides.  The trans fatty acids are unnatural to the body and have been consistently linked to an increase risk of chronic diseases, especially cancer and heart disease.  Some of this research has involved measuring the amount of trans fatty acid present in the adipose tissue.  As these fatty acids are not naturally found in the body (i.e., we do not make them), any present in the adipose would be from the diet.  Your writer has long felt that as any food with trans fatty acids is not a healthy food, counseling people to eat a more healthy diet would minimize the intake of trans fatty acids.

Cholesterol is a lipid that is a sterol.  It is only found in animal foods and does not supple any energy.  Cholesterol is used to make some hormones (estrogen, testosterone); is a starting compound for vitamin D synthesis in the body; it is part of bile; it is an essential structural part of cell membranes; and it is part of lipoproteins.

Lipoproteins are made to carry lipid in the blood.  All lipoproteins contain lipids (cholesterol, triglycerides, phospholipids) and protein, which are called “apoproteins”.  The amount of each component varies by the lipoprotein.

Chylomicrons are made in the small intestines and are used to transport exogeneous (dietary) triglyceride.  The rest of the lipoproteins are named by density or weight; the weight being the apoprotein content.

Very low density lipoprotein cholesterol (VLDL) is made in the liver to carry primarily endogenous triglyceride which is made in the liver from extra calories we consume.  VLDL triglyceride is the triglyceride measured in fasting blood.  VLDL levels are increased with a low-fat, high carbohydrate diet; the carbohydrate consumed in excess of need or ability to store as glycogen is converted to fatty acids, which are then converted to triglyceride.  How high VLDL increases with a high carbohydrate diet depends on the starting level for fasting triglycerides and how well insulin is working; insulin resistance would make theVLDL increase greater compared to when there is not insulin resistance.

When sufficient triglyceride is removed from the VLDL (i.e., either stored in adipose or used for energy) there is a decrease in density, and the particle becomes a low-density lipoprotein (LDL). LDL particles are mainly cholesterol.

Effect of diet on LDL:

  1. saturated fats can increase LDL levels with the increase mainly dependent on the diet of comparison.  There is also thought to be a genetic effect on the change with some people being more responsive to diet than others.
  2. polyunsaturated fats can decrease LDL more than other dietary fats will; however, PUFA will become part of the lipoproteins, which leads to oxidation of the particle.
  3. monounsaturated fats tend to decrease LDL, but they definitely do not lead to oxidation.
  4. a low-fat diet will lower LDL because the VLDL is not being efficiently converted to LDL.  When a low-fat diet decreases LDL, you will see an increase in fasting triglycerides (VLDL).

High levels of LDL have been related to an increase risk of CHD, but it is the oxidized form of LDL that leads to an increase in risk of CHD.

High density lipoprotein cholesterol (HDL) has an inverse relationship to heart disease, however, the reason why is not known.  The possible reasons include:

  1. reverse cholesterol transport – HDL is thought to bring cholesterol from the peripheral back to the liver for disposal.  Your reader has not found the evidence for this being the main health benefit of HDL very convincing.
  2. block oxidation of LDL – HDL carries antioxidants and may prevent LDL from oxidizing.
  3. Marker for efficient triglyceride catabolism – triglyceride levels have been inversely related to heart disease in some studies.  Triglycerides do have an inverse relationship to HDL so when triglycerides are high, HDL is low and vice versa.  It is possible that the HDL is just a stable marker for efficient triglyceride catabolism so higher levels of HDL mean there is better catabolism of VLDL; triglyceride values can vary greatly from day to day and HDL does not.

High levels of HDL are primarily genetically determined; only small (5 to 10%) changes can be achieved with diet or lifestyle.  Weight loss that lowers fasting triglycerides can result in a small increase in HDL, due to the inverse relationship discussed above.   The loss of weight could be by change in diet and/or increase in physical activity.  However, it is not correct to say that physical activity will increase HDL to levels found in endurance athletes.

Effect of diet on HDL:

A moderate / high fat diet will increase HDL and a low-fat (less than about 25% of total energy) diet will decrease HDL.  All types of dietary fat, except trans fats will increase HDL, but extra virgin olive oil has been shown to have an independent effect on increasing HDL.