Cholesterol is an essential component for life but can also be fatal if you have too much of the wrong type. Our cells require cholesterol for proper cell wall structure. We get it in our diet and our bodies produce virtually all we will ever need.
Certain types of cholesterol indicate high risk for cardiovascular disease. You may have had your cholesterol checked as part of a wellness exam. There are several components that are evaluated when looking into your cardiovascular risk factors.
Total Cholesterol (TC) – this is the total cholesterol measured on a cholesterol or lipid panel. The typical goal for TC is <200.
Triglycerides (TG) – also known as triacylglycerol. These are 3 fatty acids attached to a glycerol backbone. This is how fats are transported in the blood. Recall that blood is largely composed of water. Water & oil (fat) don’t mix. Lipoproteins carry the TGs to their destination. The goal for TG is certainly <200 but we would like <150.
Low-Density Lipoproteins (LDL) – this is the ‘bad’ cholesterol particle. Lipoprotein molecules are composed of Apoproteins, Triglycerides, Phospholipids, and Cholesterol. LDL is considered ‘low density’ because it is composed of a larger amount of TGs. The goal for LDL for standard risk people is 130 or less. If you have risk factors for heart disease or strokes, such as diabetes or previous heart attack, then your goal will be lower, less than 100. Some have suggested that we get the LDL less than 70 in some people. The formation of atherosclerotic plaques ceases when LDL is less than 100. The plaques actually regress and get smaller with an LDL of less than 70.
However, we have to remember the fact that cholesterol is a vital component to our health. It is essential for optimal function of the cell membrane (helps ensure fluidity) and it is needed for the production of bile and numerous hormones such as testosterone, progesterone, DHEA, estrogen, etc. Therefore, decreasing cholesterol has implications and potential risks. We have to be very careful about decreasing these substances and the risks and benefits of these changes should be thoroughly evaluated.
High-Density Lipoproteins (HDL) – these are the ‘good’ cholesterol. These are playing an increasingly important role in reducing cardiovascular risk. Normal values are typically between 35 and 70. My goal is to get my patients over 60. An HDL over 60 removes one risk factor in the ATP III guidelines. In other words, if you smoke (which is a risk factor) you would get a point for smoking. But if your HDL is over 60 then that would negate that risk factor.
High LDL and/or low HDL is a risk factor for heart attacks and strokes. In accordance with the ATP III guidelines, treatment is geared toward lowering LDL first and then focusing on TGs and HDL (generally).
The first intervention (depending on your LDL and risk factors) is Therapeutic Lifestyle Changes (TLCs). There are 3 components of TLCs
- Saturated fat <7% of total calories per day. For the average 2000 kcal/day diet that would be a total of 140 kcal of saturated fat or 15 grams of saturated fat. Make sure you know how to read the nutrition labels – they will all indicate the amount of saturated fat per serving – and total it for the entire day
- Total daily cholesterol intake <200 mg per day
- Soluble fiber intake of 10-25 grams per day. You want SOLUBLE fiber, not insoluble fiber. Insoluble fiber is the stuff in metamucil, salads, etc. Good sources of soluble fiber are found in:
- oats, oat cereals – this is why Cheerios gets the healthy label
- fruits – apples, pears, citrus fruits, berries, apricots, prunes
- vegetables – carrots, cabbage, brussel sprouts, sweet potatoes
- beans, legumes, lentils, chickpeas, and peas
- Plant Stanols & Sterols – shoot for 2 grams per day. These work by block cholesterol absorption in the gut. They are generally available as a supplement from most vitamin and health food stores.
Weight Management – the goal is to get a Body Mass Index (BMI) of less than 25
Increased physical activity: all exercise and activity is good. However, the ‘magic number’ that has been studied is 17 miles per week of running, jogging, or walking. Ideally, you will want to get at least 20-30 minutes of aerobic exercise on most, if not all, days of the week.
Depending on your risk factors and lipid levels, it may be suggested that you try the TLCs first.
If, after 3 months, your lipids are still not at goal then medications may be an option.
There are currently 4 classes of medications for the treatment of lipids. Each class has its own set of benefits and challenges.
- Statins – They tend to have potent LDL reduction as well as some benefit with decreasing TGs and improving HDL. They work by inhibiting the action of HMG CoA Reductase, the rate limiting step for synthesizing cholesterol. This biochemical pathway also produces Rho (very pro inflammatory) and CoQ10. Therefore, if anyone is taking this medication they should also be taking CoQ10!
- Bile Acid Sequestrants – essentially bind cholesterol in the gut and it is eliminated in the stool. Examples include cholestyramine, colestipol, & colesevelam.
- Fibric Acids: typically used to reduce TGs.
- Gemfibrozil – this one has a high risk of rhabdomyolysis when combined with a statin and, therefore, they should not be used together.
- fenofibrate – this medicine is safe when used with statins.
- Nicotinic Acid (Niacin/Niaspan) – one of the best things we can do to improve HDL, which is often hard to do. Many people cannot tolerate the side effects which include flushing (lasts 20-30min typically), itching, and rashes. This typically resolves after a couple of weeks. This can be minimized with taking aspirin or other NSAIDs such as naprosyn 30-60min prior to taking the niacin. Applesauce has been a ‘miracle food’ to reduce, if not eliminate, the side effects associated with Niacin. You should start with a very low dose (100mg) and increase 100mg every 4 days until you reach around 1500mg. Niaspan is a controlled release Niacin. Niacin can be used with statins to improve their potency in reducing HDL.
- Rev Chol – an extremely potent Krill Oil that has been compared to several other medications and has excellent evidence supporting its use without significant side effects.
HOW TO IMPROVE YOUR HDL
This can be VERY difficult to change! HDL is often genetically determined and it is hard to change it. Here are some things that can be done:
- Exercise – at least 17 miles per week (running, jogging, or walking) has a 5% increase in HDL
- Alcohol – 1-2 glasses per day (or 1 glass per day for women) has a 12% increase in HDL
- Stop tobacco use (if you are using it) – 10 % increase
- Niacin (see above) – 10-30% increase
- Weight loss if your BMI is greater than 25. If your BMI is less than 25 then losing more weight will have no additional effect.
- Remove Trans-Fatty Acids from your diet
- Add Omega-3 fatty acids to your diet
- Add soluble fiber to your diet
- Rev Chol showed a 43% improvement in 1 study
MORE, IN-DEPTH CHOLESTEROL INFORMATION
There are 5 major classes of lipoproteins. Based on size (largest to smallest) they are:
- Very Low Density Lipoprotein (VLDL)
- Intermediate Denstiy Lipoproteins (IDL)
- Low Density Lipoproteins (LDL)
- High Density Lipoprotein (HDL)
These are lipoprotein particles that consist of triglycerides (85-92%), phospholipids (6-12%), cholesterol (1-3%) and proteins (1-2%). They transport dietary lipids from the intestines to other locations in the body. These lipoproteins enable lipids, fat, and cholesterol to be transported in the blood (fats don’t mix well with water).
Chylomicrons pick up dietary cholesterol & triglycerides from the intestine and transport them to the tissues. As they circulate they exchange products with HDL (HDL donates an Apolipoprotein C-II (APOC2) and an Apolipoprotein E) and become ‘mature chylomicrons’.
An enzyme, lipoprotein lipase, removes the triglycerides from chylomicrons. Once the TGs have been distributed, the mature chylomicrons are called chylomicron remnants.
VLDL is assembled in the liver from TGs, cholesterol, and apolipoproteins. VLDL contains Apolipoprotein B100, Apolipoprotein C-I, Apolipoprotein E, Cholesterol, Cholesteryl Esters, and TGs. VLDL takes Apolipoprotein C-II and E (in the same manner as chylomicrons). Chylomicrons and VLDL are similar but chylomicrons transport exogenous products (things ingested) and VLDL transports endogenous products (things produced in the body).
VLDL transports TGs and cholesterol to the tissues. Lipoprotein lipase is the enzyme that removes the lipids from the VLDL. Once the TGs are deposited in the tissues, the VLDL becomes…
IDL is the product of removed TGs from VLDL. IDL has lost most of its TG but it retains cholesteryl esters. It also retains ApoB100 and ApoE. The ApoE has a very high affinity for the LDL receptor. When the IDL is converted to LDL it loses its ApoE.
LOW-DENSITY LIPOPROTEIN (LDL):
LDL is generally referred to as “bad cholesterol” because LDL, when elevated, increases risk of cardiovascular disease and health problems.
Each particle of LDL contains 1 molecule of Apolipoprotein B100 and has a highly-hydrophobic core consisting of polyunsaturated fatty acid known (linoleate) and about 1500 esterified cholesterol molecules.
LDL comes in multiple particle sizes. The smaller & more dense LDL, known as pattern B, are associated with increased risk of cardiovascular disease because they can more easily penetrate the endothelium. There is some evidence that elevations of these smaller, more dense LDL particles are more closely associated with cardiovascular disease than a standard measurement of total LDL. However, it is more expensive (and less available) to measure these particles so it is not routinely performed by most physicians.
There are 3 tests that will more accurately measure cholesterol & LDL:
- Nuclear Magnetic Resonance (NMR)
- Vertical Auto Profile (VAP)
- Gel Electrophoresis
LDL is formed when VLDL particles release their TGs by the action of Lipoprotein Lipase. LDL particles increase the risk for cardiovascular disease as they invade the arterial endothelium & get oxidized. A complex set of biochemical reactions, stimulated by necrotic cell debris & free radicals in the endothelium, regulates the oxidation of LDL particles.
The liver is able to synthesize cholesterol via the Mevalonic Acid Pathway. The rate limiting step in this pathway is 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA Reductase). This enzyme is inhibited by the Statin medications. HMG CoA Reductase activity is increased by insulin and decreased by glucagon adding to the multiple problems of excess insulin.
LDL is not typically directly measured but calculated by the Friedwald equation:
HDL = TC – LDL – TG(0.20)
LDL reduction is important for decreasing the risk of cardiovascular disease and atherosclerosis. The target LDL for treatment varies based on the overall risk of cardiovascular disease for the patient.
Some argue that an LDL of < 50 mg/dl decreases the risk of cardiovascular events to near zero. LDL levels of < 70 mg/dl have shown regression of atherosclerosis (plagues get smaller).
HIGH DENSITY LIPOPROTEINS (HDL):
These particles are referred to as high-density due to the amount of cholesterol relative to protein. HDL particles contain Apolipoprotein A-I and A-II. HDL transports cholesterol from other lipoproteins and tissues back to the liver and to ‘steroidogenic organs’. The steroidogenic organs need cholesterol for the production of steroids and other hormones.
The process of HDL picking up cholesterol from the tissues and taking it back to the liver is termed Reverse Cholesterol Transport (RCT).
HDL may help prevent cardiovascular disease due to its ability to pick-up cholesterol and inhibit inflammation, oxidation, activation of the endothelium, coagulation, and platelet aggregation. These factors contribute to the protective effects of HDL and why low HDL levels increase risk of CVD.
In fact, you decrease your risk of death 6% & cardiovascular events 3% for every 1 mg/dl you increase your HDL.