Even after years of healthcare guidance to patients on the importance of maintaining a healthy cholesterol level, confusion and controversy abound. Experts in the field of cholesterol management, Clinical Lipidologists, are working to educate healthcare providers and their patients about cholesterol and debunk the persistent myths generated by cholesterol skeptics. One such organization which is dedicated to enhancing the practice of lipid management in clinical medicine is the National Lipid Association (NLA).
Why is it important to understand the significance of cholesterol?
Because half of all Americans, in their lifetimes, will develop atherosclerotic cardiovascular disease (ASCVD), the leading cause of death and suffering, as well as a huge burden financially for both men and women. There are many risks for ASCVD. Besides high cholesterol, well-known risks include diabetes, high blood pressure, smoking, exposure to tobacco smoke, unhealthy lifestyle and family history. However, research has shown that the greatest risk resides in too many cholesterol-containing particles carried by a protein, apolipoprotein B, entering into and retained by the arterial wall, leading to an inflammatory response and plaque buildup (atherosclerosis). Ultimately, unstable plaque can rupture causing a heart attack or stroke. Controlling all risks, and especially the number of cholesterol-containing particles, particularly for a prolonged period, ideally, a lifetime, is important to prevent ASCVD or delay progression and these events.
So, what is cholesterol?
Cholesterol is a waxy, fat-like substance that travels throughout the blood stream carried in particles called lipoprotein particles. All of our cells can produce cholesterol; therefore cholesterol is not an essential dietary substance. Dietary cholesterol is obtained from animal products. In general, 85% of the body’s cholesterol is produced in all of the cells of our body and 15% of the body’s cholesterol is represented by animal product intake. Cholesterol is made by all cells, as it is one of several structural and functional components of cell membranes. Skin cells use cholesterol to make vitamin D. Cholesterol is the precursor to steroid hormones (estrogen and testosterone). Much of the cholesterol produced in, or delivered to, the liver is used to make bile, a biproduct that helps us in digestion of food and absorption of fat soluble vitamins. Thus, cholesterol has functions—many of which are essential for good health.
The liver is the major organ for the synthesis of cholesterol. Another substance, triglycerides, are synthesized in the liver. The synthesis of triglycerides requires the delivery of fatty acids to the liver. Fatty acids are the end-product of dietary fat digestion. Fatty acids in the digestive system are reformed into triglycerides and together with intestinal cholesterol are absorbed into the bloodstream as chylomicrons, also use as a supplier of fatty acids as an energy source for fat storage. Fatty acids are also delivered to the liver from the body’s fat deposits. Ultimately, in the liver, cholesterol and triglycerides along with a carrier protein, called apolipoprotein B, get together in a particle called very-low density lipoprotein (VLDL-C) that is released by the liver into the blood stream. The major function of this particle is the delivery of triglyceride for breakdown into an energy source, free fatty acids, utilized by the muscles of our body. These free fatty acids are also utilized by fat tissue to store fat. As the triglyceride is removed from the VLDL-C particle it becomes a small less dense intermediate density lipoprotein (IDL-C) particle and then even smaller low-density lipoprotein (LDL-C). Thus, once again cholesterol and triglyceride containing particles serve useful functions and are essential for good health.
So where does cholesterol become a problem?
Cholesterol becomes a problem, when there is an excess of these cholesterol-containing apolipoprotein B particles and then all of them (VLDL, IDL and LDL particles) can in be “bad”. The greater the numbers of “bad” particles the greater the diffusion of these particles into the arterial wall, where they can be retained and initiate or contribute to the atherosclerosis process. Most of the “bad” cholesterol is represented by LDL-C. So having the genetics of low numbers of these “bad” particles is beneficial for a lifetime of protection from ASCVD or low risk and longevity. But when one has the genetics for a high number of these “bad” particles, the burden of cholesterol shortens lifespans considerably. In some individuals with untreated Homozygous Familial Hypercholesterolemia (HoFH), ASCVD events begin in late teens and early twenties; in less severe Heterozygotes (HeFH) ASCVD events occur in their 40s. The average individual with risks, in the absence of these familial hypercholesterolemia conditions, have other genetic cholesterol issues that cause events in their 60s, disorders that affect most of the one-half of the population. In all of these conditions reducing the number of these particles, for a lifetime, is extremely important.
What’s the difference between good and bad cholesterol?
So, we’ve said when an excess of LDL-C particles, the “bad” cholesterol, circulates in your blood, an excess can diffuse into the artery wall and, ultimately, can cause plaque buildup in those arteries, eventually leading to a heart attack or stroke or death.
Another cholesterol-containing particle is called high density lipoprotein, HDL, and its carrier protein is called apolipoprotein A-1. The HDL-C is called the “good” cholesterol particle because it has several properties that appear to protect arteries; one of the most studied properties is its ability to remove an excess of cholesterol from arterial plaque. It acts like a scavenger, gathering cholesterol from the walls of arteries and carrying it back to the liver. In addition, experts believe HDL may also have some anti-inflammatory effects and antioxidant properties that are beneficial. These properties have been known to slow the buildup of plaque and even help shrink and stabilize the plaque in the arterial walls of the heart.
It’s important to understand that cholesterol, per se, is neither bad nor good, but rather the particle in which it resides may be distinguished as being bad or good.
The typical lab blood test consists of measurements of total cholesterol, triglycerides, HDL-C, LDL-C, a calculated ratio of a patient’s total cholesterol to good cholesterol ratio. The later ratio provides some insight into the contribution from good and bad cholesterol; the higher this ratio is the higher the ASCVD risk. The levels of triglycerides are also important, since the higher the triglycerides, in the presence of elevated cholesterol, the greater the number of “bad” particles of, not only LDL-C, which tend to be small, as well as numerous, but also its precursor lipoproteins, VLDL-C and IDL-C. A most important calculation is non-HDL. One subtracts the HDL-C (the “good”) value from the total cholesterol and one is left with everything that is not HDL-C (non-HDL-C), not “good” cholesterol or all of the “bad” cholesterol which includes VLDL-C, IDL-C and LDL-C. Therefore, Non-HDL-C is a more comprehensive as an ASCVD risk and a target for therapy than LDL-C. Many lipid expert also look to targeting apolipoprotein B or LDL particle numbers.
Cause for concern
Maintaining optimal cholesterol levels is a key part of maintaining overall health and should be taken seriously no matter what your age. Though many are unaware of it, the official recommendation is to get a baseline cholesterol screening between the ages of nine and 11.
Autopsies of our young soldiers, has demonstrated plaque buildup in their late teens and early 20s. Furthermore, studies of consecutive patients admitted to hospitals across the country have shown that the average LDL-C on admission is 104 mg/dL. In 2014 the NLA, Recommendations for Patient-Centered Management of Dyslipidemia, recommends an LDL-C level below 100 mg/dL, even in low-risk individuals, who have not yet suffered an ASCVD event. Very high risk individuals, patients with prior ASCVD or those with Diabetes and greater than one additional major risk, need goals for LDL-C levels below 70 mg/dL. More recent analyses and trials suggest even lower values are beneficial. Many studies also suggest that we are not reaching these goals in but a minority of patients in need.
Debunking the myths
Let’s say the results from your recent cholesterol test reveal that your HDL-C level is low—is that a good or a bad thing?
Population studies suggest that relatively high levels of HDL-C will help protect against ASCVD and vice-versa relatively low HDL-C are associated with high risk. One would, therefore, suspect that if your HDL levels are low, efforts to raise HDL-C should be employed to avoid increased risk of ASCVD. Studies to date, however, have not demonstrated that putting more cholesterol into the HDL particle reduces risk, at least with the most potent of these medicines, statins, used to lower LDL-C and reduce significantly the risk of ASCVD.
The next question would be does raising HDL-C by other methods help reduce ASCVD?
There are many ‘healthy habits’ that have been suggested to help raise “good HDL cholesterol”. Adjusting your diet may be one way you can help improve HDL-C levels.
Nuts such as almonds, walnuts and pistachios are all good sources of heart-healthy fats and are great to add to your diet to elevate HDL levels naturally. But don’t forget they are high in fat and calories, so remember to snack in moderation.
Seafood that is high in omega-3 fatty acids have been shown to be most beneficial for heart health. Health experts recommend at least two servings of fish per week.
Olive oil is high in unsaturated fats and can help you elevate your HDL. This, too, is high in fat and calories, so excessive use could lead to weight gain, which could counteract any good effects of raising HDL levels.
What you eat is important to your health, but so are other health habits. Staying active, whether for work or recreation, is a key element in health. Exercise can help to control weight, and happen to lower total cholesterol, increase the good HDL and decrease the bad LDL cholesterol. Other risk factors such as smoking cessation and moderate alcohol consumption should also be considered. You may want to seek medical advice from your physician, if you are considering making a lifestyle or dietary change.
But, while all of these good healthy habits may help reduce ASCVD risk and help to raise the HDL-C level, we do not know if simply putting more cholesterol into the HDL particle (raising HDL-C) or simply that the good healthy habits themselves, is related to the reduction in ASCVD risk. Thus, raising the cholesterol content of HDL particles, HDL-C, remains a myth, until proven otherwise. Lowering the cholesterol-containing apolipoprotein B particles (VLDL, IDL and LDL particles), however, has been proven far beyond the skeptic’s doubt.
Like everything relating to health, there are multiple factors that play into achieving and maintaining optimal cholesterol levels. For many people a few lifestyle changes can do the trick, but for others it may take meeting with a physician or taking prescribed medication to help get LDL numbers down to a desired levels. At the end of the day, everyone wants to be healthy, and it’s vital that patients take ownership of their own good health. It’s up to all of us to get our own health in check and make improvements to get our body and cardiovascular system in the best shape they can be.
Paul D. Rosenblit, MD, PhD, FACE, FNLA is the Director of the Diabetes / Lipid Management and Research Center in Huntington Beach, California. He is a Diplomate of the American Board of Endocrinology and Metabolism, has been in a private Clinical Practice setting for 28 years. He is currently an endocrinology consultant, as an active medical staff member at Hoag Hospital, Newport Beach and a courtesy medical staff at Huntington Beach Hospital, HB, Orange Coast Memorial Medical Center, Fountain Valley and St. Joseph’s Hospital, Orange, CA. Dr. Paul Rosenblit is a Clinical Professor of Medicine in the Division of Endocrinology, Diabetes, and Metabolism at the University of California, Irvine (UCI), School of Medicine, Irvine, California, and as volunteer clinical faculty, since 1990, is an attending, and Co-Director, of the Diabetes Out-Patient Clinic at the UCI Medical Center, Orange, California. Since 1987, Dr. Rosenblit has served as the volunteer Endocrinology consultant for the Laguna Beach Community Clinic in Laguna Beach, California. Dr. Rosenblit is a member of the American Association of Clinical Endocrinologists (AACE), a Fellow of the American College of Endocrinology and is currently serving on AACE education committees and task forces. Dr. Rosenblit is a member of the Professional Sections of the American Diabetes Association and the Endocrine Society. He is a member of the Councils on Arteriosclerosis, Thrombosis & Vascular Biology and Clinical Cardiology, as a Silver Heart member of the American Heart Association. Dr. Rosenblit is a member and Fellow of the National Lipid Association (NLA) and a Diplomate of the American Board of Clinical Lipidology. He is a founding member of the NLA-7-State Regional Pacific Lipid Association’s Board of Directors, and is currently serving as its President-elect. Dr. Rosenblit is active, at his research site, as principal investigator on phase II & III pharmaceutical clinical trials in the disciplines of diabetes, obesity and lipids. Dr. Rosenblit lectures as a disease state and promotional speaker faculty member of several pharmaceutical companies, and at various continuing medical education programs, with areas of interest including diabetology, clinical lipidology and cardiometabolic-cardiovascular disease. Dr. Rosenblit is a Co-Director of the Annual Fall Orange County, CA, Symposium on Cardiovascular Disease Prevention.