[Click below to listen to an audio version of this article]
Cholesterol can be a complicated topic, especially since some of the familiar narratives—based on outdated science—are not necessarily helpful. The “good” vs. “bad” cholesterol story is not only incomplete, but it also misrepresents the role cholesterol plays in our health. LDL numbers alone don’t tell us much. And statins are not a universal cure-all. Cholesterol has taken on a negative cast, but it’s crucial for our health at the cellular level. It’s also an essential metric of metabolic health, and it can even help indicate insulin resistance.
Let’s cut through the headlines and look at what cholesterol is, the role it plays in our health, and how we should think about measuring it.
What is Cholesterol?
Cholesterol is a type of waxy substance known as a lipid. It travels in your bloodstream carried by proteins.
“We all need cholesterol to survive,” writes Levels Advisor Robert Lustig, MD, in Metabolical: The Lure and the Lies of Processed Food, Nutrition, and Modern Medicine. “If you don’t consume cholesterol, your body makes it—it’s that important.”
In fact, your liver makes the bulk of it. Only about 25% of our total circulating cholesterol—LDL or HDL—is tied to what we eat. The amount we absorb from our diet varies widely depending on the food itself, our state of health, and even our genetics. Cholesterol only comes from animal-based foods.
Cholesterol’s role in the body is complex. Among its roles:
- It helps create our cell membranes and keep them fluid
- Cholesterol molecules have signaling and transport functions
- It helps make up the coating that protects our nerves
- It is the precursor to bile salts, which our body uses to break down fats
- Cholesterol is necessary to generate Vitamin D, along with steroid and sex hormones
Definitions of Common Terms
- LDL-C: Low-density lipoprotein accompanying cholesterol, sometimes called “bad” cholesterol
- HDL-C: High-density lipoprotein accompanying cholesterol, sometimes called “good” cholesterol
- Lipid: a fatty or oily organic molecule that does not dissolve in water (often used interchangeably with “fat,” however not all lipids are fats)
- Triglycerides: a type of lipid stored in fat cells when calories go unused; mainly carried through the blood by very-low-density lipoproteins (VLDL), which become LDL once they give up their triglycerides and thus may contribute to atherosclerosis
- Lipoprotein: a sphere-shaped particle made up of lipids and protein that transports cholesterol and triglycerides in the bloodstream
- Particle size and density: The size of a lipoprotein and how much more proteins dominate the particle compared to less-dense lipids
The takeaway: Cholesterol is not inherently bad, and for the vast majority of people, dietary cholesterol plays a small role in your total cholesterol levels.
Why Do We Care About Our Cholesterol Levels?
When we get a lipid panel at the doctor’s office, in addition to other metrics, we receive numbers for our LDL and HDL, often labeled the “bad” and “good” cholesterols, respectively. Here’s why:
LDL transports cholesterol to cells in artery walls. Through additional processes, these deposits of cholesterol and other substances can then lead to plaque buildup. That buildup can stiffen and narrow arterial walls, causing atherosclerosis. And atherosclerosis increases one’s risk of heart attack or stroke.
HDL, on the other hand, carries some cholesterol back to the liver, where it is broken down and passed out of the body through waste.
“If you’re like most patients I see, you’re convinced that cholesterol is the evil that causes heart disease. If you monitor your cholesterol levels and avoid the foods that are purported to cause cholesterol to rise, you hope you’ll be safe from America’s number one killer.
People fear cholesterol because for years, well-meaning doctors, echoed by the media, have emphasized what they long believed is the intimate link between cholesterol and death by heart disease.
The truth is much more complex. Cholesterol is only one factor, and not even the most important one of many contributing to your risk of getting heart disease.” —Hyman, The Cholesterol Solution (5)
The LDL Myth
A high level of LDL-C has long been considered a risk factor for heart attack and other cardiovascular concerns. And that may hold for folks who have an LDL-C over 200 mg/dL, according to Lustig. In those cases, genetics are usually at play, he adds, but data show it’s not a risk factor until it gets to that level.
“But for the rest of the population, LDL-C is not a great predictor of who will suffer a heart attack. It’s true that the HR ratio (hazard risk ratio; a measure of difference in risk versus the general population) of LDL-C is 1.3, which means that if your LDL-C is high, you have a 30 percent increase in risk for a heart attack. But correlation doesn’t mean causation. For example, if LDL-C is truly the bad boy of heart disease, as the Medical Establishment says, then why, when you remove younger people from the analysis and just look at older people (greater than sixty years), do high LDL-C levels correlate with longevity? Maybe, once you factor out the people with genetic reasons for high LDL-C (like those with genetic disorders), then LDL-C isn’t really so bad. Or maybe we’re measuring the wrong biomarker.”—Lustig, Metabolical (35)
LDL isn’t solely responsible for atherosclerosis either, explains Levels advisor Ben Bikman, PhD, in Why We Get Sick: The Hidden Epidemic at the Root of Most Common Disease—And How To Fight It. Yes, LDL certainly plays a role, but it’s not the only factor.
“Atherosclerosis is the most essential process in the development of heart disease. Our great fear of cholesterol stems from the theory that it leads to atherosclerosis, a process wherein the blood vessels become hardened and narrowed. But let’s look at this process more closely.
To be pathogenic, cholesterol must pass into the blood vessel wall. However, cholesterol being deposited in the endothelium [blood vessels wall] isn’t in itself the cause of disease. When they enter the endothelium, cholesterol and fats are benign—they appear to elicit no negative response. Indeed, the cells that line blood vessels, like all other cells in the body, need cholesterol and fats to maintain healthy function! Nevertheless, the lipids may not be benign for long. In certain people, something happens to the cholesterol and fats to make them noxious.”—Bikman, Why We Get Sick (20)
Both Bikman and Hyman say the real problem occurs when cholesterol and fat are oxidized, causing plaque buildup. And the culprit is inflammation brought on by any number of lifestyle factors or underlying conditions.
“Inflammation is the main cause of heart disease and is what makes cholesterol dangerous. Inflammation can arise from poor diet (too much sugar and trans and saturated fats), a sedentary lifestyle, stress, autoimmune disease, food allergies, or hidden infections such as gum disease, or even toxins such as mercury. A major study done at Harvard found that people with high levels of C-reactive protein (CRP, a marker of inflammation) had higher risks of heart disease than people with high cholesterol. Normal cholesterol levels were not protective to those with high C-reactive protein. The risks were greatest for those with high levels of both CRP and cholesterol.”— Hyman, The Cholesterol Solution (6)
Hyman says diabesity—the comorbidities of obesity and pre-diabetes or diabetes—is the real reason for “bad” cholesterol. Diabesity causes HDL to drop while bringing up your triglycerides, increasing dangerous small LDL particles and further driving inflammation and oxidative stress, creating a vicious cycle. A key phrase here is “dangerous small LDL particles.” Not all LDL particles are created equal, Bikman explains.
“Though it’s called “low density,” LDL cholesterol actually comes in various sizes and densities. Measuring this is getting easier and easier. We’ve known for decades that our characterization of LDL is more meaningful in predicting heart disease when it is categorized by size and density, which we refer to as a “pattern.” There are two patterns, termed A and B, that represent the ends of a spectrum: pattern A refers to an LDL molecule that is larger and less dense, and B refers to the LDL being smaller and denser [sometimes called small density LDL or sdLDL]. Now, for a cholesterol carrier to cause disease, it must pass from the blood and into the blood vessel wall; we can appreciate that a smaller, denser lipoprotein would do this more easily than a bigger one.”—Bikman, Why We Get Sick (18)
There’s a connection between particle size and metabolic health. According to Bikman, “Insulin selectively drives the production of LDL pattern B [small, dense LDL particles] from the liver (where almost all cholesterol is made). As insulin levels steadily climb with increasing insulin resistance, the liver is getting the signal to shift the individual toward a pattern B LDL profile.”
What are the Critical Numbers?
Unfortunately, standard cholesterol tests you might get at a physical don’t contain the level of detail that would be helpful, such as LDL particle testing. Advanced lipoprotein testing that produces a vertical auto profile (VAP) is sometimes available, though insurance often does not cover it. However, Bikman says we can use a “poor man’s method” by doing some math with our TG and LDL numbers.
- TG to HDL ratio
“By dividing the level of triglycerides (in mg/dL) by HDL (in mg/dL; TG/HDL), we get a ratio that is surprisingly accurate in predicting LDL size. The lower the ratio (e.g., ~<2.0), the more prevalent the larger, buoyant LDL particles; that is to say, LDL A predominates. But as the ratio climbs (~>2.0), the small, dense LDL B particles are more common. Virtually every blood test will include TG and HDL, which means we can readily get an idea of our individual LDL pattern type without requiring a specialized test.”—Bikman, Why We Get Sick (18–19) “The TG:HDL (high-density lipoprotein) ratio—the real ratio of bad to good cholesterol—is the … best surrogate marker of insulin resistance and metabolic syndrome. For reasons that are completely unclear, race matters with TG levels. If it’s over 2.5 in Caucasians or over 1.5 in African Americans, that’s a correlate of metabolic syndrome.If [your LDL] is between 100 and 300, then you need to look at the TG level.
If the TG level is above 150, that’s metabolic syndrome until proven otherwise. The reason TGs were ignored until now is that we had statins as treatment for high LDL-C, but until about fifteen years ago, we didn’t have treatment for high TG levels other than diet, which doctors didn’t employ.”—Lustig, Metabolical (143)
- Total HDL
If it’s over 60, it almost doesn’t matter what the other fractions are, as this is a sign of good cardiovascular health. If the HDL is under 40 (men) or under 50 (women), then your predisposition for heart disease is much higher. —Lustig, Metabolical (143)
- Total LDL
If it’s below 100, the small dense fraction can’t be high enough to be harmful. If it’s over 300, you might have the rare genetic disease familial hypercholesterolemia (FH) and you can’t clear your LDL, in which case a low-fat diet, and likely a statin added, will be essential to prevent a future heart attack. If it’s between 100 and 300, then you need to look at the TG level. If the TG level is above 150, that’s metabolic syndrome until proven otherwise. —Lustig, Metabolical (143)
- Total cholesterol to HDL ratio
Your ratio of total cholesterol to HDL should be less than 3.0.—Hyman, The Cholesterol Solution (10)
Hyman recommends the following general guidelines in his ebook, How to Work with Your Doctor to Get What You Need:
- Total cholesterol < 180 mg/dL
- LDL cholesterol < 70 mg/dL
- HDL cholesterol > 60 mg/dL
- Triglycerides < 100 mg/dL
- Total cholesterol/HDL ratio < 3.0
- Triglyceride to HDL ratio < 4
The takeaway: Get a full lipid panel if you can, but if you can only get a standard cholesterol test, make sure you’re looking at the correct numbers and your family history.
The Role of Statins
If you have a high LDL level, you might be prescribed a statin. Statins block an enzyme in the liver, HMG-CoA (3-hydroxy-3-methyl-glutaryl-coenzyme A) reductase, that controls the body’s production of cholesterol.
Statins do lower total LDL. But, Lustig argues, only because they lower the large particles (pattern A), which make up about 80 percent of our circulating LDL, and those aren’t the ones we need to be concerned with. The remaining 20 percent of LDL is the small and dense pattern B particles, which drive atherosclerosis.
“No argument, if the goal is reducing [total] LDL-C, statins are a simple way to do it. And if you have a genetic disorder, they’re a necessary way to do it. But do they reduce the risk of heart attack across the board? Without a doubt, they don’t!”—Lustig, Metabolical (36)
Statins aren’t a cure-all. And Lustig says they could be doing more harm than good in some cases.
“There’s now a burgeoning literature that statins increase glucose intolerance and risk for both diabetes and weight gain. Is it that, by acting on the liver, statins worsen insulin resistance? Or could it be the inverse—that statin use makes people think they can eat whatever they want because they are now impervious to any cardiovascular risk? It could be both.
So, are statins good or bad? If you don’t need to take statins, then why would you incur risk of a side effect, which could include muscle breakdown, kidney failure, and type 2 diabetes?”—Lustig, Metabolical (36–37)
The takeaway: Statins can help in limited circumstances but are not the cure-all for heart disease.
How to Think about Cholesterol and Diet
In addition to recommending statins, doctors commonly tout a low-fat diet for lowering LDL. But Levels advisors agree that fat isn’t the enemy here. It’s sugar.
“When you eat sugar—particularly fructose or high fructose corn syrup—it causes the cholesterol-producing factory in your liver to turn on. By default, a low-fat diet is going to be a higher-sugar diet.
If you have high triglycerides, low HDL, or high total cholesterol, getting off sugar and flour (which converts to sugar) becomes the best way to fix this problem.
Despite what we’ve been brainwashed to think, fat isn’t the problem. Studies show that eating more fat can actually fix your cholesterol by increasing the good kind and lowering the bad kind.”—Hyman, The Cholesterol Solution (8)
A low-fat diet may lower your LDL—but likely not in a way that is genuinely beneficial. As with statins, a low-fat diet will only reduce the large A-type LDL, not the small B-type.
“In fact, small dense LDL rises because they are responsive to dietary refined carbohydrates (i.e., fiberless food) and especially sugar consumption, which is what is substituted in lieu of the dietary fat. One of the most compelling arguments against LDL-C as the primary target of CVD prevention or treatment is the Lyon Diet Heart Study. The adoption of a Mediterranean diet for secondary prevention (after you’ve already had a heart attack) reduced the risk for recurrence. It’s clear that eating a Real Food diet, devoid of processed food (how they eat in Lyon) delivered far more impressive results when compared with statins—without the side effects and at a much lower cost. And this diet is decidedly not low-fat. Given that statins can give the illusion of CVD protection yet cause serious side effects, stopping statins and eating Real Food may paradoxically save more lives and improve quality of life.”—Lustig, Metabolical (38)
Combating oxidative stress and inflammation should be another dietary strategy for improving overall health. Remember, oxidized fat and cholesterol allow those B-type small, dense LDL-C particles to cause plaque buildup. “A rainbow of fruits and vegetables,” Hyman says, is full of antioxidants. Antioxidants scavenge free radicals that cause oxidative stress. But in addition to loading up on micronutrients, skip the fats that are easily oxidized.
“At the risk of complicating the problem, as much as the focus has been on cholesterol, it’s more valid (and fair) to spread the blame to include noncholesterol fats. In particular, the polyunsaturated fat called linoleic acid (very common in seed oils, such as soybean oil) is the most readily oxidized fat—far more so than cholesterol—and is likely a main culprit. In fact, when cholesterol gets oxidized, it’s often due to a linoleic acid being bound to a cholesterol molecule—as though our neutral cholesterol is forced to give the naughty child, oxidized linoleic acid, a piggyback ride. Nevertheless, even here, insulin resistance is relevant.”—Bikman, Why We Get Sick (21)
The takeaway: You will do more to improve your health by paying more attention to the quality of food you eat and the amount of sugar and refined carbohydrates than by worrying about cholesterol.