Over the last 50 years, the public has been subjected to a dizzying confusion of explanations of the role of cholesterol in cardiovascular disease. First we were told that our blood vessels were like pipes and cholesterol was like the calcium in hard water, causing clogs. Then we were told that, no, actually cholesterol only accumulates in arteries, not veins, and just in small segments of arteries a few millimeters (a fraction of an inch) long. We were told that cholesterol is bad and we need to get our total cholesterol levels down. Then we were told that cholesterol is actually good, HDL, or bad, LDL. We need more HDL and less LDL. Then it became common knowledge that not every kind of LDL cholesterol is harmful in our arteries, just the slightly less fluffy pieces of LDL called apo-A1. It was just these higher-low-density lipoprotein particles that are actually injurious to blood vessels, well, arteries, well, small segments of arteries under stress, when they are consumed by white blood cells, more specifically macrophages, and subjected to calcification.
What does all this mean in practical terms of staying healthy? It's probably a good idea to go back to the beginning.
"Cholesterol" Isn't the Enemy
Cholesterol is not toxic. It's essential to every cell in the human body. The body creates hormones by starting with cholesterol. Cholesterol is incorporated into the membrane lining every cell. The profound usefulness of cholesterol really is not hard to understand. The bloodstream consists mostly of plasma, which is mostly water. Cells would dissolve into the bloodstream if they didn't have a "raincoat." Cholesterol isn't soluble in water, so it can be used to protect cells from dissolution.
Because cholesterol isn't soluble in water, it can't circulate through the bloodstream without first being coated with something that is soluble in water. Cholesterol circulates through the bloodstream in a "balloon" of lipoprotein. Protein surrounds cholesterol and carries it where it needs to go. The glob of cholesterol can be large and light, surrounded by very low density lipoprotein (VLDL), or a little smaller, surrounded by low-density lipoprotien (LDL), or tight and compact, surrounded by high-density liproprotein (HDL). Each sphere of cholesterol matches to a different receptor on cell surfaces. It has a unique docking site. Receptors that capture VLDL don't capture LDL, and receptors that capture LDL don't capture HDL. Atherosclerosis involves "smaller LDL" called apo-A1. Other forms of cholesterol aren't involved in atherosclerosis (and more than just cholesterol is needed for atherosclerosis to occur).
When You Lower Your Cholesterol, Where Does It Go?
So, when you lower your cholesterol, it does not disappear. The body makes most of its own cholesterol. Only about 15 percent, at most, comes from food. "Extra calories" from carbohydrate and fat become the triglycerides that are the building blocks of cholesterol, which starts as VLDL cholesterol.
The statin drugs that every doctor prescribes to nearly every patient can actually increase the production of VLDL cholesterol, but they reduce the amount of LDL cholesterol in circulation in the bloodstream. That's usually a good thing, because both the larger and smaller pieces of LDL cholesterol become less numerous in most people. However, it's possible to have "normal" or "low" total LDL and too much apo-A1 LDL and still have elevated risk for atherosclerosis.
The Relationship Between Sugar And LDL Cholesterol
Why would someone have too much of the "really bad cholesterol" and still have normal amounts of LDL? The answer turns out to be that sometimes the body benefits from having LDL in the bloodstream rather than inside cells that use it.
Only the smaller pieces of LDL cholesterol "fit" the receptor sites that line the arteries. There is a part of the LDL molecule that fits inside the molecule on the surface of the receptor, something like a lock in a key. If the LDL "key" matches with the receptor's "lock," then it is absorbed into the cell from the bloodstream.
When there's a lot of sugar in the bloodstream, however, the LDL molecule can become glycated. This process is a little like getting "gunk" on a key, so much that it won't fit into its lock any more. A specific, 67-atom segment of the LDL molecule is susceptible to glycation by sugars that change its shape so it cannot be taken up by receptors and taken out of the bloodstream.
When you consume a lot of sugar, LDL stays in your bloodstream. When you consume a lot of fructose, the problem is magnified even more.
Glucose is among the least reactive of all the sugars that circulates in your bloodstream. Fructose is 12 to 13 times as likely to "stick" to LDL cholesterol. Fructose is the kind of sugar in fruit, and it's also the kind of sugar in high-fructose corn syrup, used to sweeten cereals, baked goods, and snack foods in the United States and Canada. There is research that suggests that the critical level of sugar is 13 to 25 percent of total calories, or about what a typical American eats every day. If you were to reduce other forms of carbohydrate consumption to make up for sugar consumption, the effects would not be as severe, but very few people do.
The first 25 grams or so of fructose you consume (that's the equivalent of two pieces of most kinds of fruit) is used as fuel by the liver. This relatively small amount of fructose actually accelerates your liver's ability to deal with glucose, which the body digests from other kinds of carbohydrate foods. More than 25 grams of fructose overwhelms the liver, and fructose is left in circulation, where it can interact with LDL.
Since the liver also is a major clearing house for LDL cholesterol, chemically altering LDL gives the liver greater opportunity to clear out fructose, which would be more damaging to the body than LDL. However, it's very simple to keep this unexpected elevation of LDL levels from every happening in the first place: Don't eat products sweetened with high-fructose corn syrup. Don't eat too much table sugar, either, because sucrose breaks down into the relatively safe glucose and the relatively toxic fructose.
For most of us, it really isn't fatty foods that raise our cholesterol, particularly our "bad" cholesterol. It's sugar. Even if you were to eat 24 eggs a day, your body simply cannot absorb enough cholesterol from the food you eat to give you high cholesterol (except in the case of a relatively rare genetic condition called familial hypercholestolemia). Your body has to make most of its cholesterol. It can't use that cholesterol, however, when sugar levels are too high. Lower your sugar consumption to lower your LDL.
Sources & Links
- Chiavaroli L, de Souza RJ, Ha V, Cozma AI, Mirrahimi A, Wang DD, Yu M, Carleton AJ, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Beyene J, Kendall CW, Jenkins DJ, Sievenpiper JL. Effect of Fructose on Established Lipid Targets: A Systematic Review and Meta-Analysis of Controlled Feeding Trials. J Am Heart Assoc. 2015 Sep 10. 4(9):e001700. doi: 10.1161/JAHA.114.001700.
- PMID: 26358358 DiNicolantonio JJ, Lucan SC, O'Keefe JH. The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease. Prog Cardiovasc Dis. 2015 Nov 13. pii: S0033-0620(15)30025-6. doi: 10.1016/j.pcad.2015.11.006. [Epub ahead of print] Review. PMID: 26586275.
- Photo courtesy of miguel_discart: www.flickr.com/photos/miguel_discart/17299031871/
- Photo courtesy of miguel_discart: www.flickr.com/photos/miguel_discart/14791222687/