They draw cholesterol out of plaque and stabilize plaque, Blaha says. Plaque is a waxy substance consisting mainly of cholesterol deposits that can build up within the walls of the arteries, interfering with blood flow to and from the heart and leading to heart attack and stroke. Early on, plaque build-up can be controlled by healthy lifestyle choices, such as switching to a heart-healthy diet, exercising and not smoking. If those efforts are unsuccessful over time, doctors will introduce treatment with statins to benefit the arteries and prevent further damage.
Being prescribed statins is no longer simply a result of having poor cholesterol numbers. Instead, doctors use a variety of ways to identify high-risk patients. You will have a cholesterol check to see if your cholesterol level has changed, and a liver function test to see if your liver is healthy.
It is recommended that you have these tests again a year later to keep any eye on your cholesterol and liver. Statins can sometimes interact with other medicines and cause side effects. It is quite understandable to have questions if you need to take a new medicine.
Statins are the most widely used medicine to lower cholesterol and they have been around for a long time. There have been a lot of news stories about them which sometimes puts people off taking them.
We are often asked if statins are safe and if there are any side effects. It's up to you whether you start taking them or not, so we've put together some answers to common questions to help you decide. Questions and answers about statins.
By continuing to browse the site you are agreeing to our use of cookies. Continue Find out more. What are statins? Statins have been around for a long time and they have been changed and improved over the years.
How do statins work? Statins can lower your triglycerides As well as lowering your LDL-cholesterol, statins can lower your triglycerides too, and high triglycerides are linked to liver disease, heart disease and diabetes. This lipid makes up a crucial component of biological membranes and serves as a precursor for other necessary substances, including the sex hormones estrogen and testosterone.
Indeed, because of its necessity cholesterol does not come exclusively from dietary sources but is also manufactured by the liver and to a lesser extent by a few other tissues, including the intestine. Figure 3. Atherosclerosis arises from a cascade of biochemical and cellular processes in which low-density lipoproteins LDLs trigger inflammation. When their levels in the blood are excessive, LDLs infiltrate the arterial wall where they accumulate and undergo chemical modifications, especially oxidation.
The modified LDLs then stimulate the expression of receptors red on the innermost, or endothelial, cells lining the artery. In the blood, monocytes—immune cells that participate in general inflammatory responses—dock onto these receptors and enter the arterial wall. Inside the arterial wall, the monocytes mature into macrophages that engulf the modified LDLs to form fat-filled macrophages called foam cells.
The foam cells secrete inflammatory substances that promote the production of a tough fibrous matrix that caps the fatty core to generate a plaque. Acute problems arise when the inflammatory substances secreted by the foam cells weaken the cap. If the cap springs a leak, blood enters, makes contact with foam-cell proteins that promote clotting and a blood clot develops in the artery. The clot that forms can plug the artery at the site of the plaque or travel downstream and obstruct blood flow at another location.
Second, it is not cholesterol in general that is the problem, but rather the form it is in that matters. Atherosclerosis "hardening of the arteries" arises from the low-density lipoprotein LDL form of cholesterol. These LDLs—globules of about 20 nanometers or so across—encapsulate cholesterol derivatives called cholesteryl esters. When the bloodstream contains a surplus of LDLs, they enter the innermost layer of cells of the arterial wall and accumulate.
Eventually, these lipids oxidize, which triggers metabolic and structural changes in the arterial wall, not unlike those elicited by infection from a pathogen. The immune system identifies these changes as damage, driving the formation of capped plaques replete with fat-engorged white blood cells.
It is when these plaques are disrupted that trouble arises: Blood leaks through the fissure into the lipid-rich core of the structure to make contact with proteins that promote coagulation, resulting in clots.
That is the downside. The upside of cholesterol comes from the high-density lipoprotein HDL form, which, unlike its LDL counterpart, is cardioprotective.
HDLs—globules only nanometers across—pick up cholesterol from the blood and prevent or impede plaque progression by retrieving arterial cholesterol deposits and limiting the rate and extent of LDL oxidation. Higher levels of HDLs thereby reduce the risk of cardiovascular disease. Of course, that is not to say that there can never be too much of a good thing: Some studies indicate that very high levels of HDLs also increase the risk of cardiovascular diseases.
Third, cholesterol tightly regulates its own production. A seminal finding in the science of cholesterol came in when Marvin D. Siperstein and Violet M. Fagan—both then at the University of Texas Southwestern Medical School—showed how the body controls cholesterol levels. These investigators discovered that the enzyme that converts a substance named HMG-CoA to mevalonic acid, the immediate precursor of cholesterol, is inhibited by cholesterol.
By feedback inhibiting the pacemaker enzyme that catalyzes the first committed and rate-limiting step in the pathway, cholesterol downregulates its own synthesis. A major culprit in heart disease—cholesterol—and a potential therapeutic target—the enzyme HMG-CoA reductase—had been discovered.
When Endo returned to Sankyo in , he was to bring together his lifelong passion for mycology and his newfound interests in lipid metabolism.
Although other researchers had the same thing in mind, Endo took a fungal angle. He speculated that there must be at least a few fungal species capable of elaborating compounds—niche-carving antimetabolites—that target HMG-CoA reductase to do battle with fungal competitors that require cholesterol-like compounds for survival.
By , Endo and his Sankyo colleague Masao Kuroda had started their search for fungal compounds that interfered with cholesterol production—via HMG-CoA reductase—in rat-liver extracts. After two years spent painstakingly screening 6, microbial strains, Endo and Kuroda at last found two promising cultures. The first came from Pythium ultimum. It inhibited HMG-CoA reductase and decreased cholesterol levels in rats, but it was eventually shown to be extremely toxic to the liver.
The second, a true hit this time, came from Penicillium citrinum , a relative of the organism responsible for the blue in blue cheese and the fungal mats that grow on old oranges—surely a thrilling result if only because of Endo's admiration for Fleming's exploits with this genus more than 40 years previously.
By purifying active compounds from 2, liters of filtered liquid drawn from P. This is the compound that became known as mevastatin, signifying a substance that stops where "stat" suggests static, or not changing mevalonic acid synthesis. With such a potentially promising inhibitor in hand, Sankyo faced two make-or-break questions: Does mevastatin do what it should in vivo , and if so is it free of deleterious side effects?
Endo started exploring these questions in depth with rats. Much to his dismay, he found that mevastatin was effective only in the short term. Over longer trials, even at relatively high doses, it produced no consistent effect. That was very bad news—news that could have easily brought work on this compound as a cholesterol-lowering drug to an abrupt end.
By chance, though, one of Endo's colleagues offered some hens for testing. Given the high levels of cholesterol in chicken eggs, these birds seemed perfect for studying this strategy for cholesterol reduction.
So Endo and his colleagues fed egg-laying hens with commercial chicken feed supplemented with mevastatin and then measured their blood cholesterol levels. It worked—decreasing cholesterol by as much as 50 percent, while leaving body weight, food intake and egg production unaffected. Before further examining the history of the statins, it is instructive to consider a perplexing question, or at least a question that is perplexing with the benefit of hindsight. That is, if statins diminish all types of cholesterol, why do they reduce the risk of cardiovascular diseases?
Well, the short answer to this question is: Luckily, these drugs are more selective than could have been anticipated when they were first discovered. Figure 4. Cholesterol's biosynthesis starts with acetyl-CoA. Then, a series of enzyme-catalyzed reactions convert acetyl-CoA to cholesterol.
The empirical results speak for themselves. Treatment with statins does appreciably decrease LDLs, as expected. But, in addition, statins increase HDLs, and by more than 7.
The liver is the hub when it comes to LDLs. And because the liver cells have fewer LDLs entering to contribute to the cholesterol pool, they generate more LDL receptors on their surfaces to grab more of this substance from the blood.
The combination of producing less cholesterol in general—including the LDL fraction—and pulling more LDLs from the blood into liver cells serves to deplete circulating levels of LDL cholesterol. All other things being equal, high numbers of LDL receptors in liver cells equate with low levels of LDLs in the blood. All well and good, but if a statin decreases the overall production of cholesterol, shouldn't circulatory HDL levels also decrease?
Logically they should, but fortunately they don't. Instead, circulatory HDLs increase, making statins even more cardioprotective than they might otherwise be. Currently, there is no consensus on just how statins increase blood HDL levels. Some scientists suspect that statins inhibit the transfer protein responsible for unloading the cholesteryl ester cargo of HDLs.
A variety of experiments on animals and humans show that blocking the cholesteryl ester transfer protein triggers increases in the levels of HDLs. Another possibility is that statins stimulate the expression of HDL transport proteins, which in turn ferry this form of cholesterol from the liver to the blood.
It is intriguing to consider that the mechanisms that nearly stalled Endo's first screens of mevastatin, because they were done on rats, are the very mechanisms that make these drugs so effective therapeutically in humans.
Rats are an exception because their steady-state blood levels of LDLs are low; most of their blood cholesterol is in HDLs. What this means is that even if statins decreased blood LDL levels enough to be noticeable in the short term in rats, any long-term effects at the level of total blood cholesterol would be offset by a subsequent increase in HDLs.
As Endo's work with chickens and subsequently other animals including humans and other primates was to show, a lowering of total blood cholesterol is typically seen because LDL cholesterol ordinarily represents a sizeable fraction of the total—a much larger fraction than in rats and other rodents.
Health Conditions Discover Plan Connect. Cholesterol Control: 4 Natural Statins. Medically reviewed by Debra Rose Wilson, Ph. What are statins Natural statins Red yeast rice Psyllium Fenugreek Fish oil Lifestyle changes Overview Having high cholesterol puts you at risk for a heart attack or stroke. What are statins? The natural options. Red yeast rice.
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