Understanding Hdl The ‘good’ Cholesterol
HDL is considered the “good” type of cholesterol. Women generally have higher levels of HDL, and that’s good with HDL you want higher, not lower, levels. A number of factors can lower HDL levels, including smoking, excess weight, too little physical activity and type 2 diabetes. Your genes can also influence your HDL levels, according to the AHA.
Most adult men are advised to have an HDL level above 40 milligrams per deciliter. For adult women, that target is 50 or higher, according to the National Heart, Lung, and Blood Institute.
Dr. Mercurio recommends exercising more often to raise your HDL levels. The NHLBI says that losing weight and managing stress also may improve HDL levels.
Read more:How to Raise Good Cholesterol Numbers
Why Do You Want To Stop
First, know that it’s OK to ask your doctor if you can stop taking meds once youâve met the blood sugar goals you’ve both set, says Robert Gabbay, MD, PhD, chief medical officer of the Joslin Diabetes Center in Boston.
And it can be done, he adds.
The first step: Tell your doctor why you want to stop. Then theyâll ask you some questions.
The doctorâs looking for specific answers, says endocrinologist Gregg Faiman, MD, of University Hospitals Case Medical Center in Cleveland. They want to know:
- Is it too hard for you to keep up with taking your medicine?
- Do the side effects lower you quality of life?
- Is the medication too expensive?
After that, you and your doctor have to agree about how youâre going to keep your blood sugar under control. You wouldnât be on the drug if you didnât need it, Faiman says. âStopping a medication requires an in-depth discussion. You have to commit to keeping your diabetes under control.â
Ask Your Doctor How To Best Stop Your Medication
Some drugs can be stopped immediately without a special discontinuation schedule, but many medications require a taper, which is a slow reduction in dose or frequency over a longer period of time. Slow tapers help to avoid disagreeable side effects or even withdrawals that you might experience if you stopped the drug quickly.
If you are stopping several medications, you may want to taper them one at a time to avoid added side effects — always check with your doctor.
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Do Statins Cause Muscle Pain And Weakness
Muscle aches occur in about 10 percent of people who take statins. Its the most common side effect of statins, but another way to look at it is that nine out of 10 patients dont experience it at all.When patients do have muscle pain:Actual muscle damage occurs in only 1 in 10,000 patients. In the rare event that muscle damage occurs, it is almost always reversible. To correct it while still protecting you from heart attack or stroke, we can adjust your medication or try a different statin. There also are many strategies to effectively manage muscle symptoms while continuing to take your medication.If you experience muscle pain while taking a statin, dont stop taking it without first talking with your doctor. For almost all patients, were able to find an effective medication that the body can tolerate. If you simply cant tolerate statins, there are other cholesterol medications we can prescribe.
- The symptom is often resolved by adjusting the medication dosage or switching to a different statin.
- Occasionally, the statins have to be stopped altogether.
- When the medication is switched or stopped, the symptoms go away and there is no damage to the muscle.
Effect Of Bempedoic Acid On Clinical Outcomes
Currently there are no outcome studies determining the effect of bempedoic acid on atherosclerotic cardiovascular disease. The effect of bempedoic acid on cardiovascular disease is currently being evaluated in a large ~3.5-year clinical trial . In animal models of atherosclerosis, treatment with bempedoic acid had favorable effects on atherosclerosis . Moreover, genetic variants that mimic the effect of ATP citrate lyase inhibitors lower LDL-C levels and are associated with a decrease in cardiovascular disease suggesting that bempedoic acid will have favorable effects on reducing the risk of cardiovascular disease .
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Are Statins Really Worth Taking For High Cholesterol
Research has shown that statins are highly effective in reducing the risk of fatal heart attack and stroke. But some people are reluctant to take these life-saving drugs. They worry about taking medicine every day for the rest of their life or have heard that statins have undesirable side effects. What does science have to say about these concerns and others surrounding statins? We talked to UH interventional cardiologist Ian Neeland, MD, Director of the Center of Cardiovascular Prevention at University Hospitals, to learn more.
Effect On Statins On Lipid And Lipoprotein Levels
The major effect of statins is lowering LDL-C levels. The effect of the various statins at different doses on LDL-C levels is shown in . As can be seen in different statins have varying abilities to lower LDL-C with maximal reductions of approximately 60% seen with rosuvastatin 40mg. Doubling the dose of a statin results in an approximate 6% further decrease in LDL-C levels. The percent reduction in LDL-C levels is similar in patients with high and low starting LDL-C levels but the absolute decrease is greater if the starting LDL-C is high. Because of this profound ability of statins to lower LDL-C levels, treatment with these drugs as monotherapy is often sufficient to lower LDL-C below target levels.
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Effect Of Pcsk9 Inhibitors On Clinical Outcomes
It should be noted that that the duration of the FOURIER trial was very short and it is well recognized from previous statin trials that the beneficial effects of lowering LDL-C levels takes time with only modest effects observed during the first year of treatment. In the FOURIER trial the reduction of cardiovascular death, myocardial infarction, or stroke was 16% during the first year but was 25% beyond 12 months. Thus, long-term benefit may be greater than observed during the study.
SUMMARY OF OUTCOME TRIALS
It should be noted that that the duration of the PCSK9 outcome trials were relatively short and it is well recognized from previous statin trials that the beneficial effects of lowering LDL-C levels takes time with only modest effects observed during the first year of treatment. In the FOURIER trial the reduction of cardiovascular death, myocardial infarction, or stroke was 16% during the first year but was 25% beyond 12 months. In the ODYSSEY trial the occurrence of cardiovascular events was similar in the alirocumab and placebo group during the first year of the study with benefits of alirocumab appearing after year one. Thus, the long-term benefits of treatment with a PCSK9 inhibitor may be greater than that observed during these relatively short-term studies.
Cautions With Other Medicines
Some medicines affect the way atorvastatin works and can increase the risk of serious side effects.
Medicines that may not mix well with atorvastatin include:
If you’re taking atorvastatin and need to take one of these medicines, your doctor may:
- prescribe a lower dose of atorvastatin
- prescribe a different statin medicine
- recommend that you stop taking atorvastatin for a while
These are not all the medicines that can interfere with atorvastatin. For a full list see the leaflet inside your medicine packet or check with your pharmacist.
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Effect Of Bile Acid Sequestrants On Lipid And Lipoprotein Levels
The major effect of bile acid sequestrants is to lower LDL-C levels in a dose dependent fashion. Depending upon the specific drug and dose the decrease in LDL-C ranges from approximately 5 to 30% . The effect of monotherapy with bile acid sequestrants on LDL-C levels observed in various studies is shown in .
Effect On Mipomersen On Lipid And Lipoprotein Levels
In the pivotal trial, 51 patients with Homozygote Familial Hypercholesterolemia on treatment were randomized to additional treatment with mipomersen or placebo and followed for 26 weeks . Mipomersen lowered LDL-C levels by 21% and apolipoprotein B levels by 24% compared to placebo. In addition, non-HDL-C was decreased by 21.6%, triglycerides by 17%, and Lp by 23% while HDL and apolipoprotein A-I were increased by 11.2% and 3.9% respectively.
Mipomersen has also been studied in patients with Heterozygous Familial Hypercholesterolemia. In a double-blind, placebo-controlled, randomized trial, patients on maximally tolerated statin therapy were treated weekly with subcutaneous mipomersen 200 mg or placebo for 26 weeks . LDL-C levels decreased by 33% in the mipomersen group compared to placebo. Additionally, mipomersen significantly reduced apolipoprotein B by 26%, triglycerides by 14%, and Lp by 21% compared to placebo with no significant changes in HDL-C levels. In an extension follow-up study the beneficial effects of mipomersen were maintained for at least 2 years .
In a meta-analysis of 8 randomized studies with 462 subjects with either non-specified hypercholesterolemia or Heterozygous Familial Hypercholesterolemia, Panta and colleagues reported that mipomersen decreased LDL-C levels by 32% compared to placebo . Additionally, non-HDL-C was decreased by 31%, apolipoprotein B by 33%, triglycerides by 36%, and Lp by 26% with no effect on HDL levels.
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Mechanism Accounting For The Lomitapide Induced Lipid Effects
Lomitapide is a selective inhibitor of microsomal triglyceride transfer protein . MTP is located in the endoplasmic reticulum of hepatocytes and enterocytes where it plays a key role in transferring triglycerides onto newly synthesized apolipoprotein B leading to the formation of VLDL and chylomicrons . Loss of function mutations in both alleles of MTP results in abetalipoproteinemia, which is characterized by the virtual absence of apolipoprotein B, VLDL, chylomicrons, and LDL in the plasma due to the failure of the liver and intestine to produce VLDL and chylomicrons . Lomitapide by inhibiting MTP activity reduces the secretion of chylomicrons by the intestine and VLDL by the liver leading to a decrease in LDL, apolipoprotein B, triglycerides, non-HDL-C, and Lp .
Eat A Plant Based Diet
The first step may surprise you because its not demanding at all. Its a step, however, that many never take or fail to sustain. Build a relationship with your physician. Let him/her know that you want to know how to get off statin drugs and where you stand in regard to heart-healthy targets. Then, in consultation with your doctor, put together a game plan for doing so. As Ive said, this will demand lifestyle modification. Without changing the way you live, theres no solid reason to get off your statin medication
Part of this game plan must be eating a plant-based diet. Depending on a patients particular profile, I recommend either the Dean Ornish Heart Disease Reversal Diet or the South Beach Diet. If you have known heart disease, the Ornish diet is better because it most effectively cleanses the system of excess fat. The South Beach Diet is usually for those with risk factors but no known heart disease. This diet allows more latitude and can still get a person to the recommended targets. Although the Ornish Diet puts no restrictions on calorie intake mainly because its hard to consume too many calories eating fruits and vegetables, youll need to limit your calories on the South Beach Diet or a Mediterranean diet . A typical unrestricted diet for the average adult contains about 2,400 calories per day. Aim to keep your calorie intake between 1,500 and 1,800 calories. The lower end is for women the higher end is for men.
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Who Can And Cannot Take Atorvastatin
Atorvastatin can be taken by adults and children over the age of 10 years.
Atorvastatin isn’t suitable for some people. Tell your doctor if you:
- have had an allergic reaction to atorvastatin or any other medicines in the past
- have liver or kidney problems
- are trying to get pregnant, think you might be pregnant, you’re already pregnant, or you’re breastfeeding
- have severe lung disease
- have had muscular side effects when taking a statin in the past
- have had, or have, a muscle disorder
Lipitor chewable tablets contain a substance called aspartame – check with your doctor before taking these if you have phenylketonuria .
Mechanism Accounting For The Pcsk9 Inhibitor Induced Lipid Effects
The linkage of PCSK9 with lipoprotein metabolism was first identified by Abifadel and colleagues in 2003, when they demonstrated that certain mutations in PCSK9 could result in the phenotypic appearance of Familiar Hypercholesterolemia . Subsequent studies demonstrated that gain of function mutations in PCSK9 are an uncommon cause of Familiar Hypercholesterolemia . In 2005 it was shown that loss of function mutations in PCSK9 resulted in lower LDL-C levels and this decrease in LDL-C levels is associated with a reduction in the risk of cardiovascular events .
The main route of clearance of clearance of plasma LDL is via LDL receptors in the liver . When the LDL particle binds to the LDL receptor the LDL particle- LDL receptor complex is taken into the liver by endocytosis . The LDL particle and the LDL receptor then disassociate and the LDL lipoprotein particle is delivered to lysosomes where it is degraded and the LDL receptor returns to the plasma membrane . After endocytosis LDL receptors recirculate back to the plasma membrane over 100 times.
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Mechanisms Accounting For Bile Acid Sequestrants Induced Lipid Effects
Bile acid sequestrants bind bile acids in the intestine, preventing their reabsorption in the terminal ileum leading to the increased fecal excretion of bile acids . This decrease in bile acid reabsorption reduces the size of the bile acid pool, which stimulates the conversion of cholesterol into bile acids in the liver . This increase in bile acid synthesis decreases hepatic cholesterol levels leading to the activation of SREBPs that up-regulate the expression of the enzymes required for the synthesis of cholesterol and the expression of LDL receptors . The increase in hepatic LDL receptors results in the increased clearance of LDL from the circulation leading to a decrease in serum LDL-C levels . Thus, similar to statins and ezetimibe, bile acids lower plasma LDL-C levels by decreasing hepatic cholesterol levels, which stimulates LDL receptor production and thereby accelerates the clearance of LDL from the blood.
The mechanism by which treatment with bile acid sequestrants improves glycemic control is unclear .
Effect Of Evinacumab On Clinical Outcomes
There are no cardiovascular outcome studies.
Homozygosity for loss-of-function mutations in ANGPTL3 is associated with significantly lower plasma levels of LDL-C, HDL-C, and triglycerides . Heterozygous carriers of loss-of-function mutations in ANGPTL3, which occur at a frequency of about 1:300, have significantly lower total cholesterol, LDL-C, and triglyceride levels than noncarriers . Moreover, patients carrying loss-of-function variants in ANGPTL3 have a significantly lower risk of coronary artery disease . Additionally, in an animal model of atherosclerosis treatment with evinacumab decreased atherosclerotic lesion area and necrotic content . Taken together these observations suggest that inhibiting ANGPTL3 with evinacumab will reduce cardiovascular disease.
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Mechanism Accounting For The Statin Induced Lipid Effects
Statins are competitive inhibitors of HMG-CoA reductase, which leads to a decrease in cholesterol synthesis in the liver. This inhibition of hepatic cholesterol synthesis results in a decrease in cholesterol in the endoplasmic reticulum resulting in the movement of sterol regulatory element binding proteins from the endoplasmic reticulum to the golgi where they are cleaved by proteases into active transcription factors . The SREBPs then translocate to the nucleus where they increase the expression of a number of genes including HMG-CoA reductase and, most importantly, the LDL receptor . The increased expression of HMG-CoA reductase restores hepatic cholesterol synthesis towards normal while the increased expression of the LDL receptor results in an increase in the number of LDL receptors on the plasma membrane of hepatocytes leading to the accelerated clearance of apolipoprotein B and E containing lipoproteins . The increased clearance of LDL and VLDL accounts for the reduction in plasma LDL-C and triglyceride levels. In patients with a total absence of LDL receptors statin therapy is not very effective in lowering LDL-C levels.
Isolated Hypercholesterolemia In Primary Prevention
In patients with isolated hypercholesterolemia without cardiovascular disease initial drug therapy is with a statin. The statin dose should be chosen based on the percent reduction in LDL-C required to lower the LDL-C level to below the target goal . As discussed earlier, the side effects of statin therapy increase with higher doses so one should not automatically start with high doses, but instead should choose a dose balancing the benefits and risks. Generic statins are inexpensive drugs and are very effective in both lowering LDL-C levels and reducing cardiovascular events. Additionally, they have an excellent safety profile. If the initial statin dose does not lower LCL-C sufficiently, one can then increase the dose. If the maximal statin dose does not lower LDL-C sufficiently adding ezetimibe is a reasonable next step if the LDL-C level is in a reasonable range and an additional 20-25% reduction in LDL will be sufficient. High dose statin and ezetimibe will lower LDL-C by as much as 70%, which will lower LDL-C to goal in the majority of patients who do not have a genetic basis for their elevated LDL-C levels. If the combination of statin plus ezetimibe does not lower the LDL-C to goal one can add a third drug, such as bempedoic acid or colesevelam. If the patient has diabetes with a moderately elevated A1c level using colesevelam instead of ezetimibe or in combination with ezetimibe could improve both glycemic control and further lower LDL-C levels.
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