Hypercholesterolemia: Wikis


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Classification and external resources

ICD-10 E78.0
ICD-9 272.0
DiseasesDB 6226
eMedicine med/1073
MeSH D006937

Hypercholesterolemia (literally: high blood cholesterol) is the presence of high levels of cholesterol in the blood.[1] It is not a disease but a metabolic derangement that can be secondary to many diseases and can contribute to many forms of disease, most notably cardiovascular disease. It is closely related to the terms "hyperlipidemia" (elevated levels of lipids) and "hyperlipoproteinemia" (elevated levels of lipoproteins).[1]

Elevated cholesterol in the blood is due to abnormalities in the levels of lipoproteins, the particles that carry cholesterol in the bloodstream. This may be related to diet, genetic factors (such as LDL receptor mutations in familial hypercholesterolemia) and the presence of other diseases such as diabetes and an underactive thyroid. The type of hypercholesterolemia depends on which type of particle (such as low density lipoprotein) is present in excess.[1]

High cholesterol levels are treated with diets low in cholesterol, medications, and rarely with other treatments including surgery (for particular severe subtypes). This is also increased emphasis on other risk factors for cardiovascular disease, such as high blood pressure.[1]


Signs and symptoms

Elevated cholesterol does not lead to specific symptoms unless it has been longstanding. Some types of hypercholesterolemia lead to specific physical findings: xanthoma (deposition of cholesterol in patches on the skin or in tendons), xanthelasma palpabrum (yellowish patches around the eyelids) and arcus senilis (white discoloration of the peripheral cornea).[1]

Longstanding elevated hypercholesterolemia leads to accelerated atherosclerosis; this can express itself in a number of cardiovascular diseases: coronary artery disease (angina pectoris, heart attacks), stroke and short stroke-like episodes and peripheral vascular disease.[1][2][3]


see High-density lipoprotein#Recommended range

see Low-density lipoprotein#Normal ranges

There is no specific level at which cholesterol levels are abnormal. Cholesterol levels are found in a continuum within a population. Higher cholesterol levels lead to increased risk of specific disease, most notably cardiovascular diseases. Specifically, high LDL cholesterol levels are associated with increased risk. When speaking of hypercholesterolemia, most people are referring to high levels of LDL cholesterol.[citation needed]

When measuring cholesterol, it is important to measure its subfractions before drawing a conclusion as to the cause of the problem. The subfractions are LDL, HDL and VLDL. In the past, LDL and VLDL levels were rarely measured directly due to cost concerns. VLDL levels are reflected in the levels of triglycerides (generally about 45% of triglycerides is composed of VLDL). LDL was usually estimated as a calculated value from the other fractions (total cholesterol minus HDL and VLDL); this method is called the Friedewald calculation; to be specific: LDL ~= Total Cholesterol - HDL - (0.2 x Triglycerides).

Less expensive (and less accurate) laboratory methods and the Friedewald calculation have long been used because of the complexity, labor, and expense of the electrophoretic methods developed in the 1970s to identify the different lipoprotein particles that transport cholesterol in the blood. In 1980, the original methods, developed by research work in the mid-1970s cost about $5,000, in US 1980 dollars, per blood sample/person.

With time, more advanced laboratory analyses that do measure LDL and VLDL particle sizes and levels have been developed, and at far lower cost. These have partly been developed and become more popular as a result of the increasing clinical trial evidence that intentionally changing cholesterol transport patterns, including to certain abnormal values compared to most adults, often has a dramatic effect on reducing, even partially reversing, the atherosclerotic process. With ongoing research and advances in laboratory methods, the prices for more sophisticated analyses have markedly decreased, to less than $100, US 2004, by some labs, and with simultaneous increases in the accuracy of measurement for some of the methods.



Fredrickson classification

Classically, hypercholesterolemia was categorized by lipoprotein electrophoresis and the Fredrickson classification. Newer methods, such as "lipoprotein subclass analysis" have offered significant improvements in understanding the connection with atherosclerosis progression and clinical consequences.

If the hypercholesterolemia is hereditary (familial hypercholesterolemia), there is more often a family history of premature, earlier onset atherosclerosis, as well as familial occurrence of the signs mentioned above.

Secondary causes

There are a number of secondary causes for high cholesterol:

Dietary influence

While part of the circulating cholesterol originates from diet, and restricting cholesterol intake may reduce blood cholesterol levels, there are various other links between the dietary pattern and cholesterol levels. The American Heart Association compiles a list of the acceptable and unacceptable foods for those who are diagnosed with hypercholesterolemia.

Dietary changes can potentially be very strong: when a group of Tarahumara Indians from Mexico with no obesity or cholesterol problems were exposed to a Western diet, their risk profile worsened significantly, with cholesterol levels rising over thirty percent.[4]


Evidence is accumulating that eating more carbohydrates - especially simpler, more refined carbohydrates - increases levels of triglycerides in the blood, lowers HDL, and may shift the LDL particle distribution pattern into unhealthy atherogenic patterns. [5]

Trans fats

An increasing number of researchers are suggesting that a major dietary risk factor for cardiovascular diseases is trans fatty acids, and in the US the FDA has revised food labeling requirements to include listing trans fat quantities.[6]


Clinical Evidence has summarized treatment for both primary prevention[7] and secondary prevention.[8] Two factors have been put forward for consideration when choosing therapy are the patient's risk of coronary disease and their lipoprotein pattern.

  1. Risk of coronary disease. To calculate the benefit of treatment, there are two online calculators that can estimate baseline risk.[9][10] Combining the baseline risk with the relative risk reduction of a treatment can lead to the absolute risk reduction of number needed to treat. For example, one of the calculators projects that a patient had a 10% risk of coronary disease over ten years. As noted below, the relative risk reduction of a statin is 30%. Thus, after 4–7 years of treatment with a statin, a patient's risk will drop to 7%. This equates to an absolute risk reduction of 3%, or a number needed to treat of 33. Thirty three such patients must be treated for 4–7 years for one to benefit.
  2. Lipoprotein patterns. (See hyperlipoproteinemia for details) The treatment depends on the type of hypercholesterolemia. Clinical trials, starting in the 1970s, have repeatedly and increasingly found that normal cholesterol values do not necessarily reflect healthy cholesterol values. This has increasingly lead to the newer concept of dyslipidemia, despite normo-cholesterolemia. Thus there has been increasing recognition of the importance of "lipoprotein subclass analysis" as an important approach to better understand and change the connection between cholesterol transport and atherosclerosis progression. Fredrickson Types IIa and IIb can be treated with diet, statins (most prominently rosuvastatin, atorvastatin, simvastatin, or pravastatin), cholesterol absorption inhibitors (ezetimibe), fibrates (gemfibrozil, bezafibrate, fenofibrate or ciprofibrate), vitamin B3 (niacin), bile acid sequestrants (colestipol, cholestyramine), LDL apheresis and in hereditary severe cases liver transplantation.

Multiple clinical trials, each, by design, examining only one of multiple relevant issues, have increasingly examined the connection between these issues and atherosclerosis clinical consequences. Some of the better recent randomized human outcome trials include ASTEROID, ASCOT-LLA, REVERSAL, PROVE-IT, CARDS, Heart Protection Study, HOPE, PROGRESS, COPERNICUS, and especially a newer research approach utilizing a synthetically produced and IV administered human HDL, the Apo A-I Milano Trial,[11][12][13][14] the results of which were published in JAMA in 2003.


In strictly controlled surroundings, such as a hospital ward dedicated to metabolism problems, a diet can reduce cholesterol levels by 15%. In practice, dietary advice can provide a modest decrease in cholesterol levels and may be sufficient in the treatment of mildly elevated cholesterol.[15]


Many primary physicians and heart specialists will initially prescribe medication in combination with diet and exercise. According to various resources, statins are the most commonly used and effective forms of medication for the treatment of high cholesterol. The U.S. Preventive Services Task Force (USPSTF) estimated that after 5 to 7 years of treatment, the relative risk reduction by statins on coronary heart disease events is decreased by approximately 30%.[16][17] More recently, a meta-analysis reported an almost identical relative risk reduction of 29.2% in low risk patients treated for 4.3 years.[18] A relative risk reduction of 19% in coronary mortality was found in a meta-analysis of patients at all levels of risk.[19]

Clinical practice guidelines

Various clinical practice guidelines have addressed the treatment of hypercholesterolemia. The American College of Physicians has addressed hypercholesterolemia in patients with diabetes.[20] Their recommendations are:

  • Recommendation 1: Lipid-lowering therapy should be used for secondary prevention of cardiovascular mortality and morbidity for all patients (both men and women) with known coronary artery disease and type 2 diabetes.
  • Recommendation 2: Statins should be used for primary prevention against macrovascular complications in patients (both men and women) with type 2 diabetes and other cardiovascular risk factors.
  • Recommendation 3: Once lipid-lowering therapy is initiated, patients with type 2 diabetes mellitus should be taking at least moderate doses of a statin (the accompanying evidence report states "simvastatin, 40 mg/d; pravastatin, 40 mg/d; lovastatin, 40 mg/d; atorvastatin, 20 mg/d; or an equivalent dose of another statin")[21].
  • Recommendation 4: For those patients with type 2 diabetes who are taking statins, routine monitoring of liver function tests or muscle enzymes is not recommended except in specific circumstances.

The National Cholesterol Education Program revised their guidelines[22]; however, their 2004 revisions have been criticized for use of nonrandomized, observational data.[23]

In the UK, the National Institute for Health and Clinical Excellence (NICE) has made recommendations for the treatment of elevated cholesterol levels, published in 2008.[24]

Alternative medicine

A survey released in May 2004 by the National Center for Complementary and Alternative Medicine focused on who used complementary and alternative medicine (CAM), what was used, and why it was used in the United States by adults age 18 years and over during 2002. According to this survey, CAM was used to treat cholesterol by 1.1% of U.S. adults who used CAM during 2002 ([1] table 3 on page 9). Consistent with previous studies, this study found that the majority of individuals (i.e., 54.9%) used CAM in conjunction with conventional medicine (page 6).

A review of 84 clinical trials with phytosterols and/or phytostanols reported an average of 8.8% lowering of LDL-cholesterol with a mean daily intake of 2.15 grams/day, administered 2-3 times a day with meals. The dose:response figure shows that more than half of the response is achieved once intake is more than 1.0 g/day.[25] In 2000 the Food and Drug Administration approved a Qualified Health Claim for labeling of foods containing specified amounts of phytosterol esters or phytostanol esters as cholesterol lowering; in 2003 an FDA Interim Health Claim Rule extended that label claim to foods or dietary supplements delivering more than 0.8 grams/day of either esterified or non-esterified ("free") phytosterols or phytostanols divided over two doses per day. Some researchers, however, are concerned about diet supplementation with plant sterol esters and draw attention to significant safety issues. This is why Health Canada, the federal department responsible for helping Canadians maintain and improve their health, has not allowed these foods to be sold in Canada.[26]


Screening for a disease refers to testing for a disease, such as hypercholesterolemia, in patients who have no signs or symptoms of the disease.

In patients without any other risk factors, moderate hypercholesterolemia is often not treated. According to Framingham Heart Study, people with an age greater than 50 years have no increased overall mortality with either high or low serum cholesterol levels. There is, however, a correlation between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). This, however, does not mean that a decrease in serum levels is dangerous, as there has not yet been a recorded heart attack in the study in a person with a total cholesterol below 150 mg/dL.

The U.S. Preventive Services Task Force (USPSTF) has evaluated screening for hypercholesterolemia.[16][17]


  1. ^ a b c d e f Durrington P (2003). "Dyslipidaemia". Lancet 362 (9385): 717–31. doi:10.1016/S0140-6736(03)14234-1. PMID 12957096. 
  2. ^ Grundy SM, Balady GJ, Criqui MH, et al. (19 May 1998). "Primary prevention of coronary heart disease: guidance from Framingham: a statement for healthcare professionals from the AHA Task Force on Risk Reduction. American Heart Association". Circulation 97 (18): 1876–87. PMID 9603549. http://circ.ahajournals.org/cgi/content/full/97/18/1876. 
  3. ^ http://labrador.eu/peripheral_vascular_disease_en.html
  4. ^ McMurry MP, Cerqueira MT, Connor SL, Connor WE (1991). "Changes in lipid and lipoprotein levels and body weight in Tarahumara Indians after consumption of an affluent diet". N. Engl. J. Med. 325 (24): 1704–8. PMID 1944471. http://content.nejm.org/cgi/content/abstract/325/24/1704. 
  5. ^ TJ Starc, S Shea, LC Cohn, L Mosca, WM Gersony and RJ Deckelbaum (1998). "Greater dietary intake of simple carbohydrate is associated with lower concentrations of high-density-lipoprotein cholesterol in hypercholesterolemic children". American Journal of Clinical Nutrition 67: 1147-1154. http://www.ajcn.org/cgi/content/abstract/67/6/1147. 
  6. ^ Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC (April 2006). "Trans fatty acids and cardiovascular disease". N. Engl. J. Med. 354 (15): 1601–13. doi:10.1056/NEJMra054035. PMID 16611951. 
  7. ^ Pignone M (2005). "Primary prevention: dyslipidaemia". Clin Evid (14): 142–50. PMID 16620402. http://clinicalevidence.com/ceweb/conditions/cvd/0215/0215.jsp. 
  8. ^ Gami A (2006). "Secondary prevention of ischaemic cardiac events". Clin Evid (15): 195–228. PMID 16973010. http://clinicalevidence.com/ceweb/conditions/cvd/0206/0206_guidelines.jsp. 
  9. ^ Pignone MP; Sheridan SL. "med-decisions.com". http://www.med-decisions.com/. Retrieved February 26, 2007. 
  10. ^ National Cholesterol Education Program. "10-year CVD Risk Calculator (Risk Assessment Tool for Estimating 10-year Risk of Developing Hard CHD (Myocardial Infarction and Coronary Death) Version)". http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=prof. Retrieved February 26, 2007. 
  11. ^ url=http://jama.ama-assn.org/cgi/content/full/290/17/2292
  12. ^ url=http://www.lipidsonline.org/commentaries/al_abstract.cfm?abs_id=abs047
  13. ^ url=http://content.onlinejacc.org/cgi/content/short/44/7/1436
  14. ^ url=http://www.lipidsonline.org/commentaries/ppt/milano.ppt
  15. ^ Tang JL, Armitage JM, Lancaster T, Silagy CA, Fowler GH, Neil HA (April 1998). "Systematic review of dietary intervention trials to lower blood total cholesterol in free-living subjects". BMJ 316 (7139): 1213–20. PMID 9552999. PMC 28525. http://www.bmj.com/cgi/content/abstract/316/7139/1213. 
  16. ^ a b Pignone M, Phillips C, Atkins D, Teutsch S, Mulrow C, Lohr K (2001). "Screening and treating adults for lipid disorders". Am J Prev Med 20 (3 Suppl): 77–89. doi:10.1016/S0749-3797(01)00255-0. PMID 11306236. 
  17. ^ a b U.S. Preventive Services Task Force. "Screening for Lipid Disorders: Recommendations and Rationale". http://www.ahrq.gov/clinic/ajpmsuppl/lipidrr.htm. Retrieved February 26, 2007. 
  18. ^ Thavendiranathan P, Bagai A, Brookhart M, Choudhry N (2006). "Primary prevention of cardiovascular diseases with statin therapy: a meta-analysis of randomized controlled trials". Arch Intern Med 166 (21): 2307–13. doi:10.1001/archinte.166.21.2307. PMID 17130382. 
  19. ^ Baigent C, Keech A, Kearney PM, et al. (2005). "Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins". Lancet 366 (9493): 1267–78. doi:10.1016/S0140-6736(05)67394-1. PMID 16214597. 
  20. ^ Snow V, Aronson M, Hornbake E, Mottur-Pilson C, Weiss K (20 April 2004). "Lipid control in the management of type 2 diabetes mellitus: a clinical practice guideline from the American College of Physicians". Ann Intern Med 140 (8): 644–9. PMID 15096336. http://www.annals.org/cgi/content/full/140/8/644. 
  21. ^ Vijan S, Hayward RA (2004). "Pharmacologic lipid-lowering therapy in type 2 diabetes mellitus: background paper for the American College of Physicians". Ann. Intern. Med. 140 (8): 650–8. PMID 15096337. http://www.annals.org/cgi/content/full/140/8/650. 
  22. ^ Grundy SM, Cleeman JI, Merz CN, Brewer HB, Clark LT, Hunninghake DB, Pasternak RC, Smith SC, Stone NJ (2004). "Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines". J. Am. Coll. Cardiol. 44 (3): 720–32. doi:10.1016/j.jacc.2004.07.001. PMID 15358046. 
  23. ^ Hayward RA, Hofer TP, Vijan S (2006). "Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem". Ann. Intern. Med. 145 (7): 520–30. PMID 17015870. 
  24. ^ National Institute for Health and Clinical Excellence. Clinical guideline 67: Lipid modification. London, May 2008.
  25. ^ http://www.ncbi.nlm.nih.gov/pubmed/19091798
  26. ^ Weingärtner O. et al. Controversial role of plant sterol esters in the management of hypercholesterolaemia. European Heart Journal 2009 30(4):404-409; doi:10.1093/eurheartj/ehn580. http://eurheartj.oxfordjournals.org/cgi/content/extract/30/4/404

See also

Simple English

Hypercholesterolemia means that the cholesterol level is too high in the blood.



Cholesterol is a molecule that is found in cells. It is a type of lipid which is a fat or fat-like molecule. Cholesterol is a special type of lipid that is called a steroid. Steroids are lipids that have a special chemical structure. This structure is made of four rings of carbon atoms.

Other steroids include hormone steroids like cortisol, estrogen, and testosterone. In fact, all steroid hormones are made from changing the basic chemical structure of cholesterol. When scientists talk about making one molecule from changing simpler ones, they sometimes call it synthesis.

Where does it come from?

Cholesterol is usually found in the walls of cells. It is only found in animals. Plants do not synthesize cholesterol. So the cholesterol in the food people eat can only come from eating food from animals. But even vegans who eat only plant foods can have cholesterol. This is because most of the cholesterol that is in our bodies is synthesized by our bodies.

What does it do?

Cholesterol does many important jobs in a cell. Cholesterols main function is as a structural component of cell membranes. It is also the starting material for bile acids that are made by the liver and used to digest fats, and for steroid hormones. However, it is best known for something bad that it does. High levels of cholesterol can lead to atherosclerosis. This is an inflammatory disease of artery walls in which white blood cells invade the vessel wall and become engorged with cholesterol and other lipids. These areas can slowly close off a blood vessel or can suddenly rupture and trigger formation of a blood clot.

Types of cholesterol

Not all cholesterol is bad. There are different kinds of cholesterol in the blood. Doctors often measure these different types to see if someone has hypercholesterolemia.

HDL, an acronym for 'high density lipoprotein' is sometimes called 'good cholesterol' because people with high levels of HDL cholesterol have less atherosclerosis.

LDL (low density lipoprotein) is sometimes called 'bad cholesterol' because people with high levels of LDL cholesterol have more atherosclerosis.

High blood levels of VLDL (very low density lipoprotein) also causes more atherosclerosis. However, measuring its level in blood is more expensive. So the blood level of triglycerides (a kind of fat) is used instead. High triglycerides (TG) are found in people with high VLDL.

Why is atherosclerosis bad?

When atherosclerosis gets bad enough, it can cause blockage of blood flow in arteries. This can hurt whatever the artery brings blood to. The organ or tissue that the blocked artery brought blood to can even die. If the organ or tissue dies, doctors call this an infarction. If it is hurt from low blood flow, but not enough to die, it is called ischemia.

If the artery brought blood to the heart, people can have angina or a heart attack. A heart attack is also called a myocardial infarction. Myocardial means relating to the heart muscle. Infarction means death of a tissue or organ. So a myocardial infarction or heart attack is when blood flow to part of the heart stops. Then that part of the heart dies. Angina is when the blood flow is low but not totally blocked.

If the blocked artery brought blood to the brain, people can have a stroke. If the blocked artery is to the kidneys, it can cause kidney failure. If the blocked artery is to an arm or leg, they may also die. If this happens, the arm or leg may need to be amputated (cut off) if the blood vessel cannot be fixed by doctors.

How is atherosclerosis treated?

The best way to treat it is to not get it! Some people develop atherosclerosis faster than others. Some develop it very slowly. Many things make those differences between people. Some are things people can change. Some are not.

  • Unchangeable things
    • Genetics (whether people have good genes or bad ones from their parents.)
    • Sex (men get atherosclerosis earlier than women)
  • Changeable things

However, once someone gets hypercholesterolemia which means high blood cholesterol, doctors treat them. The first way to treat hypercholesterolemia is to exercise, quit smoking, and eat better foods. If these work and the cholesterol blood levels become normal, no more treatment is needed. If these do not work, sometimes medicines are also needed. But even if medicine is used, it is still important to stop smoking, eat better, and exercise.

Once someone gets atherosclerosis from hypercholesterolemia, a better diet, exercise, and quitting smoking may not be enough. If people already have atherosclerosis that causes problems like heart attack or strokes, medicine is almost always needed.

People with atherosclerosis must also be watched by doctors to make sure they do not get ischemia or infarction. Since they are more likely to get a myocardial infarction (heart attack) or stroke, they must watch for signs of these. Sometimes if a doctor thinks a person has atherosclerosis she may do tests to find atherosclerosis before it causes symptoms of ischemia or infarction. But if people get symptoms of these problems, it is important to see a doctor immediately.

For all of these types of ischemia or infarction, doctors can try to reopen the blocked artery. This may be done my surgery or sometimes with very strong medicines to make the blood less able to make clots. If this is not done fast enough, the tissue or organ with ischemia may be too badly hurt to save.

Medicines to treat hypercholesterolemia

The most common type of medicine to treat hypercholesterolemia are 'statin' drugs. They are called 'statins' because their names all end in -statin. They are also called HMG-CoA Reductase Inhibitors. This is because they work by inhibiting the enzyme HMG-CoA Reductase. Inhibiting an enzyme means to make it work less well.

The HMG-CoA Reductase enzyme causes the body to make more cholesterol. If it is inhibited, the body makes less cholesterol. So statin drugs lower the amount of LDL (bad) cholesterol in the blood which stops atherosclerosis from getting worse. Statin drugs can even help make atherosclerosis better. However, statins are not as good at increasing the HDL (good) cholesterol. Low HDL is hard to treat with medicines, but goes up with more exercise!

There are two big problems with taking statins: Liver problems and 'Rhabdomyolysis.'

Rhabdomyolysis means a disease where muscle cells are damaged and die. Statins can cause damage to muscle cells. This can cause weakness and muscle pain. The worse problem though is that when muscle cells die, they release cell proteins into the blood. The kidney removes the muscle protein from the blood. If the kidney takes up too much protein, it can be hurt. If it is bad enough it can cause kidney failure. So if people take statins and get muscle pain or weakness, stop the medicine and see a doctor.

Statins can also cause liver problems. They can cause mild irritation of the liver. They can rarely cause very bad liver damage. Because of this, when someone starts taking a statin, doctors check liver blood tests after six weeks. Doctors also warn patients to watch for the signs of liver damage: pain in the right side of the abdomen, nausea, vomiting, and jaundice.

However, both of these problems are rare. In someone with hypercholesterolemia, the benefit from statins is more than the risk. This means that someone is more likely to prevent problems than cause problems by taking them. There are many big scientific studies of this problem that show the same thing: if people have hypercholesterolemia and take statins, they are more likely to live longer and be healthier.

There are other kinds of medicines to treat hypercholesterolemia. But statins are the most effective treatment.

Fibrates are medicines that lower cholesterol levels. They may also help people with Type II Diabetes. This is a good effect because diabetes and hypercholesterolemia cause some of the same problems. If both diabetes and hypercholesterolemia happen in the same person the problems from these diseases can be much worse. Fibrates can have rhabdomyolysis like the statins and also can cause upset stomach. Use of fibrates and statins at the same time makes rhabdomyolysis happen much more often.

Niacin is a vitamin that lowers cholesterol levels. It is also called Vitamin B3 or nicotinic acid. Severe niacin deficiency in the diet can cause a disease called Pellagra. This is rare in the developed world today. However, less bad deficiency of niacin can cause high blood pressure, weight gain, and hypercholesterolemia. So sometimes Niacin is used to treat hypercholesterolemia. Niacin is one of the medicines that may make HDL (good) cholesterol go up. The biggest problem with taking enough Niacin to help cholesterol is that it causes severe flushing (hot, red, sometimes itchy skin). This 'side-effect' is so bad, sometimes people stop taking the medicine.

Bile Acid Resins are medicines that make people not absorb as much bile when they digest food. This causes them to take up less cholesterol also, which lowers blood levels of cholesterol.


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