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Niacin
I want to get back to discussing lipid modulating drugs. I have been getting many questions regarding niacin on my message board and what it exactly does. I know there is a lot of information out there that it is some kind of wonder drug that raises your HDL-C (good cholesterol) and keeps you from having heart attacks. This is only partly true. As I have said many times before, there is no way to measure how well HDL-C functions. We only measure a number. In other words there is no qualitative test to measure how well the HDL-C works in our bodies, but only a quantitative test. There has never been a prospective randomized study done to correlate an HDL-C level with an outcome. I am not sure that following the HDL-C in patients on niacin tells us anything. Let's talk about what niacin really does.
First of all, niacin is a member of the B-vitamin family and is sometimes referred to as vitamin B3. It is a soluble B vitamin that impacts all lipid subfractions but is not widely used because of the associated side effects. Niacin-induced flushing, which is the result of vasodilatation of the blood vessels, is the most common side effect and usually occurs within 20 minutes following ingestion and may last for up to 60 minutes.
The way niacin works is rather complicated, but in addition to its antiatherogenic activity, the primary use of niacin is to lower triglyceride levels. Niacin reduces the mobilization of free fatty acids from fatty tissue resulting in reduced secretion of VLDL-P from the liver which is a precursor of LDL-P. While it does lower LDL-C, LDL-P, and apoB, this occurs through its triglyceride lowering abilities. Niacin also increases HDL-C. Although niacin does lower Lp(a), in my previous posting I stated that the goal is to lower LDL-P and statins are the primary to drug to perform this function.
Niacin has been associated with abnormal liver tests and causes significant liver toxicity. It should be discontinued if the liver enzymes (ALT/AST) exceed 3X the upper limit of normal. The use of over-the-counter niacin should be discouraged. Many of these preparations are not labeled as sustained release and when combined with a fiber (an example would be oat bran) can become sustained release and adversely affect the liver enzymes. Food maximizes the availability of niacin. It can raise uric acid levels and should be used cautiously in patients with gout.
As I stated earlier, the most common complaint is flushing and this occurs in all patients treated with therapeutic doses of niacin. This is also the most common reason patients stop using the medication. This can be minimized by pretreatment with aspirin or Motrin. Flushing is increased when taken with hot beverages. Gastritis and peptic ulcer disease are also some of the most common reasons for inability to tolerate niacin. Hyperglycemia occurs in patients taking niacin. Patients who are borderline diabetics can become overtly diabetic although data from the ADMIT trial indicate that it can be used safely in diabetics.
Although we still await serious outcome data with niacin, there is good data from very small trials that adding niacin to a statin lessens the thickness of the carotid arteries (CIMT), improves findings on angiograms, and reduces clinical events (the FATS and HATS trials). We await confirmation of this in the much larger AIM HIGH trial which is currently underway. They are not seeing the 90% reduction in clinical events in the AIM HIGH trial that occurred in HATS or the trial would have been stopped for ethical reasons.
In conclusion, while niacin is a drug that should be kept in the armamentarium of a physician that practices lipidology, it should not be used as a first line drug to lower LDL-C or LDL-P. I primarily use it in patients with high triglycerides with known coronary artery disease - in addition to a statin. As I write about in every posting, the name of the game to ensure cardioprotection is to lower LDL-P or apoB and this is now recommended by the American Diabetic Association and American College of Cardiology as a standard of care in patients with moderately high, high, or very high cardiometabolic risk. The full text can be found on my website at www.lipidcenter.com.
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First of all, niacin is a member of the B-vitamin family and is sometimes referred to as vitamin B3. It is a soluble B vitamin that impacts all lipid subfractions but is not widely used because of the associated side effects. Niacin-induced flushing, which is the result of vasodilatation of the blood vessels, is the most common side effect and usually occurs within 20 minutes following ingestion and may last for up to 60 minutes.
The way niacin works is rather complicated, but in addition to its antiatherogenic activity, the primary use of niacin is to lower triglyceride levels. Niacin reduces the mobilization of free fatty acids from fatty tissue resulting in reduced secretion of VLDL-P from the liver which is a precursor of LDL-P. While it does lower LDL-C, LDL-P, and apoB, this occurs through its triglyceride lowering abilities. Niacin also increases HDL-C. Although niacin does lower Lp(a), in my previous posting I stated that the goal is to lower LDL-P and statins are the primary to drug to perform this function.
Niacin has been associated with abnormal liver tests and causes significant liver toxicity. It should be discontinued if the liver enzymes (ALT/AST) exceed 3X the upper limit of normal. The use of over-the-counter niacin should be discouraged. Many of these preparations are not labeled as sustained release and when combined with a fiber (an example would be oat bran) can become sustained release and adversely affect the liver enzymes. Food maximizes the availability of niacin. It can raise uric acid levels and should be used cautiously in patients with gout.
As I stated earlier, the most common complaint is flushing and this occurs in all patients treated with therapeutic doses of niacin. This is also the most common reason patients stop using the medication. This can be minimized by pretreatment with aspirin or Motrin. Flushing is increased when taken with hot beverages. Gastritis and peptic ulcer disease are also some of the most common reasons for inability to tolerate niacin. Hyperglycemia occurs in patients taking niacin. Patients who are borderline diabetics can become overtly diabetic although data from the ADMIT trial indicate that it can be used safely in diabetics.
Although we still await serious outcome data with niacin, there is good data from very small trials that adding niacin to a statin lessens the thickness of the carotid arteries (CIMT), improves findings on angiograms, and reduces clinical events (the FATS and HATS trials). We await confirmation of this in the much larger AIM HIGH trial which is currently underway. They are not seeing the 90% reduction in clinical events in the AIM HIGH trial that occurred in HATS or the trial would have been stopped for ethical reasons.
In conclusion, while niacin is a drug that should be kept in the armamentarium of a physician that practices lipidology, it should not be used as a first line drug to lower LDL-C or LDL-P. I primarily use it in patients with high triglycerides with known coronary artery disease - in addition to a statin. As I write about in every posting, the name of the game to ensure cardioprotection is to lower LDL-P or apoB and this is now recommended by the American Diabetic Association and American College of Cardiology as a standard of care in patients with moderately high, high, or very high cardiometabolic risk. The full text can be found on my website at www.lipidcenter.com.
Related Topics:
