If you are like most people you take your heart for granted.  That's because your heart works day in and day out, pumping blood through your circulatory system.  However, we tend to neglect and abuse our hearts, that's why heart disease is the number one cause of death in the world, more than those killed by war, accidents, cancer, added together.  The National Heart, Lung and Blood Institute reported that approximately 1.25 million heart attacks occur each year in the United States.  Billions of dollars are spent on research every year, and yet modern medicine still has not been able to control the disease and treat it effectively.  Many conditions can result from neglect and abuse of the heart, including heart attacks, strokes, angina, atherosclerosis, heart failure, etc.

There are several factors that have been identified by research that contribute to heart disease, such as high cholesterol levels, diet, physical condition, smoking, consumption of alcohol, genetics or family history, etc..

Therefore, a person must do certain things, sometimes easy and simple, to protect his/her heart and keep it functioning optimally:

• control the cholesterol levels - ensuring that they don't go beyond certain levels;
• adopt a healthy lifestyle, avoiding foods determined to be unhealthy while consuming foods identified as contributing to good health, and consider supplementation with vitamins, etc.;
• avoid smoking and consume alcohol in moderation;
• become aware of your cardiovascular genetics or family history.

Controlling  Cholesterol Levels

Cholesterol is a waxy, fat-like substance called lipid.  Nowadays, it's often regarded as a villain, a poison to be got rid of.  However, your body can't live without it as it is used to build your body's cell membranes, insulate your nerves, and produce certain hormones. It's used by your liver to make bile acids, which help digest your food. The confusion that clouds cholesterol is partly due to the way some people use the word. There are actually two sources of cholesterol -- your body makes cholesterol and it also gets it from food, bu the term "cholesterol" is often a catch-all term for both the cholesterol you eat and the cholesterol that ismanufactured in your body.  Cholesterol is actually vital to your body functions, but recent research has determined that an excess of cholesterol puts you at risk of cardiovascular disease.  Therefore, it is vital that the cholesterol in your body is controlled so that one of the first things that your doctor does is to order tests for your cholesterol levels.

Currently, the test that your doctor relies on for total cholesterol levels is obtained from tests for three cholesterol groups:  low-density lipoproteins (LDL), high-density lipoproteins (HDL) and triglycerides.  The levels obtained are then grouped together and a total cholesterol level is calculated.  These are compared against the minimum/maximum benchmarks and based on the result your doctor advises you whether you are at risk or safe.  However, many specialists now believe these tests are often misleading, and more dangerously, they create a false sense of worry or security. Dr. Roger Superko, a cardiologist who advocates a new type of blood analysis at a Bay-area clinic, identified 12 different subclasses of cholesterol-carrying particles, plus other substances that influence heart disease.  Dr. Superko claims that "total cholesterol and even levels of HDL and LDL were too general to be dependable predictors of cardiovascular trouble, often misleading, creating a false sense of worry or security."

To better control your cholesterol levels, ask your doctor, in addition to testing for LDL, HDL, and triglycerides, about testing for the following substances as well:

    a) LDL IIIa and IIIb;
    b) Apolipoprotein B;
    c) Lipoprotein(a);
    d) Fibrinogen;
    e) C-reactive Protein (CRP;
    f) Homocysteine;
    g) Insulin.

Because cholesterol  itself can't dissolve in watery liquid, it must be transported by a substance called lipoprotein, which can dissolve in blood serum.  Lipoproteins contain cholesterol at the core and an outer layer of protein, called apolipoprotein. Therefore, lipoproteins are the "packages" in which cholesterol travel throughout the body. Measuring the amount of cholesterol carried by each type of lipoprotein helps determine a person's risk for cardiovascular disease (also called CVD, a disease that affects the heart and blood vessels).

Lipoproteins

There are four major classes of lipoproteins: chylomicrons, very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). There are also less commonly measured classes such as lipoprotein(a) and subtypes of the main classes. Each lipoprotein has characteristics that make the cholesterol it carries a greater or lesser risk. Measuring each type of
lipoprotein helps determine a person's risk for cardiovascular disease more accurately than measuring total cholesterol alone. When a person is determined to be at risk, treatment by diet or medication can be started and his or her response to treatment monitored by repeated testing.

Chylomicrons

Chylomicrons are made in the intestines from the triglycerides in food. They contain very little cholesterol. Chylomicrons circulate in the blood, getting smaller as they deposit the triglycerides in fatty tissue. Twelve hours after a meal, they are gone from circulation. Serum collected from a person directly after eating will form a creamy layer on the top if left undisturbed and refrigerated overnight. This creamy layer is the chylomicrons.

Very low-density lipoproteins (VLDL)

VLDL are formed in the liver by the combination of cholesterol, triglycerides formed from circulating fatty acids, and apolipoprotein. This lipoprotein particle is smaller than a chylomicron, and contains less triglyceride but more cholesterol (10-15% of a person's total cholesterol). As the VLDL circulates in the blood, triglycerides are deposited and the particle gets smaller, eventually becoming a low-density lipoprotein (LDL). Serum from a person with a large amount of VLDL will be cloudy.

Low-density lipoproteins (LDL)

LDL, often called "bad" cholesterol, carries cholesterol in the blood and deposits it in body tissues and in the walls of blood vessels, a condition known as atherosclerosis. The amount of LDL in a person's blood is directly related to his or her risk of cardiovascular disease. The higher the LDL level, the greater the risk. LDL is the lipoprotein class most used to trigger and monitor cholesterol lowering therapy.    LDL is formed primarily by the breakdown of VLDL.  LDL contains little triglycerides and a large amount of cholesterol (60-70% of a person's total cholesterol). Although the particles are much smaller than chylomicrons and VLDL, LDL particles can vary in size and chemical structure. These variations represent subclasses within the LDL class. There are seven subclasses of LDL particles, with such catchy names as I, Iia, Iib, IIIa, IIIb, Iva, and Ivb.  Serum from a person with a large amount of LDL will be clear.

LDL IIIa and IIIb (15.6 percent)

Overall, LDL is bad cholesterol, but LDL IIIa and LDL IIIb are the most destructive types.  They are the most dangerous because they are the smallest, densest particles – the ones most likely to work their way into artery walls and form plaques, creating arterial lesions, contributing to the growth of existing ones, and making plaque less stable and more susceptible to rupture. They are the worst of the seven subclasses of LDL cholesterol particles that can now be measured.  People with lots of small, dense lipoprotein are classified as pattern B and have a threefold greater risk of developing heart disease.

Apolipoprotein B (107 mg/dl)

Apolipoprotein is the outer layer, or the protein cap that each LDL particle wears. Over 90% of low density lipoprotein (LDL) particle is composed of Apo B. It serves the function of solubalizing cholesterol within the LDL complex, which in turn increases the transport capacity of LDL for subsequent deposit on the arterial wall.  Apo B is therefore a convenient marker for assessing the cholesterol depositing capacity of the blood, and studies have clearly indicated it as a better discriminator of angiographically documented coronary artery disease than LDL cholesterol. By counting these, you get a precise measure of the LDL particles in the bloodstream, a truer indication of your genetic predisposition to heart disease.  These particles may damage your arteries and cause blockages, so it helps to know how many you’ve got.

Lipoprotein(a), or Lp(a) (3 mg/dl)

Lipoprotein(a) (Lp(a)), unlike Apo AI or Apo B, whose levels vary as a result of diet, exercise, etc. is predominantly a genetic trait whose level remains more or less constant after puberty.  More than 13 phenotypes of Lp(a) have been identified having molecular weight of 300-800 Kd.  It is bound to both HDL and LDL. Lp(a) interferes with plasminogen, the clot dissolving enzyme, which binds to the arterial endothelial lining.  This in turn contributes to blood clot formation, and over a prolonged period of time would lead to significant damage to the coronary arteries.  Levels of greater  than 30mg/dl have been demonstrated to independently increase the risk of CHD by six fold.  Lp(a) a form of LDL that’s so predictive of coronary disease that it’s been called “heart attack cholesterol.”  Researchers at Oxford University in England found that among 5,400 people with heart disease, those with the highest levels had a 70 percent greater chance of having a heart attack.  It accumulates around arterial lesions and promotes clotting.  Lp(a) alone can raise your risk of heart attack by as much as 70 percent, as it does not respond to diet and exercise.  It is recommended that Lp(a) be kept below 20.  Niacin is the best way to treat it – 4 to 5 grams of niacin daily is recommended.
 

OTHER SUBSTANCES

Heart disease experts like Dr. Roger Superko and Dr. Richard Fogoros indicate that, aside from cholesterol, there are other substances that are equally considered factors contributing to cardiovascular disease and should be testing for them as well.

Fibrinogen (324 mg/dl):

Fibrinogen is a protein molecule that promotes clotting and also thickens the blood.  The more there is, the greater the likelihood that your heart is struggling to pump sludge.  High levels seem to correlate with cigarette smoking, obesity, inactivity, aging, and diabetes.  Levels above 350 double the risk of coronary disease.  It is recommended that fibrinogen be kept below 324 mg/dl.  Currently, high fibrinogen levels cannot be treated.

C-reactive Protein (CRP):

CRP is substance produced in the liver when arteries become inflamed.  The more of it there is, the greater the chance of arterial plaque rupturing and causing a heart attack. C-Reactive Protein (CRP) has been demonstrated to be a general indicator of major
tissue damage. Hence, it can be used to indicate a stroke or heart attack because major blood vessels leading to the heart or brain are damaged and release large quantities of CRP during these disease states. CRP is a particularly useful indicator of CHD in women and in patients that demonstrate no other plasma circulating biochemical indicators. Levels above 2.5 mg/dl convey a two-to fourfold increase in risk and are capable of predicting first heart attacks 6 to 8 years in advance.  As with fibrinogen, high CRP levels cannot be treated at the present time.  Regarding CRP levels, it is not the CRP level itself that is thought to be the problem, but the presumed inflammation in the coronary arteries that is reflected by the high CRP level.  So the real question is whether the inflammation (and not the CRP) can be treated.  There is some evidence that infection with an organism called Chlamydia pneumoniae may be a factor in the development of coronary artery disease.  If so, then antibiotics might be effective in eliminating the infection and reducing the risk of heart attacks (and, dentally, in reducing CRP levels). It is recommended that CRP be kept below 0.07 mg/dl.

Homocysteine (11.9 micromoles per liter):

Homocysteine is an amino acid that promotes clotting.  It appears to work in conjunction with fibrinogen and Lp(a).  Levels above 14 can increase your risk of  heart attack and stroke by two to four times.  Fortunately, it’s one of the easiest of the new blood components to control.  It responds well to folate and B vitamins.

Homocysteine is a non-essential amino acid; high levels have been associated with cardiovascular disease. Excessive homocysteine levels can be caused by a deficiency of folate and/or vitamin B12.  Deficiencies of folate can arise because a person is not eating enough fruits and leafy green vegetables. Vitamin B12 deficiency can occur in vegetarians (since this vitamin is not found in plant sources), but deficiencies are more commonly caused by poor absorption, which can result from HIV disease, aging, and other causes.

Many studies of non-HIV infected individuals have shown elevated serum homocysteine levels to be a risk factor for vascular disease. In particular, a review article by Boushey et al. (1995) highlighted homocysteine as a causal factor for arteriosclerotic vascular disease. [1] Individuals with a high level of serum homocysteine had 2.5 times the risk of developing vascular disease as those with
a normal level; this makes serum homocysteine levels a stronger risk factor for vascular disease than serum cholesterol. In another study, Stubbs et al. (2000) demonstrated that for patients being admitted for acute cardiac events, serum homocysteine levels were an excellent predictor of later cardiac events such as another heart attack or death from a heart attack.

The mechanism by which homocysteine acts is still unclear. However, research suggests that it affects the lining of blood vessels.  Increased serum homocysteine levels may damage this lining or make it hard for blood vessels to relax, making it easier for arteriosclerotic plaques to develop. Homocysteine may also change factors in blood itself so that the blood becomes more prone to clotting.

Some drugs may also increase homocysteine levels. Examples of such drugs include nicotinic acid (niacin), theophylline (used for asthma. emphysema and bronchitis), methotrexate and L-Dopa.

The most important and easiest treatment is taking dietary supplements of Vitamin B12, Vitamin B6, folic acid and TMG (betadine), in addition to eating a balanced diet including fruits and green leafy vegetables.  While there are suggested daily amounts of supplements, the only reliable way to know if a patient is taking the right amounts to control a high serum homocysteine level is by
having a blood test for homocysteine.

Insulin (4 micrograms per mililiter – 12 mcg/ml):

Insulin is a hormone secreted by the pancreas to regulate blood sugar and it is important in regulating diabetes.  However, when combined with high triglycerides, low HDL, high fibrinogen, and high levels of small, dense lipoprotein, high insulin levels strongly predispose you to atherosclerosis.  Keep this under 12 mcg/ml.  Testing for insulin isn’t new, but it’s important.

The study, "Effects of Insulin and Acipimox on VLDL1 and VLDL2 Apolipoprotein B Production in Normal Subjects", by  Raija Malmström, Christopher J. Packard, Muriel Caslake, Dorothy Bedford, Philip Stewart, Hannele Yki-Järvinen, James Shepherd, Marja-Riitta Taskinen, was aimed at was to examining the potential differential effect of insulin and acipimox (both of which reduce free fatty acid [FFA] availability) on VLDL apolipoprotein (apo) B metabolism. They studied eight healthy men (age 40 ± 4 years, BMI 25.8 ± 0.9 kg/m2, plasma triglycerides 1.30 ± 0.12 mmol/l) after an overnight fast (control study, n = 8), during inhibition of lipolysis with an antilipolytic agent, acipimox (n = 8), and under 8.5-h euglycemic-hyperinsulinemic conditions (n = 5). Plasma FFAs were similarly suppressed in the acipimox and insulin studies (~70% suppression).2H3-leucine was used to trace apo B kinetics in VLDL1 and VLDL2 subclasses (Svedberg flotation rates: 60–400 and 20–60), and a non­steady-state multicompartmental model was used to derive the kinetic constants. The mean rate of VLDL1 apo B production was 708 ± 106 mg/day at the beginning and 602 ± 140 mg/day at the end of the control study. Production of the lipoprotein decreased to 248 ± 93 mg/day during the insulin study (P < 0.05 vs. control study) and to 375 ± 92 mg/day (NS) during the acipimox study. Mean VLDL2 apo B production was significantly increased during the acipimox study (399 ± 42 vs. 236 ± 27 mg/day, acipimox vs. control, P < 0.05) but not during the insulin study (332 ± 51 mg/day, NS). The fractional catabolic rates of VLDL1 and VLDL2apo B were similar in all three studies. They concluded that acute lowering of FFAs does not change the overall production rate of VLDL particles, but there is a shift toward production of smaller and denser VLDL2 particles, and, thus, the amount of total VLDL particles secreted remained constant. Insulin acutely suppresses the total production rate of VLDL apo B by decreasing the production of large triglyceride-rich VLDL1 particles. Based on these findings, they postulate that insulin has a direct suppressive effect on the production of VLDL apo B in the liver, independent of the availability of FFAs. Diabetes 47:779–787, 1998.

Triglycerides:

Triglycerides are the primary form of fat (lipid) and comprise the bulk of fat in foods, stored fat in the body, and the primary form of fat in the blood. Triglycerides are the lipids that provide calories or energy to the body. Triglycerides exist in many shapes and sizes, but they all exhibit a similar structure which is a glycerol molecule with three fatty acids attached. The physical characteristics of a given fat are determined by the degree of saturation of its fatty acids. It is recommended that it be kept below 150 for safety.  The Rush Medical College in Chicago has shown that levels of triglycerides above 190mg/100 ml significantly increases the thickness of blood. Viscous blood is more prone to produce blood clots, which can result in cardiac and/or cerebrovascular problems. (Remember, an aspirin a day helps thin blood.)  As with cholesterol, most cases of extremely high triglycerides are the result of genetics as opposed to diet.  A mildly overweight individual could have levels in the range of 18,000 mg/dL (milligrams per deciliter) and above.

High-density lipoprotein (HDL)

High-density lipoprotein (HDL) is often called "good" cholesterol. HDL removes excess cholesterol from tissues and vessel walls and carries it to the liver, where it is removed from the blood and discarded. The amount of HDL in a person's blood is inversely related to his or her risk of cardiovascular disease. The lower the HDL level, the greater the risk; the higher the level, the lower the risk. The smallest lipoprotein, it contains 20-30% of a person's total cholesterol and can be separated into two major subclasses.  It is recommended that a HDL levels be maintained above 35 mg/dl.

Several studies have suggested that low levels of HDL-C without high levels of low-density lipoprotein cholesterol (LDL-C) characterizes between 20 and 30% of the population with coronary artery disease (CAD).  From this research, it appears that increased HDL-C levels are not only protective against CAD but also lead to a reduced risk of ischemic stroke in the elderly and among different racial and ethnic groups. HDL-C is an important modifiable stroke risk factor.

Several large-scale clinical trials involving both primary and secondary prevention have assessed the effects of lipid lowering on
clinical coronary endpoints and have also measured total cholesterol, triglyceride, or HDL-C throughout the study. None of
these trials was designed specifically to test the hypothesis that altering triglyceride or HDL-C concentrations would reduce
coronary risk. Hence, none of the studies selected patients based solely on elevated triglyceride or low HDL-C. Instead, most
studies sought to test the efficacy of lowering the LDL-C, and most subjects were chosen based on elevations of total
cholesterol, LDL-C, or apolipoprotein B concentrations. Each of the interventions affected total cholesterol and/or LDL-C and
one or more of the other components of the lipid profile. However, in only one of these studies, the Stockholm Ischaemic Heart
Disease Secondary Prevention Study, was there a clear relationship between triglyceride levels in the treated group and
beneficial change in CHD event rates. Since this study did not measure HDL levels, no conclusions could be drawn with regard
to HDL. In the Lipid Research Clinics' Coronary Primary Prevention Trial, the overall decline in CHD risk was 19 percent, 2
percent of which was attributable to an increase in HDL that was correlated with a 2 percent decline in CHD risk, and the
benefit was greatest in those with a baseline HDL > 50 mg/dL. It should be noted that significant correlations were
demonstrated also between lowering of LDL cholesterol and coronary risk. In the Helsinki Heart Study, a mean 12 percent rise
in HDL-C and an 11 percent fall in LDL-C were both correlated with a 34 percent decline in CHD events. After correcting for
HDL-C and LDL-C, no relationship between CHD events and triglyceride concentrations was found. Approximately 10
percent of the treated subjects had LDL-C/HDL-C ratios > 5 and triglyceride > 200 mg/dL. These patients had a 70 percent
lowering of their CHD risk with gemfibrozil therapy, suggesting that a subgroup at especially high risk and particularly sensitive
to therapy had been identified. The relative lowering of risk in other subgroups was considerably less.

Apolipoprotein A1 (Apo AI) is primarily found in high density lipoprotein (HDL) particle.  It serves the function of preventing the accumulation of cholesterol loaded macrophages which deposit on the arterial wall as foam cells.  This is the prominent early feature of atherosclerotic lesion formation ultimately resulting in atherosclerosis.  Apo AI, is a single polypeptide with a molecular weight of 28 Kd.  Its primary function is to activate LCAT within the HDL complex, which catalyzes the esterification of cholesterol.  This results in a more soluble cholesterol-HDL complex which increases the cholesterol transport capacity of the HDL particle for subsequent removal by the liver.  Apo AI is therefore a convenient marker for assessing the cholesterol clearing capacity of the blood, and studies have clearly indicated that it is a better discriminator of angiographically documented coronary artery disease than HDL
cholesterol.

HDL2b (21 percent)

Overall, HDL is good cholesterol, but HDL 2b is the most beneficial.  The more you have of it, the less likely you are to suffer a heart attack. There are five subclasses of HDL particles, labelled 2a, 2b, 3a, 3b, and 3c.

Treatments

Niacin, also known as Vitamin B3, is important for the normal function of many bodily processes. Like other B vitamins, it is water-soluble and plays a role in turning food into energy, as well as in the metabolism of fats and carbohydrates.  Niacin can also act as an antioxidant within cells, which means it can destroy cell-damaging free radicals. In conjunction with riboflavin and pyridoxine, it helps to keep the skin, intestinal tract and nervous system functioning smoothly.   Niacin is the best way to treat high levels of Lipoprotein(a) – 4 to 5 grams of niacin daily is recommended.

question regarding your new cholesterol-lowering supplement, Policosanol - Life Extension Magazine, 11/01 - "Studies show that niacin (B3) in doses of 1.5 grams to 3 grams lower triglycerides levels and raise HDL concentrations. Those who tolerated higher doses of niacin (nicotinic acid) showed even more improvement in lipid levels. Some people taking just 1000 mg of flush-free niacin see an elevation in beneficial HDL. Green tea also has been shown to elevate levels of HDL while lowering serum triglyceride levels. In the Journal of Molecular Cell Biochemistry, curcumin has been demonstrated, in vivo, to decrease triglycerides and increase HDL. In a study published in 1989 by the Journal of Associated Physicians-India, 125 patients receiving gugulipid showed a drop of 16.8% in triglycerides, and a 60% increase in HDL cholesterol within three to four weeks. Make sure you are taking at least six Mega EPA
fish oil capsules daily, as low dose fish oil may not adequately suppress triglycerides. Finally, there are some lifestyle changes you may wish to consider. If you are overweight, weight loss would be recommended, as it would help to lower triglycerides and raise HDL. Also, try reducing carbohydrates, which can raise triglycerides" .

General use

The recommended daily allowance (RDA) of niacin for infants under six months is 5 mg. Babies from six months to one year of age require 6 mg. Children need 9 mg at one to three years of age, 12 mg at four to six years, and 13 mg at seven to 10 years. Women need 15 mg from 11-50 years, and 13 mg thereafter. Somewhat more is required for pregnancy (17 mg) and lactation (20 mg). Men require 17 mg from 11-14 years of age, 20 mg from 15-18 years, 19 mg from 19-50 years, and 15 mg at 51 years and older.

Niacin, in the form of nicotinic acid, can be taken in very large doses to decrease cholesterol and reduce the risk of heart attack . The amount required is between 2 and 3 g. This is not a therapy that should be undertaken without professional medical advice and supervision. Certain conditions preclude the use of high doses of niacin. These include gout, diabetes, peptic ulcer, liver or kidney disease, and high blood pressure requiring medication. Even in the absence of these conditions, a patient on high doses of niacin should be closely monitored to be sure the therapy is both effective and without complications. A frequent side effect of this        therapy is extreme flushing of the face and neck. It is harmless, but can be unpleasant. An alternative form of nicotinic acid that does not cause flushing is inositol hexaniacinate. "Slow release" niacin also causes less flushing, but should not be taken as there is higher risk of liver inflammation.

There is some evidence that niacinamide used on a long-term basis can prevent the onset of juvenile diabetes in many susceptible children. Those who have been newly diagnosed with juvenile diabetes may also benefit by extending the time that the pancreas continues to produce a small amount of insulin. The advice of a health care provider should be sought for these uses.

Inositol hexaniacinate can be helpful for people suffering from intermittent claudication. This condition causes leg pain with exercise due to poor blood flow to the legs. Dilation of the blood vessels caused by the inositol hexaniacinate relieves this condition to some extent, allowing the patient to walk farther with less pain.

Natural sources

Tuna is one of the best sources of niacin, but many foods contain it. Most processed grain products are fortified with niacin, as well as other B vitamins. Although niacin is not destroyed by cooking, it does leach into water, so cooking with minimal liquid best preserves it. The amino acid tryptophan is widely found in foods high in protein, and about half of the tryptophan consumed is used to make niacin. Cottage cheese, milk, fowl, and tuna are some of the foods that are highest in tryptophan.

Supplemental sources

Niacin can be purchased as an oral single vitamin product. A balanced B complex supplement is preferred over high doses of an individual vitamin unless there is a specific indication. Supplements should be stored in a cool, dry place, away from light, and out of the reach of children.

Deficiency

A serious deficiency of niacin causes a condition called pellagra. Once quite common, it has become rare outside of areas where poor nutrition is still the norm. The symptoms include dermatitis, dementia, and diarrhea.  Milder deficiencies of niacin can cause similar, but less severe symptoms. Dermatitis, especially around the mouth, and other rashes may occur, along with fatigue, irritability, poor appetite, indigestion, diarrhea, headache, and possibly delirium.

Risk factors for deficiency

Severe niacin deficiency is uncommon in most parts of the world, but some people may need more than the RDA in order to maintain good health. Vegans, and others who do not eat animal protein, should consider taking a balanced B vitamin supplement. Others that may need extra niacin and other B vitamins may include people under high stress, including those experiencing chronic illnesses, liver disease, sprue, or poor nutritional status. People over 55 years old are more likely to have a poor dietary           intake. Certain metabolic diseases also increase the requirement for niacin. Those who abuse nicotine, alcohol or other drugs are very frequently deficient in B vitamins, but use of niacin with alcohol can cause seriously low blood pressure. A health care professional can determine if supplementation is appropriate.

Precautions

Niacin should not be taken by anyone with a B vitamin allergy, kidney or liver impairment, severe hypotension, unstable angina, arterial hemorrhage, or coronary artery disease. Supplemental niacin can exacerbate peptic ulcers. Diabetics should use caution as supplements of either niacin or niacinamide can alter medication requirements to control blood glucose. Supplements can raise uric
acid levels, and aggravate gout in people with this condition. Pregnant women should not take high doses of niacin, or any supplement, except on the advice of a health care provider.

Health care should be sought immediately if certain symptoms occur following niacin supplementation. These include abdominal pain, diarrhea, nausea, vomiting, yellowing of the skin, faintness, or headache. Such symptoms may indicate excessively low blood pressure or liver problems. Heart palpitations and elevated blood sugar are also potential effects.

Side effects

High doses of niacin can cause a harmless, but unpleasant, flushing sensation and darkening of the urine. The "no-flush" form can lessen this complication.

Interactions

Niacin supplements should not be taken by anyone on medication for high blood pressure, due to the potential for hypotension. Isoniazid, a drug used to treat tuberculosis, inhibits the body's ability to make niacin from tryptophan. Extra niacin may be required. Supplements may also be needed by women taking oral contraceptives. Concomitant use of niacin with statin class drugs to lower
cholesterol can cause myopathy. Cholestyramine and cholestipol, older medications to lower cholesterol, should be taken at a different time than niacin or they will reduce its absorption. Transdermal nicotine used with niacin is likely to cause flushing and dizziness. Carbamazepine, an antiseizure medication, is more likely to cause toxicity in combination with niacin.

If you have a family history of heart disease and/or basic cholesterol numbers that are suspicious, ask your doctor about these specialized tests.  Take niacin only under a doctor’s care; it can cause liver damage in the large doses that are necessary to be effective.