Triglycerides less than 40

Understanding Triglycerides

Triglycerides are the form in which fat is stored in your body’s fat cells. Your triglyceride level is almost always strongly influenced by lifestyle. A low-fat, high-refined carbohydrate actually elevates your triglycerides. Two decades ago, when I first began putting my patients on this type of diet, which was recommended back then, I was often dismayed to see their triglycerides go up. This, of course, was the opposite of what I was hoping to achieve. We now know that it was not the carbohydrates per se that raised the triglycerides, but the bad carbohydrates — sugars and starches devoid of fiber and other nutrients — that did it.

The same thing happened when I experimented with an extremely low fat diet that was also popular at the time. When I put one patient with a moderately high triglyceride level of 220 mg/dL on it to lose weight, he did not lose weight, and his triglycerides soared to over 500. His was just one of many cases like this that made me begin to question the conventional dietary wisdom of the time. Today, I recommend a diet that contains lean protein and moderate amounts of good fats (those found in oily fish, olive oil, and nuts) and good carbs (those found in vegetables, fruits, and whole grains). If patients follow this plan, reductions in triglycerides can be dramatic.

If you have high triglycerides (over 150 mg/dL is borderline high) and low HDL (less than 40 mg/dL if you’re a man and less than 50 mg/dL if you’re a woman), your risk of heart disease is compounded. To find out if you have this added risk, divide your triglyceride count by your HDL count. Ideally, the resulting number will be 2 or lower. For example, if your triglyceride level is 200 and your HDL is 40, divide 200 by 40 and you get 5. This is much higher than the desirable ratio, and it tells you that you have a heightened risk of a heart attack that will need to be addressed.

Your triglyceride level can also give you insight into your LDL particle size. In general, the higher your triglycerides and the lower your HDL, the smaller and denser your LDL and the greater your risk of heart disease. If your triglycerides are higher than 200 and your HDL is lower than 45, it is very likely that you have too much small, dense LDL.

There are a number of ways to lower your triglycerides. In addition to eating the healthy diet that I describe in Step 1, losing weight and getting more exercise can help. Medications such as niacin and fibrates are also effective at lowering triglycerides, increasing HDL, and enlarging LDL particle size.


149 mg/dL or under is normal.

150–199 mg/dL is borderline high.

200–499 mg/dL is high.

500 mg/dL is very high.

Ask the Diva: Can Triglycerides Be Too Low?

Q. The American Heart Association guidelines say that normal triglyceride levels are less than 150 mg/dL. My triglyceride level is 40 mg/dL. Is that too low? If so, how can I raise my levels in a healthy way?

A. Very low triglyceride levels can signal problems. Diets that don’t contain enough fat, for example, can cause triglyceride levels to dip dangerously low. (See also: How Much Fat Should You Eat?) There are also some medical problems that can cause abnormally low triglycerides, such as an inability to absorb fats or hyperthyroidism. But a triglyceride level of 40 is considered perfectly normal—ideal, in fact! Although levels up to 150mg/dL are within the ‘normal’ range, the AHA recommends that we aim for triglyceride levels below 100.

If your levels had been a concern, either on their own or in view of other test results or symptoms, I’m sure your doctor would have ordered follow up tests to rule out any other problems. And, of course, if you have any lingering worries, you should check in with her! But in and of itself, a triglyceride reading of 40 isn’t anything to worry about. It’s something to crow about!

Blood screening results photo from

Triglyceride Levels Greater Than 10,000 mg/dL in a 49-Year-Old Female without Evidence of Pancreatitis


We present a rare case of a 49-year-old female with very severe hypertriglyceridemia (HTG) having a total triglyceride (TG) count of > 10,000 mg/dL in the absence of pancreatitis. Based on literature review, this is one of the highest recorded TG counts in an adult without evidence of pancreatitis. HTG is a common occurrence in clinical practice, but rarely do numbers exceed 2000 mg/dl. It is crucial to evaluate and rapidly lower TG levels to prevent potentially life-threatening complications such as severe pancreatitis. Removal of potential predisposing medications, control of underlying diseases known to cause HTG, and maintenance therapies are essential to prevent reoccurrence.

1. Introduction

HTG is a common form of dyslipidemia with the potential to cause significant morbidity and mortality. In cases of severely elevated TG levels, rapid lowering to levels < 500–1000 mg/dL can be achieved with aggressive use of intravenous insulin and heparin (caution needs to be exercised when using heparin in cases of pancreatitis) and fasting.

2. Case Description

Our case is a 49-year-old Hispanic female who presented to our hospital with multiple episodes of chest pain. The onset of her pain was 5 days prior to admission. She complained of left sided pain “5 out of 10” intensity described as chest tightness. The pain was nonradiating and not precipitated by activity, inspiration, or position. The patient stated that she would have almost 5 episodes of pain daily with each episode lasting 2-5 minutes in length. This was not associated with any diaphoresis, shortness of breath, vomiting, or abdominal pain. The frequency and intensity of her pain episodes increased which led her to come to the emergency department. Her past medical history is significant for hypertension and difficult-to-control asthma requiring frequent hospital admissions. In the past she was on medication for “high cholesterol” but stopped taking it years ago as she was never told she had very high cholesterol levels. She denied any history of abnormal lipid profile, myocardial infarction or angina, congestive heart failure, or diabetes mellitus. Her medications included inhaled fluticasone and vilanterol combination, albuterol inhalation as needed, losartan, meloxicam, montelukast, verapamil, omalizumab, and intermittent short courses of prednisone for asthma exacerbations. She denied any alcohol consumption or illicit drug use. She admitted to smoking about a quarter pack a day for 15-20 years and quit 13 years ago. Family history was significant for hypertension in her mother, and a sister with stroke at the age of 44. There was no family history of dyslipidemia.

On physical examination she was found to have temperature of 97.8 degrees F, heart rate of 92 bpm, respiratory rate of 19/min with oxygen saturation of 96% on room air, and blood pressure of 152/98 mmHg. Her body mass index (BMI) was 27.7 on admission. Cardiovascular examination revealed chest wall tenderness to palpation on the upper left side. On auscultation there were no significant murmurs. Slight wheezing was audible in bilateral lung fields on auscultation. Examination of the skin did not reveal any xanthomas or xanthelasmas. Ophthalmologic examination did not reveal corneal arcus or lipemia retinalis. The examination of the nervous system and the head and neck was within normal limits.

Relevant laboratory results on admission were as follows. Initial blood draw when centrifuged on gross examination was heavily lipemic (see Figure 1). Subsequent lipid panel studies were ordered which were significant for serum triglyceride (TG) of >10,000 mg/dL, serum cholesterol of 1,029 mg/dL, direct measure low density lipoprotein (LDL) of 33 mg/dL, and high-density lipoprotein (HDL) of 22 mg/dl. Other pertinent lab values included WBC count 7900/cumm, Hb of 11.6 g/dL, serum lipase of 160 units/dL, which was 46 units/dL when repeated and consistently remained within normal limits during hospitalization, serum sodium 130 mmol/L, serum magnesium of 5.2 mg/dL, and blood glucose of 111 mg/dL (random). Serum TSH was 2.39 mcIU/mL and HbA1c was of 5.3%. Initial troponin was of <0.03 ng/mL. Bicarbonate on admission was 22 mmol/L. EKG showed normal sinus rhythm with no ST-T wave changes. Chest X-ray was normal.

Figure 1

The patient was started on conservative management. She was kept nothing by mouth except medications for one day and started on IV regular insulin drip at a rate of 4 units/hr with IV fluids containing 5% dextrose to prevent hypoglycemia along with heparin 5000 units subcutaneously every 8 hours. Heparin drip was not initiated because PTT could not be accurately measured secondary to lipemia. She was also started on gemfibrozil, atorvastatin, and niacin at the time of admission. All of her home medications were stopped. A cardiac diet with no fats and no carbohydrates was initiated by day 2. Cardiology was consulted. Echocardiogram was done which was normal with an EF of 72%.

The patient’s old medical record was reviewed to obtain previous lipid panel test results. Her lipid panel from 2016 revealed a serum triglyceride of 212 mg/dL and serum cholesterol of 182 mg/dL.

Lipid panel was repeated daily over the course of 9 days with significant decrease in patient’s triglyceride and cholesterol levels. On day 9, serum triglyceride levels came down to 825 mg/dL and serum cholesterol was noted to be 360 mg/dL (see Table 1). Her diet was slowly advanced to a low fat and low carbohydrate diet which she tolerated well.

Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7 Day 8 Day 9
TG Levels (mg/dL) >10,000 8,887 4,119 1,617 1,315 1,120 1,138 937 825
IV Drip Insulin Insulin Insulin Insulin Insulin Insulin Insulin Insulin None
Diet NPO 0 fat
0 carb
0 fat
0 carb
0 fat
0 carb
0 fat
0 carb
Low fat
Low carb
Low fat
Low carb
Low fat
Low carb
Low fat
Low carb
Oral Medication G & A G & A G & A G & A
G & A
G & A
G & A
G & A
F & R
G = Gemfibrozil; A = Atorvastatin; F = Fenofibrate; R = Rosuvastatin.

Table 1 Patient’s HTG trend along with therapies used and diet.

The patient also underwent treadmill myoview stress SPECT study once the serum triglyceride levels were < 2000 mg/dL in view of chest pain, which was normal. The patient’s chest pain and serum triglyceride levels improved. She did not require any other interventions besides insulin drip and subcutaneous heparin. She was discharged on day 9 in medically stable condition and was closely monitored as outpatient. She was discharged on Rosuvastatin, Fenofibrate, and prescription omega-3 fatty acids. Repeat lipid panel was done in one month after discharge and the serum triglyceride levels were found to be 142 mg/dL and serum cholesterol of 117 mg/dL. Apolipoprotein B level was measured at 186 mg/dL. The patient was instructed for further genetic testing after discharge but did not follow up after this.

3. Discussion

Hypertriglyceridemia (HTG) is one of the most common lipid abnormalities and has been known to be associated with other metabolic derangements. It is estimated that the number of patients with HTG who have levels exceeding 500 mg/dL has risen to >4 million Americans and that this is more common in the Hispanic-American population . The presence of very severe HTG (TG levels greater than 2000 mg/dL) is estimated to be 1.8 cases per 10,000 white adults . Hypertriglyceridemia is defined as TGs >150 mg/dL. The Endocrine Society 2010 guidelines further classify HTG into mild (150–199 mg/dL), moderate (200–999 mg/dL), severe (1000–1999 mg/dL), and very severe (greater than or equal to 2000 mg/dL) . Severe and very severe HTG have been shown to increase the risk for acute pancreatitis and cardiovascular disease. When levels are > 1,000 mg/dL, the risk of pancreatitis rises to approximately 5%, and, when levels are >2000 mg/dl, the risk significantly rises to 10-20% .

The etiologies of HTG can be further classified into primary and secondary. The Fredrickson classification scheme is commonly used to organize various primary hypertriglyceridemias into different categories (Table 2). In the United States, the most common primary HTGs include familial combined hyperlipidemia (Fredrickson type IIb) and familial hypertriglyceridemia (Type IV) . Secondary causes frequently include medical conditions such as obesity, untreated diabetes mellitus, excessive alcohol intake, hypothyroidism, nephrotic syndrome, liver disease, and pregnancy . Certain medications are also well known to cause elevations of TG levels such as estrogens, glucocorticoids, thiazides, beta-blockers, antipsychotics (Olanzapine), immunosuppressants, protease inhibitors, isotretinoin, and bile acid resins .

I – Familial chylomicronemia Chylomicron TC +
TG +++
Presents in infancy, eruptive xanthomas, recurrent pancreatitis, failure to thrive <1%
II b – Familial Combined Hyperlipidemia LDL, VLDL, Apo-B TC ++
TG ++
Xanthomas less common. Risk of premature CVD 40%
III – Familial dysbetalipoproteinemia IDL TC ++
TG ++
Palmar xanthomas, risk of premature CVD <1%
IV – Familial Hypertriglyceridemia VLDL TC +
TG ++
Associated w/ DM, insulin resistance, obesity, HTN 45%
V – Primary Mixed Hyperlipidemia Chylomicron, VLDL TC +++
TG +++
Similar to type I but develops in adulthood 5%
TC = total cholesterol; TG = triglycerides; DM = Diabetes Mellitus; HTN = Hypertension; CVD = cardiovascular disease; LDL = low-density lipoprotein; VLDL = very low-density lipoprotein; IDL = intermediate density lipoprotein; Apo-B = apolipoprotein B.

Table 2 Fredrickson classification of primary hypertriglyceridemia .

There is a broad spectrum of clinical manifestations of HTG, the most common of which being patients who are asymptomatic. Other symptoms may include mid-epigastric abdominal pain, nausea, and vomiting in relation to acute pancreatitis. Cutaneous manifestations are usually associated with elevations of LDL levels and include eruptive cutaneous xanthomas, palmar crease xanthomas, tendinous xanthomas, tuberous xanthomas, and eyelid xanthelasmas . Ophthalmologic features can include lipemia retinalis. The risk of pancreatitis increases when TG levels exceed 1000-2000 mg/dL and is the third leading cause of pancreatitis after alcohol and gallstones. There are also moderate to highly significant associations between triglyceride values and the risk of coronary heart disease. We theorize that our patient experienced chest pain possibly as a result of accumulation of chylomicrons in the coronary arteries leading to ischemia which was relieved with rapid lowering of TG levels.

Diagnosis of specific HTG disorders requires extensive and costly workup. Therefore, the most critical initial step is to exclude secondary causes. This includes medication review, evaluation of body mass index (BMI), hemoglobin A1c, TSH, and renal and liver function testing . When potential secondary causes have been ruled out, patients should be evaluated for various primary HTG.

Management of severe and very severe HTG involves rapidly lowering total TG levels to prevent development of acute pancreatitis. This comprises of both immediate dietary modifications and use of TG lowering medications which may require hospitalization . During acute rapid lowering of TG levels, patients are typically kept NPO, and a no-fat diet is generally introduced when TG drops to <1000 mg/dL. For chronic maintenance, patients are instructed to avoid simple carbohydrates completely as well as reducing fat intake to less than 10% of daily caloric intake . This is to decrease the risk of postprandial chylomicronemia since lipoprotein lipase (LPL) levels are maximally saturated from existing severe elevations of TG levels . Rapid lowering of TG levels can be achieved with administration of IV Insulin drip with glucose and IV Heparin which are potent activators of LPL to effectively remove TGs from circulation . The effective goal to reduce the risk of pancreatitis is to reduce TG levels to less than 500-1000 mg/dL . Concomitantly, oral TG lowering medications should be initiated. First line medical therapy of isolated HTG is fibrates . The preferred fibrate is Fenofibrate of which the onset of action may take a few weeks . For patients with associated elevations of low-density lipoprotein (LDL) levels, a statin medication can be given. With this combination, risk of myopathy should be assessed with baseline creatinine kinase (CK) levels, and again if patients become symptomatic . Suggested prescriptions of Omega-3-fatty acids and Niacin can be added as well. For patients who develop acute pancreatitis secondary to HTG, plasmapheresis can be performed to rapidly lower TG levels .

We postulate that our patient had a form of familial dyslipidemia which was exacerbated by the use of estrogens and steroids. Given her elevated apolipoprotein B levels, it is more likely that she had type IIb familial combined hyperlipidemia (FCHL).

4. Conclusion

Hypertriglyceridemia is frequently encountered in clinical practice. Very severe hypertriglyceridemia above 1000-2000 mg/dL should be evaluated for primary and secondary causes. Rapidly lowering triglyceride levels is essential to prevent serious complications such as acute pancreatitis. Long term effects of elevated TG count have also been associated with coronary artery disease. Rapid lowering can be achieved with intravenous insulin drip, even in nondiabetic patients, and intravenous heparin. Maintenance therapy with dietary changes and medications such as fibrates is highly recommended.

Conflicts of Interest

The authors declare that they have no conflicts of interest.


What are triglycerides?

Triglycerides are a type of fat, which come into your bloodstream three different ways:

  1. Consumption of foods that contain fat
  2. Consumption of extra calories, carbohydrates, and simple sugars
  3. Release from fat stores in the body

How are triglycerides different from cholesterol?

Triglycerides and cholesterol are both types of fat in your blood known as lipids. Triglycerides provide much of the energy for cell function and metabolism of alcohol, and cholesterol is used to build cells and several hormones.

Your health care provider can check your cholesterol and triglyceride levels by taking a sample of blood. The blood is analyzed and provides triglyceride level, total cholesterol level, HDL cholesterol (high-density lipoprotein or “good” cholesterol) and LDL (low-density lipoprotein or “bad” cholesterol).

Following a meal, blood triglyceride levels are normally elevated. For an accurate reading, blood samples for a triglyceride test should be taken after a 12-hour period of not eating or drinking.

What are the guidelines for triglyceride levels?

Guidelines for triglyceride levels in healthy adults are:

  • Normal: under 150 mg/dL
  • Borderline high: 150-199 mg/dL
  • High: 200-499 mg/dL
  • Very high: 500 mg/dL or higher

Is a high triglyceride level a health problem?

Yes. Current research reveals elevated triglycerides may contribute to hardening the artery wall, which increases risk for stroke, heart attack, and heart disease. Often, high triglycerides are a sign of other conditions such as obesity, poorly controlled diabetes, low thyroid hormones, and liver or kidney disease.

How can triglycerides be lowered?

You may be able to reduce high triglycerides without medication by reducing sugar, alcohol, and fat intake, and following a low-fat, low-cholesterol diet. If you currently smoke, stopping may decrease your triglyceride level and your risk for heart disease. Weight loss may also decrease your triglyceride level and your risk for heart disease.

Dietary modifications

To reduce fat and cholesterol in your diet, here are some suggestions:

  • Eat fewer calories if you are overweight. Excess calories are converted into triglycerides and stored as fat.
  • Avoid refined foods and foods that contain sugar (such as white flour, desserts, candy, juices, fruit drinks, soda pop, and sweetened beverages).
  • Choose carbohydrates that have 2 grams fiber or more per serving, such as brown rice, whole wheat bread, and whole grain cereals.
  • Follow your doctor’s advice regarding alcohol. Alcohol increases triglyceride levels for some individuals. If you have high triglycerides and do consume alcohol (such as red wine), it is recommended to limit intake to 5 ounces per day or limit it entirely.
  • Decrease total amount of fat you eat to 20-35% of your total calories (<15% if triglycerides are higher than 500 mg/dL); saturated fat should provide 7% or less of your total calories. For example, a person eating 2,000 calories per day would eat 65 grams or fewer total fat and 16 grams of saturated fat.
  • Avoid trans fats, which are partially hydrogenated oils found in some fried foods and commercial baked products. The goal is 1% of calories (or less) per day. For example, if following a 2,000-calorie diet, aim to consume 2 grams or fewer per day.
  • Replace saturated fat (found in animal fat and some tropical oils) for monounsaturated fat (found in olive/canola/peanut oils, etc.).
  • Limit cholesterol intake to 300 mg per day, 200 mg/day or less if you have heart disease.
  • Consume at least 2 servings of cold water fish each week, such as salmon, mackerel, tuna, lake trout, herring, and sardines (all of which are high in omega-3-fatty acid). Include into your diet other foods high in omega-3 fatty acid, such as ground/milled flaxseed, walnuts, almonds, canola or soybean oil, etc.
  • Aim for 3 servings of low-fat dairy per day, such as 8 oz. milk or yogurt.
  • Choose up to 6 ounces per day of lean protein, such as fish, skinless poultry, lean beef, or lean pork.
  • Consume at least 2-3 cups of vegetables and 1 cup of fruit each day.
  • Exercise to burn excess calories, aiming for at least 30 minutes of physical activity on most days of the week.


People who have high triglycerides and low HDL or high LDL levels may require medications as well as diet modifications. Patients with triglycerides in the very high range (over 500 mg/dL) generally will require medications, because triglyceride levels this high may cause an acute inflammation of the pancreas.

Is it possible to combine a triglyceride-lowering diet with a heart-healthy style of eating?

Absolutely! Following a heart-healthy diet, reducing alcohol and sugar intake, complete with physical activity and a healthy body weight, is recommended for all individuals. If you have other questions about triglycerides, consult your doctor or registered dietitian.

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Should We Treat Moderately Elevated Triglycerides? Yes: Treatment of Moderately Elevated Triglycerides Is Supported by the Evidence

The normal physiologic concentration of triglyceride in human serum is 10 to 70 mg per dL (0.11 to 0.79 mmol per L; mean 30 mg per dL ).1 Values greater than 150 mg per dL (1.69 mmol per L) are considered abnormal, and values between 200 and 500 mg per dL (2.26 and 5.65 mmol per L) are considered by the National Cholesterol Education Program (NCEP) to be high.1 The question for physicians is whether or not patients benefit from treatment of elevated levels.

At values greater than 500 mg per dL, triglycerides may cause pancreatitis. At lower values (200 to 500 mg per dL), especially with normal lipid subfractions, the risk of hypertriglyceridemia is not clear. Patients with familial hypertriglyceridemia (Fredrickson type IV) do not appear to have higher cardiovascular risk. However, patients with abnormal triglyceride values typically have other lipid derangements, such as high levels of low-density lipoprotein (LDL) and low levels of high-density lipoprotein (HDL; e.g., atherogenic dyslipidemia). Additionally, patients with hypertriglyceridemia often have metabolic syndrome (e.g., abdominal obesity, hypertension, insulin resistance, low HDL, high triglycerides), which is a risk factor for developing coronary heart disease (CHD).2 In this sense, a triglyceride level can be thought of as a lifestyle biomarker identifying patients who are sedentary, have high-carbohydrate diets, and are overweight or obese.

Multiple studies have identified elevated triglyceride levels as an independent risk factor for CHD.3–5 This risk seems to be greater in women, and in patients with diabetes mellitus or known CHD. Most of this risk occurs in patients with low HDL cholesterol and high LDL cholesterol. Although the risk associated with elevated triglyceride levels is largely attenuated by controlling for low HDL levels, residual risk remains.

In the largest study to evaluate risk associated with triglycerides, there was a 14 percent increased risk in men and a 37 percent increased risk in women for every 88 mg per dL (0.99 mmol per L) increase in triglyceride concentration above normal.6 The most likely reason for this residual risk is that hypertriglyceridemia is a surrogate marker for patients with an excess of atherogenic remnant particles and other proatherogenic conditions. Using conventional lipid testing, a patient’s total atherogenic load can be estimated by calculating the non-HDL cholesterol concentration (total cholesterol minus HDL). The NCEP Adult Treatment Panel III (ATP III) guidelines recommend calculating the non-HDL cholesterol value in patients with a triglyceride level greater than 200 mg per dL.1 Some argue that the non-HDL cholesterol level should be calculated for all patients because it is more closely linked to CHD risk than LDL cholesterol.7

Treatment of severe hypertriglyceridemia (greater than 500 mg per dL) should begin immediately to reduce the risk of pancreatitis. Usually, a fibrate is tried first with therapeutic lifestyle changes. Treatment of modest hypertriglyceridemia (200 to 500 mg per dL) should begin with therapeutic lifestyle changes and a search for underlying causes or contributing factors, such as obesity, hypothyroidism, or diabetes. If triglycerides remain elevated, the NCEP-ATP III guidelines recommend treating the LDL cholesterol first, and then the non-HDL cholesterol to reach goals based on the patient’s Framingham risk assessment. Drug therapy in these cases should begin with a statin, which should be titrated accordingly. Combination therapy with a fibrate should follow if needed. It is safest to add fenofibrate (Tricor), because there is a chance of rhabdomyolysis with gemfibrozil (Lopid). Omega-3 fish oil (n-3 fatty acid) was recently approved for the treatment of hypertriglyceridemia and can be added to the statin. Niacin is another therapeutic option and is now available in a combination product with simvastatin (Simcor).

There are no specific guidelines from the NCEP-ATP III about treating isolated moderate hypertriglyceridemia. However, if the triglyceride level remains elevated once LDL and non-HDL cholesterol concentrations are normalized, it may be worthwhile to pursue further triglyceride-lowering treatment, especially in high-risk patients with CHD or type 2 diabetes.

In the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction (PROVE IT-TIMI) 22 trial of patients after acute coronary syndrome, a final triglyceride level less than 150 mg per dL was associated with a 27 percent relative reduction in coronary events.8 In the Baltimore Coronary Observational Long-Term Study there was an association between increased coronary events and moderate hypertriglyceridemia.9 Recent findings from the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study show a 27 percent relative reduction in CHD and a 38 percent relative reduction in nontraumatic leg amputation in patients with diabetes treated using fenofibrate.10 The NCEP-ATP III final report states that drugs that modify atherogenic dyslipidemia yield moderate reductions in CHD risk.1

Until more refined laboratory techniques become available to clearly identify patients who would benefit from treatment, it seems prudent to aggressively treat high-risk patients by normalizing their LDL cholesterol, non-HDL cholesterol, and triglyceride levels. Moderate- and low-risk patients should be monitored regularly and given the option for treatment if their lipid levels worsen. All patients with hypertriglyceridemia should be encouraged to stop smoking, exercise regularly, and adhere to their prescribed diet.

Address correspondence to Rade N. Pejic, MD, MMM, at [email protected] Reprints are not available from the author.

Author disclosure: Nothing to disclose.

show all references

1. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106(25):3143–3421….

2. Alexander CM, Landsman PB, Teutsch SM, Haffner SM; Third National Health and Nutrition Examination Survey (NHANES III); National Cholesterol Education Program (NCEP). NCEP-defined metabolic syndrome, diabetes, and prevalence of coronary heart disease among NHANES III participants age 50 years and older. Diabetes. 2003;52(5):1210–1214.

3. Assmann G, Schulte H, Funke H, von Eckardstein A. The emergence of triglycerides as a significant independent risk factor in coronary artery disease. Eur Heart J. 1998;19(suppl M):M8–M14.

4. Castelli WP. Epidemiology of triglycerides: a view from Framingham. Am J Cardiol. 1992;70(19):3H–9H.

5. Fontbonne A, Eschwège E, Cambien F, et al. Hypertriglyceridaemia as a risk factor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Results from the 11-year follow-up of the Paris Prospective Study. Diabetologia. 1989;32(5):300–304.

6. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996;3(2):213–219.

7. Kastelein JJ, van der Steeg WA, Holme I, et al.; TNT Study Group; IDEAL Study Group. Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment. Circulation. 2008;117(23):3002–3009.

8. Miller M, Cannon CP, Murphy SA, Qin J, Ray KK, Braunwald E; PROVE IT-TIMI 22 Investigators. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2008;51(7):724–730.

9. Miller M, Seidler A, Moalemi A, Pearson TA. Normal triglyceride levels and coronary artery disease events: the Baltimore Coronary Observational Long-Term Study. J Am Coll Cardiol. 1998;31(6):1252–1257.

10. Rajamani K, Colman PG, Li LP, et al.; FIELD study investigators. Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. Lancet. 2009;373(9677):1780–1788.

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