By Guest Contributor Justin Groce MSN,NP-C,CSCS

With cardiovascular disease being the main cause of mortality in the United States it’s no wonder that statins and other lipid-lowering agents have become the victim of both positive and negative attitudes.  Although low-density lipoproteins (LDLs) have become the forefront target of treatment in regards to lipids one must wonder why triglycerides (TGs) take the backseat.

So, what’s the big deal about “trigs?”

Well, they’ve been rising over the last few decades.  As a matter of fact, while LDLs have been decreasing over the last several years, most likely attributed to the use of statins, triglycerides have been gradually increasing.  It’s postulated that this increase is due to the increased prevalence of diabetes, obesity, and metabolic syndrome (excessive alcohol intake receives an honorable mention).  Metabolic syndrome and diabetes increase TGs by both inhibiting lipoprotein lipase (LPL) and upregulating apo C-III; LPL breaks down TGs and apo C-III inhibits LPL. 

Why treat and when to treat?

Hypertriglyceridemia (HTG) can be predictive of coronary heart disease (CHD) risk. This is because very-low density lipoproteins are the primary vehicle for TG transport throughout the body.  Since VLDLs are considered atherogenic particles, more TGs = more atherogenic particles. 

The first and foremost consideration for treatment is what are the patient’s trigs?  Are they considered very high (>500mg/dL) or extremely high (>885mg/dL)?  When the TGs are above 500mg/dL the initial goal is to prevent acute pancreatitis.  Around 10% of pancreatitis occurrences are secondary to HTG.  With each subsequent 100mg/dL reduction in TGs there is a 5% reduction in pancreatitis risk.  Since the purpose of this article is geared towards treating HTG in the outpatient clinic treating acute pancreatitis secondary to HTG is beyond the scope of this article.

If the patient’s TGs are <500mg/dL, treatment is targeted towards lowering LDL. If the patient’s TGs are >=200mg/dL, then you will have non-HDL as the secondary target of treatment. Use risk calculators to determine the patient’s LDL target given their comorbidities and health status. If the patient has TGs between 200-499mg/dL, then non-HDL will be their secondary target.  Add 30mg/dL to their LDL target to get their non-HDL target (e.g. if their LDL goal is 70, then their non-HDL goal is 100).

Ready to get started?  Good, here’s a simple algorithm to follow.

  1. Are the patient’s TGs >500mg/dL?
    1. Yes:  TGs are the primary target of treatment
      1. Initiate fibrate, niacin, or omega-3 therapy (bile acid sequestrants contraindicated when TGs >500mg/dL)
        1. Did you get TGs <500mg/dL?
          1. Yes:  continue current therapy
            1. Next target is LDL goal; begin statin therapy
              1. Proceed to step 2
          2. No:  intensify fibrate, niacin, or omega-3 therapy until TGs <500mg/dL
            1. Next target is LDL goal; begin statin therapy
              1. Proceed to step 2
    2. No, but the TGs are <200mg/dL:
      1. LDLs are the primary target
        1. Initiate statin therapy
          1. Proceed to step 2
    3. No, but the TGs are between 200-499mg/dL:
      1. LDLs are the primary target with non-HDLs being the secondary target
        1. Initiate statin therapy
          1.  Proceed to step 2
  2. Did you get the LDLs to goal?
    1. Yes:  continue current therapy; proceed to non-HDL
      1. Proceed to step 3
    2. No:  intensify statin therapy
      1. Continue until goal achieved
        1. When goal is achieved proceed to non-HDL goal
          1. Proceed to step 3
  3. Did you get the non-HDLs to goal (if applicable)?
    1. Yes:  continue current therapy; proceed to TG goal <150mg/dL
      1. Proceed to step 4
    2. No:  maximize statin therapy until goal achieved
      1. Once goal non-HDL achieved targeting TGs <150mg/dL is goal
        1. Proceed to step 4
  4. Did you get the TGs to goal <150mg/dL?
    1. Yes:  Yay!
      1. If LDL and non-HDLs are at goal, then you’re done!
        1. If not, then begin/intensify statin therapy
          1. See step 2
    2. No:  Intensify fibrate, niacin, or omega-3 pharmacologic therapy (bile acid sequestrants cautioned when TGs >300mg/dL)

What about therapeutic lifestyle changes (LTC)?

I integrate these at the beginning of all therapy regardless of the patient’s goal, whether it be targeting TGs, LDLs, or non-HDLs.  Patients are encouraged to exercise 150-200 minutes a week with a combination of both cardiovascular training and resistance training.  Literature has shown that the best determinants for positive lipid improvements from exercise is the overall volume (time spent, calories expended) of exercise.  Furthermore, exercise reduces TGs by increasing LPL activity while reducing hepatic lipase (HL) activity.  HL is responsible for hydrolyzing the TGs carried by HDLs, thus making them smaller, less capable of carrying cholesterol and TGs, and are more readily disposed of. 

Weight loss is critical to managing a patient’s TGs.  Initial weight loss of 5-10% can be achieved with a 500-1000 calorie per day deficit, which can contribute up to a ~20% reduction of TGs.  Greater TG reductions can be observed in those with higher starting TGs and those with greater weight loss reductions.  Weight loss should be achieved through a combination of both exercise and nutritional compliance.  Weight loss medications can be used as well, but are beyond the scope of this article.

Lastly, dietary modifications are critical to long-term outcomes.  Lower simple-carbohydrate and lower fat diets are encouraged in patients with HTG.  Patients are advised to limit sugary beverages (e.g. sweet tea, sodas, fruit juices) to no more than 36oz per week.  Simple carbohydrates including snack bars, cakes, candy, and those that have added sugars should be reduced, if not, avoided completely (I loosely refer to these as “vending machine foods”).  Replacing low-glycemic carbohydrates with monounsaturated and polyunsaturated fats can reduce TGs and increase HDLs.  Trans fats (hydrogenated and partially hydrogenated oils) should be avoided altogether.  Remember, even “trans fat-free” products can still contain up to 0.5g of trans fat.  Alcohol restriction is important as it increases the risk of pancreatitis in the patient with HTG, esp when the TGs >500mg/dL. 


Justin Groce is a nurse practitioner providing primary care, functional medicine, and weight loss coaching in middle Tennessee.  He is a graduate of Vanderbilt University and holds board certifications in Adult/Gero NP (AANP), cardiovascular NP (ABCM), and lipidology (ACCL).  He is also certified as a strength and conditioning specialist (CSCS-NSCA) and has 10 years of personal training experience.



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Bays, H. et al (2013). Obesity, adiposity, and dyslipidemia:  A consensus statement from the National Lipid Association. J Clin Lipid 7, pp 304-383.

Brown, V., Bays, H., and Bray, G. (2014). JCL Roundtable:  Clinical mgmt of individuals with obesity. J Clin Lipid 8, pp 237-248.

Cohen, J., Cziraky, M., Cai, Q., et al (2010). 30-year trends in serum lipids among United States adults: results from the national health and nutrition examination surveys II, III, and 1999-2006. Am J Cardiol. 106.

Grundy, M. et al (2018). 2018 ACC/AHA/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the mgmt of blood cholesterol:  A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. DOI:  https://doi.org/10.1016/j.jacc.2018.11.003

Karalis, D. (2017). A review of clinical practice guidelines for the management of hypertriglyceridemia:  A focus on high-dose omega-3 fatty acids. Adv Ther. 34(2).

Milne, V. (2012). Practicing Pearls:  Primary HTG – Treating triglycerides when it’s not the usual suspects. DOI:  http://nlaresourcecenter.lipidjournal.com/Content/PDFs/1-Milne-Pearls.pdf


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