Although treatment strategies for high triglyceride levels in the blood are well established, new clinical practice guidelines from the Endocrine Society released today in the Journal of Clinical Endocrinology and Metabolism recommend that more attention should be paid to the ways each person's unique history, physiology and lifestyle interact to affect risk.
High triglyceride levels in the blood, or hypertriglyceridemia, greatly increase the likelihood of heart disease, but the causes of elevated levels and the degree of risk they pose can differ from person to person, the researchers stress. Genetics, for example, may play a critical role for one patient while the interaction of different drugs may be key for someone else.
The guidelines emphasize the need to scrutinize the way each patient's genetic profile, diet, lifestyle and medications interact to determine net risk.
"The take-home is that we need to look at all these things in a more personalized way to understand a patient's risk," said Lars Berglund, a prominent endocrinologist, senior associate dean for research and director of the Clinical and Translational Science Center at UC Davis Health System. Berglund chaired the task force that assessed the current state of diagnosis and treatment for high blood triglyceride levels to set the new guidelines.
Triglycerides are fatty molecules that circulate in the blood as a natural result of the breakdown of food in the gut. They are essential for providing energy to muscles and other tissue. But like LDL cholesterol, excess triglycerides can lodge in arterial walls and increase the risk for atherosclerosis and other cardiac diseases.
The task force pointed out that the causes of excess triglycerides in the blood are not fully understood, but that many aspects of diagnosis and treatment are well established. Fatty foods, smoking and poor exercise, for example, all clearly contribute to risk for high triglyceride and high LDL cholesterol levels. But a diet high in simple sugars, such as from eating lots of white bread or sugary sodas, boosts triglyceride levels without affecting cholesterol.
Similarly, alcohol is a boon to healthy levels of HDL ― the "good" cholesterol ― but alcohol consumption leads to higher triglyceride counts, the task force reports. Patients who share some of the same risk factors can face different levels of overall risk because of unique differences between them. Understanding the importance of a given risk requires a full profile of each patient.
Certain inherited genetic mutations also can contribute to overall risk, but lifestyle, diet and other factors appear to account for more cases of high triglyceride levels than do genetics, Berglund said. When combined with smoking, poor diet or limited exercise, genetic vulnerabilities pose particularly high risks.
The task force pointed out that statins are effective against high triglyceride levels, but unusually high levels call for stronger medicines. Drugs known as fibrates are the first line of defense against excessive triglyceride levels, which can cause pancreatitis, an inflammation that poses severe health problems and is often fatal.
A concern that is often under the radar is how drugs prescribed to treat other medical conditions can interact to raise blood triglyceride levels, the report stresses. For example, a drug called a bile acid sequestrant, prescribed for high LDL, can raise borderline triglyceride to potentially dangerous levels.
"Perhaps the most pressing under-addressed concern is the need to consider all of a patient's history and risk-factor burden in assessing vulnerability to atherosclerosis," Berglund said.
The task force included seven U.S. and European university endocrinologists, including a scientist representing the American Heart Association. Coauthors on the study were John D. Brunzell, University of Washington; Anne C. Goldberg, Washington University; Ira J. Goldberg, Columbia University; Frank Sacks, Harvard University; Mohammad Hassan Murad, Mayo Clinic; and Anton F. H. Stalenhoef, Radboud University, The Netherlands.