![]() ![]() The knowledge that apoB may be a more direct metric of CV risk than TGs should prompt the medical community to rethink conventional interpretations of TG levels when apoB information is not available. Although these data further indicate that truly “optimal” TG levels may be even lower than 100 mg/dL and may differ significantly between men and women, the critical point is now to recognize that lipoprotein-related CV risk is more accurately reflected by the number of apoB-containing lipoproteins rather than their TG content. However, the statement suggested a threshold for “optimal” at <100 mg/dL, a reduction that is supported by the study conducted at Duke. Over a decade ago, the American Heart Association released a statement suggesting a new designation of TG levels: a range of “optimal” TGs, distinct from the range of “normal.” The proposed definition for “normal” remained at <150 mg/dL, continuing to reflect the majority of the American population despite the knowledge that such a level approaches (males) or exceeds (females) the 75th percentile population cutpoint. These remarkable differences strongly signal a need for gender-specific guidelines for what constitutes “optimal” TG levels.įigure 3: Association between the average TG level and CVD risk based on sex. Astonishingly, the risk in men appeared to increase steeply with rising TGs well below 100 mg/dL, at which point it began to level off. In women, the CV-risk rose more gradually with TG levels than in men, yet continued to increase over a much broader TG range, up to 200 mg/dL (Figure 3). Interestingly, the relationship between TG and CVD risk varied significantly between men and women, with a stronger association for women vs. ![]() Unfortunately, apoB is often not included in standard lipid panels, and thus, TGs (and, if available, non-HDL-C) may provide valuable – albeit imperfect – information on CVD risk in the absence of apoB measurements. Over time, the guideline-recommended TG threshold for considering treatment has dropped from 250 to 150 mg/dL, and currently, TG levels 500 mg/dL) levels, which would signal high risk of pancreatitis. Indeed, there has long been a debate on whether serum TG constitutes an independent risk factor for CVD – and if so, at what levels. TGs affect the structure, size, composition, catabolism, plasma residence time, clearance, functionality, and concentration of all lipoproteins, including both the potentially atherogenic apolipoprotein B (apoB) family and the apoA-I (HDL family), yet historically, unlike all cholesterol metrics, TGs have not been included as part of CV-risk algorithms apart from their contribution to the definition the metabolic syndrome (though it’s always noted that at fairly extreme levels, typically >500-800 mg/dL, TGs increase the risk of acute pancreatitis). Serum TG is a component of a standard lipid panel, which, in addition to TG, typically reports several cholesterol metrics – total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and non-HDL cholesterol. Triglycerides – also known as triacylglycerols – are composed of three fatty acid molecules bound to a glycerol backbone. (Two centuries ago, a normal life expectancy was around 30-40 years, but I doubt anyone would call that normal or optimal today.) This semantic problem was highlighted in a 2020 study investigating the relationship between serum triglycerides (TG) and cardiovascular disease (CVD) risk: is “normal” really “optimal?” What are triglycerides (TG)? In medicine, “normal” is often erroneously used interchangeably with “optimal.” Not only are these two words not necessarily synonyms, their individual definitions – and how closely one approximates the other – are subject to change with changing populations and advancements in scientific knowledge. ![]()
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |