Within the ancestral health and functional medicine communities, an ample intake of high-quality saturated fats is emphasized as being quite important for the promotion of optimal health. While this view lies in stark contrast to what the conventional medical community has led us to believe in regards to saturated fat (i.e. that consumption of saturated fat drives the development of heart disease), recent high-quality scientific research opposes this long-held conventional view and has concluded that saturated fat is not in and of itself associated with an increased risk of heart disease. This has led to a surge in enthusiasm for the consumption of saturated fats, including foods such as butter, eggs, and full-fat dairy products. However, in the rush to jump on the high-fat bandwagon, we seem to be overlooking a crucial fact, which is that while increased saturated fat intake is not a driving force in heart disease, it still can have varied effects on biomarkers of health from one person to another. One biomarker that is affected differently from one person to another in response to saturated fat intake is LDL particle number and distribution.
What is LDL and how does it affect our health?
“LDL,” as you may know, stands for “low density lipoprotein,” and is a substance consisting of protein and fat that transports cholesterol throughout the body so that the cholesterol can be used for important bodily processes. LDL particle “distributions” refer to the specific types of LDL particles in the bloodstream, such as small dense LDL and large “fluffy” LDL. Increased small, dense LDL particles, as well as a high total LDL particle number, have been associated with an increased risk of high cholesterol and heart disease and are thus undesirable.
Previous studies examining the replacement of saturated fat for carbohydrates or unsaturated fat in the diet have found that this dietary modification promotes increases in large-cholesterol LDL (the more benign form of LDL), with very minimal changes in small, dense LDL and apolipoprotein B. Small LDL particles and apolipoprotein B are more highly associated with an increased risk of heart disease than are large LDL particles. Therefore, this previous research was suggestive that increased saturated fat intake should not be an overly concerning factor in regards to heart disease risk.
When some people increase their saturated fat intake in response to ancestral health or functional medicine guidelines, their LDL levels remain steady, or sometimes even decrease. However, in other people, their LDL and total cholesterol numbers soar upon increasing saturated fat intake. So, what gives? How can there be such dramatic differences in a single biomarker in response to increased saturated fat intake? The answer lies with the unique metabolic differences that exist amongst people. Researchers have found that certain metabolic traits impact LDL particle distributions quite differently from one individual to another in response to saturated fat intake, thus affecting heart disease risk. Therefore, we need to be careful about promoting fad diets and one-size-fits-all dietary recommendations, as a dietary recommendation that helps one person may ultimately be detrimental to another person.
A 2017 study published in PLoS One emphasizes the point that saturated fat intake should not be a one-size-fits-all recommendation, due to the metabolic differences that affect how peoples’ bodies handle saturated fat (1).
In examining the impact of saturated fat intake on LDL particle distribution, the researchers involved in the study focused on a particular metabolic trait called LDL phenotype B. LDL phenotype B, also referred to as “LDL pattern B,” is a lipoprotein pattern in which one has a substantial proportion of abnormally small LDL particles in the bloodstream, relative to other types of LDL particles. The flipside of this is called LDL phenotype A, in which one has a preponderance of large LDL particles relative to other sizes of LDL particles. LDL phenotype B is associated with increased concentrations of plasma triglycerides, decreased levels of HDL, and increased risk of heart disease compared to LDL phenotype A. The development of LDL phenotype B is influenced by genetic predisposition, overall macronutrient intake, and body weight. In this randomized controlled trial, the researchers examined the effects of saturated fat intake on individuals with atherogenic dyslipidemia (a condition characterized by high triglycerides and small dense LDL) who presented with LDL phenotype B, in order to determine how saturated fat consumption might interact with this particular metabolic trait in regards to CVD risk.
- Fifty-three LDL phenotype B men and postmenopausal women were recruited through internet advertisements and from a database of previous study participants. LDL phenotype B was determined through ion mobility, a test that detects and quantifies lipoprotein particle sizes and concentrations.
- The participants ate a baseline diet consisting of 55% carbohydrate, 15% protein, 30% fat, and 8% saturated fat for three weeks. At the three-week mark, the subjects were randomized to consume either a moderate carbohydrate, very high saturated fat diet (39% carbohydrate, 25% protein, 36% fat, 18% saturated fat), or a low saturated fat (37% carbohydrate, 25% protein, 37% fat, 9% saturated fat) experimental diet for another three weeks. Clinical and laboratory measurements were taken both at the end of the baseline diet and at the end of the experimental diet.
- The low saturated fat and high saturated fat diets were designed to have similar amounts of carbohydrate, protein, and total fat, so that the only difference was the amount of saturated fat. In the low saturated fat group, saturated fat was exchanged for monounsaturated fat.
- High vs. low or non-fat dairy products provided the major source of differences in saturated fat intake.
- Compared to the low saturated fat diet, consumption of a diet high in saturated fat resulted in statistically significant increases in plasma concentrations of proatherogenic apolipoprotein B, medium, small, and total LDL particles. However, there were no changes in the concentrations of large or very small LDL particles.
- In the high saturated fat group, LDL-cholesterol and total cholesterol were increased
- Increased plasma cholesteryl ester transfer protein (CETP) was significantly associated with a preponderance of proatherogenic small and medium LDL particles in participants on the high saturated fat diet compared to those on the low saturated fat diet. CETP is responsible for transferring cholesteryl esters from HDLs to apolipoprotein B and is therefore considered proatherogenic.
This research suggests that saturated fat intake recommendations are not one-size-fits-all. A very high saturated fat intake may increase the risk of heart disease in individuals with the metabolic trait LDL phenotype B. LDL phenotype B individuals experienced increased medium and small LDL cholesterol particles in response to high saturated fat intake, a response that is associated with an increased risk of CVD. The findings of this study differ from previous studies that found no significant effect of saturated fat on LDL particle size distribution. This is due to the fact that the participants in this study were LDL phenotype B, whereas participants in previous studies largely expressed the metabolic trait LDL phenotype A. This research indicates that the presence of metabolic traits such as LDL phenotype B, which is shaped by factors such as genetic predisposition and overall macronutrient intake, must be taken into account by practitioners when they are making recommendations to their patients regarding saturated fat intake. Rather than consuming high amounts of saturated fat, people with LDL phenotype B may want to focus more on monounsaturated fats such as olives, olive oil, and avocado, and consume a "Mediterranean Paleo" diet rather than the more popularized high-fat Paleo diet, which tends to be high in saturated fats. This individualized approach to saturated fat intake appears to be crucial in regards to managing the risk of heart disease in people who have this particular metabolic trait.
I plan on writing more blog posts in the near future regarding my thoughts on the role of fats (and other macronutrients) in the context of an Ancestral diet. Stay tuned!