Model offers new perspectives on saturated fat and heart disease
It has been thought that saturated fats in the diet promote heart disease by increasing blood cholesterol. However, a new model explains why this so-called "diet-heart hypothesis", which has had a major influence on dietary guidelines, may have an alternative explanation, according to new research published in the American Journal of Clinical Nutrition.
To understand why saturated fats increase blood cholesterol, and why should this be dangerous, researchers from the University of Bergen in Norway developed a model, the Homeoviscous Adaptation to Dietary Lipids (HADL).
The basis of the model is that when saturated fats replace polyunsaturated fats in the diet, less cholesterol is needed in the cell membranes, according to Marit Zinöcker, lead author of the study at Bjørknes University College in Oslo, Norway. The opposite is true when eating more polyunsaturated fatty acids, which include omega-3 and omega-6 fatty acids. This is because polyunsaturated fats from the diet enter cell membranes and make them more fluid. The cells adjust the fluidity of their membranes by incorporating cholesterol recruited from the bloodstream, Zinöcker said.
According to the model, this can explain why blood cholesterol levels decrease when we eat more polyunsaturated fats. Cells need to adjust their membrane fluidity according to changes in their environment, such as the access to different types of fat, said Simon Dankel, study co-author and researcher at the University of Bergen. This phenomenon is called homeoviscous adaptation, and has been described in both microorganisms, vertebrates and in human skin cells. We argue that this is a critical principle in human physiology. Our cells are normally capable of adjusting their cholesterol content according to changes in dietary fats.
Nutrition research often focuses on what changes in the body, but the question of why something, such as the blood cholesterol, changes, is of equal importance, according to Karianne Svendsen, study co-author and postdoctoral fellow at the University of Oslo.
This is where the new HADL model comes into play, providing an explanation based on adaptive human physiology. From the perspective of the HADL model, we find logical explanations for why cells need to change their cholesterol content, and thereby the blood cholesterol, when fats in the diet change, the researchers said.
In the paper, other reasons for elevated LDL-cholesterol in people with cardiovascular disease are discussed, such as low-grade inflammation and insulin resistance. This indicates that elevated blood cholesterol caused by metabolic disruptions must be uncoupled from elevated blood cholesterol caused by a major change in intake of dietary saturated fatty acids. It also questions the benefit of lowering blood cholesterol by adding polyunsaturated fatty acids to the diet, and not addressing the root cause, according to the study.
The authors state that although the model is based on existing knowledge of cellular mechanisms, the model still needs to be verified. The authors therefore urge researchers to discuss and test the HADL model.
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